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Epidemic Ceeebro-spinal Meningitis 
 
 AND ITS RELATION TO 
 
 Othee Forms of Meningitis. 
 
 LIBRARY 
 
 OF THE 
 
 PATHOLOGICAL LABORATORY, 
 
 THE PRESBYTERIAN HOSPITAL, 
 
 IN THE CITY OF NEW YORK. 
 
 A REPORT 
 
 State Board of Health 
 
 OF aiASSACHUSETTS. 
 
 BOSTON : 
 
 WRIGHT & POTTER PRINTING CO., STATE PRINTERS, 
 
 18 Post Office Square. 
 
 1898. 
 
LIBRARY 
 
 OF THE 
 
 PATHOLOGICAL LABORATORY, 
 
 THE PRESBYTERIAN HOSPITAL, 
 
 IN THE CITY OF NEW YORK. 
 
 TABLE OF CONTENTS. 
 
 PAGE 
 
 Preface, . 5 
 
 History of the Disease, 9 
 
 Epidemic Character of the Disease, . 17 
 
 Sporadic Cases, 26 
 
 Clinical Cases, 30 
 
 Bacteriology, 70 
 
 Lumbar Puncture, 79 
 
 Gross Pathological Anatomy, 82 
 
 Pathological Histology, 101 
 
 Classification of the Disease, 125 
 
 Symptomatology, 131 
 
 Lesions of the Eyes, 141 
 
 Lesions of the Ears, ' 148 
 
 Diagnosis, 161 
 
 Summary, 162 
 
 Other Forms of Meningitis 165 
 
 Pneumococcus Meningitis, 166 
 
 Streptococcus Meningitis, 171 
 
 Tubercular Meningitis, 172 
 
 Anthrax Meningitis, 172 
 
 Description of Plates, 174 
 
 Bibliography 176 
 
UBRARY 
 
 OF THE 
 
 PATHOLOGICAL LABORATORY, 
 
 THE PRESBYTERIAN HOSPITAL, 
 
 IN THE CITY OF NEW YORK. 
 
 INTRODUCTORY. 
 
 The prevalence of epidemic cerebro-spinal meningitis in 
 Massachusetts has been marked with much irregularity. An 
 epidemic of unusual severity i5 1873 gave rise to an inves- 
 tigation and report by Dr. J. B. Upham, which appeared 
 in the report of the State Board of Health for that year. 
 A summary of 517 cases reported by different physicians 
 throughout the State was given in that report. Dr. Upham 
 was particularly well qualified for this investigation by his 
 previous acquaintance with the disease in Newbern, North 
 Carolina, during the civil war. In considering the causes 
 of the disease he paid particular attention to the influence 
 of insanitary conditions as an active or predisposing cause. 
 With regard to this he says : — 
 
 The relation of insanitai'y conditions in and around the abode 
 of the patient to its origin or supposed cause demands the most 
 careful consideration. In weighing the evidence contained in the 
 returns, I find the scale to be pretty evenly balanced in this par- 
 ticular. The cases are distributed among all classes and grades 
 of society, — the high and low, the rich and the poor, locations 
 unexceptionable for situation, open to abundant light and air, 
 and the pent-up hovels of the lowly and wretched, have all con- 
 tributed to the material of the epidemic. We believe, therefore, 
 that the primal origin of the disease is atmospheric, and, for the 
 present, beyond our ken. 
 
 Since Dr. Upham's report, great discoveries in regard to 
 the aetiology of many of the infectious diseases have been 
 made. The bacterium which can now be regarded as the 
 
Vlll 
 
 essential cause of epidemic cerebro-spinal meningitis was 
 discovered in 1887, but the first important confirmation of 
 that discovery was not made until 1895. There has always 
 been a great deal of obscurity in the relations between 
 cerebro-spinal meningitis which appeared in an epidemic 
 form and sporadic cases which sometimes appeared alone 
 or in connection with other diseases, and which were very 
 similar in their clinical manifestations and pathological 
 lesions to the epidemic form. With the view of clear- 
 ing up this and some other obscure points in the general 
 aetiology and pathology of tke disease, the present inves- 
 tigation has been undertaken by the State Board of Health. 
 The present epidemic is the only one of considerable impor- 
 tance which has been seen since the advance in bacteriology 
 and pathology has made such an investigation possible. In 
 this investigation only the cases which were seen in the 
 principal hospitals and in which the diagnosis of the disease 
 could be regarded as certain have been considered at any 
 length. 
 
 The accuracy of the statistics relating to this disease must 
 necessarily be questioned, as presenting a history of its actual 
 prevalence, for the following reason : — 
 
 The confusion of medical terms by physicians, together 
 with the fact that all returns made to the State authorities 
 are copies of certificates, and not originals, and that these 
 copies are in the majority of instances made by men who 
 have little or no knowledge of the significance of medical 
 terms, give to the information obtained in regard to this dis- 
 ease a great measure of uncertainty. This is peculiarly true 
 of epidemic cerebro-spinal meningitis, — a disease which is 
 liable to be confounded with several other forms of brain 
 disease, in consequence of the similarity in nomenclature of 
 the terms employed to define such diseases. In addition to 
 this, the disease is not a common one, and the clinical 
 
IX 
 
 manifestations of it are liable to be confounded either with 
 other cerebral diseases or with forms of diseases in which 
 cerebral s^^mptoms predominate. 
 
 The whole number of deaths reported in the State as due 
 to cerebro-spinal meningitis during the period of nearly 
 twenty years, ending with Oct. 1, 1897 (nineteen years and 
 nine months), was 2,909, or nearly 150 per year. In this 
 summary the deaths from this cause in the fraction of the 
 year 1897 are those which were reported directly to the 
 State Board of Health by local authorities. The numbers 
 for the years 1878 to 1896, inclusive, were fairly uniform, 
 the maximum being 171 in 1888 and the minimum 78 in 
 1878. But in the first nine months of 1897 the number 
 reported to the State Board of Health was 405, those in 
 Boston alone being 184. 
 
 That these numbers are probably much too large is shown 
 by a classification of the deaths by ages. For this purpose 
 the deaths occurring in the nine years, 1887-95, are selected, 
 since the finer distinction of separating the deaths in each of 
 the first five years of life was first introduced into the State 
 Kegistration Eeport in 1887. The deaths recorded in those 
 years by ages were as follows : — 
 
 Deaths from Cerebrospinal Meningitis, Massachusetts, 1887-95. 
 
 AGE PERIODS. 
 
 0-1 year, 
 
 1-2 years, . 
 
 2-3 years, . 
 
 3-4 years, . 
 
 4-5 years, . 
 
 5-10 years, . 
 10-15 years, . 
 15-20 3'ears, . 
 20-60 years, . 
 All over 60 years, 
 
 Totals, . 
 
 Deaths. 
 
 Males. 
 
 316 
 
 180 
 
 146 
 
 74 
 
 99 
 
 51 
 
 77 
 
 41 
 
 38 
 
 19 
 
 132 
 
 59 
 
 81 
 
 47 
 
 61 
 
 36 
 
 186 
 
 89 
 
 43 
 
 12 
 
 1,179 
 
 608 
 
 136 
 72 
 48 
 36 
 19 
 73 
 34 
 25 
 97 
 31 
 
 571 
 
By the foregoing table it appears that 316 deaths from 
 this disease, or 26 -\- per cent, of the whole number, were 
 reported as having occurred among children under one 
 year. This fact necessarily vitiates the accuracy of the 
 returns to a considerable degree, since the disease is ex- 
 tremely rare among infants as well as among those of ad- 
 vanced years. 
 
 The reported deaths from this cause occurred mainly in 
 the large cities and towns, the whole number reported 
 from towns of less than 5,000 inhabitants being only 136, 
 or less than 5 per cent, of the whole number. 
 
 The map of Boston which faces the title page of this 
 monograph presents the locality of those cases only which 
 were treated at certain hospitals of Boston during the 
 spring of 1897. A similar map could not have been 
 prepared with accuracy for the State, for the reason, as 
 already stated, that very many cases reported in towns 
 and cities elsewhere and not under hospital supervision 
 were not genuine cases of this disease. 
 
Epidemic Cerebeo-spinal Meningitis 
 
 AND ITS RELATION TO 
 
 Othee Foems of Meningitis. 
 
EPIDEMIC CEREBRO-SPIML MEXIXGITIS AXT) ITS 
 EELATION TO OTHER EOEMS OE MENINGITIS. 
 
 PREFACE. 
 
 We shall endeavor in tbis paper to describe the epidemic of 
 cerebro-spinal meningitis which has prevailed in this community 
 during the past winter and spring, aud also to consider other 
 forms of meningitis allied to the epidemic form. The disease 
 has a peculiar interest here, from the fact that in the United 
 States it was first recognized as an independent disease in 
 Medfield, Mass., a year after the appearance of the disease 
 in Geneva, by Danielson and Mann,^'^* whose observations 
 were made independently of those of Vieusseaux^* in Geneva. 
 In the epidemic at the beginning of the century the disease 
 was more prevalent in the New England States than elsewhere 
 in this country, and in subsequent epidemics there have been 
 many cases in these States. 
 
 The literature of the disease has been enriched by the care» 
 ful studies of these epidemics in New England. The clear 
 objective description of the character of the disease by Daniel- 
 son and Mann, with the records of autopsies, served, as much 
 as the somewhat earlier description of Vieusseaux, to establish 
 the disease as an entity. The most complete of the earlier 
 descriptions is contained in the report of a committee of the 
 Massachusetts Medical Society, appointed in 1809 to investigate 
 the disease. The secretary of the committee and the author 
 of the report was James Jackson. ^^ The committee carefully 
 investigated the symptoms and course of the disease, its relation 
 to other diseases, its pathology and most approved mode of 
 
 • The small numbers refer to the bibliography. 
 
6 
 
 treatment. The report contains the records of eight post- 
 mortem examinations, made by J. C. Warren/^^ one of the 
 members of the committee. Another report on the disease, 
 which is one of the classics in medicine, is that of Elisha 
 North^^ of Goshen, Conn., in 1811. In a small book, now 
 very rare, he gives the result of his own observations, together 
 with reports from others, both physicians and laymen, which 
 appeared in the various newspapers of the day. A committee 
 appointed by the Massachusetts Medical Society made a report 
 on the epidemic which appeared in this State in 1864 and 
 1865.^® In reference to the same epidemic a Boylston prize 
 essay by Dr. S. G. Webber^^ gives the best account which 
 has ever appeared of the history of the disease and its relation 
 to other epidemics. In this paper Dr. Webber takes the 
 ground that the disease is probably identical with some of 
 the earlier and imperfectly described epidemics of Europe. 
 It is to be regretted that this paper of Dr. Webber's, which 
 aj)peared in the form of a long serial in the " Boston Medical 
 and Surgical Journal," should have so generally escaped the 
 notice of subsequent writers. There is further a careful study 
 of the epidemic of 1874 by Upham,"*^ who had previously 
 become acquainted with the disease in Newbern, N. C, during 
 the civil war. We should have some hesitation in adding 
 to the voluminous literature of the disease, were it not for 
 the fact that the recent advances in the technique of 
 investigation, and the possibility, which the discovery of the 
 organism of the disease has given us, of studying the 
 lesions and symptoms in relation with the setiological 
 factor, have enabled us to fill out some points only touched 
 upon by the earlier investigators. 
 
 We wish to express our deep indebtedness to the physicians 
 of the City Hospital, the Massachusetts General Hospital and 
 the Children's Hospital, who have generously placed their 
 clinical observations and cases at our disposal. Our work has 
 been further materially assisted by the zeal and enthusiasm 
 of the assistants in the laboratories of the City and Massa- 
 chusetts General hospitals. 
 
"We are indebted to Dr. Wentwortb for bis notes on spinal 
 puncture, witb descriptions of tbe cbaracter of tbe fluid witb- 
 drawn. Dr. Edwin Jack bas allowed us to publish bis 
 observations on tbe cbaracter of tbe eye complications of tbe 
 disease wbicb be observed at tbe Cbildren's Hospital. 
 
 Tbe plates wbicb accompany tbe article with one exception 
 are from water-color paintings made by Miss Byrnes. Tbey 
 were drawn by tbe camera lucid a, with little or no assistance 
 from tbe autbors, and represent actual conditions. 
 
 Under tbe term meningitis is understood inflammation of the 
 pia-aracbnoid, tbe membrane wbicb forms tbe immediate invest- 
 ment of tbe brain and spinal cord. Tbe separation of tbis mem- 
 brane into tbe pia and arachnoid is artificial, although there is more 
 justification for such a separation in tbe spinal cord than in the 
 brain. Considered as a single membrane, it consists of a serous 
 surface (arachnoid) in contact with the dura, forming one side of 
 the sub-dural space, and beneath tbis a loose connective tissue (pia 
 mater) containing numerous and large lymph spaces and carrying 
 the blood vessels for tbe brain and cord. In tbe spinal cord there 
 is a single large space between tbe upper serous surface and the 
 tissue which closely invests the cord, crossed by numerous fibrous 
 trabeculse. The lymph spaces in the membrane communicate with 
 the lymph sheaths around tbe vessels of the brain and cord, and 
 by means of the lymphatics accompanying the nerves, with the 
 general lymphatic system of tbe body. The membrane in the form 
 of tbe choroid plexus passes into the ventricles of the brain. 
 
 The surface forming part of the sub-dural space is covered with 
 a single layer of endothelial cells ; beneath this there is a more or 
 less definite layer of connective tissue, which passes into tbe loose 
 connective tissue of the pia with its numerous lymph spaces and 
 blood vessels. This tissue contains the single connective tissue 
 cells of the fibrous tissue, tbe cells of tbe blood vessels and lym- 
 phatics, and a variable number of lymphoid cells which are found 
 in the lymphatics and in the lymph spaces around the vessels. 
 
 There are various means by which infectious agents can gain 
 access to this tissue. Tbey may enter into it by means of the 
 blood or by the extension of infectious processes from adjacent 
 
8 
 
 regions. The extension may be direct, or by means of lym- 
 phatics which communicate directly or indirectly with those of 
 the membrane. 
 
 All inflammatory processes in the pia-arachnoid, however pro- 
 duced, agree more or less in their anatomical features ; and in so 
 far as the symptoms depend upon the purely local lesions, there is 
 considerable uniformity in the symptoms produced. There are, 
 however, certain minor differences in the anatomical lesions which 
 are sufficient to differentiate certain forms of meningitis from 
 others. These differences depend in general upon the extent and 
 character of the exudation, upon the varying degree in which the 
 blood vessels and nerves are involved, and upon the direct exten- 
 sion of the process in the meninges into the adjacent tissues of the 
 brain and cord. In some cases the lesions are limited to the mem- 
 branes ; in others there is a tendency for the process to extend into 
 the adjacent nervous tissue and along the nerves. There is little 
 doubt that all cases of meningitis are cerebro-spinal, the meninges 
 of the cord being affected as well as those of the brain. The cord 
 lesions are, however, so much more marked in certain cases that 
 these have been especially distinguished by the name cerebro- 
 spinal meningitis. 
 
 In epidemic cerebro-spinal meningitis there are sufficient differ- 
 ences in the character of the exudation, in the greater degree of 
 involvement of the meninges of the cord, in the extension of the 
 inflammation along the nerves, and in the participation of the 
 tissue of the brain and cord in the process, to enable us to dis- 
 tinguish anatomically most cases of this from other forms of 
 meningitis. There is a further difference between the epidemic 
 cerebro-spinal meningitis and all other forms of meningitis, in 
 the general absence of inflammatory lesions in the intima of 
 the arteries in the epidemic variety, while it is common in all 
 the other forms. 
 
 The peculiarity of all lesions produced by the tubercle bacillus 
 enables us to distinguish tuberculous meningitis from the other 
 forms. There are few differences between the inflammations pro- 
 duced by the streptococcus, the staphylococcus aureus and the 
 diplococcus lanceolatus. There are certain peculiarities in the 
 
9 
 
 anatomical processes in all forms of meningitis which are depend- 
 ent upon the character of the tissue affected. Inflammations of 
 the meninges due to the action of certain organisms differ some- 
 what from the lesions produced by the same organisms elsewhere 
 in the body. Tuberculosis of the membrane appears both in the 
 form of tubercle formation along the vessels, and as a diffuse 
 inflammation due to a fibrino-purulent exudation ; the latter may 
 be present to such an extent that the tubercles may be overlooked. 
 In all forms of meningitis the inflammatory exudation is more 
 marked on the base than over the convexity of the brain, and 
 along the posterior than the anterior surface of the cord. 
 
 EPIDEMIC CEREBRO-SPINAL MENINGITIS. 
 
 It is usually considered that epidemic cerebro-spinal meningitis 
 first appeared in 1805 in G-eneva. Vieusseaux"^ described an 
 uncommon disease which appeared in Geneva in the winter and 
 spring of 1805. The disease commenced suddenly with loss 
 of strength, vomiting, violent pains in head and along spine, 
 and, in infants, with convulsions. The course of the disease 
 was rapid in fatal cases, lasting from twelve hours to five 
 days. In the greater number of patients who died in twenty- 
 four hours the body was covered with violet spots. 
 
 Mathey"^ gives an account of a post-mortem examination made 
 of one of the fatal cases. He describes a gelatinous exudation 
 covering the convex surface of the brain, and a yellow puri- 
 form matter upon its posterior aspect, upon the optic commis- 
 sure, and the inferior surface of the cerebellum and the medulla 
 oblongata. The description of Vieusseaux combined with the 
 post-mortem examination described by Mathey can leave no 
 doubt as to the character of the disease. 
 
 Although this is generally regarded as the beginning of epidemic 
 cerebro-spinal meningitis, there can be little doubt that the disease 
 existed previously. Among the early accounts of epidemics sim- 
 ilar to cerebro-spinal meningitis, Bascome,^ in his history of 
 " Epidemic Pestilences," speaks of a local epidemic at Roettinggen 
 in Franconia in the autumn of 1802, in which the young and 
 
10 
 
 strong were suddenly seized U^ith pain and anguish at the heart 
 and pain in the nape of the neck. In the fatal cases the patient 
 fainted, the limbs became rigid, and death sometimes took place 
 twenty-four hours from the commencement of the attack. It is 
 interesting, as showing the probably greater distribution of the 
 disease, to note that in the same volume of the " Medical and 
 Agricultural Register" which contains the description of Danielson 
 and Mann there is a letter from Indiana, describing a severe 
 epidemic which appeared there in Vincennes. The disease 
 especially affected young females, and some of the symptoms 
 would point to meningitis. The editor of the magazine very per- 
 tinently asks if this be not the same disease described by Daniel- 
 son and Mann. In the histories of the great epidemics of Europe, 
 from the thirteenth century on, symptoms are described which 
 almost certainly point to this disease. A very interesting account 
 of these early epidemics and their affinity to or identity with 
 cerebro-spinal meningitis is given by Webber in his admirable 
 account of the history of the disease. The descriptions of 
 these epidemics are exceedingly obscure, and, in the general 
 absence of the records of post-mortem examinations, it is im- 
 possible to say exactly what disease they represent. The descrip- 
 tions of the clinical symptoms could apply equally to typhus, 
 typhoid or cerebro-spinal meningitis. Webber attaches consider- 
 able importance to the description of the skin lesions, but these 
 are not sufficiently constant or sufficiently characteristic to serve 
 as a means of diagnosis. 
 
 In his work on the diseases of the army, published in 1752, 
 Sir John PringalP" gives an account of a jail or hospital 
 fever, which in many respects was similar to cerebro-spinal 
 meningitis. On post-mortem examination suppuration of the 
 brain was found. 
 
 The classification of a disease should always be made from 
 an astiological point of view ; the recognition of a definite in- 
 fectious agent establishes the identity of a disease. In the 
 absence of this, a definite class of symptoms, based on certain 
 anatomical lesions, is our only method of classification. The 
 insufficiency of this method of classification is shown by the fact 
 
11 
 
 that before the recognition of the infectious agent causing epi- 
 demic cerebro-spinal meningitis there was no way of separating 
 sporadic cases and small epidemics of this disease from menin- 
 gitis caused by other infectious agents. 
 
 After the epidemic at Geneva the disease next appeared in 
 Medfield, Mass., and was described by Danielson and Mann in 
 1806. The publication of Danielson and Mann was made in- 
 dependently of the work of Vieusseaux, with which they were 
 not familiar. They described carefully the symptoms of the 
 disease, and gave the results of five post-mortem examinations. 
 They speak particularly of the uniformity of the symptoms and 
 the mode of attack. The disease soon became rapidly diffused 
 in the New England States. It extended to nearly all the towns 
 in Massachusetts, and was particularly severe in "Worcester ; 
 then it appeared in New Hampshire, Connecticut, New York, 
 New Jersey, Vermont and Maine, and kept up continuously in 
 one place or another in New England until 1816. 
 
 There are two classical descriptions of the epidemic of this 
 period. One is by Elisha North"^ and the other by a' com- 
 mittee appointed by the Massachusetts Medical Society^"^' to 
 investigate the new disease. The committee was composed of 
 Drs. James Jackson, J. C. Warren and Thos. "Welch, and the 
 report was written by James Jackson, the secretary. The com- 
 mittee sent letters to various physicians all over the State, and 
 analyzed their replies. The disease was described as beginning 
 suddenly with great prostration, intense pai-i in the head and 
 along the spine, and vomiting. Many of the cases died sud- 
 denly in ten to twelve hours ; others in twenty-four to forty- 
 eight hours after the first symptoms. Almost all the fatal 
 cases died before the third day. The disease affected espe- 
 cially young persons of both sexes, but not generally very 
 young infants or aged persons. The committee reported in 
 all eight autopsies, most of which were made by J. C. "Warren. 
 
 Jackson thinks that the description of malignant fever by Sen- 
 nert^^ agrees in many respects with this disease. He thinks the 
 seat of the disease is not in the skin lesions but in the mem- 
 branes of the brain, the skin lesions being secondary and symp- 
 
12 
 
 tomatic. Notwithstanding the infrequency of the skin lesions 
 and their varying character, the disease continued to be named 
 petechial or spotted fever. 
 
 North describes the disease from his personal experience with 
 it, and appends to this various other accounts which have been 
 given by contemporaneous authors. North divided the disease 
 into two types depending on the more or less rapid course of 
 the disease and the intensity of the symptoms. 
 
 Dr. Samuel Woodward,^^ in a newspaper printed in Hartford, 
 describes an epidemic in Litchfield County in 1807. In the 
 same paper, Dr. Bestor, after giving an excellent account of 
 the clinical course of the disease, says that, though it has been 
 attributed to various causes, he is convinced that the "immediate 
 cause of the disease is the increase in the sensorial power of sen- 
 sation with the decrease of the sensorial power of irritation." The 
 book of North also contains a description of the disease by Dr. 
 Fiske, " Sketch of Spotted Fever" ("Massachusetts Spy," April 
 9, 1810), " Observations on Anomalous and Irregular Diseases," 
 by Dr. Williamson (Baltimore, 1808 ; letter to Philadelphia Med- 
 ical Museum), and a collective report from Drs. Haskel, Spooner 
 and Holmes, who were a committee appointed at Farmington, 
 Conn., to investigate the disease. 
 
 Hirsch^" divides the history of the disease into four periods. 
 The first, from 1805 to 1830, shows the disease in isolated epidem 
 ics in various places in Europe, but more generally in the United 
 States. In the second period, from 1837 to 1850, the disease 
 became prevalent in wide-spread epidemics in France, Italy, 
 Algiers, the United States and Denmark. During the third period, 
 from 1854 to 1875, it reached its widest diffusion throughout most 
 of Europe, the adjoining countries of Asia, the United States and 
 some parts of Africa and South America. The fourth period, from 
 1876 to the present day, shows a return in slight epidemics of more 
 or less considerable groups of cases in various countries, but par- 
 ticularly in the United States, Germany and Italy. In this last 
 period there has been very little of the disease in France. In the 
 first period it was seen in Canada in 1807 ; in Virginia, Kentucky 
 and Ohio, in 1808 ; in New York and Pennsylvania, the year after. 
 
13 
 
 The year 1816 forms the close of these series of epidemics, with 
 the exception of one at Middletown, Conn., in 1823, and one at 
 TrnmbuU, O., in 1828. The United States was free from epidemic 
 cerebro-spinal meningitis until the year 1842. In Europe in the 
 first period there was an epidemic in Paris in 1814,^^^ in 1815 at 
 Metz,^*^ and in subsequent years in two or more villages in the 
 province of Geneva, and in a few places in Germany. 
 
 Lichtenstern*^^ gives Sibergundi^^ the credit for the first descrip- 
 tion of the disease in Westphalia, Germany. In the second 
 period, from 1837 to 1850, the disease first broke out in two 
 localities in the south of France^ in Bayonne and the department 
 of the Landers on one hand, and the districts of Foix and 
 Narbonne on the other. It extended all over France, most of 
 the cases being among the garrisons, and next to France its 
 greatest ravages were in southern Italy. The only other country 
 in Europe in which meningitis was prevalent to any extent during 
 this period was Denmark, and from here it was probably carried 
 to Iceland. In Germany there are references to a few slight epi- 
 demics of encephalitis and acute hydrocephalus, which in all 
 probability were cerebro-spinal meningitis. In the United States 
 in this period the disease appeared principally in small epi- 
 demics in the western and southern States. The most extensive 
 epidemic was seen at New Orleans, in a regiment of recruits 
 which had come there from Mississippi. In 1848 it was seen 
 in the towns of Millbury and Sutton, in Worcester County, 
 Mass., and described by Sargent. ^^ 
 
 The second period was characterized chiefly by the prevalence 
 of the disease among the troops. The epidemic was most 
 prevalent in France, and in nearly all cases it appeared first 
 in the military, and from there in some cases, notably in Metz, 
 extended to the civil population. 
 
 The descriptions of the disease by French authorities during this 
 time are of great value. They devoted their attention chiefly to 
 the description of the course of the disease, the rare symptoms, 
 the manifold complications, the ordinary and the rarer pathologi- 
 cal lesions. The most prominent of the French treatises are 
 those of Rollet,^-^*^ Tourdes,^^'' Forget^^^ and Broussais.^^^ 
 
14 
 
 In the third period the disease began in Sweden, a country 
 hitherto free from it, and prevailed there in extensive epidemics 
 for ten years (Hirsch) . Another one of its principal seats was 
 Germany, where it reached its height in 1864 and 1865. 
 Here it first appeared in Silesia, and broke out almost simul- 
 taneously at a number of points in east and west Prussia, 
 gradually extending throughout south Germany. 
 
 In this period the best descriptions are those of Wunderlich^*' 
 of the disease in Leipzig, and of Ziemsen and Hess^*^ of the 
 epidemic in Erlangen. The disease appeared in Berlin in 1864, 
 and the pathological lesions were carefully described by Klebs,^* 
 who reported the results of twenty-six autopsies. Kotsonopulos^^ 
 described an epidemic of the disease in Nauplia, Greece, in 1869, 
 and in 1873 he gave a further account, showing that the epi- 
 demic of 1869 continued with a number of single cases and 
 small epidemics until 1873. 
 
 The United States was free from the disease from 1850 to 
 1857, when it again appeared in two such widely separated 
 areas as North Carolina'^^^ and the western part of New York.^^ 
 During the civil war, from 1861 to 1864, the disease became 
 widely spread. In the winter of 1861 and 1862 it appeared 
 in the Army of the Potomac and in camp near Washington,"^ 
 and was especially severe among the negroes sent by the 
 Confederates to Memphis. 
 
 Upham"'' gives an account of the disease as it appeared in 
 the winter and spring of 1862 and 1863 in the camps in and 
 around Newbern, N. C. He compares the symptoms observed 
 in this epidemic with those of the Massachusetts epidemic in 
 1810, and concludes that both diseases were the same. He 
 made a number of post-mortem examinations, and gives a 
 careful description of the anatomical lesions. 
 
 The disease appeared again in Massachusetts in 1864 and 
 1865, and a report was made on it in 1865 by a committee 
 appointed by the Massachusetts Medical Society. The report 
 of this committee, unlike that of 1810, did not make any 
 material addition to our knowledge of the disease. The disease 
 was also described at this time by Webber, whose article is 
 
15 
 
 chiefly valuable for his study of the history of the disease and 
 the relations of early epidemics to it. 
 
 From 1865 there was a period of quiescence in Massachusetts 
 until 1872 and 1873, when there was another severe epidemic in 
 Boston, which was reported by Upham."*' In Philadelphia and 
 other parts of Pennsylvania there was a severe epidemic in 
 
 1863, which was described by Stille."^ 
 
 The disease took the character of a very wide-spread epidemic 
 in Ireland in the first half of the year 1866, appearing in Dublin 
 and the surrounding country. It was spoken of by the people as 
 the " black death." It appeared first among the troops, and 
 extended from these to the civic population, being most prominent 
 among the troops in 1866 and among the population in 1867. 
 
 From 1860 to 1874 epidemics of the disease were seen in almost 
 all parts of the United States. The epidemics usually appeared in 
 the winter and reached the greatest extension in the spring. 
 Hirsch thinks that in the last period, beginning in 1876, the 
 disease is retreating into narrower limits, so that it nowhere 
 retains a character of a prevalent disease of the people. A review 
 of the literature since 1884, the date of the publication of his 
 work, shows numerous, for the most part small, epidemics, in 
 widely different localities. In this period also reports of a great 
 many sporadic cases of the disease have been published. The 
 reports of so many sporadic cases are probably due in part to 
 the closer observation and better recognition of the disease, and 
 the greater interest which the development of our knowledge of 
 bacteria has brought about. In 1876 there was a small epi- 
 demic at Birmingham, reported by Forster^*^ and at Galston 
 near Glasgow, reported by Frew.^ 
 
 Striimpel,^^ in an article on " Pathology of Cerebro-spinal 
 Meningitis," says that the disease has continued in Leipzig since 
 
 1864, a few cases being seen every year. In the first half of 
 the year 1879, at the same time with the extensive epidemic of 
 recurrent fever, the disease became more common and prevailed 
 to a slight extent up to the summer of 1880. In 1881 he saw 
 four cases. Frolik-*^ reports a small epidemic in the garrison in 
 Leipzig. The disease began to appear in 1877, and up to 
 
16 
 
 October, 1879, sixteen cases were taken to the hospital, of which 
 five died and eleven recovered. Leyden''^ says there has been 
 in recent years slight epidemics of the disease in Berlin, espe- 
 cially in the year 1885 and the spring of 1886. Bliimm^ re- 
 ports a small epidemic in Sulzbach, and says that at the same 
 time single cases or small epidemics were observed in the 
 surrounding towns. In Ziemssen's clinic in Munich in 1890 
 there were seventeen cases and three deaths, and in the clinic 
 of Bauer in the same city there were twenty-four cases and 
 eight deaths. > 
 
 Leichtenstern^^ gives an account of cerebro-spinal meningitis 
 on the Rhine from 1885 to 1893. The disease appeared in 
 Cologne in 1885, and reached an epidemic extension. One hun- 
 dred and eleven cases occurred, with thirty-seven deaths. There 
 were thirty-four cases in 1886, twenty-six in 1888, and in other 
 years a varying small number of cases. 
 
 In 1890 the disease extended from Cologne to the neighboring 
 village of Diisseldorf, where there was a small epidemic of twenty 
 cases with six deaths. Panienski^ reports a small epidemic in 
 Karlsruhe in the winter of 1892 and 1893, in which there were 
 sixteen cases and seven deaths. A small epidemic of thirty 
 cases appeared in Copenhagen in 1891, which was described by 
 Friis.-^ Austria has generally been more or less free from the 
 disease. 
 
 Karg"'' reports a small epidemic in the Orphanage of Vienna 
 in 1863. Warschauer^^^ reports an epidemic in Cracow, which 
 prevailed principally among the Jews, whom he considers more 
 susceptible to the disease than the Slavonic population. In 
 1867 Baxa^ describes an extensive epidemic which prevailed in 
 Pola in Bohemia. One hundred and twenty-nine cases occurred, 
 with a mortality of sixty-six per cent. In 1868 a similar epi- 
 demic prevailed at the same place. At various other places in 
 the Austrian monarchy there are reports of small scattered epi- 
 demics, none of them reaching any considerable extent. In the 
 United States since 1876 sporadic cases and small epidemics have 
 been seen in various places. The most extensive epidemics dur- 
 ing this period have been those of New York^ in 1893, that in 
 
17 
 
 Lanaconing, McL, in the same year, and the recent epidemic 
 in Boston, 1896 and 1897. Many of the epidemics have not 
 embraced more than four to six cases, and most of the accounts 
 concern only sporadic cases. 
 
 The Character of the Epidemic. 
 
 Considered as an epidemic, cerebro-spinal meningitis has many 
 features which distinguish it from epidemics of the other infectious 
 diseases. As a rule, none of the epidemics has shown a con- 
 tinuous extension, this being noticeably the case with the first 
 recognized epidemics. After the disease had appeared in Geneva 
 in 1805 its next appearance was in Medfield, Mass., and shortly 
 after this it appeared in other towns in New England, Illinois, 
 New York, New Jersey and Maryland. In some cases, as in the 
 French epidemics from 1840 lo 1845, it appeared to extend with 
 the movements of the troops. It was undoubtedly carried into 
 Algiers in this period by the French troops. In almost all cases 
 it appeared first among the troops, and from these it extended to 
 the civic population. Hirsch, in his study of the disease, has 
 found only one instance in which an epidemic has followed a regu- 
 lar course. In the diffusion of the disease through central Fran- 
 conia it travelled somewhat regularly from north-east to south-west. 
 As a rule, the outbreaks of the disease have been seen as perfectly 
 isolated epidemics in places which had been hitherto free from it. 
 
 Almost all of the epidemics have appeared in the winter and 
 spring. Vieusseaux pointed out that the disease in Geneva dis- 
 appeared on the approach of mild spring weather. All of the 
 early epidemics in Massachusetts were seen in the winter and 
 spring. "Woodward speaks of the disease in Litchfield County 
 appearing in April, when the frost was dissolving and the ground 
 breaking up, and says the disease seemed to be more common in 
 rainy weather. 
 
 Love"^ has pointed out that the epidemic in New Orleans in 
 the winter of 1847 was confined to one regiment newly arrived 
 from Mississippi, who were quartered in bad barracks, on damp 
 ground, and exposed in their wet clothes to the cold. Other 
 troops quartered near them, which were seasoned to the weather 
 
18 
 
 and supplied with woollen clothing, remained absolutely free from 
 the disease. 
 
 Baxa^ shows that the epidemic in Pola commenced in January 
 and lasted until the end of May. There were no cases in the 
 summer, and in 1868 the disease broke out again. Although 
 the disease frequently begins in the winter, it usually reaches its 
 height in the spring months, April and May. 
 
 In the epidemic in New York, both in 1892 and 1893 the 
 greatest number of cases was found in May. In the epidemic 
 of Cologne, in 1885, the greatest number of cases was seen in 
 April, although there were but slight differences in May and 
 June. In the Strassburg epidemic among the soldiers in 1841 
 the greatest number of cases was seen in March, there being 
 in that one month sixty-five out of a total of one hundred and 
 ninety-eight cases. 
 
 Hirsch reports a few exceptions to this general rule. At Bor- 
 deaux, 1839, Toulouse, 1842, Dublin, 1850, and Chrzanow, 1874, 
 the disease first appeared in the summer. The weather in itself 
 probably has little to do with the disease, because the number of 
 cases has frequently increased with the approach of warm spring 
 weather and an increase in the temperature. 
 
 This supposed relation between the period of the year and the 
 appearance of the epidemic led people to suppose that cold in 
 itself could be an exciting cause. Lowy^ says cold and heat, 
 rain and sunshine have nothing to do with the appearance and 
 extension of the epidemics. 
 
 Table I. 
 
 
 Jan. 
 
 Feb. 
 
 March 
 
 April 
 
 May 
 
 June 
 
 July 
 
 Aug. 
 
 Bept. 
 
 Get. 
 
 Nov. 
 
 1896, , . 
 
 - 
 
 - 
 
 - 
 
 • - 
 
 - 
 
 1 
 
 - 
 
 - 
 
 1 
 
 - 
 
 - 
 
 1897, . . 
 
 1 
 
 10 
 
 23 
 
 29 
 
 21 
 
 14 
 
 7 
 
 
 
 3 
 
 - 
 
 - 
 
 Dec. 
 
 The preceding table gives the date of the appearance of the 
 disease in the cases observed in the hospitals of Boston in the 
 present epidemic. From this it will be seen that the greatest 
 number of cases was in the spring months. The first case seen 
 
19 
 
 ■was in June, but the epidemic character of the disease was not 
 recognized until the following February. 
 
 Age. 
 In general the disease has been most prevalent in children 
 and young adults. The cases occurring in the military epi- 
 demics were mostly young soldiers, from the age of eighteen to 
 twenty-four years. Leichtenstern found, in the epidemic in Cologne 
 in 1885, out of one hundred and eleven cases, only twenty- 
 three which occurred after the thirtieth year. More than half 
 of his cases occurred before twenty-one. The following table, 
 taken from Leichtenstern, gives the ages of cases seen in the 
 epidemic in 1885, and in the small epidemics which followed 
 this. 
 
 Table II. 
 
 
 
 
 
 
 rt 
 
 e 
 
 n 
 
 e 
 
 m 
 
 9 
 
 m 
 
 e 
 
 w 
 
 e 
 
 ifl 
 
 e 
 
 
 to 
 
 
 , 
 
 e 
 
 w( 
 
 et 
 
 « 
 
 M 
 
 M 
 
 * 
 
 * 
 
 w 
 
 la 
 
 e 
 
 e 
 
 *>i 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 w^ 
 
 « 
 
 H 
 
 IS 
 
 >« 
 
 «S 
 
 w* 
 
 e 
 
 w( 
 
 n 
 
 pN 
 
 « 
 
 o 
 
 o 
 
 
 "* 
 
 9 
 
 rt 
 
 FK 
 
 « 
 
 « 
 
 M 
 
 M 
 
 ■* 
 
 e 
 
 Iffl 
 
 19 
 
 e 
 
 « 
 
 t' 
 
 H 
 
 1885, 
 
 
 
 17 
 
 14 
 
 10 
 
 19 
 
 18 
 
 10 
 
 6 
 
 6 
 
 4 
 
 1 
 
 1 
 
 4 
 
 - 
 
 1 
 
 - 
 
 111 
 
 1886, 
 
 
 
 - 
 
 3 
 
 3 
 
 11 
 
 7 
 
 2 
 
 1 
 
 2 
 
 1 
 
 2 
 
 1 
 
 1 
 
 - 
 
 - 
 
 - 
 
 34 
 
 1887, 
 
 
 
 - 
 
 2 
 
 1 
 
 - 
 
 - 
 
 - 
 
 - 
 
 - 
 
 1 
 
 - 
 
 - 
 
 - 
 
 - 
 
 - 
 
 - 
 
 4 
 
 1888, 
 
 
 
 2 
 
 2 
 
 1 
 
 7 
 
 9 
 
 3 
 
 - 
 
 2 
 
 - 
 
 - 
 
 - 
 
 - 
 
 - 
 
 - 
 
 - 
 
 26 
 
 1889, 
 
 
 
 - 
 
 - 
 
 1 
 
 1 
 
 1 
 
 - 
 
 - 
 
 1 
 
 - 
 
 - 
 
 - 
 
 - 
 
 1 
 
 - 
 
 - 
 
 5 
 
 1890, 
 
 
 
 - 
 
 - 
 
 1 
 
 - 
 
 - 
 
 1 
 
 - 
 
 - 
 
 - 
 
 - 
 
 - 
 
 - 
 
 1 
 
 - 
 
 1 
 
 4 
 
 1891, 
 
 
 
 1 
 
 - 
 
 - 
 
 1 
 
 1 
 
 1 
 
 - 
 
 - 
 
 - 
 
 
 - 
 
 - 
 
 - 
 
 - 
 
 - 
 
 4 
 
 1892, 
 
 
 
 2 
 
 - 
 
 - 
 
 3 
 
 1 
 
 - 
 
 - 
 
 - 
 
 - 
 
 - 
 
 - 
 
 - 
 
 - 
 
 - 
 
 - 
 
 6 
 
 Totals, 
 
 
 22 
 
 21 
 
 17 
 
 42 
 
 37 
 
 17 
 
 7 
 
 11 
 
 6 
 
 3 
 
 2 
 
 5 
 
 2 
 
 1 
 
 1 
 
 194 
 
 Of twenty-eight cases reported by Rollet,^^^ sixteen were from 
 eighteen to twenty-two years, eleven from twenty-three to 
 twenty-seven years, and only a single case of thirty years. 
 The cases seen by him extended from January to August. 
 
 Striimpel™ observed thirty-two cases, twenty-four of which were 
 between ten and thirty years. The youngest case was in a child 
 four and one-half months ; the two oldest cases were fifty-two and 
 sixty-six years. 
 
20 
 
 The epidemics in the early part of the century were particu- 
 larly prevalent in children. At more advanced periods of life 
 meningitis is very rare. 
 
 The following table gives the ages of the cases seen in the 
 present epidemic. Only those cases which were seen in the hos- 
 pitals are considered. A separate tabulation of those under five 
 years of age shows but five .cases under three years and one 
 under one year. Nothing shows the inaccuracy of mortality 
 tables of cerebro-spinal meningitis more than the analysis of 
 ages in the cases in which diagnosis is certain. Epidemic 
 cerebro-spinal meningitis is exceedingly rare under one year 
 of age. All other forms of meningitis, though rare at this age, 
 are more common than the epidemic. In mortality statistics of 
 the disease a large percentage of cases is put down as under 
 one year. In the present epidemic no cases were seen in the 
 infant hospital. 
 
 Table III. 
 
 
 e 
 
 10 
 
 S 
 
 m 
 
 e 
 
 iffl 
 
 e 
 
 10 
 
 © 
 
 rt 
 
 © 
 
 « 
 
 LO 
 
 wH 
 
 1-1 
 
 w 
 
 w 
 
 M 
 
 M 
 
 ^ 
 
 "K 
 
 rt 
 
 ffl 
 
 © 
 
 
 © 
 
 e 
 
 w4 
 
 e 
 
 p4 
 
 (S 
 
 pH 
 
 <c 
 
 J^ 
 
 e 
 
 M 
 
 © 
 
 © 
 
 
 
 I"l 
 
 m 
 
 W 
 
 M 
 
 M 
 
 M 
 
 * 
 
 * 
 
 US 
 
 w 
 
 
 18 
 
 12 
 
 6 
 
 11 
 
 16 
 
 20 
 
 13 
 
 s 
 
 1 
 
 3 
 
 1 
 
 2 
 
 
 
 
 There is a general agreement among writers on the disease as to 
 contagion. Vieusseaux"* says the extension of the disease shows 
 that it is not contagious. In G-eneva it began among the poor 
 population, living generally under bad hygenic conditions, and did 
 not extend from case to case. The attendants on the sick and the 
 neighbors remained free from it. Even when there were two sick 
 in the same house, the disease usually appeared at the same time, 
 and they did not acquire it from one another. 
 
 North''^ says, in speaking of the epidemic character of the dis- 
 ease : "I have known more than one instance in which persons 
 coming from a part of the country where the epidemic has never 
 prevailed, and resting a short time in a town where the disorder 
 has been epidemic, have had the disease at a season when the 
 inhabitants of the said town had been free from it. I have also 
 
21 
 
 known persons who resided in sections of the country where this 
 epidemic appeared, after having been on a journey to places 
 where it had never been, attacked with it soon after returning 
 home, and at a season when it did not attack those in different 
 circumstances." 
 
 Stevenson and Smith^"'' reported a small epidemic in Davonport 
 in 1885. The first cases were seen on some ships moored there, 
 and then the troops in the barracks became infected without 
 there having been any communication between the ships and the 
 troops. 
 
 Berg,^ in the epidemic in New York in 1893, could not find a 
 single case in which two or more members of the same family were 
 affected. The outbreaks occurred in widely separated parts of the 
 city, and no relation could be traced between the various outbreaks. 
 
 Panienski** reports an epidemic in Carlsruhe. The disease 
 began among the soldiers, and after a number of cases had 
 occurred a portion of the garrison which had not been affected 
 were sent to Rastatt. One of the men in the garrison there was 
 affected the next day, and then after a pause of four weeks 
 there were three other cases, all of which recovered. In the 
 town of Carlsruhe there were sixteen cases. Coleman^^" gives 
 the following observations on contagiousness : — 
 
 No. 1. Man, aged sixty-one years, typical case of the disease. In; 
 the same house several weeks later the eighteen-year-old son became 
 affected, and one week later the daughter. 
 
 No. 2. Fourteen-year-old boy died with typical disease. His mother 
 became attacked with croupous pneumonia, which was followed two 
 days afterwards by meningitis.. 
 
 No. 3. Girl, seventeen years, died with typical disease, Body re- 
 mained in the house four days. Clothes from the house were lent tO' 
 other people, among whom several cases of the disease appeared. 
 
 Herman and Kober^^ in reporting the epidemic of cerebro- 
 spinal meningitis in upper Sicilia, in Beuthen, say that the 
 epidemic was not limited to a definite place, but broke out in 
 a number of places, most cases coming from crowded and filthy 
 parts of the city. Several cases appeared in the same house or 
 room. No infections were observed in the hospitals. 
 
22 
 
 Singer^''^ reported in tbe epidemic in Tirgul Frumor that eight 
 members of the same family died of the disease. Baxa^ found 
 in one house four deaths, in another three, in three others two. 
 
 Friis,^ in the epidemic in Copenhagen, 1891, found that the 
 disease generally occurred in small family or house epidemics of 
 from two to five cases. 
 
 Peterson*'' studied the epidemic which prevailed in Berlin in 
 1895 and 1896, and thinks that infection takes place by per- 
 sonal contact or by visiting infected localities. The disease 
 may be given to children by intermediate conveyors who remain 
 healthy. 
 
 Gahlberg,^ in the epidemic in Mailberg, found there were 
 numerous cases from the same house, and the disease was 
 especially virulent in certain streets. 
 
 Nowlin^^^ found in the small epidemic of five cases of Shelby- 
 ville, Tenn., that two cases arose in the same house. 
 
 Leichtenstern'^^ has collected the cases bearing on contagion 
 in the epidemic studied by him. In this epidemic there was a 
 small house-epidemic in the hospital, in which four nurses on the 
 medical side of the house, four employees of the house who in no 
 way came in contact with the sick, and one patient who was care- 
 fully isolated in the syphilitic division, became affected. In one 
 hundred and eighty cases in which the dwelling could be ascer- 
 tained, one hundred and fifty came each from one house. 
 
 In the Strassburg epidemic, in 1840, the disease appeared 
 among the soldiers in October. The first case in the civic popula- 
 tion appeared in January, 1841. Hirsch^^ gives the following 
 interesting observations : — 
 
 On the 8th of February, " K," twenty years old, in Sczakan, became 
 infected with meningitis, and was cared for by a woman from Sullen- 
 cyen. After the death of " K," " W," who had cared for him, returned 
 to Sullencyen and died there of meningitis on the 26th of February. A 
 family, " K," accompanied by the boy " D " and the four-year-old daugh- 
 ter of a teacher, " O," came to the funeral of this girl. Shortly after the 
 return to Podgass a small child of the family " K," the boy " D " and the 
 daughter " O " all died of the disease. 
 
 Herman'*^ gives a case of house infection in the epidemic in 
 Breslau in 1887. A family in which there had been meningitis 
 
23 
 
 moved from a house and another family moved into it. In this 
 family there were several cases. He thinks that the epidemic 
 in 1887 was a continuation of the one in 1879, there being 
 sporadic cases between the two epidemics. 
 
 In the epidemic in Beuthen, reported by Richter/^^ there were 
 fifty-six cases and twenty-four deaths. Seventeen of the cases 
 came from tap rooms, and he thinks that in such localities there 
 may be foci of infection. 
 
 Richter^^ thinks that the disease may be contagious. He often 
 found cases in the same family, and the disease spread most in 
 places where people congregated. He gives one case which 
 speaks strongly for contagion. A woman visited at a house 
 where two children had been sick with the disease ; she stayed 
 in the house one day, and then visited an uncle. She had 
 meningitis on the fourth day. In the last days of her disease, 
 on November 6, she was visited by a young man; on the 10th 
 he had a light case ; after five days he returned to his business, 
 and on the 19th an apprentice in the same shop was affected. 
 The period of incubation he thought was about five days. 
 
 In a question of the probability of transmission of an in- 
 fectious disease we should consider the location of the disease 
 and the ways in which the organism causing it can pass from 
 the lesions of the disease to the outside ; further, the viability 
 of the organisms and their possibility of leading a saprophytic 
 existence. The lesions of meningitis are chiefly in the meninges 
 of the brain and cord, and confined to these organs in most cases. 
 While located in the meninges, there is little or no opportunity 
 for the organism to infect the outside. In a certain number of 
 cases there are lesions in the lungs, ears and nose, in which 
 large numbers of organisms are present, and from which an 
 infection of neighboring objects or persons could easily take 
 place. The organism, as far as we have been able to tell 
 from its behavior in culture media and in the tissues, has a 
 feeble vitality, and would not be capable of leading a sapro- 
 phytic existence. In the report on the bacteriology of the dis- 
 ease will be found some observations bearing on the vitality of 
 the organism producing it, when subjected in pure culture to 
 
21 
 
 various external conditions. Still, it must be remembered that 
 we cannot reproduce artificially all the conditions which organ- 
 isms might find in nature. It is certain that the disease is an 
 infectious disease, and is produced by a definite micro-organism. 
 This organism increases in the body of the affected individual, 
 and in a certain number of cases may infect his surroundings, 
 and may in a manner which we do not know be conveyed to 
 the tissues of a susceptible individual and there produce the 
 disease. Why this takes place in some cases and not in others, 
 and the conditions under which it takes place, we do not know. 
 The evidence, on the whole, is not conclusive that the disease 
 is incapable of being transmitted from one individual to another. 
 In the present epidemic there were but few cases in which sev- 
 eral individuals in the same house were affected. In one case 
 a mother was attacked two days after the death of her child 
 from the fulminating form. In two other cases there were 
 cases in the same family, and in one case it was said that 
 children in the same neighborhood had died of brain fever. 
 
 We have been able to find but little in the literature bearing 
 on the subject of immunity in this disease. North,^^ in his de- 
 scription of individual cases, gives one undoubted case in which 
 there was an attack twenty-five months previously. Another 
 case had the disease in August, 1808, and was again attacked 
 in May, 1810. Herman and Kober^ report that a girl who had 
 the disease in May, 1886, died in the second epidemic the fol- 
 lowing year. Lowy^ reports a second attack three weeks after 
 apparent recovery. Warshauer"^ reports a case in a woman 
 who had the disease in an epidemic five years previously. 
 From the fact that second ' attacks are so rarely mentioned, it 
 would appear that a relatively high degree of immunity must 
 be conferred by a single attack. In the present epidemic there 
 was no history of a previous attack. 
 
 Hygienic conditions do not appear to play much part in influ- 
 encing the epidemics. Randolph found, in the epidemic in Lana- 
 coning, that virulent types of the disease appeared in such widely 
 different localities and under such different hygienic conditions 
 that he thinks that hygienic conditions can have but little to do 
 
25 
 
 with the extension of the disease. Claverie,^^ in the epidemic 
 observed in Rocheford, found that the disease was not more 
 prevalent in the crowded parts of the city. In Barden the dis- 
 ease seemed to shun the most crowded streets and only appeared 
 in the best streets. He quotes Laveran as saying. that the dis- 
 ease once appeared in the barracks when very few troops were 
 in them, and disappeared when they filled up again. The re- 
 ports of most epidemics show that the disease is more prevalent 
 in the poorer and more crowded parts of the cities. The map 
 at the end shows the distribution of the cases in this city 
 which came to the hospitals. It is seen from this that with 
 the exception of a small area along the water front, the cases 
 were pretty equally distributed over the city. 
 
 Rollet^'^ gives the mortality in all the epidemics in France up 
 to 1844. At Nancy, where Rollet observed his cases, the mor- 
 tality was 28 per cent. ; Le Mans, 33^ per cent. ; Ancenis, 33^ 
 per cent. ; Montbrison, 34 per cent. ; Caen, 40 per cent. ; Poi- 
 tiers, 40 per cent. ; Versailles, 48 per cent. ; Metz, 55 per cent. ; 
 Perpignan, 56 per cent. ; Strassburg Military Hospital, 58 per 
 cent. ; Strassburg, inhabitants, 60 per cent. ; Laval, 63 per cent. ; 
 Colmar, 71 per cent. ; Bayonne, 75 per cent. ; Aigues-Mortes, 75 
 per cent. General average of all cases, 51 per cent. The mor- 
 tality varies greatly in different epidemics. Hirsch'^^ gives it as 
 from 20 to 75 per cent. In this epidemic one hundred and eleven 
 cases were seen in the three hospitals. Of these, seventy-six died 
 and thirty-five recovered, a mortality of 68|^ per cent. 
 
 With the view of ascertg.ining the prevalence of the disease in 
 the State, the following circular letter was sent to three hundred 
 and fifty physicians : — 
 
 COMMONWEALTH OF MASSACHUSETTS. 
 
 State Board of Health, 
 State HorsE, Boston, Mass., Sept. 1, 1897. 
 
 Dear Doctor : — During the past year an epidemic of cerebro-spinal 
 meningitis has prevailed in Massachusetts, a large number of cases 
 having been seen in the hospitals of Boston. With the view of ascer- 
 taining the extent of the epidemic and the prevalence of the disease in 
 private practice, the following circular letter has been addressed to a 
 number of physicians : — 
 
26 
 
 1. Have you seen any cases of epidemic cerebro-spinal meningitis in your practice 
 
 in 1896 or 1897 ? (If the cases were seen in Boston, give their residence, 
 street and^number.) 
 
 2. Under what form of the disease did these cases come ? 
 
 3. Among what class of the population did such cases arise ? 
 
 4. Were you led to believe that the disease is communicable ? 
 
 5. "What was the mortality ? 
 
 6. Were autopies made, and result ? 
 
 Remarks : — 
 
 One hundred and fifty replies were received from physicians 
 in all of the large cities and a number of the towns. Positive 
 reports, in most cases giving short and adequate clinical his- 
 tories, were received from twenty-one physicians. Cases of 
 the disease were reported in Springfield, Gardner, Marlborough, 
 Framingham, Lowell, Lexington, Weston, Tewksbury, Waltham, 
 Newton, Melrose, Somerville, Gloucester, Rockland, Cambridge 
 and Quincy. With the exception of Springfield, where one 
 case was reported, and Gardner, where two cases were reported, 
 all of the reports come from towns within a radius of thirty 
 miles of Boston. With the exception of Rockland and Quincy, 
 all are to the west of or north of the city. Of course a 
 number of cases reported in the practice of single physicians 
 represent but a small fraction of the total number of cases 
 which may have occurred. It is seen from this that the epi- 
 demic was not confined to Boston, but that cases occurred in 
 other parts of the State. 
 
 Sporadic Cases. 
 
 The accounts given of epidemics of cerebro-spinal meningitis 
 show that they are not of short duration. In the table given by 
 Leichtenstern^^ (Table II.) he shows the number of cases which 
 were observed in Cologne from 1885-92. It will be seen from 
 this that in 1887, 1889, 1890, 1891 and 1892 there was a small 
 number of cases each year, and in 1888 a larger number. The 
 epidemics appear in many cases to have been preceded and fol- 
 lowed by a number of sporadic cases. 
 
 Striimpel,"^ in 1882, says that, since the appearance of the dis- 
 ease in Leipzig in 1863 and 1864, single cases have been seen 
 almost every year, but they never rose to an epidemic extension 
 
27 
 
 until the first half of the year 1879. At that time and with the 
 epidemic of recurrent fever the disease became more frequent, and 
 in the months from April to June thirteen cases were taken into 
 the hospital. Then the epidemic extended in small numbers until 
 the summer of the following year, during which time fifteen more 
 cases were taken in ; finally, after a still longer pause in February 
 and March of 1881, four cases were received. Leyden,"^ in 1887, 
 says that sporadic cases have still remained after the great epi- 
 demic in 1864 and 1865. In recent years there have been slighter 
 epidemics in Berlin, embracing a considerable number of cases. 
 This was especially in the year 1885 and in the spring of 1886, 
 when there were several cases. Mason*^^ reports five cases of 
 cerebro-spinal meningitis occurring from 18S1 to 1883 in Boston, 
 and says there has been a steady decline in the number of cases of 
 this disease since 1874, but a small number are seen in every part 
 of the State except on Cape Cod. Herman and Kober^ say that 
 sporadic cases have been observed in the years preceding the epi- 
 demic extension. 
 
 These reports as to the sporadic cases, coming from observers 
 who are well acquainted with the epidemic form, are interesting. 
 Omerod^^ reports ten cases of sporadic meningitis, with autopsies. 
 Four of these cases occurred between March and June, 1890, and 
 in the summer of the same year there was an epidemic of the 
 disease in the eastern counties of P^ngland. He thinks that the 
 sporadic cases do not differ from the epidemic cases. In all of 
 Omerod's cases the cord was examined and spinal meningitis 
 found. They all had the same clinical history, and the same con- 
 ditions were found at autopsy, as in the epidemic cases. Both the 
 clinical and the gross anatomical descriptions of Omerod are 
 excellent, and it is greatly to be regretted that they were not com- 
 pleted by bacteriological cultures. Osler^ reports a case of spo- 
 radic meningitis of a chronic form, which was followed by total 
 blindness which was gradually recovered from. Rotch,"^ in an 
 article on meningitis, in his text-book gives an admirable pict- 
 ure of a chronic case of sporadic meningitis, with recovery, 
 which would seem almost certainly to have been the epidemic 
 form. Senator^"^ reports a case of sporadic meningitis in which 
 
28 
 
 the clinical history conforms exactly to the type of the chronic 
 epidemic disease. The disease lasted from May 13 to August 
 8, and was characterized by great emaciation. 
 
 Sinclair also reports a case of sporadic meningitis in the Dundee 
 Royal Infirmary. Both from the clinical history and the autopsy 
 this seems to have been of the epidemic form, and there were no 
 other cases of meningitis in the vicinity at that time. 
 
 May, Schmidt and Kastner^^ reported twenty-four cases of 
 sporadic cerebro-spinal meningitis from the clinic of Professor 
 Bauer between 1885 and 1889. There was acute swelling of the 
 spleen in eight cases. It is probable that many of these cases 
 represent sporadic cases of the epidemic form, but in the absence 
 of bacteriological examinations it must remain uncertain. The 
 same may be said of the seventeen cases reported from Ziemmsen's 
 clinic in the same period. * The comparatively small mortality 
 would show that the cases were of the epidemic form. In Bauer's 
 cases there were eight deaths out of twenty-four, and in Ziemm- 
 sen's three out of seventeen. Senator^"^ reports several sporadic 
 cases in Berlin in 1886, with two autopsies. Reichmann^^^ gives a 
 number of sporadic cases in which the symptoms were in all 
 respects similar to the epidemic form. One case lasted from the 
 5th of June to the 14th of August. Laboulene®* says that most of 
 the epidemics have left in their trail sporadic cases analogous to 
 Asiatic cholera. There is but one report of a case of sporadic 
 meningitis in which the diplococcus intracellularis was found ; 
 this is by Stoeltzner, who found these organisms in a typical 
 sporadic case. 
 
 In going over the literature of the disease we find a great many 
 reports of sporadic cases, some of them of single, others of 
 multiple cases. Of course it is very difficult to say whether these 
 cases were of the epidemic form or some one of the other forms. 
 Neither the clinical history nor the autopsy without cultures are 
 absolutely conclusive. In going over the clinical histories of 
 large numbers of cases one receives an impression of the epi- 
 demic form which differs somewhat from that of the pneumo- 
 coccus form and the streptococcus form, but the clinical history 
 
29 
 
 alone is not conclusive. Autopsy accounts would be more con- 
 clusive had they been accompanied with cultures or even with 
 careful histological investigations. The importance of combined 
 clinical and pathological investigation is very evident in going 
 over these reports. There are careful clinical histories given with 
 imperfect accounts of autopsies and without bacteriological investi- 
 gation, and in those cases in which the latter were carried out the 
 clinical histories were either absent altogether or very meagre. In 
 the reports of these sporadic cases it may be generally assumed 
 that the recoveries were of the epidemic form. So far we have 
 not been able to find a case which certainly could be regarded, 
 from the accompanying pneumonia or endocarditis, as pneumococ- 
 cus meningitis, which has recovered. Of course there is a certain 
 number of cases of pneumococcus meningitis in which the affection 
 of the meninges is primary, and it is impossible to say with regard 
 to these cases whether there are any recoveries among them. In 
 the same way there are no recoveries noted from cases of menin- 
 gitis secondary to thrombosis of the lateral sinuses or disease of 
 the middle ear. Those sporadic cases which have been followed 
 by eye and ear lesions are probably the epidemic form and due to 
 the diplococcus intracellularis. 
 
 In going over the cases of meningitis which have occurred in the 
 City Hospital in the five years previous to the appearance of the 
 epidemic, and in which bacteriological examinations were made 
 at the post-mortem examination, no cases due to the diplococcus 
 intracellularis were found. 
 
 This matter of the relation of sporadic cases to the epidemic 
 form is one of the greatest importance, and can only be deter- 
 mined by a careful bacteriological examination of the organs 
 of the cases which die, and bacteriological examination of the 
 fluid obtained from the spinal puncture in all cases. This is one 
 gap in our knowledge of the disease which remains to be filled up. 
 It seems probable that there must be a large number of sporadic 
 cases of epidemic meningitis constantly occurring, which, under 
 certain conditions, the nature of which we are not aware of, may 
 so increase in number as to form an epidemic. Nothing can be 
 
30 
 
 learned with regard to these cases from an examination of the 
 mortality tables. One gets the impression from such tables that 
 the disease is very frequently not recognized when it occurs, and 
 that ma;ny cases are reported as meningitis which are not so. 
 The large percentage of cases under one year in such tables 
 shows how unreliable they are. 
 
 CLINICAL CASES. 
 
 The description of individual cases is taken from the records in 
 the three hospitals in which the cases occurred. They are not 
 reported in full, but the most important of the phenomena noted 
 in the records are described. These records have been made by 
 a number of physicians, and they represent the routine hospital 
 examinations of patients. There is a certain advantage in having 
 the observations of a number of men, because a single individual 
 would almost certainly have his attention directed to single clinical 
 phenomena which seemed to him of special importance and inter- 
 est. The cases reported by Dr. Williams^^^ are included in this 
 report. A number of charts, which are illustrative of the pulse 
 and temperature of the disease, is given with the individual 
 cases. 
 
 In estimating the duration of disease, the time of onset as given 
 in the history of the patient before entry into the hospital is taken. 
 Many of the patients were brought into the hospital in an uncon- 
 scious condition, and were without relatives or friends from whom 
 their previous history could be obtained. Many of them were 
 foreigners, and many belonged to a class in which there would be 
 but little attention paid to the early symptoms of the disease. The 
 charts which are given were taken after the patients had entered 
 the hospital, and after the disease had existed a variable length of 
 time. It is greatly to be regretted that we could obtain no chart 
 which represented the entire duration of the disease, nor could we 
 find any such in the literature. 
 
 Case 1. Female, age fifty years. Entered hospital June 21, 1896. 
 Present illness began three days before admission. At that time frontal 
 
31 
 
 headache, constant vomiting, pain in small of back and both calves. On 
 admission, puj^ils regular ; some general tenderness in muscles of calves 
 and thighs ; great rigidity of neck ; Avhole body can be raised without 
 bending neck ; movement of head from side to side painful. June 
 22, pujiils contracted ; great pain in lumber region ; very restless. 
 Blood count showed 15,000 leucocytes. June 23, noisy and delirious. 
 June 24, delirium continued. June 25, dysphagia ; pupils react alike ; 
 patient cannot be roused. Died 4.52 P.M The chart shows slight 
 irregular fever, with terminal rise. Post-mortem examination. 
 
 Case 2. Female, age fourteen years. Entered hospital October 6, 
 1896. September 21, complained of headache and pain in abdomen. 
 After one week, continual nausea and vomiting, followed by complete 
 annorexia. At the beginning of the illness, had a severe chill. On 
 admission, complained of pain in head, neck, and generally over body ; 
 said it pained her to move ; pupils equal ; tenderness on pressure over 
 cervical and upper dorsal vertebrae ; attempts to flex or move head from 
 side to side causes pain. October 10, patient has moaned and cried 
 almost continually since admission. When spoken to, complains of 
 pain. From this time until death, on October 17, the condition remained 
 about the same, the patient becoming gi-adually weaker. The chart 
 shows slight increase in temperature, with great irregularity. Post- 
 mortem examination. 
 
 Case 3. Male, age twenty-six years. Entered hospital Dec. 31, 1896. 
 He had not been feeling well for three weeks ; was found unconscious 
 on bath-room floor (no date given), and was still unconscious when 
 brought into the hospital. UiDon admission, eyes showed slight diverg- 
 ent strabismus ; pupils much contracted-, equal, do not react ; slight 
 retraction and rigidity of neck, slight rotation to left; reflexes increased. 
 January 2, patient had two or three convulsions ; extremities rigid ; 
 still unconscious ; very restless ; retraction of neck increased. January 
 3, condition worse ; still unconscious. January 4, has had convulsions 
 nearly all day, with short intermissions ; twitching of hands and face. 
 January 4, died. 
 
 Case 4. Male, age twenty-three years. Entered hospital Dec. 30, 
 1896. Three days before, had a chill, Avent to bed, and soon began to 
 have severe headache and vomiting. Two days previous, had been 
 taking care of a child which died of " inflammation of the brain." 
 Upon admission, very restless, complained of severe pain in head and 
 neck; eyes normal. December 31, blood count showed 16,500 whites. 
 January 6, temperature higher ; epistaxis ; delirious for past two 
 days. January 11, much improved. January 15, improving slowly. 
 January 23, temperature normal. January 26, discharged well. The 
 appended chart shows the highest temperature found in any case in the 
 
32 
 
 series, with the exception of some terminal tempei-atiires. 
 parison of the pulse with the temperature is interesting. 
 
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 Case 5.* Male, age forty years. Entered hospital January 2. Dec. 
 27, 1896, went to work as usual, when severe headache came on ; next 
 day delirious, and knew no one. On admission, he was in a semi-coma- 
 tose condition, and remained so until death, January 5. Post-mortem 
 examination. 
 
 Case 6. Female, age seven years. Entered hospital February 11. 
 Three weeks before admission, violent headache and vomiting Four 
 days after this, became deaf, and had pain in both ears. No discharge 
 from ears ; has had marked opisthotonos. On admission, head retracted 
 and drawn to right side ; eyes bulging ; perfectly deaf ; complains much 
 of pain. February 13, examination of ear shows otitis media on right 
 side ; left ear shows an old otitis media. Child sent to surgical wards 
 
 * The following cases in the series are In 1897. 
 
33 
 
 for operation. Re-entered April 3, after mastoid operation, wound 
 healed. Child very much emaciated ; abdomen retracted ; no retraction 
 of head ; understands very little ; seems to have no perception of light ; 
 hears but little, if any. On May 20, can recognize light and shade. 
 May 30, much stronger. June 6, can stand alone. Can see contour and 
 light and shade. June 10, hearing somewhat improved ; sees somewhat 
 better. June 20, discharged. This case is evidently one of the very 
 chronic forms of cerebro-spinal meningitis. Three lumbar punctures 
 were made, the turbidity of the fluid withdrawn diminishing in the suc- 
 cessive punctures. No organisms obtained ; first spinal puncture made 
 four weeks after onset 
 
 Case 7. Male, age forty years. Entered hospital February 10. 
 For a week before entrance, intense nausea, severe pain in back and 
 legs. A day after onset, was unconscious, and moved hands and feet 
 convulsively. Became conscious again three days later, and talked 
 rationally, but still had intense pain in head, back and legs. From the 
 onset there was frequent vomiting. On admission, somewhat delirious ; 
 head retracted ; pupils react slightly to light ; patellar reflex normal ; 
 marked tenderness of back of neck, head and along sjDinous processes. 
 February 15, much worse. For a day or two after admission was de- 
 lirious, but now is semi-conscious. There is paralysis of the right side. 
 Passes urine involuntarily. February 17, temperature high ; oedema of 
 lungs ; unconscious, cyanotic : head retracted and turned to right ; no 
 strabismus. Died at 4 p.m. Post-mortem examination. 
 
 Case 8. Male, age forty-nine years. Entered hospital February 7. 
 Was found in his room unconscious, and brought to the hospital. 
 Pupils contracted, and do not react; patellar reflex absent; stiff- 
 ness of muscles of neck ; pulse of good strength and volume. Patient 
 remained unconscious, breathing heavily during the day, and towards 
 night moaned and had convulsive movements of ai'ms. Lungs began 
 to fill up in the afternoon. Died at 1.30 a.m., February 11. Post-mortem 
 examination. 
 
 Case 9. Male, age twenty -five years. Entered hospital February 12, 
 with a diagnosis of acute articular rheumatism and unresolved pneu- 
 monia. About that tim,e had headache, pains and swellings in hands 
 and knees. Physical examination ; septic odor to nasal discharge ; 
 throat injected ; pupils dilated ; mai'ked tremor of hands and slight 
 twitching of muscles ; seems dull, somnolent, but when roused answers 
 questions ; reflexes present. February 16, condition about the same as 
 at entrance. February 20, condition much improved. Pain and swell- 
 ing in joints much better. March 1, examination shows flatness under 
 right scapula and a few sub-crepitant rales. March 6, dullness in right 
 back not so marked. March 16, condition same as at last note. Blood 
 count shows 20,000 w^hites. March 21, growing gradually weaker; 
 dyspnoea came on in evening, for which no cause could be found. Died 
 at 12.45 A.M. 
 
34 
 
 Case 10. Male, age ten years. Entered hospital February 23. Four 
 days before admission, headache, pain in stomach, restlessness, vomit- 
 ing, and constipation. On admission, delirious and unmanageable ; head 
 retracted ; muscles of neck tense and contracted ; quite deaf since en- 
 trance. There Tvas very little increase of temperature throughout the 
 disease; eyes normal. Lumbar puncture, March 22, thirty-one days 
 after admission and thirty-five days from beginning of disease, showed 
 slightly clouded fluid ; no organisms found. There was great emacia- 
 tion. Child discharged relieved, though x^erfectly deaf, April -4. 
 
 Case 11. Male, age thirty-one years. Entered hospital March 5. 
 Has been having severe chills for two weeks. One week before 
 entrance, went to bed complaining of pains in back and neck and 
 
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35 
 
 shows 19,000 whites. March 9, has severe headache and pain in back 
 of heck. March 12, pain not so severe; lumbar puncture negative. 
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 April 10, discharged well. 
 
 Case 12. Male, age twenty-one years. Entered hospital Mai-ch 4. 
 Gave up work two weeks before admission. Complained of head- 
 ache, pain in neck, loss of appetite. The headache was mainly in 
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 weak ; pulse dicrotic. March 8, noisy delirium. Movement of head 
 more free. OiDhthalmoscopic examination showed slight optic neuritis. 
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 of neck and back very marked. March 19, rigidity still marked; 
 patient occasionally cries out. March 19, still delirious, but more 
 rational than before. March 23, ap^jarently has less pain ; answers 
 
36 
 
 questions intelligently. On the 27th, decidedly better, no pain, head 
 moved freely. From this time the patient steadily improved, and was 
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 showed no oi'ganisms on microscopic examination. In the cultures 
 
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 Bee Case 14. 
 
 aj^parently no growth after twenty-four hours, but after this there was 
 an abundant growth of typical diplococci just above the water of con- 
 densation. The appended chart shows a rather high and irregular 
 temperature, with dro23 to sub-normal at the last. The pulse is low 
 throughout. 
 
37 
 
 Case 13. Female, age three years. Entered hospital April 19. On 
 February 22, acute attack ; convulsions, vomiting, high fever ; right 
 eye sw^ollen, but aftervi^ards became sunken. On admission, retraction 
 of head. Choroiditis found on examination. Lumbar puncture, April 
 22, gave practically clear fluid ; no oi-ganisms found. Child discharged 
 unrelieved April 29. 
 
 Case 14. Male, age seventeen years. Entered hospital March 6. 
 Ten days before admission, pain in back of neck, followed by a chill 
 and extension of pain to head and back. Three days before admission, 
 diplopia and deafness in left ear. Eight days before, vomiting and 
 vertigo. Had been in bed since onset. Was more or less delirious 
 during first seven days. On admission, muscles of neck tense ; pupils 
 equal and reacted ; ptosis of left eye, and photophobia. March 10, less 
 pain in the head. March 12, double optic neuritis. Blood count, 
 March 11, showed 16,000 leucocytes. March 12, left ear congested over 
 the whole extent of drum March 14, mild delirium. March 15, blood 
 count showed 22,000 whites. March 18, condition much worse ; patient 
 in stupor, which continued to increase until March 21. Death at 
 1.10 P.M. Spinal puncture, March 15, showed 8 cubic centimeters of 
 clear, watery fluid. No sediment Mici'oscopic examination showed no 
 cells. Cultures sterile. March 18, lumbar puncture gave 6 cubic centi- 
 meters of a slight opalescent wateiy fluid, with trace of albumen. No 
 cellular elements No organisms. Cultures sterile after forty-eight 
 hours. In this case spinal punctures, made nineteen days, twenty days, 
 and twenty-two daj^s after acute onset, were negative, both for organ- 
 isms and pus cells. The temperature in this case is interesting, showing 
 a rapid fall to normal on third day of entrance, after which there were 
 slight, irregular rises. The pulse is equally irregular. 
 
 Case 15. Male, age fifteen yeai's. Entered hospital March 19. 
 Three weeks before admission, complained of continuous pain in head 
 and back. For three days before admission was semi-conscious, but 
 responded when spoken to. Vomited frequently. On admission, semi- 
 conscious ; convergent strabismus of right eye ; some diplopia; pupils 
 unequal, and did not react alike ; tache cer6brale well marked ; all 
 reflexes absent ; no tenderness along spine ; at times mai'ked retrac- 
 tion of head. March 21, purpuric spots observed on knees and flexure 
 side of forearm ; complete unconsciousness ; urine and fseces passed 
 involuntarily. March 22, patient steadily failed, and died at 1.30 p.m. 
 Lumbar puncture made March 20 gave 6 cubic centimetei'S of an opal- 
 escent watery fluid, which deposited slight sediment. Microscopic 
 examination showed pus cells and diplococci. Cultures positive. 
 
 Case 16. Male, age 30 years. Entered hospital March 18. Twenty 
 days befoi'e admission, general malaise and headache, which increased 
 in severity, and neck became stiff and rigid. A few days before 
 entrance, became delirious. On entrance, noisy and delirious. At times 
 
38 
 
 violent rigidity of muscles of neck ; head retracted ; tenderness along 
 cervical and dorsal region; pupils equal and i-eacted alike; eyeballs 
 rolled up ; rigidity of muscles of extremities. March 22, continuous 
 delirium and coma a few hours before death. Death, 4 p.m. Lumbar 
 puncture on March 22, shortly after death, gave 5 cubic centimeters of 
 clear straw-colored fluid, with slight flocculent sediment. On micro- 
 scopic examination, numerous lymphoid cells ; no pus cells ; no organ- 
 isms ; cultures sterile. In this case the lumbar puncture was made 
 twenty-four days after acute onset. 
 
 Case 17. Female, age twelve years. Entered hospital March 8. 
 One week before entrance, headache ; burning feeling in head ; pain 
 about eyes ; vomiting ; rather stupid three days before entrance ; stiff- 
 ness of neck. On admission, marked retraction of head, with stiffness ; 
 slight convergent strabismus ; could answer questions intelligently. 
 Blood count showed 9,800 whites. Herpes of lips; large patches of 
 herpes on left arm; few hsemorrhagic spots on abdomen. March 11, 
 brighter; no tenderness along spine. Lumbar puncture negative 
 Blood count gave 19,0U0 whites. Eye examination showed atrophy of 
 optic nerve on left side. Another blood count gave 22,000 whites. On 
 March 23, blood count gave 26,000 whites. Condition changed con- 
 stantly ; one minute would complain of headache, and then of no pain, 
 April 1, vomited. April 2, no vomiting. No change. April 5, blood 
 count gave 20,000 whites. April 8, vomited during night. April 9, 
 vomiting continued. April 1 1 , headache most of the day. April 13, more 
 comfortable. April 16, severe headache ; retraction of head diminished. 
 April 23, culture from nasal mucous membrane negative. April 26, 
 temperature practically normal. May 6, still complained of headache ; 
 vomiting. May 20, much better. May 22, pain in legs. Blood count 
 showed 14,000 whites. Patient discharged well June 12, Some tendency 
 to walk on heels. 
 
 Case 18. Male, age eight years. Entered hospital March 5, Three 
 days before enti'ance, headache, pain in stomach, vomiting. On ad- 
 mission, tenderness over entire body, chiefly in neck ; head retracted. 
 For next three days retraction continued ; muscles tense. Lumbar 
 puncture on Mai-ch 9, eight days after acute attack, gaA^e cloudy fluid. 
 April 3, macular eruption noted over legs and trunk. Continued to gain 
 gradually. Discharged well on May 10, 1897. In this case lumbar 
 puncture was performed three times at different periods of the disease. 
 There was constant diminution in the turbidity of the fluid : 1st, very 
 turbid, with thick purulent sediment ; 2d, less marked ; 3d, slightly 
 cloudy; some fibrin formed in the fluid, but there was no purulent 
 sediment. Diplococci uncertain. 
 
 Case 19, Male, age twenty-two years. Entered hospital March 5. 
 Day before admission, pain, slight cough, vomiting, headache, chill in 
 evening. Tried to work morning of admission, but became drowsy 
 
39 
 
 and vomited several times. Oa admission, conjunctivEe injected ; skin 
 hyper^emic ; reflexes normal. In evening, several convulsive attacks ; 
 eyes varied ; part of time left pupil dilated, at other times equal ; right 
 eye turned in at times. March 6, worse ; head somewhat retracted. 
 Died at 8.45 P.M. Post-mortem examination. 
 
 Case 20. Male, age five years. Entered hospital March 11. One 
 week before entry, vomited and had chilly sensation ; pain in stomach 
 and headache. Herpes on admission ; red spots on abdomen ; held head 
 stiffly ; no retraction ; pupils equal ; slight tenderness in back of neck, 
 none along lower part of spine or mastoids ; irritable ; patellar reflexes 
 diminished. Blood showed 36,0U0 whites. Eye examination showed 
 indistinct discs, more marked in right eye. Face congested. March 15, 
 optic discs more distinct than at first examination. March 16, neck not 
 so stiff. March 18, blood count showed 24,000 whites. March 22, neck 
 painful ; stiffness of neck, but no retraction. Blood count showed 
 22,000 whites. Discharged well April 1. Last blood count, March 30, 
 showed 8,100 whites. 
 
 Case 21. Male, age twenty-three years. Entered hospital March 
 10. Five days before, complained of pain in head, neck, back and limbs ; 
 on the same day became delirious. Upon admission, eyes normal ; 
 physical examination negative ; mental condition seemed dull ; he talked 
 strangely. March 14, delirium less ; resisted treatment. Lumbar punct- 
 ui'e, milky fluid withdrawn. March 18, patient got out of bed and 
 wandered about; seemed brighter. March 26, patient remained in a 
 condition of semi-stupor, March 81, vomited yesterday, and seemed 
 weaker. April 4, abdomen " scaphoidal." Died April 6. 
 
 Case 22. Male, age twenty-five. Entered hospital March 9. Twenty- 
 four hours before admission he complained of headache, and during the 
 evening was found unconscious on the floor of his room. On admission 
 into hospital, unconscious ; muscles of back and neck stiff' and rigid ; 
 head retracted ; pupils dilated ; patellar reflex increased. March 10, 
 condition the same. A blood count showed 19,800 leucocytes. On 
 March 12, patient still unconscious ; became comatose, and died at 
 11.15 a.m. on March 13, The temperature was 100*^ at time of admis- 
 sion, and showed a gradual increase, reaching 104° on the last day. 
 Post-mortem examination. 
 
 Case 23. Male, age 23 years. Entered hospital March 11. Three 
 days before admission, complained of pain in back, headache and ner- 
 vousness ; on night before admission, became delirious and vomited a 
 great deal. On admission, was very restless; no retraction of head; 
 pupils equal, and reacted alike ; patellar reflex absent ; legs held rigidly. 
 Patient resisted examination. March 12, patient very stupid ; lay on left 
 side ; no apparent tenderness over ma.stoid region. March 13, dark-red 
 eruption over trunk and extremities ; patient rational ; tongue protruded 
 
40 
 
 slightly to the left. March 15, general condition better. Mental condi- 
 tion improved ; slight convergent strabismus of right eye. All the 
 sym^Dtoms continued to improve, and he was discharged well April 13. 
 Spinal puncture, made March 20, gave 8 cubic centimeters of clear 
 watery fluid, with very slight floculent sediment. Microscopic examina- 
 tion showed a few lymphoid cells, but no polynuclears. No organisms 
 found microscopically. On cultures after several days there developed 
 very small colonies of diplococci, which varied considerably in size, but 
 which showed the characteristic staining. 
 
 Case 24. Female, age five years. Entered hospital March 18. 
 Ten days before admission, poor appetite on returning from school ; 
 next day, dull, cried much ; kept eyes closed most of the time ; screamed 
 once or twice, as if in severe pain ; herpes of lips. Retraction of head 
 and inequality of pupils noticed on day of entry. The mother said that 
 another child in her neighborhood had similar symptoms, and died in 
 eight days. On admission, head retracted; eyes closed; pupils large 
 and equal, and changed from time to time ; reacted sluggishly to light ; 
 slight convergent strabismus ; no tenderness of mastoids or along spine ; 
 purulent secretion on conjunctiva. Blood count showed 18,000 whites. 
 March 21, no change in condition; spoke occasionally to nurse; eyes 
 closed most of the time. March 26, evidence of broncho-pneumonia. 
 March 30, blood count showed 16,000 whites. April 2, no particular 
 change ; left chest still dull ; retraction of head the same. April 5, 
 blood count showed 21,000 whites. April 8, left lung cleared up. April 
 13, fretful ; retraction continued. April 14, discharge from right ear. 
 April 16, both ears discharging. April 19, discharge from ears much 
 less. April 21, retraction of head extreme; eye symptoms the same. 
 April 28, ear discharge slight. April 30, ear discharge profuse. May 
 9, severe cough, with rapid respiration. May 10, collapse during morn- 
 ing; continued to grow weaker, and died at 10.30 a.m. of the 12th. 
 April 23, cover-slips from nose and from ear discharge showed dip- 
 lococci decolorized by Gram in the leucocytes. No diplococci found in 
 the sputum examined May 9. The temperature chart of the case is 
 interesting, as showing a continuous high temperature, running above 
 103^. 
 
 Case 25. Female, age seventeen years. Entered hospital March 11. 
 March 9, had chill, headache, pain all over body, pain in eyes, and throb- 
 bing in ears which interfered with hearing ; vomited several times. On 
 admission, slight nystagmus ; pupils equal and reacted alike ; reflexes 
 normal ; tache cerebrale well marked. March 12, intense pain in back 
 and neck. March 13, vomited several times ; slight delirium ; dijilopia, 
 convergent strabismus and slight ptosis ; tenderness on pressure along 
 spine. Blood count showed 31,000 white corpuscles on Mai'ch 14. Deli- 
 rium continued ; could be roused to answer questions. March 16, patient 
 much duller, and died at 3.30 p.m. Spinal puncture, March 14, gave 8| 
 cubic centimeters of cloudy fluid, with slight sediment. On microscopic 
 
41 
 
 examination, abundant pus cells were found containing numbers of 
 diplococci. Cultures showed abundant pure growth of diplococci. The 
 chart shows a rise to 105|° the second day after entering hospital, then 
 a fall to normal, followed by a rise to 1U2" at death. 
 
 Case 26. Female, age 25 years. Entered hospital March 17. Sick 
 four days before entrance ; com^Dlained of headache and of indefi- 
 nite pain all over body ; this was followed by delirium and vomiting. 
 On admission, pupils regular and reacted ; reflexes normal. March 20, 
 slight nystagmus and diplopia ; marked tenderness in back of neck. 
 March 25, sixth nerve paralyzed on right and partially on left side ; 
 constant variable nystagmus ; answered questions slowly ; was lethargic. 
 March 26, paresis of third nerve ; optic nerves showed slight swelling and 
 congestion. March 30, vomiting ; patient much weaker ; stupor appear- 
 ing. April 2, stupor increased, and patient died at 5.55 A. M., April 3. 
 Lumbar puncture, April 3, shortly after death, gave a small amount of 
 turbid fluid. No microscopic examination made of the fluid. It was 
 sterile in cultures. 
 
 Case 27. Female, age two and one-half years. Entered hospital 
 April 8. Sickness began twenty-five days before entry into hospital 
 with headache, loss of vision and vomiting. On admission, emaciated ; 
 head not retracted, but some resistance to flexion, April 11, lumbar 
 puncture gave turbid fluid with slight deposit of pus at bottom of tube ; 
 diplococci in pus cells. Chart shows irregular sharp rise in tempera- 
 ture up to 106" before death. 
 
 Case 28. Male, age thirty-seven years. Entered hospital March 20. 
 One week before admission, headache, pain and stifl'ness in neck ; 
 three days before admission, was delirious. On admission, head rigid, 
 patient cried out with pain on attempting to move it ; delirium ; head 
 retracted ; jjupils contracted, but reacted alike ; patellar reflex absent. 
 March 24, continued delirium ; back and neck painful to touch. Blood 
 count gave l'i,000 whites. On March 28, quieter and more rational. 
 April 1, less tenderness and rigidity; no special change of mental condi- 
 tion ; no optic neuritis. April 5, still delirious and restless, April 9, 
 some improvement ; the mind clear at times. April 13, continuous im- 
 provement. April 17, mental condition better, but at times delirious. 
 The patient continued to gain in strength, and on May 17 was dis- 
 charged, to go into country. At the time of discharge, irritable and 
 childish. Lumbar puncture, March 24, was negative for organisms both 
 on microscopic examination and cultures. There were abundant pus 
 cells in the fluid. 
 
 Case 29. Female, age four and one-half years. Entered hospital 
 March 20. Attack began three days before entrance ; vomiting ; 
 after that great pain in head and neck ; opisthotonos. Lumbar puncture 
 made March 20. Optic neuritis of both sides on May 15. Child con- 
 
42 
 
 tinued to improve, and was discharged well June 6. Temperature of 
 the case is interesting, as showing a very low temperature, rising only 
 •once to 101°. Fluid from lumbar puncture, March 20, was cloudy but 
 not very turbid ; only slight deposit. 
 
 Case 30. Female, age three years. Entered hospital March 24. 
 Four days before admission, tenderness of neck muscles ; hyperesthesia 
 of entire body, Lumbar jjuncture positive. Herpes of lips. Condition 
 improved rapidly, temperature falling to normal on March 28. Dis- 
 charged well April 12. 
 
 Case 31. Female, age eight years. Entered hospital March 23. 
 Three days before admission, vomiting, pain in back, headache and 
 constipation. Strabismus two days before admission. .On admission, 
 strabismus of both eyes ; hyperesthesia of entire body, chiefly back 
 of neck ; patellar reflexes normal. Lumbar puncture, March 26, nega- 
 tive. At this time, temperature was gradually going down. Lumbar 
 I^uncture, April 3, positive. Discharged well July 5. The spinal punct- 
 ure was made during an exacerbation of fever. 
 
 Case 32. Female, age seventeen years. Entered hospital March 2.5. 
 ]March 21, came home from work complaining of pain in head, 
 chilliness and vomiting. On the following morning, rigidity of arms 
 and legs, with slow movements ; was in stupor and unconscious for 
 most of the day. On third and fourth days, delirious, and complained 
 of pain in head and neck. On admission, muttering delirium ; marked 
 retraction of head ; pupils equal and reacted to light ; convergent strabis- 
 mus. Patient died suddenly at 6,30 a.m., March 26. Temperature on 
 admission, 100^ ; pulse, 120. Post-mortem examination. 
 
 Case 33. ]\Iale, age twenty- five years. Entered hosj)ital March 30. 
 Eight days before admission, feeling of malaise, with headache. Two 
 daj's before entrance, delirious ; in the evening was nauseated. On 
 admission, semi-conscious ; fever and headache, pain in neck ; herpes 
 on lips and nose; puj^ils equal, occasionally strabismus of left eye; 
 knee jerk not obtained. April 2, patient unconscious. Blood count 
 showed 21,600 whites. Became gradually weaker, and died at 10 p.m. 
 Spinal puncture, made April 2, gave temporary relief. Puncture 
 showed considerable cloudy fluid. Smears showed abundant pus and 
 dijDlococci. 
 
 Case 34. Female, age seven years, two months. Entered hospital 
 March 26. Two days before admission, face flushed, complained of 
 headache, vomiting. There were convergent strabismus and opisthot- 
 onos. On admission, child crying, with eyes partly closed and hands to 
 head. Easily roused ; answered questions. Pain in forehead ; jjupils re- 
 acted alike ; convergent strabismus ; tenderness of neck ; tache cerebrals 
 well marked ; patellar reflexes unequal. Blood count showed 25,000 
 
43 
 
 whites. March 27, restless ; tenderness of right wrist, which was swollen 
 and red ; moderate retraction of head ; internal strabismus ; stupor ; 
 complained of tenderness of right ankle. March 28, vomiting ceased ; 
 stupor increased. March 29, large patch of hei-pes just below and 
 anterior to lobe of left ear. Culture from fluid from hei'petic vesicles 
 negative. April 15, much better. Discharged well May 4. Tempera- 
 ture was high until April 2, then gradually declined. 
 
 Case 35. Male, age five years. Entered hospital April 3. Nine 
 days before admission, headache ; irritable. Two days before, went 
 to Eye and Ear Infirmary and was sent to hospital. On entrance, 
 right pupil slightly larger than left ; no herpes ; no ecchymosis ; slight 
 stifi"ness of neck. April 4, much pain in head and neck; at 6 p.m., 
 delirious; quieter afterwards. April 5, less delirious. April 7, left pupil 
 larger than right ; strabismus ; slight stiftness of neck ; backward and 
 forward movement caused jjain. April 8, did not recognize relatives ; 
 seemed more stupid ; no strabismus. Discharged against advice. 
 
 Case 36. Male, age nineteen years. Entered hospital March 30. 
 Five days before admission, pain in side, severe headache ; vomiting, 
 with delirium and retraction of head. On admission, delirious and deaf ; 
 herpes labialis ; pupils equal and reacted alike ; patellar reflex slightly 
 increased. Blood count showed 9,350 whites. April 3, retraction less 
 marked; had grown more deaf. April 6, head moved without pain- 
 April 12, better. Ophthalmoscopic examination, April 16, showed slight 
 optic neuritis. April 19, discharged. 
 
 Case 37. Male, age twelve years. Entered hospital April 1. Vomit- 
 ing and headache three days before entrance. On entrance, photophobia ; 
 hyperjBthesia of skin, no eruption ; delirious, unconscious. Herpes de- 
 veloped, general condition became much woi'se. Died April 7. No 
 post-mortem examination. Purulent discharge from eyes. Tempera- 
 ture irregular, with sharp terminal rise. Lumbar puncture, immedi- 
 ately after death, gave thick purulent fluid with diplococei in pus cells 
 
 Case 38. Male, age thirty -thi-ee years. Entered hospital April 1. 
 Three days before admission, began to vomit, and continued to do 
 so since; pain in back of head. On admission, pupils equal, slight 
 convergent strabismus of left eye; patellar reflex absent; stiffness 
 of neck ; pain limiting motion in all directions ; no tenderness ; no 
 retraction. April 4, very delirious, tearing his bed. April 5, rapid 
 failure ; death in coma, 3 p.m. 
 
 Case 39. Male, age thirteen months. Entered hospital April 13. 
 
 Two weeks before admission grew feverish ; loss of appetite ; cried a 
 
 great deal. Four days before admission, slight convulsion. Head re- 
 
 ' tracted five days before admission. Eyes reacted alike ; tache cerebrale 
 
 on admission; skin clear. Grew gradually worse; died May 18. 
 
44 
 
 Case 40, Male, age three and one-half years. Four days before 
 admission, fever and chills; vomiting day before admission; head re- 
 tracted; slight discharge from both ears. Lumbar puncture, April 8; 
 fluid very turbid, with thick pus at the bottom of test tube ; diplococci. 
 Died June 14. Post-mortem examination. 
 
 Case 41. Female, age fifteen years. Entered hospital April 3. On 
 April 2 she was irritable, had intense headache and vomiting. On day 
 of admission, was delirious and had marked muscular spasm. No 
 retraction of head, although flexion was resisted, and there was con- 
 siderable pain and tenderness in back of neck. At times divergent 
 strabismus and slight nystagmus. Pupils dilated, of equal size and 
 reacted alike. April 4, the same condition ; frequent vomiting and com- 
 plained of headache. Died suddenly. Post-mortem examination. 
 
 Case 42 Male, age nineteen years. Entered hospital April 3. Well 
 up to night before admission. Sickness began with chill, followed by 
 nausea and vomiting. He became stupid and somewhat 
 delirious. On admission, pupils somewhat dilated, 
 reacted to light ; jaws closed ; no retraction of head ; 
 knee jerks noi-mal. April 4, delii'ious ; in semi-lucid 
 intervals complained of head ; tenderness of muscles 
 in back of neck. April 5, breathing somewhat labored. 
 Blood count showed 18,000 whites. Died at 3 p.m. 
 Post-mortem examination. 
 
 EL 
 
 Case 43. Male, age thirty five years. Entered hos- 
 pital April 5. Two days before admission complained 
 of headache and intense pain through head ; jDain also 
 in back and limbs. The day before admission, became 
 delirious and later unconscious. On admission, vmcon- 
 scious, pulse full ; neck retracted ; pupils slightly 
 conti'aeted, reacted alike ; extremities rigid ; pain on 
 pressure along back of neck and spine. April 6, 
 very cyanotic. The removal of exudation by lumbar 
 puncture was followed by relief, but the patient soon 
 grew worse, and died at 6.20 pm. About 5 cubic 
 centimeters of distinctly cloudy, purulent fluid was 
 obtained from lumbar puncture. Smears showed pure 
 pus, many of the pus cells very large and filled with 
 flattened diplococci. 
 
 Case 44. Male, age fifty years. Entered hospital 
 April 4. No previous history could be obtained. On 
 admission, the head was drawn down to the right 
 posteriorly, rotation to the left caused intense pain ; 
 marked tenderness on pressure below mastoids ; pupils equal and reacted 
 alike ; nystagmus jiresent ; patellar reflex absent. Patient failed rapidly, 
 and died April 9. Post-mortem examination. 
 
45 
 
 Case 45. Female, age four and one-half years. Entered hospital 
 April 9. Sudden attack day before entrance, with headache, etc., 
 then became unconscious, delirious and stupid. Marked hyperesthesia; 
 tonic spasms of arms and legs Lumbar puncture, April 22, showed 
 cloudy fluid, with jdus cells and diplococci. Child continued to grow 
 worse. Died May 24. 
 
 Case 46. Female, age eight years. Entered hospital April 9. 
 On admission, unconscious ; head retracted. Condition became worse, 
 and child died April 11. Lumbar puncture, April 11, showed very thick 
 purulent fluid, with pus cells and diplococci. Post-mortem examination. 
 
 Case 47. Female, age twenty years. Entered hospital April 14. 
 Headache and constant vomiting four days before admission, then 
 became unconscious and delirious. Cried out with pain in her head, 
 which was slightly retracted; muscles of neck tense; eyes partially 
 closed; slight divergent strabismus ; both pupils somewhat contracted ; 
 herpes about lips ; patellar reflex normal ; tache cerebrale marked. 
 April 15, vomiting continued ; rather brighter ; answered questions intel- 
 ligently. April 17, more stupid; delirious. Blood count, April 18, 
 showed 13,000 whites. April 21, slept well; no vomiting; less rigid. 
 Blood count showed 20,000 whites. April 23, vomiting during night. 
 Patient continued to improve slowly, and was discharged relieved 
 June 23. Covei'-slip examination of nasal secretion showed diplococci 
 decolorized by Gram in leucocytes and free. 
 
 Case 48. Female, age six years. Entered hospital April 19. 
 Eight days before admission, fever and vomiting ; severe headache ; 
 retraction of head the night before admission, with frequent vomiting. 
 After admission, had slight convulsion and became unconscious ; after- 
 wards hyperassthetic, and then unconscious again. Died shortly after- 
 wards, on day of admission. Lumbar puncture, after death, gave slightly 
 cloudy fluid ; no organisms found. 
 
 Case 49. Male, age thirty-five years. Entered hospital April 22. 
 Ten days before admission, comj^lained of headache and vomiting ; 
 vomiting persisted for several days. On admission, patient in stupor ; 
 answered no questions ; muscles of back of neck not tense except when 
 head was bent forward ; abdomen retracted. Blood count showed 14,000 
 whites. April 23, rigidity of back of neck quite marked. April 25, bed 
 sore developed. Died April 26, Fluid from spinal puncture, made 
 April 24, was slightly cloudy. Direct examination for bacteria negative. 
 Polynuclear leucocytes present in moderate numbers. Cultures on two 
 tubes sterile ; in one, colonies of staphylococcus albus, evidently skin 
 contamination. The temperature shows a rapid terminal rise to 107 -. 
 
46 
 
 Case 50. Female, age tliirty-six years. Entered hospital April 22. 
 On April 12, had chill; headache and pain running down the ba^'k 
 into the extremities. Vomited up to four days before admission ; was 
 delirious the day before admission. On admission, herpes labialis ; 
 pupils equal and reacted ; reflexes normal ; stiffness of neck ; motion 
 
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 Case 50. 
 
 limited by pain. April 24, slight delirium ; no eye symptoms, no i-etrac- 
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47 
 
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 Case 50 Concluded. 
 
 Case 51. Male, age fifty years. Entered hospital April 13. Patient 
 found in a vacant building. On admission, unable to talk ; pupils small 
 and equal; slight fibrillar twitchings of muscles; partial anassthesia. 
 April 14, patient fairly i-ational. April 16, optic neuritis, with con- 
 vergent strabismus. April 20, delirious ; herpes on face ; some petechias 
 on buttocks ; no vomiting, no headache. Steadily failed, and died 9.25 
 P.M. Lumbar puncture, April 15, gave 15 cubic centimeters of slightly 
 cloudy, watery fluid, with slight sediment. Microscopic examination 
 showed pus cells, with occasional diplococci. Cultures showed very 
 feeble growth of typical diplococci. 
 
 Case 62. Male, age twenty-seven years. Entered hospital April 14. 
 On day before admission, had a chill; delirious; face cyanotic; 
 tongue dry ; left pupil smaller than right, both reacted alike ; no en- 
 
48 
 
 largement of spleen ; legs covered with reddish hypersemic blotches ; 
 similar condition on arms, but less marked; patellar reflex normal. 
 Condition grew rapidly worse. Died at 7.15 p.m. Temperature on 
 entrance, 105^. Post-mortem examination. 
 
 Case 53. Male, age twenty-four years. Entered hospital April 17. 
 Headache and vomiting three days before admission. Upon ad- 
 mission, stiffness of neck, pain on bending neck forward ; herpes 
 labialis ; pupils equal and regular, reacted alike ; reflexes normal ; 
 hgemorrhagic peteehise on elbow and buttocks. On April 21, patient 
 was delirious ; required restraint, but was occasionally brighter and 
 answered questions intelligently. Gradually became worse, and died 
 at 3.45 P.M., April 23. Post-mortem examination. 
 
 Case 54. Male, age twenty-six years. Entered hospital April 15, 
 Three days before admission, severe headache ; excessive vomiting ; 
 jjain in back, especially in right lumbar region. No reti'action of neck 
 when admitted into hospital ; mai'ked resistance to movement of head ; 
 tenderness over mastoids and right lumbar muscles ; slight ptosis of 
 light lid ; pupils reacted slowly, but equally. April 20, condition im- 
 proved. Aj^ril 23, complained of pain in right wrist. May 3, marked 
 nausea and vomiting. May 7, vomiting and intense headache. May 11, 
 very delirious. iMay 13, severe frontal headache. May 14, difi'use 
 sweating, weaker pulse. May 17, nausea and vomiting continued. 
 Lumbar puncture, made April 19, showed a small amount of clear 
 serous fluid : cultures of this sterile. Condition gradually imj)roved, 
 and j)atient discharged May 15. This case is not clear. The history is 
 strongly suggestive of mening'itis, but the clear serous fluid withdrawn 
 by spinal i^uncture sj)eaks against it. 
 
 Case 55. Female, age forty years. Entered hospital May 6. Head- 
 ache three weeks before. Head held somewhat backwards. Vomiting 
 for a week. Day before entrance, fell unconscious. On admission, 
 pupils reacted ; tenderness of back of neck ; very slight rigidity ; knee 
 jerks diminished. White corpuscles, 19,000. Continued more or less 
 unconscious. Died May 8. 
 
 Case 56. Female, age three and one-half years. Entered hosj)ital 
 April 19. Hlness began four days before admission, with incessant 
 vomiting. Three days before admission, stiffness of neck, with great 
 pain on motion. No strabismus. On entry, cyanotic ; dulness at 
 base of both lungs ; no retraction of head ; no especial tenderness 
 along spine. One hour after admission, pupils contracted ; cyanosis 
 worse. Gradual improvement up to 6 p.m., when the respiration be- 
 came diflBcult ; unconsciousness developed. Died on morning of 20th. 
 Post-mortem examination. 
 
 Case 57. Male, age twenty-four years. Entered hospital April 17. 
 Perfectly well up to day before admission, when he awoke with intense 
 
49 
 
 headache, vomited several times, was very restless. On admission, 
 almost complete unconsciousness, turning from side to side, burying his 
 head in the pillow. No retraction of head and no tenderness at back of 
 neck. The pupils were normal. Patient continued very restless, turning 
 from side to side : restraint was necessary. He suddenly showed signs 
 of failure, cyanosis, weak pulse, and died at 4 15 p.m., three hours after 
 admission. Post-mortem examination. 
 
 Case 68. Male, age twenty-eight years. Entered hospital April 
 23. One week before admission, complained of headache, which 
 was followed by delirium two days later. On admission, high 
 delirium, patient struggling violently ; rigidity of muscles of neck ; 
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 and opisthotonos. Patient became less noisy after spinal puncture. 
 April 28, blood count showed 11,400 leucocytes. April 30, patient spemed 
 better ; a third puncture was made. May 4, slight change ; patient dull, 
 could not answer questions. Patient continued to improve, and was dis- 
 
50 
 
 charged on May 22. At the time of discharge he was rational, but his 
 mind was evidently impaired. Lumbar puncture was made on April 23, 
 on the 2t)th, and on April 30. On the 23d two test tubes were filled with 
 a bloody, serous fluid containing large clots. There was a great deal of 
 blood and abundant pus cells. No organisms found on microscopic 
 examination or in cultures. On April 26, 15 cubic centimeters of cloudy, 
 yellow, serous fluid removed. Microscopically, showed abundant pus and 
 epithelioid cells ; diplococci contained in pus cells and in cultures. This 
 puncture made during an exacerbation of temperature. The puncture 
 on April 3U was negative. The chart shows rise after entering hospital, 
 with decline to sub-normal, marked by exacerbations. 
 
 Case 59. Male, age twenty-nine yeai's. Entered hospital April 21. 
 April 17, chill, headache, general pain and vomiting ; delirious at 
 night. On admission, delirious ; head retracted; muscles of neck stiff; 
 tenderness on pressui-e over cervical and dorsal vertebrae ; j^atellar re- 
 flex absent ; pupils contracted. Lumbar puncture made April 22, and 
 gave some relief. Died April 23. The lumbar puncture gave 20 cubic 
 centimeters of bloody fluid. Cover-slips and cultures from this showed 
 diplococci. Post-mortem examination. 
 
 Case 60. Female, age five years. Entered hospital April 18, at 
 3.15 A.M. Day before admission, convulsions and high fever; vomit- 
 ing and diarrhoea. At 10.30 of night of admission, numerous small 
 hsemorrhages into skin appeared all over body. On entrance, child was 
 moribund. Two minutes after death, rigor mortis to a marked degree 
 in both legs. Rigor mortis was present in both ankles before death. 
 Rigor rapidly extended to muscles of neck. Skin all over body covered 
 with i^unctate hsemorrhages from the size of a pin's head up to that of a 
 pea. Lumbar puncture, Aj^ril 18, immediately after death, gave a puru- 
 lent fluid with numerous diplococci. This case was most like the fulmi- 
 nating cases described in previous epidemics. 
 
 Case 61. Male, age nineteen years. Entered hospital April 21. 
 Three days before admission, headache and slight chill ; general pain, 
 esijecially in back; vomiting. On admission, slightly irrational; 
 marked tenderness over mastoids and bcick ; pupils small ; abdomen 
 rigid, tympanitic ; tender on pressure over recti muscles ; purplish 
 maculse on skin. April 29, complained of headache. May 7, severe 
 headache and chill ; broncho-pneumonia. Patient continued to improve, 
 and was dischai'ged June 8. The temperature chai't shows irregular 
 fever, not over lUl", then sharp rise to 102°, corresponding to broncho- 
 pneumonia. Lumbar puncture, April 23, gave 35 cubic centimeters 
 of turbid, slightly yellowish fluid. Microscopic examination showed 
 abundant pus cells and large epithelioid cells. Diplococci found in pus 
 cells in considerable numbers and sometimes free. Cultures showed 
 abundant typical development of diplococci. 
 
51 
 
 Case 62. Female, age four and one-half years. Entered hospital 
 April 20. One day before admission, attack began ; no vomiting ; ma- 
 laise ; anorexia; coryza, On admission, restless, delirious and at times 
 unconscious ; head retracted. Died April 22. Lumbar puncture, post- 
 mortem, gave cloudy fluid, and cultures showed pure gi'owth of di- 
 plococci. 
 
 Case 63. Male, age twenty-seven years. Entered hospital April 30, 
 Nine days before admission, complained of severe headache and pain in 
 neck, with vomiting. Headache had not been constant since, but there 
 had been stiffness of muscles and retraction of head. April 29, became 
 delirious. On admission, unconscious, marked retraction of head with 
 rigidity of neck ; conjunctivas injected ; pupils equal, moderately di- 
 lated, did not react; patellar reflex normal. May 1, retraction of head 
 less marked ; mental condition improved ; slight nystagmus ; no stra- 
 bismus. May 2, condition more unfavorable. Spinal puncture May 2. 
 May 5, sane mentally, hiccoughs ; Cheyne-Stokes respiration. May 8, 
 temperature fell to normal. Died May 8. Spinal puncture gave 6 cubic 
 centimeters of cloudy fluid, containing considerable blood Microscopi- 
 cally, single pus cells and many mononuclear cells. None of the large 
 cells found. On culture, most of the tubes sterile. One tube gave four 
 colonies of staphylococcus albus, probably a contamination of the skin. 
 Puncture negative twelve days after attack. 
 
 Case 64. Female, age three years. Entered hospital April 21. A 
 cousin of this child died four days before this with " brain fever" in the 
 same house in which the i^atient was living. On admission, unconscious ; 
 head strongly retracted ; could not be flexed ; convergent strabismus of 
 both eyes. Continued to fail. Died April 22. 
 
 Case 65. Female, age ten years, Entered hospital April 25. Two 
 days before admission, fever, pain in back, vomiting. Lumbar punct- 
 ure April 27. Very cloudy fluid. Typical diplococci in cultures. 
 Died April 29. 
 
 Case 66. Female, age twenty-eight years. Entered hospital April 26. 
 Headache and vomiting three days before admission. On admis- 
 sion, tenderness over mastoids ; rigidity of neck, without retraction ; 
 conjunctiviB injected; pupils rather small, but equal ; petechiae of skin, 
 April 20, continuous delirium ; severe conjectivitis in both eyes. There 
 was a sudden rise of temperature during the visit of the physician, 
 going from normal up to 105°. Patient comatose, and died suddenly 
 April 29. Post-moi*tem examination. 
 
 Case 67. Male, age two and one-half years. Entered hospital April 
 24. No previous history. On admission, unconscious ; eyes open and 
 fixed ; some retraction of head. Spinal puncture, on April 26, gave 
 cloudy fluid, containing pus cells and diplococci. Temperature showed 
 very sharp terminal rise to 108°. 
 
52 
 
 Case 68. INIale, age ten years. Entered hospital May 5. Present 
 illness began six days ago, with pain in right leg, followed by head- 
 ache ; vomiting ; delirium ; three days after this, herpes developed. On 
 entry, herpes about lips ; muscles at back of neck tender and rigid ; no 
 tenderness along spine. Blood count showed 1.5,000 whites. May 7, 
 seemed better. May 9, 1'igidity of neck less ; less pain Blood count on 
 the 15th showed 14,000 whites ; a count on the 17th showed 17,000 
 whites. Discharged well May 18. Temperatui'e came down on day 
 after admission, and remained normal. 
 
 Case 69. Male, age thirty-five years. Entered hospital May 5. 
 Five days before admission, complained of pain in back and headache ; 
 had one chill the first day and one on day of admission ; vomited on 
 three days before admission. On admission, pain in eyes, throbbing pain 
 in back and occasional pain in ears; pupils equal, regular and reacted 
 alike ; reflexes normal ; stifi"ness of neck and whole back ; slight herpes 
 and petechise on nose. May 15, for some days had no pain for several 
 hours each day. May 19, marked impi'ovement. Discharged well 
 May 22. Lumbar puncture made May 7, no fluid obtained. 
 
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53 
 
 Case 70. Male, age twenty-seven years. Entered hospital May 7. 
 Four days before admission, began to have jiain in arms and legs ; the 
 next day, vomited, had headache and pains in back ; on day following 
 this, eijistaxis ; tenderness in parotid region and lower down in neck ; 
 delirium ajjpeared. On entrance, stuj^id and irrational ; no retraction of 
 head, but tenderness on jDressure below mastoids ; lack of motion and 
 expression on right side of face ; herpetic eruption on mouth ; slight 
 ptosis of right eye, conjunctivae injected ; pupils equal and reacted nor- 
 mally. May 9, patient was delirious and noisy, complained of head- 
 ache, the pain extending down the back ; nose bled several times. 
 On May 12, marked improvement; at night of 12th, more delirious, 
 could not be kept in bed. May 17, general condition better ; patient in- 
 telligent when aroused. A slight hsemorrhagic eruption appeared on 
 upper part of abdomen. On the 20th, delirious, stupid, not easily 
 roused ; involuntary micturition. May 24, clear mentally. May 27, 
 jDatient did not respond to questions ; comj^lete paralysis of right arm 
 and leg ; occasional slight nystagmus ; eyes turned towards the left ; 
 inability to swallow. May 29, cyanosis of face. Died at 2.32 p.m. 
 Spinal puncture, May 9, 60 cubic centimeters of yellow, cloudy fluid ob- 
 tained. On microscopic examination, abundant pus and ef)ithelioid cells, 
 and a few lymphoid cells. Many of the pus cells contained diplococci 
 in considerable numbei's. Fifteen tubes were inoculated with large 
 amounts of the fluid ; three of these showed a growth. On two of these 
 tubes two, and on one ten, colonies of typical diplococci. The chart 
 shows complete intermission of fever for two days, coincident with 
 marked improvement of the patient. 
 
 Case 71. Male, age two years. Entered hospital May 7. May 5, 
 suddenly attacked with headache, pain in abdomen and vomiting. May 
 6, became drowsy, stupid and finally unconscious. On admission, per- 
 sistent retraction of head and irregular temperature, varying from nor- 
 mal to 106°. Lumbar puncture May 7. Fluid cloudy, cultures showed 
 diiDlococci in pus cells. The child's condition gradually improved. 
 Emaciation was marked. On May .30, an enlarged cervical gland was 
 noticed ; examination of throat showed membrane on both tonsils. Bac- 
 teriological examination showed K.L. bacilli. Entered south depart- 
 ment of Boston City Hospital June 1. Condition gradually grew worse ; 
 death on June 3, in convulsions. No urine passed while in south 
 depai'tment hospital, and none found in bladder by catheterization, 
 Post-mortem examination. 
 
 Case 72. Female, age six years. Entered hospital May 12. Illness 
 began seven days before admission with abdominal pain, fever and 
 vomiting ; two days before admission there was headache, slight retrac- 
 tion of head and delirium. On admission, slight strabismus ; tache 
 cerebrale well mai'ked ; legs flexed ; pain on attempting to straighten 
 them. Lumbar puncture, May 15, gave cloudy fluid with pure culture 
 of diplococci. Discharged well June 21. The temperature chart is in- 
 teresting, in showing a very shai'p evening rise, somewhat resembling 
 
54: 
 
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 Case 73. Male, age twenty-six years. Entered hospital May 21. 
 Fourteen days before, began to have pain in the back and head, which was 
 continued with varying severity ; movements of head painful ; constant 
 vomiting from the first. On admission, dull and slightly delirious; 
 herpes on lips and around nose ; pupils equal, and reacted ; marked con- 
 junctivitis ; head held stiffly ; motion limited by pain ; no tenderness on 
 pressure over vertebrse. May 24, active delirium ; rigidity of head and 
 back more marked. May 28, less delirious ; no vomiting ; head could 
 not be touched without pain ; no eye symptoms. June 1, mild delirium 
 continued. June 5, occasional delirium ; rigidity of neck had in large 
 measure passed away. On June 9, head could be moved without pain. 
 Patient continued to improve, and on June 21 was dischai-ged well. 
 
 Case 7-4. Female, age ten years. Entered hospital May 9. Illness 
 began night before admission, with chills and vomiting. On entrance, 
 high fever; erythematous blotches on legs. Child rapidly grew worse, 
 and died May 13. Lumbar puncture. May 12, gave cloudy fluid. Cult- 
 ures of this showed typical diplococci. 
 
 Case 7.5. Male, age forty years. Entered hospital May 12. Three 
 days before admission, complained of headache and sore throat; became 
 deaf the following day ; there was retching, but no vomiting. On night 
 before admission, delirious. On admission, pupils small, equal, re- 
 sponded slightly to light ; slight nystagmus and divergent strabismus 
 of right ej-e; deafness; head stiff; pain on motion; no retraction; 
 slio-ht tenderness along vertebrse ; reflexes absent. May 15, herpes on 
 
55 
 
 lips increased; delirious. May 18, eyes again normal; involuntary 
 micturition. Patient slowly failed, and died at 7.30 pm., May 19. 
 
 Case 76. Male, age thirty years. Entered hospital May 17. Patient 
 was in bed one week before entrance, with severe headache and pain in 
 neck, with limited and painful motion of head ; pain in back extending 
 into legs ; vomiting daily before admission into hospital. On admission, 
 head held fixedly ; flexion limited by pain ; eyes normal ; patellar re- 
 flex normal ; abdomen tender. May 20, no vomiting since entrance ; 
 
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 headache continued ; patient dull and quiet. INIay 23, slight delirium. 
 May 27, lay in apparent sttipor. May 28, delirious again ; rigidity of 
 head and back. May 31, stupor continued June 3, patient steadily 
 continued to fail, and died at .5.30 P M. Lumbar puncture. May 19, showed 
 15 cubic centimeters of a slightly cloudy fluid, which after some hours 
 
56 
 
 deposited a yellowish clot. The sediment contained many pus cells, 
 with a few lymphoid and large cells. A few diplococci found. They 
 were occasionally free, usually in pus cells, several j)airs of them 
 grouped about the nucleus. Cultures on every tube showed abundant 
 growth of tyiDical colonies. The chart shows a fever of medium degree, 
 with slight variation, then fall to normal, with slight terminal rise. 
 
 Case 77. Female, age nineteen years. Entered hosjiital May 14. 
 For three days before admission, pain in head and neck and stiffness in 
 neck and back ; slightly stupid. On admission, evident pain, some re- 
 traction of head ; could be roused to answer questions ; pupils equal and 
 reacted ; answered questions, but was dull. May 15, seemed somewhat 
 better, but became rajDidly cyanotic, and died at 2.40 p.m. Lumbar punct- 
 ure on May 1-5 gave 12 cubic centimeters of slightly cloudy fluid with 
 yellow flocculent precipitate. On microscopic examination abundant pus 
 cells and lai'ge epitheloid cells. Diplococci were found microscoj)ically 
 and in cultures. 
 
 Case 78. Male, age twenty-three years. Entered hospital May 25. 
 Two weeks before entrance, gradual onset of temporal headache and 
 pain in back of neck ; vomiting ; headache constant. On admission, 
 left pupil dilated, reacted sluggishly to light ; slightly enlarged spleen ; 
 patellar reflex absent, other reflexes exaggerated ; faint reddish mottling 
 over back and upper arms : headache persisted until May 30. May 31, 
 signs of paralysis on left side of face ; eye did not shut ; corner of 
 mouth immobile : tongue deviated to left. June 4, facial paralysis ; 
 frontalis muscle involved. June 17, slight pain on left side of head. 
 June 18, pain more severe, localized about ear ; mastoid tender ; vessels 
 of tympanum slightly injected. June 19, paracentesis. June 20, ear 
 discharging freely. June 21, tenderness over mastoid. June 24, slight 
 tenderness. June 25, almost no mastoid tenderness. June 26, slight sero- 
 purulent discharge from ear. June 27, pain in back of neck. July 2, no 
 discharge from ear. July 3, discharge fairly free ; jDain in neck moder- 
 ate. July 6, no pain ; slight tenderness ; continuous sero-purulent dis- 
 charge from ear. July 8, comfortable. July 10, no discharge ; much 
 pain and tenderness ; mastoid operation done ; a large amount of 
 purulent material ran from nose during the operation, supposed to be 
 from antrum. July 16, returned to medical side. From the 16th to 
 the 19th, slight bronchitis. July 20, vomiting, swelling of feet and 
 legs ; mastoid better. July 28, oedema of scrotum. August 12, urine 
 shows evidence of acute nephritis. August 16, swelling continued. 
 August 18, better. September 3, discharged relieved. On the 19th of 
 June, microscopic examination of jdus from left ear obtained by para- 
 centesis showed leucocytes and diplococci. June 15, microscopic ex- 
 amination of the purulent nasal secretion showed a few intracellular 
 diplococci and few leucocytes. The dij^lococci did not grow on culture. 
 
 Case 79. Male, age fifty-eight years. Entered hospital May 13. 
 The previous history of the patient could not be obtained, as he could 
 
57 
 
 speak no English. On admission, was semi-conscious and at times 
 delirious; ptosis of left eye, left pupil smaller than right; neither 
 reacted to light ; pulse regular, of good strength and volume ; patellar 
 reflex diminished on left side ; superficial reflexes diminished. May 
 16, still delirious ; incontinence of urine and fteces ; condition much 
 the same as at entrance. May 19, patient much weaker ; stupor deepened, 
 and patient died at 6 a.m.. May 19. The temperature was sub-normal 
 while in hosjDital, Post-mortem examination. 
 
 Case 80. Female, age thirty years. Entered hospital May 21. 
 Seven daj^s before, headache ; vomited several times ; neck not stiff. On 
 admission, right pupil slightly larger; both reacted normally; slight 
 strabismus ; head retracted, but could be forced forward without pain ; 
 cried out, groaned, etc. ; no enlargement of spleen ; reflexes more 
 marked on right side. Blood count gave 14,800 whites. Delirious. 
 May 22, delirious ; headache. May 23, no change in condition. May 
 24, picking at bed clothes. May 25, weak, pulse not so good. Died 
 May 25. The temperature was 102*^ on entrance ; with slight remissions 
 it rose to 105° before death. 
 
 Case 81. Female, age twenty-six years. Entered hospital June 14. 
 Illness began four weeks ago, with headache ; no vomiting. Patient 
 stupid ; eyes closed ; pupils small ; head stiffly retracted ; no tender- 
 ness ; res]Diration irregular ; patellar reflexes diminished ; conjunctivte 
 injected. Blood count showed 10,000 whites. June 15, mild delirium. 
 June 19, pulse weak. June 21, mental condition better. June 22, 
 more stupid ; passed urine and fasces involuntarily. June 24, blood 
 count showed 14,000 whites. July 4, failed all day ; died at 4.45 p.m. 
 Several examinations were made from the superior nasal passages. No 
 diplococci found on the early examinations. Examination on June 15 
 showed a few leucocytes ; no intracellular organisms. There was a 
 high terminal temperature, reaching to 106°. 
 
 Case 82. IMale, age fifty-eight years. Entered hospital May 17. 
 The day before admission, complained of pain in right leg and chilly 
 sensation ; was very weak, and vomited ; found unconscious at 1 p.m:. 
 On admission, was unconscious and cyanotic ; conjunctivte slightly in- 
 jected ; tenderness over cervical vertebrte ; neck stiff, but no retraction ; 
 pupils equal ; did not react alike ; limbs rigid ; patellar reflex absent. 
 Became gradually weaker, and died at 4.50 p.ii.. May 18. Lumbar 
 puncture. May 18, produced 14 cubic centimeters of bloody, cloudy 
 fluid, containing a large trace of albumin. On microscopic examina- 
 tion, pus cells with diplococci. Cultures from fluid showed diplococci. 
 Post-mortem examination. 
 
 Case 83. Male, age sixteen years. Entered hospital May 21. Three 
 days before admission, sudden severe headache in frontal region, ex- 
 tending down middle of neck to middle of shoulders ; retraction of head, 
 with pain on motion. On admission, conscious ; tenderness over sterno- 
 
58 
 
 mastoid and lumbar muscles ; herpes labialis : eyes and reflexes nor- 
 mal. May 24, marked delirium; retraction of head less marked. May 
 
 26, delirium increased ; frequent 
 vomiting. May 27, somewhat bet- 
 ter. May 29, i^atient became worse, 
 and died at 12.45. 
 
 Case 84. Female, age thirty- 
 one years. Entered hospital May 
 22. Three days before entrance, 
 l^ain in head and back of neck, and 
 vomiting ; became unconscious. 
 On admission, pupils equal ; con- 
 vergent strabismus on right side ; 
 head partially retracted ; no ten- 
 derness over cervical vertebrse ; 
 spleen not enlarged ; diminished 
 patellar reflex. Blood count 
 showed 18,000 whites. May 23, 
 still unconscious ; quiet most of 
 the time, groaned if moved; re- 
 traction of head more marked than 
 at entry. Died May 24. Temper- 
 ature chart shows steady rise from 
 time of admission to death. Post- 
 mortem examination. 
 
 Case 85. Male, age twenty- 
 five years. Entered hospital May 
 22. Two days before admission, 
 felt tired, remained in bed, com- 
 plained of general tendernpss of scalp and soreness of head. On May 
 21, complained of numbness, and became delirious in the evening. On 
 entrance, semi-conscious, dull and restless ; pupils of equal size, and 
 reacted alike ; patellar reflex normal ; no rigidity of extremities ; some 
 stiffness of neck, which was not tender on pressure. On the 26th, con- 
 vergent strabismus of both eyes Lumbar jjuncture, May 24, gave about 
 60 cubic centimeters of clear, serous fluid, which deposited a yellow viscid 
 sediment. It contained many piis cells and a few large mononuclear 
 cells with vesicular nuclei. There were few large, flat diplococci in the 
 pus cells, and cultures gave abundant growth of typical dijDlococcus 
 colonies In this case thei'e was extensive diplococcus iDueumonia. The 
 chart shows a terminal rise of temperature. Post-mortem examination. 
 
 i Days of 
 Mon*. 
 
 Zl 
 
 n 
 
 13 
 
 nWs- 
 
 ^C,Vi\vr IH\ li 
 
 Days of _, 
 D'4.ease. 
 
 3 
 
 
 
 
 
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 Case 86. Female, age thirteen years. Entered hospital May 24. 
 Two days before admission, vomited ; this was followed by pain in neck, 
 with retraction. Night before admission, unconscious ; lay on right 
 side, with her face buried in pillows. Slight retraction of head, with 
 tenderness in back of head and neck ; herpes labialis ; slight bulging 
 
59 
 
 of left eye ; slight nystagmus ; pupils normal. May 25, small purplish 
 spots in right axila. May 26, quieter; not easily aroused; pulse rapid 
 and feeble ; unconsciousness continued. Death at 12.46 p.m. 
 
 Case 87. Male, age thirty-five years. Entered 
 hospital May 30. Six days before admission, com- 
 plained of pain all over body ; four days before 
 had chill ; headache and pain in neck and back 
 had been constant and severe ; vomited every 
 day ; several times had nose-bleed. On admission? 
 pupils and reflexes normal. June 2.3, headache ; 
 pain and rigidity in neck and back. June 2, spinal 
 puncture. June 7, patient not so well ; seemed 
 dull. June 11, patient had evidently failed ; he was 
 dull, unresponsive, and had been delirious for one 
 or two nights ; neck held rigidly. June 15 to 
 June 23, the condition continued. On the 26th, 
 chill ; temj^erature and pulse rose, and death oc- 
 curred at 11.45 P.M. Spinal puncture made June 
 2. About 20 cubic centimeters of cloudy serous 
 fluid removed. Examination showed abundant pus 
 and large epithelioid cells. A few diplococci wei'e 
 found in the pus cells. Cultures gave abundant 
 typical growth. There is complete intermission 
 in temperature on June 11, 12 and 13, coincident 
 with evident failure of patient. 
 
 Case 88. Male, age seventeen years. Entered 
 hospital May 30. Had had weakness and general 
 m.alaise four days before admission On day be- 
 fore admission, complained of obstruction of nose^ 
 and frontal headache and vomiting ; on day of bj.j. c^gg 35. 
 
 admission, became unconscious. On admission, 
 
 complained of intense pain in back and neck and across forehead; 
 stiffness of muscles of neck, slight retraction of head ; tenderness 
 over mastoid region; pupils equal and reacted alike. May 31, slightly 
 conscious ; marked convergent strabismus of left eye. Died at 9.40. 
 Lumbar puncture, made just after death, gave 20 cubic centimeters of a 
 rather thick, bloody fluid, in which a thick clot formed after six hours. 
 Microscopic examination showed abundant pus cells and many large 
 epithelioid cells with vesicular nuclei, occasionally containing enclosed 
 pus cells. A few flattened diplococci were found within the pus cells 
 grouped about the nuclei. Cultures gave an abundant pure growth of 
 diplococci. 
 
 Case 89. Male, age thirty-seven yeai's Entered hospital May 31. 
 On May 27, complained of pain in small of back and legs; there was 
 severe headache for three days, and for two days he was unconscious 
 for a short time ; a great deal of vomiting. On admission, dull and 
 
 r 0;.ys o( 1 
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 107- 
 I06* 
 lOS- 
 104' 
 i03' 
 102- 
 
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 97' 
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 m 
 
 130 
 
 120 
 no 
 roo 
 
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60 
 
 stupid, but answered questions fairly well ; complained of pain across 
 forehead and back of neck ; stiffness of neck ; head held rigidly, pain 
 upon rotation ; not retracted ; pupils equal ; slightly contracted and 
 reacted slowly ; patellar reflex normal. On June 4, patient's general con- 
 dition improved ; no delirium. On this day had a chill, and pneumonia 
 appeared. Cultures taken from the nose showed no diploeocci. June 
 5, well-developed pneumonia ; patient delirious, noisy, violent and re- 
 quired restraint. June 7, patient weaker and cyanotic ; failed rapidly, 
 and died at 10.30 a.m. The appended chart shows a sharp rise, coinci- 
 dent with the development of the pneumonia. Post-mortem examination. 
 
 Case 90. Male, age thirty-three 
 years. Entered hospital July 5. Ill- 
 ness began five weeks before ad- 
 mission, with severe pain in foi'e- 
 head. On night before admission, in- 
 tense pain on left side of forehead. 
 While at drug store, where he went 
 to consult a doctor, had an attack of 
 dizziness and vomiting. On admis- 
 sion, face flushed ; eyes injected ; 
 walked with difficulty ; severe pain ; 
 marked rigidity ; slight divergent 
 strabismus ; no stiffness of neck, no 
 tenderness ; arms rigid ; abdomen re- 
 tracted ; patellar reflex active. Blood 
 count showed 22,000 whites. July 6, 
 temperature continued to rise ; uncon- 
 scious. Examination of nasal secre- 
 tion from upper sinuses showed pus 
 cells enclosing diploeocci. July 7, 
 still unconscious ; conjunctivae more 
 injected. Died July 7. The temper- 
 ature in this case is remarkable, 
 showing a gradual increase from time 
 of entry into hospital, reaching 109° 
 six hours before death. Post-mortem 
 examination. 
 
 1 
 
 Month, 
 
 3/ 
 
 1 
 
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 t 
 
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 7 
 
 
 
 Days ol 
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 Case 91. Male, age twenty-seven years. Entered hospital June 10. 
 One week before entry, chill, followed by headache, nausea and vomit- 
 ing. On admission, stiffness of head ; herpes ; soreness in all the limbs ; 
 pain on pressure over mastoids ; eyes normal ; patellar reflex absent ; 
 knee joints sore and stiff. June 21, blood count showed 15,800 leuco- 
 cytes. June 26, condition improved. , Blood count, 9,800 leucocytes. 
 July 2, intense headache, neck stiff, but more comfortable. July 9, pain 
 in head, mild delirium. July 30, patient was delirious ; knee very painful 
 and swollen ; much exudation present. August 9, patient up and about ; 
 knee better. Dischai-ged August 11. 
 
61 
 
 Case 92. Male, age twenty-nine years. Entered hospital June 8. 
 Four days before admission, complained of jjain in laead and abdomen ; 
 three days before, screamed and threw himself about ; day before ad- 
 mission, became suddenly deaf. On admission, eyes normal ; stiflfness 
 of neck and pain on motion ; apparent total deafness ; mental condition 
 dull and confused ; apparently in much pain, but could not definitely locate 
 it. June 10, marked herpes labialis. June 14, still deaf, but heard 
 better than at entry, June 16, chill. June 18, held head stiffly, and 
 complained of pain in head and neck. June 22, delirious for two nights. 
 June 26, bloody, purulent discharge from left ear. June 30, was losing 
 strength and becoming more stupid. Died July 4. Lumbar puncture, 
 June 9, gave 12 cubic centimeters of a cloudy, serous fluid with thick, 
 yellow, tenacious sediment, much fibrin, many pus cells, few endothelial 
 cells ; very few pairs of flattened diplococci in jjus cells. Cultures gave 
 typical diplococci. 
 
 Case 93. Male, age twenty-four years. Entered hospital June 6. 
 Two days before admission, chill, with headache and vomiting ; great 
 prostration. On examination, head not retracted ; pupils dilated and 
 reacted ; nystagmus ; pain on attempting to flex head ; rigidity of mus- 
 cles at back of neck ; patellar reflexes diminished ; tremor of hands ; 
 legs not I'igid ; moi'e or less restless ; vomiting. Blood count showed 
 10,000 whites. June 8, herpes developed. June 9, blood count showed 
 15,000 whites. June 10, 16,000 whites. Pupils at times unequal ; di- 
 vergent strabismus of left eye ; herpes marked on upper part of jaw. 
 June 11, condition about the same. June 13, whites same count. June 
 17, quieter ; slept. Blood count the same. June 18, general condition 
 not so good. June 19, diminished leucocytes, 12,000 whites. June 20, 
 condition the same ; leucocytes 13,000. June 23, 16,000. June 25, 
 10,000. July 7, stiffness of left knee ; no pain. July 8, left knee 
 swollen, fluctuating, patella floating. Condition in knee continued to 
 impi'ove. Patient discharged well July 14. Examination of nasal 
 secretion was made June 10, and showed diplococci decolorized by 
 Gram inside of leucocytes. June 15, showed numerous Gram decolor- 
 izing diplococci in leucocytes. June 26, none found. The chart is in- 
 teresting, as showing a considerable temperature on entry into hospital. 
 The temperature remained up until June 19, when there was a fall, with 
 another rise on the 22d, after which it remained normal. 
 
 Case 94. Female, age thirty-two years. Entered hospital June 16. 
 Eleven days before admission, had sudden severe headache, with pain in 
 occipital region ; more or less nausea and vomiting began soon after 
 headache ; aftei-wards pain in lumbar region and in hip developed. Day 
 before admission, became hard of hearing. No herpes ; no aj)petite ; 
 never unconscious On admission, looked dull ; cheeks flushed ; pupils 
 irregular, reacted equally ; somewhat deaf; complained of pain in occi- 
 pital region when head was flexed ; no tenderness in back of head ; no 
 rigidity. Blood count showed 12,000 whites. June 18, had ringing 
 and drumming in ears ; patient continued worse ; somewhat delirious. 
 
62 
 
 June 20, right pupil contracted ; did not react. Died June 20. Exam- 
 ination of nasal secretion on June 18 and 19 showed diplococci decol- 
 orized by Gram, within leucocytes. 
 
 Case 95. Male, age thirty-one years. Entered hospital June 12. 
 Three days before admission, pain all over body ; face flushed ; frontal 
 headache ; pain in legs ; vomiting ; on entry, eyes normal ; herpes of 
 lower lip and right nostril ; spleen enlarged. June 1.3, less headache. 
 June 14, delirious. June 15, quieter. June 16, irrational. June 21, 
 increase of temperature, and pain back of neck June 24, severe pain 
 in back and neck, not relieved by morphia by mouth, which continued 
 unabated until July 4. July 4, area of splenic dulness increased. July 5, 
 mild delirium ; tremor of hands ; slight headache. July 7, no morphia 
 for sevei'al days, July 8, did not recognize wife; did not respond 
 quickly to questions ; tremor of hands more marked. July 9, died sud- 
 denly. ^Examination of nasal secretion, July 8, showed leucocytes and 
 diplococci. Temperature extremely irregular, never very high. No 
 terminal rise. 
 
 Case 96. Female, age 
 sixteen years. Entered 
 hospital June 12. Two 
 days before admission, 
 headache, vomiting, and 
 pain in head and back. 
 On admission, slight de- 
 lirium ; retraction of head ; 
 tenderness over back of 
 neck ; herpes labialis ; eyes 
 normal ; patellar reflex 
 diminished. June 15, pa- 
 ralysis of left side of face 
 developed ; herpes on both 
 ears and sides of neck ; no 
 delirium ; patellar reflex 
 absent; left knee swollen 
 and painful. June 19, eyes 
 injected ; no complaint of 
 pain ; general condition 
 much worse. Died sud- 
 denly June 24. The chart 
 shows an exceedingly 
 irregular curve, with a gen- 
 eral downward tendency. 
 The pulse, equally irreg- 
 ular, gradually ascends. 
 
 Case 97. Female, age thirty years. Entered hospital June 11. No 
 history could be obtained, as patient was semi-conscious on admission, 
 
 Days of 
 Month 
 
 ¥1 
 
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 71 
 
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 105' 
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63 
 
 and had no friends. Patient resisted examination. Pupils regular and 
 small, and did not react ; held head stiffly, turned toward the left ; no 
 marked pain on movement of head ; no tenderness along spine ; no 
 herpes or petechias. June 15, still delirious, requiring restraint ; com- 
 jilained of pain in neck and 
 back. June 12, lumbar punct- 
 ure. On June 17 there was a 
 chill, but otherwise patient had 
 steadily improved. On the 
 20th, could move head freely 
 and seemed free from pain. 
 On the 24th, discharged well. 
 Fifteen cubic centimeters of 
 fluid AvithdraAvn by lumbar 
 puncture. The pus cells con- 
 tained diplococci. Tempera- 
 ture chart shows the sharp 
 rise with chill, then falling to 
 normal. 
 
 Case 98. Male, age twentj^- 
 five years. Entered hospital 
 June 17. On June 14, had a 
 chill, succeeded by vomiting, 
 which lasted through the night ; 
 then headache, stiff neck and 
 back, with pain and soreness 
 over limbs. On the 16th, de- 
 lirious. On admission, mind 
 clear ; complained that it hurt 
 him to lie on the back ; neck 
 was tender to touch ; slight 
 retraction of head, pain on 
 
 flexion ; pupils equal and reacted slowly ; some pain in legs and back. 
 June 18, mind still clear ; exti'eme pain in back and limbs. Died sud- 
 denly at 8. 30 A.M., June 19. Spinal puncture made post-mortem ; 5 
 cubic centimeters of a bloody fluid obtained, which showed abundant 
 pus with diplococci in pus cells. The organisms were usually in single 
 pairs, two pairs being found in only two cases. The organisms did not 
 ffrow on culture. 
 
 Mon/hi|;i.i(3 rtl/r|/t,i/7/r 
 
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 Case 99. Male, age t^venty-four years. Entered hospital June 28. 
 Seven days before admission, chill and vomiting ; since then, two more 
 chills. Complained of severe headache in back of head, pain extended 
 down spinal column. On admission, stiftness and limited motion of 
 head ; tenderness on pressure in cervical and lumbar region. Blood 
 count, June 29, showed 11,200 leucocytes; July 8, 12,400; July 9, 
 14,200. July 2, patient in mild delirium, but seemed to be free from 
 pain. July 10, head turned toward the left; general condition more 
 
64 
 
 stupid. Stupor continued until death, on July 15. Temperature chart 
 shows an irregular, generally high, temperature, with one marked inter- 
 mission. There is a gradual increase in the pulse, which shows no 
 relation to temperature. 
 
 Days of 
 Month. 
 
 ir 
 
 if 
 
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 5 
 
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 3 
 
 a 
 
 107' 
 106- 
 105° 
 104' 
 I03- 
 102' 
 101° 
 100' 
 99° 
 98° 
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 96' 
 95' 
 
 150 
 MO 
 130 
 120 
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 Case 100. Male, age twenty-six years. Entered hospital June 29. 
 Week before entiy, headache, vomiting, no chill ; pains in back of neck ; 
 became stupid two days before entry. On entry, expression dull, stupid ; 
 right pupil larger; both reacted alike; divergent strabismus more 
 marked on right side. July 1, stupid; muttering delirium; herpes on 
 forehead ; nystagmus ; reflexes more active on right than left. Steady 
 decline ; died at 6.20 p.m. The temperature shows a continual rise until 
 death, reaching 108^". Examination of nasal secretion, July 1, showed 
 some diplococci decolorized by Gram, in leucocytes. Post-mortem 
 examination. 
 
65 
 
 Case 101. Female, age nine months. Entered hospital July 4. 
 Illness began twelve days before admission, with diaiThoaa and fever. 
 Child held head backwards. Discharge from eyes developed. On ad- 
 mission, sero-pm-ulent secretion from eyes ; pupils contracted ; con- 
 vergent strabismus ; child lay with head retracted ; rigid ; no herpes. 
 July 7, hyperi^emic spots, with htemorrhages on right side of face and 
 temple ; convulsive movements more marked, as well as retraction of 
 head ; almost opisthotonos ; no herpes ; condition not much altered. 
 July 22, blood count showed 17,800 whites. Petechi^e had disajDiDeared. 
 July 23, vomiting ; purulent discharge from right ear. Examination of 
 pus from ear showed diplococci decolorizing by Gram. Death, July 23. 
 July 6, examination of nasal secretion showed a few diplococci in pus 
 cells. On examination on July 8, they were absent. Examination of 
 conjunctival pus, July 8, showed no diplococci. The temperature of 
 this case is exceedingly irregular, running a high course throughout. 
 
 Case 102. Male, age six years. Entered hospital June 30. Illness 
 began with vomiting ; retraction of head. Continued to improve. Dis- 
 charged well August 3. 
 
 Case 103. Male, age fifty-two years. Entered hospital July 7. No 
 previous history obtained, except that patient said he had been sick for 
 one week before admission. On admission, stiffness of neck ; motion 
 limited by pain ; tenderness to pressure in upper cervical region ; spas- 
 modic twitching of arms ; eyes normal, with the exception of slight con- 
 junctivitis ; reflexes exaggerated. Blood count, July 8, showed 8,000 
 whites. Blood count, July 11, showed 18,-100 whites. July 11, patient 
 became noisy, then stupid, the stupor continuing until death. Post- 
 mortem examination. 
 
 Case 104. Female, age forty-six years. Entered hospital July 12. 
 Ten days before admission, had nausea and vomiting ; pain in back of 
 neck and general weakness ; complained of double vision ; pain in neck 
 somewhat relieved when head was retracted. On admission, was con- 
 scious and rational ; tenderness in back of neck ; rotation and flexion of 
 head painful ; slight droojaing and loss of exj^ression on left side of face ; 
 mouth drawn to right; herpes labialis ; convergent strabismus; pupils 
 normal ; patellar reflex absent ; petechise over abdomen. Blood count 
 showed 19,600 leucocytes. July 14, patient still complained of pain in 
 neck, and weakness. July 15, the paresis less marked, and less diplopia. 
 July 18, patient better ; paralysis almost disappeared. July 20, mental 
 derangement ; patellar reflex still absent. July 24, patient weaker ; de- 
 lirious most of the time. Death, July 25. The appended chart shows 
 an inverse curve of pulse and temperatui'e. Post-mortem examination. 
 
 Case 105. Male, age thirty-eight years. Entered hospital July 5. 
 No history could be obtained from patient, save that he had worked 
 until three days before admission. On admission, his aspect was dull ; 
 there was herpes labialis ; eyes normal ; patellar reflex slight on left, 
 
66 
 
 absent on right side. July 8, blood count showed 15,600 leucocytes. 
 July 16, by spinal jjuncture a small amount of cloudy fluid obtained, 
 containing pus cells and diplococci. July 21, patient in mild delirium 
 since July 16. At times he was quite rational ; at others stupid. July 25, 
 patellar reflex absent. July 30, no change from last note ; patient still 
 continued stupid. The condition became somewhat better, pulse and 
 temperature became normal, and patient left hospital August 31 with 
 marked mental impairment. 
 
 Days of 
 Month 
 
 n 
 
 13 
 
 IH 
 
 /r 
 
 /fc 
 
 n 
 
 l^ 
 
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67 
 
 Case 106. Female, age twenty-seven years. Entered hospital July 6. 
 On July 3, patient's child died of cei-ebro-spinal meningitis, child being 
 ill for twelve hours. After this she appeared dazed and at times 
 delirious. In the evening she complained of pain in the back of neck ; 
 began to vomit, which continued for twenty-four hours On admission, 
 patient unconscious ; joints of wrists and ankles swollen, red and pain- 
 ful ; head jjainf ul on iiiotion ; pain on pressure on calves and thighs. 
 July 7, marked divergent strabismus Blood count showed 29,400 whites. 
 July 9, blood count showed 14,000 whites. Patient much better ; neck 
 less stiff; no strabismus. July, 19, blood count showed 19,400 whites. 
 Patient discharged well August 11. Lumbar puncture, July 7, gave 
 small amount of cloudy fluid which contained pus cells and diplococci. 
 
 Case 107. Male, aged thirty-two years. Entered hospital July 26. 
 On July 4, began to have severe headaches ; no pain or stiffness in back 
 of head or neck ; general pain in body ; weakness, loss of appetite and 
 drowsiness ; no vomiting. On admission, semi-conscious and restless ; 
 eyes rolled upwards ; reflexes normal ; no herpes ; pulse full, strong 
 and slow; jDatellar reflex absent; no retraction of head. July 27, 
 blood count showed 11,500 leucocytes. July 30, patient sank gradually 
 into deep stupor, and at times was delirious ; incontinence of urine 
 
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68 
 
 and faeces,; retraction of head appeai'ed, and at times amounted to 
 opisthotonos ; weakness increased ; death occurred at 4.15 p.m. Post- 
 mortem examination, which showed a mixed infection with tuberculous 
 meningitis. 
 
 Case 108. Male, age twenty-six years. Entered hospital July 6. 
 Two days before admission began to vomit, and complained of head- 
 ache. On admission, unconscious ; eyes, normal ; head held rigidly, with 
 slight retraction at times ; pain on motion. Blood count, July 7, showed 
 16,400 whites. July 14, slight irregularity of pupils. July 18, stupor 
 more marked. July 22, profound stupor; head retracted; eyes and 
 mouth j)artly open ; corneal reflex gone. July 26, stupor deepened, until 
 the morning of the 26th, when temperature dropped and he seemed 
 better. July 28, marked improvement, which lasted until August 1. 
 
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 August 7, temperature had remained normal for three days ; recognized 
 nurse, but was not clear mentally. August 11, pulse weaker ; respirations 
 increased in rapidity ; patient thought to be dying ; next morning, better. 
 August 15, patient increased in strength ; mild delirium. August 17, 
 blood count gave 13,400 corpuscles. August 19 to August 22, con- 
 tinued to improve physically and mentally; bed sores over sacrum. 
 
69 
 
 The imprnvcment continued, and at this time, September 20, the patient 
 is still in the ward, but his general condition is good. The apjjended tem- 
 perature and pulse curve shows the extreme irregularity which may be 
 seen in a chronic case. 
 
 Case 109. Female, age thirty-two years. Entered hospital July 24. 
 On the 22d, began to vomit, and complained of severe headache ; vomit- 
 ing continued until the morning of admission. The headache was sevei-e, 
 with darting pains in back of neck; was unconscious part of the time ; 
 eyes normal ; reflexes normal ; tenderness over spinous processes of 
 cervical and dorsal vertebrae. Blood count, July 25, showed 13,800 
 whites. July 28, herpes labialis developed. Had been in great pain^ 
 since entry, but was somewhat better. Blood count, July 29, 7,40U whites. 
 Patient became gradually better, and was dischai'ged well August 14. 
 
 Case 110. Male, age three and a half yeai's. Entered hospital Sep- 
 tember 12. Unconscious on day of admission. Died September 15. 
 Retraction of head. This case is interesting, as showing a well-marked 
 terminal rise of temperature, which reached 109.7° just before death. 
 Post-mortem examination. 
 
 Case 111. Male, age thirty-five years. Entered hospital Septem- 
 ber 18. Two days before admission, complained of headache, vomiting 
 and diarrhoea. On admission, unconscious ; face flushed ; expression 
 anxious ; head turned slightly to the left ; mouth drawn to left ; respi- 
 ration labored and noisy ; turning of head to right resisted ; no retrac- 
 tion of head ; no evidence of tenderness to pressure over vertebrae ; 
 pupils reacted alike ; slight dulness posteriorly in both lungs, more 
 marked on right side ; respiration noisy ; loud rales heard ' everywhere ;• 
 patellar reflex normal ; considerable loss of power both of arm and of 
 leg on right side. September 19, area of dulness of right base greater;, 
 bronchial respiration and moist rales : right pupil larger than left ; a 
 divergent strabismus developed. Remained unconscious until death, 
 "which occurred on 19th. Lumbar puncture made on 19th, shortly before 
 death, gave a considerable amount of slightly cloudy fluid, which in the 
 course of twelve hours developed a slight amount of whitish yellowish 
 sediment and a considerable amount of fibrin, which formed a definite 
 layer thi'ough the entire tube. Microscopic examination of the fluid 
 showed the sediment composed of polynuclear pus cells, with numbers- 
 of diplococci within them. Post-mortem examination. 
 
70 
 
 BACTERIOLOGY. 
 
 The aetiology of the disease has been involved in obscurity 
 until quite recently. Notwithstanding the numerous investiga- 
 tions made with the view of ascertaining the particular micro- 
 organism which could be regarded as a causative agent, it is 
 only recently that such an organism has been discovered and 
 its causal relation to the disease been proven. 
 
 The first description of an organism which might be con- 
 sidered as the diplococcus intracellularis was given by Leichten- 
 stern^ in his first paper on meningitis in which he describes 
 the first cases seen in the epidemic in Cologne. He found in 
 the exudation in the meninges a few cocci, sometimes single, 
 sometimes in groups similar in arrangement to gonococci, enclosed 
 in white corpuscles. Schwabach found, in pus from a case of 
 otitis media secondary to meningitis, diplococci in the pus cells. 
 It is probable that in this case also the organism was the dip- 
 lococcus intracellularis. In 1887 Weichselbaum^*^ described a 
 peculiar form of micrococcus, resembling the gonococcus, which 
 he found in six cases of acute cerebro-spinal meningitis. "When 
 these cases appeared the disease was not prevailing in Vienna 
 in epidemic form, although there was at the time an epidemic 
 in Mailberg,-'^ in lower Austria.* The organism described by 
 Weichselbaum was a diplococcus occurring almost solely within 
 the cells. It grew best on agar-agar. In pure culture it 
 formed a grayish- white, rather viscid growth, and the single 
 colonies often appeared to be formed of small confluent masses. 
 It would not grow at room temperature, and died quickly, so 
 that new cultures had to be made every two days. In 
 cultures the organisms occurred singly, in pairs and in 
 tetrads. Both in cultures and in the tissue they were de- 
 colorized by the Gram stain. They were not easily demonstrated 
 in sections of the meninges, and in most cases but few organ- 
 isms were found. Weichselbaum inoculated mice, guinea-pigs, 
 
 * Widerhoferi22 reported seven cases of cerebro-spinal meningitis in children in 
 Vienna in 1885, just before the cases seen by "Weichselbaum^-". The histories of 
 the cases given by Widerhofer and "Weichselbaum coincide with the epidemic form. 
 
71 
 
 rabbits and dogs with pure cultures of the organism. Subcu- 
 taneous inoculations were without result, but inoculation in the 
 pleural or peritoneal cavities proved fatal to guinea-pigs and 
 rabbits in from one to four days. In these serous mem- 
 branes, inflammation with sero-flbrinous exudation was pro- 
 duced. He produced meningitis and encephalitis in dogs by 
 inoculating them directly in the meninges. He found the 
 organism not only in the meninges in all six of his cases, 
 but also, in one case, in foci of broncho-pneumonia in the 
 luDgs. The plate which accompanies the article of Weich- 
 selbaum gives a very correct representation of the organ- 
 ism, showing the irregular and swollen forms which are 
 sometimes found. He called the organism the diplococcus 
 intracellularis meningitidis. Goldschmidt^^^ found the diplo- 
 coccus in a case of acute meningitis in a child of four 
 months. His description of the morphology and cultural 
 peculiarities of the organism agrees essentially with that 
 given by Weichselbaum. Netter'* investigated twenty-five cases 
 of meningitis, with reference to the bacteria present, and found 
 the diplococcus intracellularis in two of these cases. 
 
 There is no other mention made of this organism until 1895, 
 when the most important confirmation of "Weichselbaum's 
 investigation appeared. Jager^^^ described the diplococcus in 
 twelve cases of epidemic cerebro-spinal meningitis occurring in 
 the garrison in Stuttgart. His description of it agrees essen- 
 tially with that of Weichselbaum, with the exception that he 
 says a capsule was sometimes found around the organisms, and 
 that cover-slips made from the cultures could be stained with 
 Gram. In cultures there was some tendency for the organism 
 to grow in streptococcus form, and a fine line running longitu- 
 dinally could be made out along the chain. He calls attention 
 to the very slight amount of exudation which he found in most 
 of the cases. The number of organisms varied with the amount 
 of exudation, being most numerous where the exudation was 
 most abundant. In only two cases was there a microscopic 
 examination made of the meninges and in these the organisms 
 were found in small numbers. 
 
72 
 
 Heubner^^^ found the diplococcus in nine typical cases of 
 cerebro-spinal meningitis in the fluid obtained by lumbar 
 puncture. He produced acute meningitis in goats by injecting 
 pure cultures of the organism into the spinal canal. His 
 experiments on other animals were negative. There were other 
 cases of meningitis in Berlin at the time when Heubner made his 
 report. In six of Heubner's cases the diagnosis made by spinal 
 puncture was confirmed by post-mortem examination. 
 
 Holdheim^^ gives the result of spinal puncture in four cases of 
 meningitis. In all of these cases the organisms were obtained. 
 Two of the cases died, and the organisms were found on post- 
 mortem examination. He confirms Jager's description of the 
 streptococcus form and the longitudinal line found in this. 
 
 Peterson^" investigated an epidemic of the disease in Berlin in 
 1895 and 1896. In twelve post-mortem examinations he 
 found the diplococcus in the exudation in the spinal canal. 
 Furbringer^^^ found the diplococcus intracellularis in the menin- 
 geal exudation of an individual who had acute gonorrhoea at the 
 same time. The two oi'ganisms were so similar in appearance 
 that he thought they might be the same, but cultures showed 
 the difference. Kischensky^^ reports a case of cerebro-spinal 
 meningitis in which he found the diplococcus in the meninges and 
 in hsemorrhagic foci in the lungs. This article is valuable for the 
 histological description of the lesions. Kister^^^ obtained the 
 organisms in two cases from fluid removed by spinal puncture. 
 He found some difficulty in growing the organisms on agar-agar, 
 and obtained the best growth on blood-serum agar. Sub- 
 cutaneous inoculation was without result, but animals inoculated 
 in the pleura or peritoneum died in from four to six days. 
 Stoeltzner^"^ found the diplococcus in the fluid obtained by lum- 
 bar puncture in a sporadic case of meningitis in a child two and 
 one-half years old. The fluid was cloudy, and contained the 
 diplococci enclosed in pus cells. The child recovered. 
 
 Finkelstein^^ found the organism on post-mortem examination 
 of one case which died and in the fluid withdrawn by lumbar 
 puncture in a case which recovered. The diplococci wei'e found 
 within the cells. Scherer^^® investigated an epidemic of meningitis 
 
73 
 
 in an array corp in Stuttgart. He found the organisms in the 
 meninges in two eases which died, and in the nasal secretion in 
 eighteen cases. He thinlis that infection of the nose is always 
 present, and that the presence of the diplococci can establish 
 the diagnosis. 
 
 In thirty-five of our cases on which post-mortem examinations 
 were made, diplococci were found in cultures or on microscopic 
 examination of the exudation or in sections in all but four cases. 
 In most of the cases they were found in all three methods of exami- 
 nation. In one case in which they were not found they had 
 previously been found in the fluid withdrawn by spinal puncture. 
 Two of the other cases were chronic, and no acute lesions were 
 found. The fourth case was a chronic case with a mixed infection 
 with tuberculosis. The diagnosis of the mixed infection in this 
 case was made from the character of the lesions in the meningitis, 
 and from the extension of the inflammatory exudation along the 
 nerves without any evidence of tubercular lesions, although old 
 tubercles were found in the meninges. There was marked 
 infiltration of the Gasserian ganglia. 
 
 In a certain number of cases cultures failed to give the organisms, 
 although they were abundantly present both on cover-slip exami- 
 nation and in sections. As showing the diflSculty in growing the 
 organisms in cultures made from the meninges at the post-mortem 
 examination, ten cultures were made in one case from the exudation 
 on the brain and six from the cord, cover-slip examinations showing 
 abundant organisms in the cells. Only two of the cultures 
 from the brain and one from the cord showed a growth, a 
 single colony being found on each tube. In ten cultures from 
 the brain and nine from the cord in another case, but two tubes, 
 one from the brain and one from the cord, showed a growth. 
 As a rule, the organisms were more easily obtained in cultures 
 made on the acute cases than on the chronic. In a few of the 
 cases the tubes showed a very abundant growth of the organisms, 
 so abundant that on casual inspection of the tube it might have 
 been taken for a growth of the pneumococcus. 
 
 The diplococcus intracellularis of Weichselbaum has the fol- 
 lowing characteristics when grown in pure culture. It is a 
 
74 
 
 micrococcus of about the same size as the ordinary pathogenic 
 micrococci, and appears in diplococcus form as two hemispheres 
 separated by an unstained interval. It stains with any of the 
 ordinary stains for bacteria, and is decolorized by the Gram 
 method of staining. There is considerable irregularity in stain- 
 ing, some organisms being brightly stained, others more faintly. 
 Sometimes this difference in staining is seen in a single pair of 
 organisms, one being more brightly stained than the other. 
 There may also be considerable variation in size, and the larger 
 organisms stain imperfectly. In the swollen" organisms there 
 is often a brightly stained point in the centre, while the re- 
 mainder of the cell is scarcely colored. It may have been this 
 condition which was mistaken by Jager for a capsule. These 
 variations in size and in staining appear to be due to degen- 
 eration, and are more common in old than in fresh cultures. 
 
 The two organisms are usually sharply separated, but in some 
 there seems to be a small amount of material uniting them. 
 Division talies place usually in one plane giving rise to diplo- 
 cocci ; tetrads are occasionally seen. There is little or no 
 tendency to growth in the streptococcus form, although short 
 chains of four to six organisms may be found. We have never 
 seen the streptococcus formation described by Jager, and in 
 the short chains the longitudinal line on which he lays much 
 stress was not seen. 
 
 In cultures the organism does not give a profuse growth on 
 any medium. We have found the blood-serum mixture of Loeff- 
 ler prepared in the method given by Mallory the best adapted 
 for its growth. From its feeble growth on agar we are sure 
 that had this been generally used for the first cultures the or- 
 ganism in many instances would not have been found. This 
 is particularly the case when other organisms are present. In 
 all cases a large number of organisms appear to be dead, 
 or at least they do not grow. In no case was it possible to 
 obtain a continuous growth over the surface. Even when a 
 large quantity of an exudation which on microscopic examina- 
 tion contained large numbers of the organisms was smeared 
 over the surface, only single colonies would develop. The 
 
^o 
 
 same was true in transplanting colonies ; in the place of a 
 streak, single colonies would develop in the line of the needle. 
 To be sure of obtaining growth it was necessary to make a 
 number of cultures, using large amounts of the material investi- 
 gated. To keep pure cultures going, transfers were made daily 
 and four or five tubes inoculated. On some of them the growth 
 would usually fail. 
 
 On the Loeffler serum mixture the growth forms round 
 whitish, shining, viscid-looking colonies, with smooth, sharply 
 defined outlines, and may attain a diameter of 1 to 1^ mm. in 
 twenty-four hours (Plate I., Fig. 1). The colonies tend to be- 
 come confluent, and do not liquefy the blood serum. In acute 
 cases, when large numbers of the organisms are present, there 
 is in some cases an abundant growth of minute, round, trans- 
 parent colonies, bearing much resemblance to the pneumococcus 
 lanceolatus (Plate I., Fig. 2). There is a better growth when 
 the serum is freshly prepared. 
 
 The growth is feeble on plain agar, but better on glycerine 
 agar, though not so good as on blood serum. On glycerine 
 agar the organism forms round, pearly, translucent, flat, shining, 
 viscid-looking colonies, with smooth, sharply defined outlines. 
 On examination with low power they are homogeneous, semi-trans- 
 parent and faintly brownish, with transparent, sharply defined, 
 smooth margins. They rapidly become confluent. On agar it 
 is often impossible to obtain a second growth. 
 
 In bouillon the growth is feeble and the medium becomes 
 only slightly cloudy. At the bottom of the test tube there is 
 a scanty grayish-white sediment, which rises up as a viscid 
 string when the tube is shaken. On potato it has no visible 
 growth, and it produces no change in litmus milk. 
 
 In the tissues the diplococcus is almost strictly confined to 
 the interior of the polynuclear leucocytes (Plate III., Figs. 
 1 and 2). It was never found in the bodies of other cells. 
 In the cell it has no definite position, and is never found in the 
 nucleus. When smears of an exudation are made, appearances 
 suggestive of this may be found, but they result from the dis- 
 tortion of the cells in making the preparation. In paraffine 
 
76 
 
 sections, in wliich the cells are better shown, nothing similar is 
 seen. The numbers found in the cells varied from a single 
 pair in a cell to cells so packed with them that the nucleus 
 was obscured. The greatest numbers were found in the leuco- 
 cytes in the lungs in cases of diplococcus pneumonia (Plate III., 
 Fig. 2). There is no difficulty in demonstrating their presence 
 in the tissues when the method of hardening and staining 
 recommended is used. In the cells the same irregularity in 
 size and in staining was found which has been described in 
 the pure cultures. 
 
 In no case were the diplococci found except in connection 
 with the lesions of the disease. So far as could be learned 
 from cultures of blood, liver, spleen and kidneys which were 
 made at each post-mortem examination, it never produces septi- 
 caemia. It is possible that it may occasionally have been pres- 
 ent and not grown on the cultures. 
 
 Mixed infections with other organisms were not uncommon. 
 The pneumocoecus was found seven times, once in connection 
 with Friedlander's bacillus. Terminal infections with staphy- 
 lococci and streptococci were occasionally found. 
 
 The results of inoculation show that the organism has but feeble 
 pathogenic powers for rabbits and guinea-pigs. The results of 
 our inoculations would seem to show a still more feeble patho- 
 genesis than has been obtained by previous investigators. All 
 of the inoculations made in the subcutaneous tissues were nega- 
 tive. More successful results were obtained from inoculations 
 into the peritoneum and pleural cavities. The material used for 
 inoculation was in part pure twenty-four-hour cultures of the 
 organism, in part the fluid containing the organisms obtained 
 from lumbar puncture, and in part portions of the meningeal 
 exudation containing the organisms. Inoculations made into 
 the spinal canal in rabbits, guinea-pigs and cats in all cases gave 
 negative results. Out of a large number of inoculations made 
 into the peritoneal and pleural cavities, only six guinea-pigs died. 
 All of the fatal cases were inoculated wilh 1 cubic centimeter of a 
 strong bouillon suspension of a pure culture on blood serum 
 twenty-four hours old. Death took place in from twenty-four 
 
77 
 
 to forty-eight hours. In two negative cases there was marked 
 emaciation of the animals, but there were no lesions found on 
 killing them. 
 
 In the successful inoculations in the pleural and peritoneal 
 cavities, inflammation with slight fibrino-purulent exudation was 
 found. The entire peritoneum was injected, there was a small 
 amount of fluid present in the cavity and a slight fibrinous ex- 
 udation over the surface of the liver. Microscopic examination 
 of the exudation showed pus cells which contained enormous 
 quantities of the organisms. In some cases a cell was so filled 
 with these that the nucleus could not be made out. Among the 
 organisms in the pus cells there was a large number of swollen 
 and degenerated forms. The organisms were obtained from cult- 
 ures from the peritoneal cavity, but there was no invasion of the 
 tissues. The same condition was found in the pleural cavity. 
 
 The only successful inoculation resulting in the production of 
 a typical meningitis was made on a goat. This animal was in- 
 oculated in the spinal canal with 1 cubic centimeter of a bouillon 
 suspension of a pure culture of the diplococcus from an acute case 
 at the Massachusetts General Hospital. The inoculation was made 
 in the afternoon, and the animal was found dead the next morning 
 at ten o'clock, having evidently been dead for several hours. 
 
 Macroscopically nothing could be made out beyond intense in- 
 jection of the meninges of both brain and cord, with slight 
 cloudiness in the meninges of the brain along some of the ves- 
 sels and a slight increase in the meningeal fluid. Microscopically 
 in the brain there was deep injection of the blood vessels and in 
 the meninges an exudation composed principally of pus cells. 
 There was very little fibrin and only small numbers of diplococci 
 in the pus cells. The purulent infiltration extended from the 
 meninges into the brain, following along the vessels, and in the 
 outer layer of the cortex there were scattered pus cells at a dis- 
 tance from the vessels (Plate III., Fig. 3). The tissue of the 
 meninges was swollen, the fibres softened and separated, the 
 cells were swollen, and there seemed to be beginning prolifera- 
 tion, although no nuclear figures were found. No change could be 
 made out in the neuroglia. In the cord the purulent infiltration 
 
78 
 
 of the meninges was not so marked as in the brain, and here only 
 pus cells were found. A section of one of the ganglia of the cord 
 showed that the purulent exudation had extended up to this, and 
 a few pus cells were found among the ganglion cells. The sec- 
 tions stained to show degeneration showed a very slight but 
 perfectly obvious degeneration in both the anterior and posterior 
 nerve roots. In the tissues of the cord a few degenerated and 
 swollen fibres were found. 
 
 The diplococcus was obtained in pure culture both from the 
 brain and cord. The other organs were sterile, and showed no 
 change microscopically beyond slight cloudy swelling of the 
 l^idneys. 
 
 This case is interesting not only in being a positive inocula- 
 tion, but as showing how extensive a pathological condition can 
 be produced in so short a time. An inoculation made at the same 
 time in the spinal canal of a sheep with the same amount of the 
 same culture was negative. 
 
 The following observations were made on the viability of the 
 organism : — 
 
 Oct. 1, 1897. Cultures (7) made from a fluid which had been 
 obtained by lumbar i^uncture and had been kept at room temperature 
 for eight days, were sterile. (This fluid had shown an abundance of 
 organisms, and good cultures had been readily obtained from it pre- 
 viously.) 
 
 Sept. 30, 1897. Cultures on blood serum, twenty-four hours' growth, 
 were dried on sterile paper in sterile Petri dishes and placed (1) in di- 
 rect sun-light, (2) in thermostat at 37.5°, and (3) dark drawer, room 
 temperature, for twenty-four hours respectively. Plants then were 
 made on blood serum with negative result in Nos. 1 and 2, but positive 
 in 3. 
 
 Dried preparations in dark after forty-eight hours and sixty hours 
 produced growth when planted on blood serum; after seventy-two and 
 ninety-six hours, they were sterile. 
 
 1. Action of formaldehyde gas, on smears of oi'ganisms on jDaper in 
 bell jar, exposed for four to seven hours. 
 
 Dilutions of 1-7500, 1-15000, 1-30000, 1-60000, 1-20000, 1-225000 destroy 
 vitality. Plants on bouillon and blood serum sterile. 
 
 Smears of organisms on j^aper exposed to continuous action of formal- 
 dehyde for eighteen houi's, in rooms of 1,200 and 9,000 cubic feet respec- 
 tively, show no growth Avhen planted on blood serum. 
 
 2. Bouillon containing carbolic acid in proportion of 1-100, 1-300, 
 1-500, 1-600, 1-700 and 1-800 prevents development of organisms. 
 
79 
 
 LUMBAR PUNCTURE. 
 
 Lumbar puncture was performed in fifty-five cases, and in 
 some of these several punctures were made. Diplococci were 
 found either on microscopic examination or in cultures in thirty- 
 eight cases. In seventeen of the cases they were absent. The 
 average duration of time from the onset of disease before spinal 
 puncture was made was seven days in the positive cases, and 
 seventeen days in the negative cases. The longest time after 
 onset in which the puncture was positive was twenty-nine days. 
 The negative cases were most numerous in the early part 
 of the epidemic, before we had realized how difficult it was to 
 obtain cultures of the diplococci in all cases. When but few 
 organisms were present they could easily be missed on micro- 
 scopic examination, and even when present in large numbers 
 cultures made in the usual way, by spreading a loop full of the 
 exudation on the surface of the medium, frequently showed no 
 growth. How difficult it was in some cases to obtain cultures 
 is seen from the notes. In case 49, in which cultures were 
 made by pouring 1 cubic centimeter of the fluid obtained over 
 the slanting surface of the culture media, on one tube one 
 colony developed, three on a second and none on four others. 
 In case 68, fifteen tubes were used. On two of the tubes there 
 were two, and on one ten colonies of the organisms. In this 
 case microscopic examination of the fluid showed considerable 
 numbers of diplococci and pus cells. Toward the last of the 
 epidemic there were no negative results when the spinal punct- 
 ure was made early and the tubes inoculated with a large amount 
 of material. The character of the fluid obtained varied greatly. 
 In some cases, even when diplococci were found in it, it was 
 almost clear, showing only a slight turbidity when held before 
 a dark background. In most of the cases where the puncture 
 was made early in the disease the fluid was turbid, in some 
 almost like pus, and in twenty-four hours a large sediment 
 formed in the bottom of the tube. When the fluid was most 
 turbid there was little or no formation of fibrin ; in some cases 
 the fluid became gelatinous on standing, from the abundant for- 
 
80 
 
 mation of fibrin. We have not considered those cases in which 
 no fluid was found, and those in which pure blood was obtained. 
 
 Interesting results were obtained in those cases in which sev- 
 eral spinal punctures were made during the course of the dis- 
 ease. In these cases there was found a diminution in turbidity, 
 often accompanied by absence of organisms in fluids withdrawn 
 last. In one chronic case three punctures were made, one be- 
 fore, one after and one during an exacerbation. In the fluid 
 obtained before and after the exacerbation no diplococci were 
 found. The fluid obtained by the puncture during the exacer- 
 bation was more cloudy, and contained diplococci. Microscopic 
 examination of the fluid agreed perfectly with the character of 
 the lesions in the meninges. In the fluid obtained in early 
 punctures two to three days after the onset almost the only 
 cellular elements were polynuclear leucocytes. Later the large 
 epithelioid cells of the meninges were found among the pus cells, 
 often enclosing them. A small number of lymphoid cells were 
 found in many cases, and were numerous in the chronic cases. 
 The number of diplococci found on microscopic examination 
 varied greatly. In some cases they were so numerous that in 
 every field several cells containing them were found ; in other 
 cases they were found only after prolonged search for them. 
 They were occasionally found in the fluid, their presence here 
 being probably due to the rupture of pus cells containing them 
 in making the preparation. They were only found in the poly- 
 nuclear leucocytes. "We have taken the following description of 
 the technique of the operation from Wentworth's description in 
 Mallory and Wright's " Pathological Technique " : — 
 
 The operation and the subsequent examination of the fluid should 
 be as carefully performed as any other bacteriological investiga- 
 tion, in order to obtain accurate results. The back of the patient 
 and the operator's hands should be made sterile. The needle 
 should be boiled for ten minutes. The patient should lie on the 
 right side, with the knees drawn up, and with the uppermost 
 shoulder so depressed as to present the spinal column to the 
 operator. This position permits the operator to thrust the needle 
 directly forward rather than from side to side. An antitoxin 
 
81 
 
 needle, 4 cm. in length, -with a diameter of 1 mm., is well 
 adapted for infants and young children. A longer needle is 
 necessary for adults and children over ten years of age. 
 
 Aspiration of the fluid is not necessary, but some operators 
 prefer to attach a hypodermic syringe to the needle, to afford 
 a better grasp for the hand. In this case the syringe would 
 have to be detached to allow the fluid to flow. The additional 
 manipulation, and possibly the defective sterilization of the 
 syringe, might impair the subsequent bacteriological examination. 
 
 The puncture is generally made between the third and the 
 fourth lumbar vertebrae, sometimes between the second and third. 
 The thumb of the left hand is pressed between the spinous proc- 
 esses, and the point of the needle is entered about 1 cm. 
 to the right of the median line, and on a level with the thumb 
 nail, and directed slightly upward and inward toward the median 
 line. Care must be exercised to prevent the point of the needle 
 from passing to the left of the median line and striking the 
 bone. At a depth of 3 or 4 cm. in children and 7 or 8 cm. 
 in adults the needle enters the subarachnoid space, and the 
 fluid flows usually by drops. If the point of the needle meets 
 with a bony obstruction, it is advisable to withdraw the needle 
 somewhat, and to thrust again, directing the point of the needle 
 toward the median line, rather than to make lateral movements, 
 with the danger of breaking the needle or causing a haemorrhage. 
 The smallest quantity of blood obscures the macroscopic appear- 
 ance of the fluid by rendering it cloudy. The fluid is allowed 
 to drop into an absolutely clean test-tube which previously has 
 been sterilized by dry heat to 150° C. and stoppered with cotton. 
 The fluid should be allowed to drop into the tube without 
 running down the sides. From 5 to 15 cubic centimeters of 
 fluid is a sufficient quantity for examination." 
 
 No ill effects were seen from spinal punctures. Dr. Williams 
 believes that the withdrawal of the exudation may be of positive 
 benefit to the patient. A note in one case says the patient 
 became very much quieter and slept after the operation. Too 
 much cannot be said of the importance of the procedure in 
 making the diagnosis of the disease. There should always be a 
 
82 
 
 microscopical and bacteriological examination of the fluid obtained, 
 in order to determine what organism is present. If the puncture 
 be made early enough, there need be no difficulty in distinguishing 
 the organisms and the character of the meningitis. Acute 
 meningitis may. be due to a variety of organisms and it is 
 important to know which is present for this has an influence in 
 making the prognosis, and in the future it may be of importance 
 in influencing the treatment. By this means the character of 
 the meningitis in sporadic cases can be established, for there 
 is a great lack of definite information about these cases. 
 
 PATHOLOGICAL ANATOMY. 
 
 In the literature of cerebro-spinal meningitis there are 
 numerous accounts of post-mortem examinations, often with the 
 details of the microscopic examination. These examinations 
 have been made both in acute and chronic cases, and there is 
 considerable uniformity in the descriptions of the lesions. In 
 many cases special features in the pathological anatomy have 
 been most studied and a general application of the results of 
 the study of the pathological lesions to the explanation of 
 symptoms has been attempted. The descriptions of the patho- 
 logical changes in the text-books on medicine and pathology, 
 and those contained in the special treatises on the disease do 
 not seem in general to have been founded on personal obser- 
 vation, but to have been compiled from various sources. Most 
 of these articles, even those recently published, give erroneous 
 ideas of the pathological anatomy, and the diplococcus of 
 "Weichselbaum is rarely mentioned in connection with the 
 pathogenesis. Since the discovery of this organism there has 
 not been any study of the lesions of the disease in their con- 
 nection with the organisms. Certain of the lesions, especially 
 those connected with the ear, have been carefully studied. The 
 study of the eye lesions in the disease have not been so good. 
 
 "We shall make no attempt to give the entire literature of 
 the pathology of the disease, only citing the most important. 
 Mathey"* describes a yellow gelatinous exudation in the mem- 
 
83 
 
 branes of the brain, in a post-mortem examination made on one 
 of the cases of Vieusseanx. Danielson and Mann made post- 
 mortem examinations on five cases. In the first ease, in which 
 the symptoms of the disease were of twenty-two hours' dura- 
 tion, they found only hyperjemia of the meninges. In another 
 post-mortem examination, on a girl in the same family, the 
 disease was of longer duration, and they found a fluid resem- 
 bling pus between the pia and dura, together with intense 
 injection of the vessels. 
 
 The committee appointed by the Massachusetts Medical Society 
 in 1809^^ give the results of eight post-mortem examinations in 
 their report. The lesions they found differed according to the 
 duration of the disease. In those cases dying within twelve 
 hours there was intense congestion of the membranes of the 
 brain ; in the cases of longer duration there was a greenish 
 yellow, purulent exudation. The ventricles were distended and 
 the choroid plexus infiltrated. In one case there was acute 
 pericarditis and pleurisy. 
 
 The lesions were more carefully studied in the French epi- 
 demics from 1840 to 1845. Rollet^'"'' thinks that both from a 
 clinical and pathological point of view the disease can be 
 divided into two categories. In one of these, which he calls 
 eerebro-spinal meningitis, the lesions are confined to the menin- 
 ges. In the other, which he calls encephalo-meningitis, there 
 is an extension into the substance of the brain and cord. 
 These lesions of the tissue of the brain and cord seem to have 
 especially engaged the attention of the French aiithors at this 
 time. They were recognized by Faure Villar,^®' who describes 
 both general and localized softening, and thinks the brain is 
 affected in all cases in which there are symptoms affecting 
 motion. Chauffard^^^ says he has recognized alterations of the 
 cord consisting of foci of softening containing a purulent sub- 
 stance, in his study of the disease in Avignon. He was so 
 impressed with the frequency of these lesions in the cord that 
 he called the epidemic in Avignon " cerebro-spinite." 
 
 Bohmer,^ who investigated an epidemic in Cologne in 1865, 
 gives a very good description of the pathological anatomy. He 
 
84 
 
 describes the exudation as occurring in the sub-arachnoid space, 
 and most abundant over the base of the brain. The ventricles 
 were only slightly dilated, their walls were soft and the fluid 
 in them increased in amount. He was the first to describe the 
 large cells in the exudation, and thinks these ai*e the mother 
 cells for the pus cells which he often found filling them. 
 He found the same large cells in other forms of meningitis 
 than the epidemic, but they were then filled with fat instead of 
 with young cells. In some cases there was considerable fibrin 
 in the exudation. In the substance of the brain and cord 
 there was serous transudation and an increased number of cells 
 in the perivascular lymph spaces, as well as small collections of 
 cells in the brain itself. He never found enlargement of the 
 spleen or any change in the intestinal follicles. 
 
 Klebs^* investigated the pathological lesions in the epidemic 
 in Berlin in 1865. He found no exudation between the dura 
 and arachnoid. He attributed the large amount of exudation 
 found at the base of the brain to the effect of gravity. He 
 found softening and purulent infiltration in the tissue of the 
 brain and fcord and in some cases small blood extravasations in 
 the white matter. Reichman^''^ thinks there is a difference in the 
 pathological lesions between epidemic meningitis and the other 
 forms, the most marked difference being the extensive partici- 
 pation of the meninges of the cord in the process in the 
 epidemic form. 
 
 Probably the best general description of the lesions of the 
 disease is that given by StrlimpeP^ He found purulent 
 exudation in the meninges in cases which macroscopically 
 showed no abnormal condition. He calls special attention to 
 tlie participation of the tissues of the brain and cord in the 
 process. In the brain a small zone immediately beneath the 
 meninges is infiltrated with round cells, and these foci seem to 
 be independent of the vessels. The largest of the areas of 
 cellular infiltration within the brain are around the vessels. 
 There is marked hypersemia of the vessels in the interior of 
 the brain, and hsemorrhages may be found. There are histo- 
 logical changes in the nerves of both brain and cord, consisting 
 
85 
 
 in hypertrophy of the axis cylinders. He thinks that brain 
 abscesses may arise in the course of meningitis, and may be 
 the result of a meningitis which was not recognized. He 
 gives the history of three cases of apparently idiopathic brain 
 abscess which had been preceded by meningitis. 
 
 Reichman gives an account of the lesions in a chronic 
 case of meningitis which lasted from the 5th of June to the 
 14th of August. The pia arachnoid was cloudy, and over 
 the base of the brain it was infiltrated with a firm, yellowish 
 material. The same infiltration extended through the foramen 
 magnum and surrounded the cord as far as the exit of the 
 third cervical nerve. The convolutions of the convexity of 
 the brain were flattened, the ventricles dilated. The brain 
 substance was somewhat oedematous and of peculiar elastic 
 consistency. The pia in places adhered strongly to the surface 
 of the hemispheres, portions of the cortex being torn off in 
 removing it. There was thickening and exudation around all 
 of the cervical nerves. A small portion of the cervical cord 
 appeared to be softened. 
 
 Meschede™ found, in a post-mortem examination on a chronic 
 case of meningitis, characterized by marked remissions in the 
 course of the disease, partly cicatricial thickening and partly 
 exudation in the meninges with transitions between these. 
 
 ClozeP reports the examination of two chronic cases of 
 meningitis, one lasting two and the other three months. No 
 inflammatory exudation was found, but there was considerable 
 thickening of the meninges with dilatation of the lateral ventricles. 
 
 In the six cases of meningitis reported by "Weichselbaum, in 
 which he found the diplococcus intracellularis, there was an acute 
 exudation in the meninges of the brain and cord. 
 
 Hagelstaram^"'^ investigated the histological changes in the spinal 
 cord in eleven cases of epidemic cerebro-spinal meningitis in Hel- 
 singford. He found the changes most common at the edge of the 
 cord about the blood vessels coming from the pia. In this part 
 of the cord there was small cell infiltration and various degrees of 
 degeneration of the nerves. In the central part of the cord there 
 was degeneration in the nerve fibres, though of slighter degree. 
 
86 
 
 TABLE OF POST-MORTEM EXAMINATIONS. 
 
 Num- Sex Duration 
 berof and ; of 
 
 Case. Age. i Sickness. 
 
 Condition of 
 Body. 
 
 Brain. 
 
 Cord. 
 
 F. 14 
 
 M.40 
 
 M.40 
 
 M.49 
 
 M.22 
 
 il.25 
 
 P. 17 
 
 F. 15 
 
 7 days, 
 
 26 days, 
 
 7 days, 
 
 14 days. 
 
 Unknown, 
 found nn- 
 conscions. 
 
 2 days, 
 
 5 days, 
 
 5 days, . 
 
 Well nourished, 1 Weight, 1,095 grams. Overentire Slight exudation, 
 
 abundant adi- surface of pia, over both lateral most marked on 
 
 pose, muscles! convexiiies, thin purulent exuda- posterior surface, 
 pale. I tion and cloudiness. 
 
 Skin pale, ab- j Brain bulging, convolutions flat- Abundant exuda- 
 
 doraen sunken, tened. Over base and cerebel- tlon of same char 
 
 muscles thin lum, extending up over convexi- acter as in brain, 
 
 and pale. ties, a dense fibrino-purulent particularly 
 
 exudation. This extended down- marked on poste- 
 
 wards, filling the foramen mag- rior surface of 
 
 num. Lateral ventricals dilated, i dorsal cord. 
 The ependyma softened. Exu- I 
 dation in fourth ventrical. 
 
 Good muscular ' Thick fibrino-purulent exudation Exudation of same 
 development. over base; on upper surface ex- character on pos- 
 
 Over abdomen 
 small hyper- 
 aemic areas. 
 Decubitus over 
 sacrum. 
 
 Good nutrition, 
 pale. 
 
 Blight icterus, 
 
 tends over frontal lobes. 
 
 terior surface. 
 
 Good nutrition, 
 rigor mortis. 
 
 Post-mortem de- 
 compo sit ion 
 over abdomen. 
 
 Well nourished, 
 marked rigor 
 mortis. 
 
 Softening in left side of brain in- Exudation along 
 volving fissure of Rolando. Over en tire posterior 
 the base, extensive exudation, in- i surface, 
 volving cranial nerves. 
 
 Over convexity and base thick Could not be ex- 
 fibrino-purulent exudation. amined. 
 
 Very slight exudation over convex- ' Could not be ex- 
 ity occurring as faint yellowish amined. 
 streaks and cloudiness. At base i 
 and in ventricals slight amount 
 of cloudy fluid. 
 
 Tough fibrino-purulent exudation Could not be ex- 
 over base extendingup over both amined. 
 lateral convexities. 
 
 Convexities of brain showed yel- ' Exudation abun- 
 lowishexudationalongthecourse ' dant on posterior 
 of vessels. Slight exudation at surface, extend- 
 base, foci of softening and hem- | ing around nerves 
 orrhage in white matter. j of cauda equina. 
 
 3 days, . Well nourished. Along fissure of Sylvius on both ! Slight exudation 
 sides a slight yellowish infiltra- along posterior 
 tion along the vessels; at the surface of lumbar 
 base the exudation only about cord, 
 optic commissure. 
 
87 
 
 TABLE OF POST-MORTEM EXAMINATIONS. 
 
 Heart. 
 
 Lungs. 
 
 Liver. 
 
 Spleen. 
 
 Kidneys. 
 
 Cultures and Remarks. 
 
 
 Myocardi- 
 um rather 
 Boft.slight 
 a r t e r i 
 sclerosis. 
 
 Slight conges 
 lion and oede- 
 ma. 
 
 Tissue 
 opaque. 
 
 Weight, 250 
 grams; on 
 section ho- 
 mogeneous. 
 Malpighian 
 bodies not 
 visible. 
 
 Weight, 360 
 grams; cap- 
 sule easily 
 stripped, 
 opaque cor- 
 tex, pale. 
 
 Liver, spleen and heart 
 sterile. Kidney colon. 
 Brain cocci, arranged as 
 diplococci. Single or- 
 ganisms flattened. 
 
 1 
 
 Small, nor- 
 mal. 
 
 Intense conges- 
 tion posteri- 
 orly in both. 
 
 Congested, . 
 
 No rmal i n 
 size and ap- 
 pearan ce; 
 weight, 75 
 grams. 
 
 Congested, . 
 
 All organs sterile; a few 
 diplococci found in 
 sections. 
 
 2 
 
 Normal, 
 
 Lower lobe of 
 right hyper- 
 jemic, with 
 areas of bron- 
 cho-pneumo- 
 nia, some of 
 which coa- 
 lesce. 
 
 Pale, . 
 
 Rather soft ; 
 weight, 307 
 grams. 
 
 Pale, . 
 
 Lungs, multiple organ- 
 isms, chiefly staphylo- 
 cocci. Brain sterile, 
 diplococci found on sec- 
 tions. 
 
 3 
 
 Normal, . 
 
 Foci of bron- 
 cho-pneumo- 
 nia in lower 
 lobes of both. 
 
 Pale, . 
 
 Slightly en- 
 1 a r g e d ; 
 weight, 170 
 grams. 
 
 Normal, 
 
 Pneumococci in lungs, 
 spleen, kidney and 
 heart; in brain diplo- 
 cocci. 
 
 4 
 
 Weight, 
 500 gram 8. 
 Fatty de- 
 generation 
 of myo- 
 cardium. 
 Slight ar- 
 terio-scle- 
 rosis. 
 
 Beginning red 
 pneumonic 
 consolidation 
 upper lobe of 
 left, lower of 
 right. 
 
 Soft, pale, . 
 
 Soft, large, 
 adherent j 
 weight, 300 
 grams. 
 
 Pale, . . 
 
 Pneumococci in lungs. 
 Heart, liver, sterile. 
 Brain, diplococci. 
 
 5 
 
 Slightacute 
 pericardi- 
 tis, ecchy- 
 moses in 
 per icar- 
 dium. 
 
 Congestion, 
 
 Pale, . 
 
 Enlarged, 
 soft; weight, 
 302 grams. 
 
 Enl arged ; 
 hyperaemic 
 ecchymoses 
 in cortex; 
 markings 
 obscure. 
 
 In brain diplococci; 
 other organs sterile. 
 
 6 
 
 Myocardi- 
 um soft. 
 
 Broncho pneu- 
 monia of both. 
 Lax pneumo- 
 nialowerlobe 
 of right. 
 
 Pale, cloudy. 
 
 Slightly en- 
 larged and 
 soft; weight, 
 135 grams. 
 
 Pale; opaque, 
 
 Lungs, abundant staphy- 
 1 c c c i , few strepto- 
 cocci. Liver, strepto- 
 cocci ; brain, diplococci. 
 
 7 
 
 Normal, . 
 
 Muco-pus in 
 bronchi. 
 
 Rather 
 opaquewith 
 some injec- 
 tion in cen- 
 tres of lob- 
 ules. 
 
 Somewhat en- 
 larged; paler 
 foUicles dis- 
 tinct; weight, 
 195 grams. 
 
 Normal, 
 
 Liver, spleen and kid- 
 neys sterile. Brain and 
 cord, profuse growth of 
 diplococcus. Colonies 
 of streptococci also 
 found. Only diplococci 
 found in sections. 
 
 8 
 
 Normal, . 
 
 Oongestion 
 and oedema in 
 lower lobes. 
 
 Moderately 
 congested. 
 
 Enlarged ; 
 weight, 215; 
 follicles nu- 
 merous. 
 
 Injected ; 
 cloudy. 
 
 Heart, liver, kidney and 
 b rain sterile. Abun- 
 dant diplococci found 
 in sections. 
 
 9 
 
88 
 
 TaUe of Post-mortem Examinations — Continued. 
 
 Num- 
 berof 
 Case. 
 
 Sex 
 aud 
 Age. 
 
 43 
 
 M.IQ 
 
 44 
 
 M.50 
 
 S3 
 
 M.27 
 
 53 
 
 M.24 
 
 56 
 
 F. 3| 
 
 57 
 
 M.24 
 
 79 
 
 M.oS 
 
 59 
 
 M.29 
 
 66 
 
 F. 28 
 
 71 
 
 M. 2 
 
 Duration 
 
 of 
 SickncBB. 
 
 Condition of 
 Body. 
 
 Cord. 
 
 3 days, 
 
 5 days, 
 
 2 days. 
 
 9 days, 
 
 5 days. 
 
 2 days, 
 
 30 days. 
 
 6 days. 
 
 6 days, . 
 
 29 days, 
 
 Well nourished, 
 rigor mortis. 
 
 Well nourished, 
 good muscular 
 development. 
 
 Well nourished, 
 rigor. 
 
 Well nourished. 
 Herpes about 
 mouth and chin. 
 
 Well nourished. 
 
 Well nourished, 
 slight rigor. 
 
 Good muscular 
 developmen t, 
 spare. 
 
 Well nourished. 
 
 Well nourished ; 
 over various 
 parts of the 
 body h e m or- 
 rhages, some 
 ■with whitish 
 centres. 
 
 Great emacia- 
 tion. 
 
 Vessels of meninges deeply in- 
 jected. Faint yellowish streaks 
 along vessels and yellowish 
 cloudy fluid in meshes. In white 
 substance of both frontal lobes 
 ill-defined, grayish, softened 
 areas. Ecchymoses in white 
 matter generally. 
 
 Abundant gelatinous fibrino-pur- 
 ulent exudation, more abundant 
 on right side and over base. All 
 the cranial nerves involved in 
 the exudation. 
 
 Pi a over convexity and base infil- 
 trated with yellowish exudation. 
 In ventricals slight exudation 
 with fibrinous flocculi. 
 
 Over convexity faint yellowish 
 exudation along blood vessels. 
 Over the base an abundant fi- 
 brino-purulent exudation; ven- 
 tricals dilated, contain exudation. 
 Exudation along cranial nerves. 
 
 Extensive exudation over base, 
 less over cortex. Small ecchy- 
 mosis in corpus striatum and 
 optic thalamus. In white sub- 
 stance ecchymoses. 
 
 A slight, grayish-yellow exudation 
 over the convexities, along blood 
 vessels and in the sulci. Slight 
 over base; more cloudiness than 
 visible exudation. 
 
 Thickening of pia over convexity, 
 with small, opaque yellowish 
 foci in the meshes. Fibrinous 
 and in part organized exudation 
 over base and in ventricals, in- 
 duration of brain. 
 
 Similar exudation 
 in cord. 
 
 Could not.be examined, 
 
 Great amount of exudation over 
 entire surface of brain, particu- 
 larly over base. Injection of ves- 
 sels, exudation in ventricals, 
 softening of ependyma. Exuda- 
 tion around cranial nerves. 
 
 Pia thickened, cloudy; yellow foci 
 in meshes; thick exudation at 
 base and over cerebellum. Optic 
 commissure covered by thick ex- 
 udation. 
 
 Similar exudation 
 in cord, involving 
 all the nerves of 
 the Cauda equina. 
 
 Exudation well 
 marked along 
 posterior surface 
 of cord. 
 
 Abundant exuda- 
 tion along cord. 
 
 Abundant exuda- 
 tion along cord. 
 
 Very slight exuda- 
 tion along cord 
 posteriorly and 
 general clo ud i- 
 ness. 
 
 Thickening of 
 meninges of cord. 
 
 Abundant exuda- 
 tion along cord, 
 greatest amount 
 in lumbar region. 
 
 Exudation along 
 entire cord, par- 
 ticularly poste- 
 rior surface. 
 
 Thickening of me- 
 ninges; accumu- 
 lations of thick, 
 yellowish masses 
 posteriorly. 
 
89 
 
 Table of Post-mortem Examinations — Continued. 
 
 Heart. 
 
 Lungs. Liver. 
 
 Spleen. 
 
 Kidneys. 
 
 Cultures and Remarks. 
 
 
 Xormal, . 
 
 In lower lobe Cloudy, 
 
 Normal; 
 
 Cloudy; pale. 
 
 Cultures from lung and 
 
 1 
 
 
 of right lung 
 
 weight, 120 
 
 
 brain diplococci. Dip- 
 
 
 
 i 1 1-d e ti n e d 
 
 grams. 
 
 
 lococci on sections of 
 
 
 
 areas of con- 
 
 
 
 
 lung and brain. 
 
 
 
 solidatiou, 
 
 
 
 
 
 
 
 size of pea to 
 
 
 
 
 
 
 
 that of bean. 
 
 
 
 
 
 
 
 Diplococcus 
 
 
 
 
 
 
 
 pneumonia. 
 
 
 
 
 
 
 Normal, . 
 
 Ecchymoses Normal, 
 
 Soft; weight. 
 
 Cortex; 
 
 Heart, spleen, liver and 
 
 2 
 
 
 over pleura. 
 
 75 grams. 
 
 cloudy. 
 
 kidneys sterile. Diplo- 
 
 
 
 Congestion , 
 
 
 
 cocci in cultures from 
 
 
 
 posteriorly. 
 
 
 
 
 cord. 
 
 
 
 B r n c h o 
 
 
 
 
 
 
 
 pneumonia. 
 
 
 
 
 
 
 
 Bronchiecta- 
 
 
 
 
 
 
 
 tic cavities. 
 
 
 
 
 
 
 Normal, 
 
 Hyperaemic, . 
 
 Pale, . 
 
 No r m a 1 ; 
 weight, 120 
 
 grams. 
 
 Normal, 
 
 All cultures from brain 
 show pure diplococci. 
 Mixture of other organ- 
 isms in cord. All the 
 other organs sterile. 
 
 3 
 
 Very slight 
 
 Fibrous thick- 
 
 Smallcentres 
 
 Weight, 150 
 
 Injected, 
 
 Cultures from brain gave 
 
 4 
 
 fibrinous 
 
 ening at api- of lobules 
 
 grams. On 
 
 
 colon and other con- 
 
 
 exadation 
 
 ces. 
 
 injected. 
 
 section, soft 
 
 
 taminating organisms. 
 
 
 over peri- 
 
 
 
 and flabby; 
 
 
 Cord gave on four tubes 
 
 
 cardium. 
 
 
 
 follicles vis- 
 ible. 
 
 
 pure cultures of diplo- 
 coccus. 
 
 
 Normal, . 
 
 Foci of con- 
 solidation. 
 Diplococcus 
 pneumonia. 
 
 Pale, . 
 
 Weight, 29 
 grams; nor- 
 mal. 
 
 Normal, 
 
 In brain and cord pure 
 cultures of the diplo- 
 coccus. Diplococci in 
 lungs. Cultures from 
 upper nasal cavity 
 showed diplococci. 
 
 5 
 
 Normal, . 
 
 Old tubercu- 
 
 Slightly en- 
 
 Enlarged; 
 
 Injected, 
 
 Heart, liver, spleen and 
 
 6 
 
 
 lous nodule. larged. 
 
 firm on pren- 
 
 
 kidney all sterile. In 
 
 
 
 Injection. 
 
 sure; weight, 
 210 grams. 
 
 
 brain and cord a few 
 colonies of diplococcus. 
 
 
 Normal, 
 
 CEdematous, . Cloudy, lob- 
 
 Weight, 145 
 
 Normal, 
 
 All cultures negative save 
 
 7 
 
 
 ules indis- 
 
 grams ; folli- 
 
 
 a few streptococci in 
 
 
 
 tinct. 
 
 cles visible. 
 
 
 liver and kidneys. 
 
 
 
 
 
 
 
 Brain and cord sterile. 
 
 
 
 
 
 
 
 Evidently old case, — 
 
 
 
 
 
 
 
 older than history given. 
 
 
 Normal, . 
 
 Foci of consol- 
 
 Normal, 
 
 Weight, 85 
 
 Normal, 
 
 Cultures from cord show 
 
 8 
 
 
 idation with 
 
 grams; firm. 
 
 
 diplococci. Lungs 
 
 
 
 necrosis and 
 
 
 follicles vis- 
 
 
 abundant pneumococci 
 
 
 
 breaking 
 
 
 ible. 
 
 
 and other organisms. 
 
 
 
 down. 
 
 
 
 
 Other organs sterile. 
 
 
 Normal, 
 
 Injected oedem- 
 
 Large i n - 
 
 Enlarged; 
 
 Rather large. 
 
 Lung staphylococcus. 
 
 9 
 
 
 atous. 
 
 jected lob- 
 
 weight, 410 
 
 vessels in- 
 
 aureus and pneumo- 
 
 
 
 
 ules, very 
 
 grams; folli- 
 
 jected; nor- 
 
 ooccus. Liver, spleen, 
 
 
 
 
 distinct cel- 
 
 cles distinct. 
 
 m al mark- 
 
 kidney and heart ster- 
 
 
 
 
 lular intil- 
 
 
 ings. 
 
 ile. Brain and cord 
 
 
 
 
 t ration 
 
 
 
 diplococcus. 
 
 
 
 
 iu portal 
 
 
 
 
 
 
 
 spaces. 
 
 
 
 
 
 Normal, . 
 
 Congestion 
 
 Firm and 
 
 Small, smooth, 
 
 Large ; pale ; 
 
 In this case, spinal punct- 
 
 10 
 
 
 and broncho 
 
 congested. 
 
 firm; weight. 
 
 cortex swol- 
 
 ure at Children's Hos- 
 
 
 
 pneumonia. 
 
 
 25 grams. 
 
 len; con- 
 tain ecchy 
 moses. 
 
 pital gave diplococci. 
 Child acquired diphthe- 
 ria with acute glomenlo 
 nephritis. Cultures at 
 autopsy showed diph- 
 theria bacilli. 
 
 
90 
 
 Table of Post-mortem Examinations — Continued. 
 
 Num- 
 ber of 
 Case. 
 
 Sex 
 and 
 Age. 
 
 Duration 
 
 of 
 Sickness. 
 
 Condition of 
 Body. 
 
 Brain. 
 
 Cord. 
 
 F. 10 
 
 5 days, 
 
 2 days, . 
 
 "Well nourished. 
 
 Muscular; well 
 nourished ; 
 rigor mortis. 
 
 M.25 
 
 5 days. 
 
 Fairly well nour- 
 ished. 
 
 M 37 
 
 M.31 
 
 11.52 
 
 10 days, 
 
 37 days, 
 
 30 days, 
 
 9 days. 
 
 14 days. 
 
 Well nourished, 
 
 Emaciated, 
 
 Emaciated, 
 
 Well nourished, 
 
 Well nourished; 
 marked rigor. 
 
 23 days, 
 
 Well nourished; 
 marked rigor. 
 
 Abundant exudation, yellowish 
 soft sero-purulent in places; 
 serous over lateral convexities 
 and base. Cranial nerves in- 
 volved in exudation. 
 
 General serous exudation beneath 
 pla with lines of deep, thick yel- 
 low exudation along vessels at 
 base ; abundant exudation around 
 nerves. 
 
 Abundant exudation over base 
 and cerebellum, extending over 
 cortex; exudation along nerves; 
 exudation in ventricals. 
 
 Not examined. 
 
 Pia thickened ; frontal lobes ad- 
 herent; red thrombus in basilar 
 artery with softening of pons. 
 
 Pia thickened; small amount of 
 exudation along vessels. 
 
 Yellowish purulent streaks along 
 vessels over lateral convexities; 
 exudation at base not abundant. 
 
 Abundant purulent exudation ex- 
 tending along cranial nerves at 
 base; exudation in ventricals. 
 
 Pia oedematous, thickened; small 
 amount of exudation, except here 
 and there in masses; most abun- 
 dant in base. 
 
 Posterior surface 
 of cord hidden by 
 the abundant, 
 thick, yellowish 
 exudation. 
 
 Vessels of menin- 
 ges deeply in- 
 jected, with only 
 slight exudation 
 posteriorly. 
 
 Abundant exuda- 
 tion. 
 
 Abundant exuda- 
 tion on posterior 
 surface of lower 
 dorsal and lum- 
 bar. 
 
 Thickening of me- 
 nin ges , with 
 slight exudation. 
 
 Cloudy fluid in 
 canal; slight exu- 
 dation, thicken- 
 ing. 
 
 Thick exudation 
 posteriorly. 
 
 Thick exudation, 
 most abundant in 
 dorsal and lum- 
 bar. 
 
 Thick exudation 
 over posterior 
 surface of cervi- 
 cal and dorsal. 
 
91 
 
 Table of Post-mortem Examinations — Continued. 
 
 Heart. 
 
 Lungs. 
 
 Liver. 
 
 Spleen. 
 
 Kidneys. 
 
 Cultures and Remarks. 
 
 
 Normal, . 
 
 Old fibrous ad- 
 
 Normal, 
 
 Normal; 
 
 Vessels i n - 
 
 Pure cultures from brain 
 
 1 
 
 
 hesions. 
 
 
 weight, .55 
 grams. 
 
 jected ; cor- 
 tex opaque. 
 
 and cord of diplococcus. 
 
 
 X^ormal, . 
 
 Id lower lobe 
 
 Large, . 
 
 Capsule 
 
 Firm; nor- 
 
 CultTires of brain sterile. 
 
 2 
 
 
 of left lung a 
 
 
 wrin k led; 
 
 mal mark- 
 
 Diplococci found on 
 
 
 
 large area of 
 
 
 follicles visi- 
 
 ings. 
 
 cover slips and sections 
 
 
 
 conBolidation 
 
 
 ble; weight, 
 
 
 of brain and lungs. 
 
 
 
 wilh puru- 
 
 
 175 grams. 
 
 
 
 
 
 lent infiltra- 
 
 
 
 
 
 
 
 tion and par- 
 
 
 
 
 
 
 
 tial breaking 
 
 
 
 
 
 
 
 down. Diplo- 
 
 
 
 
 
 
 
 C0CCU8 pneu- 
 
 
 
 
 
 
 
 monia. 
 
 
 
 
 
 
 Normal, . 
 
 In both lungs 
 
 Normal, 
 
 Small; weight, 
 
 Cortex more 
 
 Cultures from brain and 
 
 3 
 
 
 foci of con- 
 
 
 95 grams. 
 
 opaque; 
 
 cord pure diplococci. 
 
 
 
 solidation 
 
 
 
 m arkings 
 
 Diplococci found in lung 
 
 
 
 from 1 mm. 
 
 
 
 normal. 
 
 with other organisms. 
 
 
 
 to 3 cm. in di- 
 
 
 
 
 Other organs sterile. 
 
 
 
 ameter, red- 
 
 
 
 
 
 
 
 dish-gray in 
 
 
 
 
 
 
 
 color, sur- 
 
 
 
 
 
 
 
 rounded b y 
 
 
 
 
 
 
 
 yellowish 
 
 
 
 
 
 
 
 zone. Diplo- 
 
 
 
 
 
 
 
 coccus pneu- 
 
 
 
 
 
 
 
 monia. 
 
 
 
 
 
 
 Normal, J . 
 
 Complete red- 
 
 Congested, . 
 
 Small; weight. 
 
 Opaque; 
 
 Cultures from lung show 
 
 4 
 
 
 dish - gray 
 
 
 80 grams. 
 
 pale; mark- 
 
 pneumococci; no cult- 
 
 
 
 consolidation 
 
 
 
 ings nor- 
 
 ures from cord. Micro- 
 
 
 
 of lower lobe; 
 
 
 
 mal. 
 
 scope shows diplococci 
 
 
 
 acute pleu- 
 
 
 
 
 in cord and in abscess 
 
 
 
 risy ; partial 
 
 
 
 
 in seminal vesicles, in 
 
 
 
 consolidation 
 
 
 
 
 latter with pneumo- 
 
 
 
 of upper lobe. 
 
 
 
 
 cocci. 
 
 
 Normal, . 
 
 Congested, 
 
 Normal, 
 
 Small ; weight, 
 105 grams. 
 
 Normal, 
 
 No diplococci found in 
 cultures, nor on micro- 
 scopic examination. 
 Condition one of 
 chronic meningitis with 
 abscess following. 
 
 5 
 
 Normal, . 
 
 CEdema, . 
 
 Normal, 
 
 Small; weight, 
 90 grams. 
 
 Normal, 
 
 Cultures from brain, few 
 diplococci. 
 
 6 
 
 Normal, . 
 
 Congested, 
 
 Normal, 
 
 Small; weight, 
 102 grams. 
 
 Normal, 
 
 Autopsy 3 days after 
 death. Cultures over- 
 grown with contami- 
 nating organisms. Dip- 
 
 1 
 
 
 1 
 
 
 
 lococci found in sections 
 
 
 
 
 
 
 
 of the cord. 
 
 
 Normal, . 
 
 Foci of consol- 
 idation ; yel- 
 1 wi sh cen- 
 tres with hy- 
 peraemic pe- 
 riphery up to 
 3 cm. in diam- 
 ter. D i p 1 - 
 coccus pneu- 
 monia. 
 
 Normal, 
 
 Slightly en- 
 larged; firm; 
 weight, 170 
 grams. 
 
 Congested, . 
 
 Brain, 10 cultures, 2 show 
 each 1 colony of diplo- 
 coccus. Cord, 6 cult- 
 ures, 1 shows 1 colony 
 of diplococcus. Lung, 
 diplococcus, strepto- 
 coccus, pneumococcus 
 and staphylococcus; 
 sections only diplococ- 
 cus. 
 
 8 
 
 Normal, . 
 
 Intense injec- 
 tion with foci 
 of consolida- 
 tion. Biplo- 
 coccus pneu- 
 monia. 
 
 Normal, 
 
 Soft; follicles 
 visible; 
 weight, 85 
 grams. 
 
 Normal, 
 
 Brain, 10 cultures, 1 tube 
 shows 2 colonies of dip- 
 lococci. Cord, 9 cult- 
 ures, 1 tube shows 1 
 colony of diplococcus. 
 Heart, liver, spleen and 
 kidneys sterile. Lung, 
 
 9 
 
 
 
 
 
 
 pneumococci and Fried- 
 
 
 
 
 
 
 lander's bacillus. 
 
92 
 
 Table of Post-mortem Examinations — Concluded. 
 
 Num- ' Sex j Duration 
 berof and of 
 
 Case. Age. Sickness. 
 
 Condition of 
 Body. 
 
 Cord. 
 
 110 
 
 F. 3J 
 
 M.35 
 
 M.31 
 
 F. 21 
 
 m:.43 
 
 M.32 
 
 m:.25 
 
 3 days, 
 
 3 days, 
 
 74 days, . 
 
 35 days. 
 
 Unknown, 
 estimated 
 at 7 to 10 
 days. 
 
 26 days, 
 
 Well nourished, 1 Over both lateral convexities foci 
 of yellowiBh purulent exudation 
 along vessels; abundant exuda- 
 tion at base. 
 
 Good muscular 
 development. 
 
 Greatly emaci- 
 ated. 
 
 Emaciated, 
 
 Slight muscular 
 development; 
 spare. 
 
 Emaciated, 
 
 Slight muscular 
 deve lopment; 
 poor nutrition. 
 
 Exudation abundant; intense hy- 
 persemia of brain; foci of hem- 
 orrhage in white matter; abun- 
 dant exudation at base along 
 nerves. 
 
 Firm, organized exudation at base : 
 thickening of meninges; small 
 opaque foci in meninges. 
 
 Entire pia cloudy and thickened; 
 over base firm yellowish exuda- 
 tion with more opaque foci. 
 
 Over entire anterior surface of 
 brain, extending down over lat- 
 eral surfaces and over occipital 
 lobe on left side, abundant yel- 
 lowish, gelatinous exudation; 
 large amount over base and cere- 
 bellum. 
 
 There are tubercles along vessels 
 in Sylvian fissure and elsewhere ; 
 tubercles old and caseous. Fi- 
 brino-purulent exudation over 
 base with few tubercles; puru- 
 lent exudation along cranial 
 nerves, extending to gasserian 
 ganglion, which was infiltrated 
 with pus and granulation tissue. 
 
 Firm, yellowish exudation along 
 vessels of convexity, best marked 
 laterally ; abundant exudation at 
 base. 
 
 Cervical cord free; 
 abundant exuda- 
 tion over lower 
 dorsal and lum- 
 bar. 
 
 Along posterior 
 cord ; bestmarked 
 in lumbar and 
 dorsal; ganglia 
 swollen. 
 
 Thickening of me- 
 n in ges , with 
 opaque foci. 
 
 Firm exudation 
 along posterior 
 surface. 
 
 Not examined. 
 
 Pia of cord cloudy 
 and oedemntous; 
 slight exudation; 
 no tubercles. 
 
 Not examined. 
 
93 
 
 Table of Post-mortem Examinations — Concluded. 
 
 Heart. 
 
 Lungs. 
 
 Liver. 
 
 Spleen. 
 
 Kidneys. 
 
 Cultures and Remarks. 
 
 
 Normal, . 
 
 Congestion and 
 
 Normal, 
 
 Small; weight. 
 
 Normal, 
 
 Cultures from brain and 
 
 1 
 
 
 asdema. 
 
 
 50 grams. 
 
 
 cord show abundant 
 pure cultures of diplo- 
 cocci. 
 
 
 Normal, . 
 
 Large area of 
 
 Normal, 
 
 Slightly e n - 
 
 Fale, . 
 
 Five cultures from lung 
 
 2 
 
 
 consolida- 
 
 
 larged; firm ; 
 
 
 all show abundant 
 
 
 
 tion ; cedema 
 
 
 weight, 200 
 
 
 growth of diplococcus. 
 
 
 
 and hemor- 
 
 
 grams. 
 
 
 Diplococci in cultures 
 
 
 
 rhage at pe- 
 
 
 
 
 from brain and cord. 
 
 
 
 riphery, with 
 
 
 
 
 
 
 
 confluent 
 
 
 
 
 
 
 
 areas of puru- 
 
 
 
 
 
 
 
 lent iutiltra- 
 
 
 
 
 
 
 
 tion. Diplo- 
 
 
 
 
 
 
 
 coccus pueu- 
 
 
 
 
 
 
 
 monia. 
 
 
 
 
 
 
 Normal, . 
 
 Foci of consol- 
 
 Firm, lobules 
 
 Normal; 
 
 Congestion 
 
 No cultures made. Spinal 
 
 3 
 
 
 idation with 
 
 prominent; 
 
 w e i g h t , 60 
 
 of pyra- 
 
 puncture April 8 gave 
 
 
 
 softened cen- 
 
 increase of 
 
 grams. 
 
 mids. 
 
 diplococci. Large num- 
 
 
 
 tres. Diplo- 
 
 connective 
 
 
 
 bers of diplococci found 
 
 
 
 coccus pneu- 
 
 tissue and 
 
 
 
 in sections of lungs; 
 
 
 
 monia. 
 
 foci of in- 
 fi 1 1 r a t i n 
 around por- 
 tal spaces. 
 
 
 
 none found in sections 
 of brain and cord. 
 
 
 Normal, . 
 
 Congestion 
 
 Normal, 
 
 Normal; 
 
 Normal, 
 
 Diplococci found in cult- 
 
 4 
 
 
 and broncho- 
 
 
 weight, 70 
 
 
 ures and in sections of 
 
 
 
 pneumonia. 
 
 
 grams. 
 
 
 brain and cord. 
 
 
 Normal, . 
 
 Congestion 
 
 Normal, 
 
 Firm; slight- 
 
 Normal, 
 
 Cultures and cover slips 
 
 5 
 
 
 and oedema. 
 
 
 ly enlarged; 
 weight, 130 
 grams. 
 
 
 from brain showed pure 
 diplococci. Other or- 
 gans not examined. 
 Diplococci found in sec- 
 tions. 
 
 
 Normal, 
 
 Conglomerate 
 
 Pew tuber- 
 
 Small; weight, 
 
 Congested, . 
 
 From lungs pneuraococ- 
 
 6 
 
 
 tubercles and 
 
 cles present. 
 
 65 grams. 
 
 
 cus; cultures of brain 
 
 
 
 tuberculous 
 
 
 
 
 sterile. This case was 
 
 
 
 broncho-pneu- 
 
 
 
 
 considered one of mixed 
 
 
 
 monia. 
 
 
 
 
 infection of meningitis 
 with tuberculosis. In 
 considering it epidemic 
 meningitis, the main 
 points were the charac- 
 ter of the exudation and 
 the infiltration extend- 
 ing along the nerves. 
 
 
 Normal, . 
 
 Congested, 
 
 Congested, . 
 
 Normal; 
 weight, 85 
 grams. 
 
 Congested, . 
 
 The body had been kept 
 5 days before autopsy. 
 Cultures were unsntls- 
 factory, being over- 
 grown with various or- 
 ganisms. Diplococci 
 found in pus cells in 
 the ventricals. 
 
 7 
 
94 
 
 Flexner and Barker, in two cases investigated by them in the 
 epidemic in Lanaconing, Md., described the large cells in the men- 
 inges and small foci of cellular-infiltration in the brain and cord. 
 
 When we review these brief extracts, we find that in the most 
 acute cases there is found intense hypersemic of the meninges, 
 with purulent infiltration visible only on microscopic examination. 
 In cases of longer duration fibrino-purulent exudation is present 
 most abundantly over the base. In chronic cases fibrous thicken- 
 ing of the meninges is found with or without exudation. The 
 exudation contains pus cells, fibrin and large cells of unknown 
 origin. Changes in the tissue of the brain and cord, consisting 
 of cellular infiltration, of abscesses or foci, of softening, have 
 been described. 
 
 The preceding table (pp. 86-93) gives the results of thirty- 
 five post-mortem examinations. In most cases the examina- 
 tions were made a short while after death. When the period 
 was longer most of the bodies had been kept preceding the ex- 
 amination in a room cooled by a freezing process to 32° to 35° F. 
 We have made post-mortem examinations on bodies which have 
 been kept at this temperature four days and found the tissues 
 almost perfectly preserved ; the nuclear figures showed nearly as 
 well as in fresh tissues. In a few of the bodies which were kept 
 at ordinary temperatures the tissues were not so good and the 
 cultures unsatisfactory. At every autopsy where it was possible 
 cultures were made from the brain, cord, heart, lungs, liver, 
 kidneys and spleen. For general histological purposes portions of 
 the brain, cord and other organs were hardened both in Zenker's 
 fluid and in alcohol. For the study of degenerated nerve fibres 
 small pieces of nervous tissues were hardened in Miiller's fluid 
 or in formaldehyde followed by Miiller's fluid, before staining in 
 Marchi's solution. For the fixation of ganglion cells strong 
 alcohol was employed. 
 
 For the study of the distribution of the diplococcus and of the 
 histological changes in the tissues eosin followed by Unna's alka- 
 line methylene blue solution was found to be by all odds the most 
 satisfactory stain. The advantage of Unna's solution, which is 
 considerably more alkaline than Loeffler's, is that it stains bacteria 
 
95 
 
 and nuclei in tissues hardened in Zenker's fluid, which gives a 
 much more perfect fixation of tissue elements than alcohol. 
 Imbedding in paraffin was used almost exclusively. The corro- 
 sive crystals were removed from the sections after cutting, not 
 from the blocks of tissue, so as to avoid prolonged treatment 
 with iodine, which acts injuriously. 
 
 The steps in staining are as follows : — 
 
 1. Stain paraffin sections in a five per cent, to saturated aqueous solu- 
 tion of eosin, twenty minutes to one hour. 
 2 Wash oif in water. 
 
 3. Stain in Unna's alkaline methylent blue solution (methylene blue, 
 1 ; cai'bonate of potassium, 1 ; water, 100) , one part, diluted with nine 
 parts of water, for one to two hours. 
 
 4. Wash in water. 
 
 5. Decolorize in ninety-six per cent alcohol followed by absolute 
 alcohol, until the tissue is well differentiated. 
 
 6. Xylol. 
 
 7. Balsam. 
 
 Bacteria and organisms stain a sharp, clear blue ; red blood 
 globules, protoplasm, fibrin and intercellular substance stain of 
 varying shades of pink and lilac. 
 
 A little practice is required before good results can always be 
 obtained. It is important not to carry the decolorization with 
 the alcohol too far. 
 
 Nissl's stain for ganglion cells and Marchi's stain for fatty, 
 degenerated nerve fibres require no special mention. 
 
 In the cases on which post-mortem examinations were made 
 the duration of illness varied from two days up to seventy-four 
 days. The average duration, leaving out of consideration the 
 very chronic case of seventy-four days, was eleven and one-third 
 days, this being taken, not from the stay of the patient in the 
 hospital, but from the initial symptoms of the disease. The 
 duration is really much less than this for the average number 
 of cases, being greatly increased by seven cases, which were 
 twenty-three, thirty-two, twenty-three, thirty-seven, twenty-nine, 
 thirty and twenty-six days respectively. Leaving out these, and 
 the seventy-four-day case, the average duration is six and one- 
 half days. This can be taken as the average of the acute 
 
96 
 
 cases, while twenty-eight and one-half days can be considered 
 as the average of the chronic cases, here again leaving out the 
 exceptional case of seventy-four days. 
 
 The condition of the body varied in the acute and chronic 
 cases. In the acute cases the body was generally well nourished, 
 and in some there was an abundant development of adipose 
 tissue. The chronic cases presented an almost characteristic 
 appearance ; the body was greatly emaciated, the skin was pale, 
 the abdomen sunken, the muscles thin and pale. In one case 
 of unknown duration there was slight icterus. The presence or 
 absence of rigor mortis was not always noted. When it was noted 
 it was generally very well marked in the acute cases and in 
 most of the chronic. In one case, which was of but six days' 
 duration, there was a decubitus over sacrum. Evidence of herpes 
 and other skin lesions were not as apparent at post-mortem 
 examinations as they were during life. In one case there was a 
 perfectly characteristic hsemorrhagic eruption over various parts 
 of the body. There are few observations with regard to the con- 
 dition of the muscles. They were generally pale and cloudy. 
 
 Lesions of the Nervous System. 
 
 Macroscopic lesions. 
 The lesions produced by the disease may be divided into those 
 affecting the meninges, those affecting the tissues of the brain 
 and cord, and those affecting the nerves. The lesions of the 
 meninges vary in their extent and character, this depending 
 mainly upon the differences in the intensity and acuteness of 
 the process. The pathological process consists in inflammation, 
 with purulent, sero-purulent and fibrino-purulent exudation. 
 TJie most marked lesions are found at the base of the brain, 
 extending from the optic commissure backwards over the crura, 
 the pons, and medulla. The meninges of the entire brain 
 are rarely affected ; the exudation on the convexity is usually 
 most intense on the lateral surfaces, extending for some 
 distance on either side of the fissure of Rolando. In some 
 cases it is more marked in other parts of the brain, and 
 
97 
 
 the principal exudation may be found over the parietal or 
 even the occipital lobes. There is usually little or no exudation 
 in the meninges along the longitudinal fissure. The meninges 
 of the cerebellum are always involved ; the exudation extends 
 over the under, but especially over the upper, surfaces of 
 this. Along the upper rim of the cerebellum masses of it 
 from two to six mm. in thickness may be found. Small 
 masses of it may also be found along the vessels of the 
 choroid plexus. The exudation is chiefly found in the sulci 
 along the vessels. Karely a wide-spread exudation is found 
 covering large areas of the brain. 
 
 In the most acute cases, those dying in a few days after the 
 onset, the changes are not so marked as in the more advanced 
 cases. We have not had any post-mortem examinations on fou- 
 droyant cases dying within ten to twenty-four hours after the 
 onset. In the most acute cases there is very little exudation. 
 The blood vessels of the pia-arachnoid are intensely injected ; 
 not only do the large blood vessels appear as red lines, but 
 the entire surface of the brain has a pinkish hue, due to the 
 injection of the smaller vessels. The exudation appears in 
 yellowish lines in the sulci along the vessels, and in some 
 cases there is little more than cloudiness. There is more or 
 less oedema of the entire meninges, in addition to the purulent 
 exudation ; they strip off easily from the surface, and a con- 
 siderable amount of fluid runs out. In these more acute 
 cases there seems to be but a small amount of fibrin, and 
 the exudation may easily be removed with a needle from the 
 meshes of the meninges. In the loose tissue of the meninges 
 of the base of the brain there is more exudation, and it 
 often has a distinctly purulent character, appearing either 
 diffusely spread over the surface or as larger or smaller 
 yellowish masses. 
 
 In the more advanced cases, those dying from five to twelve 
 days after the onset, the amount of exudation is much greater 
 and it contains more fibrin. It has a tough, more gelatinous 
 character, and cannot be removed from the meshes of the 
 meninges with a needle. There may be a great amount of 
 
98 
 
 it at the base of the brain and the medulla may be embedded 
 in it. The injection is marked, but not so intense as in the 
 more acute cases (Plate II., Fig. 1). 
 
 In the chronic cases in which death has taken place in 
 from fifteen to thirty days from the acute onset, the appear- 
 ance of the meninges differs widely from that in the acute 
 (Plate II., Fig. 3). In these the most marked condition is 
 the oedema and general thickening of the meninges. The 
 change is most marked in those places where the acute 
 process is most evident. Along the vessels the meninges are 
 thickened and whitish ; there is little evident exudation, 
 yellowish circumscribed foci scattered here and there in the 
 sulci marking the remains of it. The meninges at the base are 
 opaque, enormously thickened, and there are bands of organized 
 tissue extending from point to point. In one of the most 
 chronic cases, in which the duration of the disease could not 
 be ascertained with any accuracy, owing to the mental con- 
 dition of the patient when he was brought into the hospital, 
 the appearance simulated that of general paralysis. There 
 was marked thickening of the meninges over the entire frontal 
 and parietal lobes and over the base and medulla. The only 
 evidence of exudation was in the ventricles, in which masses 
 of partly organized fibrin were found adherent to the walls. 
 In one case, the duration of which, from the imperfect 
 history, was apparently over thirty days, in addition to the 
 thickening of the meninges the entire medulla was so embedded 
 in a dense mass of connective tissue that it was diflflcult 
 to remove it. 
 
 The inflammation is confined to the pia-arachnoid. The adjoin- 
 ing surface of the dura is smooth and there is little injection of 
 the vessels. The amount of fluid in the subdural space is in- 
 creased in amount, and it is more cloudy than normal. 
 
 The process in the meninges of the cord is very similar to that 
 in the brain. The cord is always affected to a greater or less 
 extent, and in some cases the lesions in the cord were more 
 marked than those in the brain. In the acute cases the injec- 
 tion of the inner meninges is not so marked as in the brain, 
 
99 
 
 but there is intense injection of the dura. The amount of fluid 
 in the sub-arachnoid space is greatly increased, and a large 
 amount escapes on opening this. The fluid is cloudy, and may 
 contain floculi of fibrin and pus. The exudation is always most 
 marked along the posterior surface of the cord, and may be found 
 here in large amount, while the anterior surface may show only 
 cloudiness and injection. All parts of the cord are not affected 
 to the same degree ; there is usually more exudation along the 
 dorsal and lumbar cord than along the cervical, though the re- 
 verse of this was often found (Plate II., Fig. 2). 
 
 In the chronic cases the same conditions were found as in the 
 brain. There was general thickening of the meninges, and in 
 the place of a general and diffuse exudation, there were scat- 
 tered yellowish patches marking the remains of the exudation. 
 
 There were few lesions of the tissue of the brain and cord 
 apparent to the naked eye, and without careful microscopic ex- 
 amination lesions which must be regarded as among the most 
 important in the disease would have been over-looked. All these 
 lesions of the brain and cord were less marked in the most acute 
 cases. The ventricles in the acute cases were slightly dilated and 
 the fluid increased and cloudy. The vessels of the ependyma 
 and choroid plexus were dilated. In the posterior cornua of the 
 lateral ventricles there was usually a small amount either of pure 
 pus or of pus and fibrin. In more advanced cases the surface of 
 the ventricles had lost its glistening appearance ; it was softer ; 
 sometimes almost mushy to the touch, and small losses of sub- 
 stance or a more or less ragged or uneven condition of the surface 
 were found. In the chronic cases the dilatation was more marked, 
 the surface of the ependyma uneven and covered with granula- 
 tions. Section of the brain tissue beneath the ependyma showed 
 this to be looser in texture, somewhat more transparent and 
 oedematous. In one chronic case there was a mass of connective 
 tissue and organized fibrin which completely closed the foramen 
 of Magendie. 
 
 In the acute cases the meninges stripped off easily from the sur- 
 face. In one chronic case they were adherent, and small bits 
 of the surface of the brain were removed on stripping them off. 
 
100 
 
 The general consistency of the brain is little altered ; it may 
 be somewhat softer to the touch, owing to the dilatation of the 
 ventricles, and there may be oedema. The vessels both of the 
 gray and white matter are injected. The gray matter on section 
 may have a pinkish tinge, and blood flows from the sections of 
 the dilated vessels. The surface may be softer, and punctiform 
 hgemorrhages may be found in it. In one case, which was 
 unfortunately not examined microscopically, there was distinct 
 softening over a considerable area of the lateral surface. In 
 eight cases there were definite macroscopic lesions in the tissue. 
 These consisted for the most part in haemorrhages, in the white 
 matter, either single or in aggregations. In one case there was 
 an area of distinct softening in the pons adjoining a thrombus 
 in the basilar artery. In two cases there was hsemorrhage with 
 softening of the cortex of the cerebellum. In one case there 
 were foci of induration in the basal ganglia. In no case was 
 there definite abscess formation. The only macroscopic lesions 
 noted in the cord were increased injection, and a softer consistency. 
 
 The cranial nerves were affected to a greater or less degree 
 in all cases. The nerves most affected were the second, the 
 fifth and the seventh and the eighth. The nerves were embed- 
 ded in the exudation which extended along them. On section 
 they were swollen and reddened. The Gasserian ganglia were 
 removed in a number of cases, and in all they were found swollen 
 and softened. The olfactory bulbs were in some cases slightly 
 swollen. The exudation could often be followed along the 
 seventh and eighth nerves into their foramina. The spinal 
 nerves were also affected. The nerve roots were embedded in 
 the exudation, and the spinal ganglia red and swollen. The 
 exudation around the nerves was often particularly prominent 
 around the nerves of the cauda equina. 
 
 In two cases the exudation from the meninges extended into 
 the sella tursica aud the periphery of the pituitary body was 
 infiltrated and softened. 
 
101 
 
 Microscopic Lesions. 
 
 The results of the microscopic examination of the tissues 
 differ according to the aeuteness of the process. In the most 
 acute cases in which there was but little change on macroscopic 
 examination, the lesions consist in purulent infiltration in the 
 meninges. Even in the advanced cases examination of the 
 meninges at the periphery of the more marked lesions shows 
 purulent infiltration as the main change. The blood vessels are 
 injected and many of the smaller veins contain numbers of 
 leucocytes both within the vessels and infiltrating the walls. The 
 leucocytes in the exudations are contained in the tissue in 
 larger and smaller masses, the largest masses being in the 
 sulci. In the meninges over the surface of the convolutions 
 there is infiltration of the tissue. The denser tissue on the 
 surface (arachnoid) is infiltrated, but there are no masses of 
 cells in this. In places the leucocytes are closely packed 
 together ; in others they are found scattered in a finely granular 
 mass, which is evidently the coagulated albuminous exudation. 
 There is little fibrin among the cells. The leucocytes are exclu- 
 sively the polynuclear variety, the nuclei stain intensely and 
 there is no evidence of degeneration. The methods used 
 brought out very distinctly the character of the granulations in 
 the leucocytes, and the absence of eosinophilic cells was remark- 
 able. In most cases not a single eosinophile cell was found. 
 In these acute cases there is little or no change in the fixed 
 cells of the tissue. Some of the cells of the walls of the ves- 
 sels are swollen, but there is no evidence of proliferation. 
 
 In more advanced cases the number of cells is much greater. 
 They appear in large masses in the meshes of the tissue. A 
 part of the mesh-work evidently represents the dilated lymph 
 spaces of the tissue, and a part, in which the meshes are much 
 smaller, represents the dilated cell spaces of the more compact 
 tissue of the surface. In some cases but little can be seen 
 of the connective tissue, the whole tissue being infiltrated 
 with cells. Here also the cells are principally polynuclear 
 leucocytes ; in most of them the nuclei stain brightly, but there 
 
102 
 
 may be masses of them in the middle of the membrane which 
 are swollen, more granular, and whose nuclei either stain im- 
 perfectly or not at all. In most cases there are no red cor- 
 puscles in the exudation, in others scattered ones may be found 
 among the leucocytes, and in one case areas were found where 
 the exudation had an almost hsemorrhagic character. There is 
 more fibrin than in the most acute cases. It appears in masses 
 by itself or as a delicate net- work among the pus cells. In 
 one case there was a considerable amount of it, and in places 
 it had undergone hyaline metamorphosis. It is never present to 
 the same extent as it is in other forms of meningitis, particu- 
 larly that produced by the pneumococcus. In addition to the 
 pus cells and the scattered red corpuscles other cells appear in 
 the exudation, and often form a large part of it. These are 
 large cells, from two to eight times the diameter of a leucocyte. 
 They are present to some extent in all cases, but very few are 
 found in the most acute cases. The nuclei of these cells are 
 large and vesicular, the protoplasm stains very faintly and is 
 finely granular. It is difficult to make out the protoplasm of 
 the largest of these cells, for they are filled with other cells 
 which they have taken up (Plate VI., Fig. 2). Polynuclear 
 leucocytes, often in considerable numbers, are found in these 
 cells. In one as many as fifteen were counted. The enclosed 
 leucocytes show various changes. Most often they are contained 
 in a vacuole of the large cell, and a clear space can be seen 
 around the periphery of the enclosed cell. Rarely lymphoid 
 cells may be found in them. The protoplasm becomes pale and 
 gradually disappears, while the nucleus may be but little changed. 
 Finally the nucleus breaks up into irregular masses of chromatin, 
 and some cells are found which are filled with irregular chromatin 
 fragments. The large vesicular nucleus of the cell may be made 
 out lying close to the periphery. In most cases the large cells 
 were well preserved, in others they were among masses of de- 
 generating leucocytes, and seemed to undergo the same degener. 
 ation. They were most numerous around the periphery of the 
 cell masses of the exudation. 
 These large cells have excited the interest of all who have 
 
103 
 
 studied the process, but their origin has been obscure. Owing 
 to the freshness and variety of the material and the use of 
 improved methods of technique, it has been possible to follow 
 the various stages of their formation. In the place of the few 
 scattered cells, with thin, spindle-shaped nuclei, seen in the con- 
 nective tissue of the normal meninges, the nuclei become large 
 and vesicular, and the protoplasm of the cells is increased in 
 amount and granular. These cells are greatly increased in num- 
 ber, there are masses of them around the blood vessels and 
 in the connective tissue. The spaces in the tissue enclosing 
 the pus cells may be lined with them. Nuclear figures in con- 
 siderable numbers and in great variety and beauty are often 
 seen in cells which are still in connection with the tissues, and 
 in those lying free among the cells in the exudation. By 
 taking different cases, and sometimes even in the same case, 
 the various steps in the formation of these large cells from 
 the cells of the connective tissue and from the cells lining 
 the lymph spaces in the tissue could be followed. The con- 
 nective tissue fibres become less evident, and, as the cells 
 multiply, they become swollen or disappear. 
 
 The vessels are dilated and in some of them thrombi are found. 
 Masses of leucocytes with a few lymphoid cells among them are 
 often found in the centre of the vessels among the red corpuscles. 
 Occasionally a few lymphoid and plasma cells are found around 
 the vessels. The proliferative changes found in the intima of the 
 arteries, which are so common in tuberculosis and pneumococcus 
 meningitis, are but rarely found here. This change consists in the 
 loosening of the endothelial layer of the intima, and the forma- 
 tion between this and the elastica of numbers of large epithelioid 
 cells, which appear to form a lining to the vessel. In one speci- 
 men the intima of a small artery was elevated and back of this 
 was a clear space filled with polynuclear leucocytes, which also 
 to some extent infiltrated the muscular coat. Some degree of 
 purulent infiltration is seen in wall of an artery (Plate III., Fig. 2) 
 which is from a case of experimental meningitis in a goat. 
 
 In the chronic cases the lesions are much less striking. The 
 exudation is confined to the small, yellowish masses mentioned 
 
104 
 
 in the macroscopic description. These are composed for the 
 most part of masses of degenerated pus cells and nuclear de- 
 tritis. At the periphery of the masses occasional leucocytes are 
 seen whose nuclei are clearly stained. The meninges are con- 
 verted into thick, dense masses of tissue, resembling cicatricial 
 tissue, which contain few cells. Here and there in the tissue, 
 especially close to the brain, there are groups of cells. In 
 these there are but few of the large cells which form such 
 a conspicuous feature in the acute cases. In the place of these 
 we find in the cell groups and around the vessels numbers of 
 lymphoid and plasma cells. We understand, under the term 
 plasma cells, cells which are similar to those described under 
 this term by Unna. They have a nucleus similar in its general 
 character to that of the lymphoid cell, and a variable amount 
 of granular protoplasm which stains blue with Unna's alkaline 
 methylene blue solution. In the cell groups there are cells which 
 seem to show transitions between the lymphoid and plasma cells. 
 It is only by means of fine sections and the use of high powers 
 that the character of the cells forming the closely packed masses 
 around the vessels can be made out. 
 
 The changes in the meninges of the cord are of the same 
 general character as those of the meninges of the brain. The 
 large cells, though present, are not so numerous as in the latter. 
 The blood vessels are injected. The greatest mass of the exu- 
 dation is invariably in the meninges on the posterior surface of 
 the cord. The pus cells lie in larger masses and the reticulum 
 is not so evident, and there is always a smaller amount of fibrin 
 than in the meninges of the brain. In cases where the macro- 
 scopic examination showed only hypersemia with slight cloudi- 
 ness of the meninges, as on the anterior surface of the cord 
 and in places over the entire surface, microscopic examination 
 showed well-marked purulent infiltration. In the more chronic 
 cases, just as in the meninges of the brain, the purulent exu- 
 dation is confined to small areas of degenerated pus cells, and 
 there is thickening of the meninges with cellular accumulations 
 around the vessels. 
 
105 
 
 Lesions of the Tissue of the Brain and Cord. 
 These lesions are interesting on account of their frequency, 
 their general bearing on pathological processes and from being 
 most marked in the particular form of meningitis which is 
 produced by the diplococcus intracellularis. In only a few cases 
 were these lesions absent. The lesions are most evident in 
 those cases in which from five to ten days elapsed from the onset 
 of the disease until death. The blood vessels of the convexity 
 are injected, the cortex in most cases wider, and the tissue more 
 loose and reticular, as though cedematous. The lymph spaces 
 around the blood vessels are dilated. In some places there is 
 a circumscribed infiltration of the tissue with pus cells which 
 extend downward from the infiltration in the meninges. The 
 spaces around the dilated vessels are often filled with pus cells 
 which extend from here into the surrounding brain tissue. The 
 infiltration was usually most marked in the outermost layer of 
 the cortex above the ganglion cells, but in some cases it was 
 found deeper down among the ganglion cells, and even in the 
 white matter. In addition to this infiltration around the vessels 
 single pus cells are often found in the brain tissue, apparently 
 remote from the areas of infiltration. There were but few haemor- 
 rhages found in the cortex of the cerebrum. In two cases there 
 was extensive softening, with purulent infiltration and haemor- 
 rhage in the cortex of the cerebellum. In these places, which 
 partly extended into the granular layer, the cortex was repre- 
 sented by scattered granular masses, among the pus cells and 
 haemorrhage, and the cells of Purkinje had disappeared, or only 
 granular fragments of them were found. The areas in the 
 white matter which showed macroscopicaUy as hsemorrhages 
 generally appeared as foci, composed of numerous fine hcemor- 
 rhages, with but little infiltration with pus cells. Around these foci 
 there were changes in the neuroglia which will be presently 
 described. In one case there was an acute focus of softening 
 with infiltration with pus cells in the pons just over a throm- 
 bus in the basilar artery. In this area the tissue was distinctly 
 
106 
 
 broken down, necrotic and infiltrated with pus cells. In the 
 most chronic case there was a firm mass resembling a gumma on 
 the upper surface of the cerebellum which completely closed the 
 foramen of Magendie. On microscopic examination, the centre 
 of this was composed of totally necrotic pus cells and fibrin, with 
 fine remains of nuclear detritis. This was surrounded by a 
 dense mass of connective tissue with infiltration of plasma 
 cells and lymphoid cells, and it extended downwards through 
 the granular layer. It seemed to have resulted from the 
 necrosis of a large purulent exudation in the meninges, com- 
 bined with superficial necrosis of the tissue of the cerebellum 
 immediately beneath. In several of the chronic cases, in which 
 there was marked thickening with cellular infiltration of the 
 meninges, the same cellular infiltration was found around the 
 vessels extending into the tissue. In one acute case, in which 
 almost complete paralysis of one side appeared twenty-four 
 hours before death, the exudation was most marked on the side 
 of the brain opposite the paralyzed side. In this place the 
 oedema and cellular infiltration of the cortex was most marked. 
 Macroscopically the cortex was much swollen and softer. Pus 
 cells were found not only in large numbers around the vessels 
 but had generally infiltrated the brain tissue. At various places 
 in the white matter and in the internal capsule there were 
 small foci of haemorrhage. 
 
 In no case in which the ventricles were examined were 
 they found free from alteration. The ependymal lining was 
 in some cases preserved, in others it was lost over greater 
 or smaller areas. The tissue beneath the ependyma was 
 loose, reticular and oedematous. The blood vessels were injected 
 and there was more or less infiltration with pus cells both 
 immediately around the vessels and at a distance. In many 
 of the chronic cases the surfaces of both the lateral and 
 fourth ventricles were covered with granulations. 
 ' The tissue of the cord was always less affected than that 
 of the brain. Only in one case did we find a purulent 
 infiltration of the cortex extending from the meninges with 
 foci of infiltration in the tissue. 
 
107 
 
 The most interesting changes concern the neuroglia. These 
 were found both in the cortex and beneath the ventricles, 
 and in the neighborhood of the foci of softening. With a 
 low power there is a distinct increase in the cells of the 
 cortex outside of the ganglion cells, which is both general 
 and more marked in certain places. With high power the 
 cells of the neuroglia are swollen, their nuclei are large, 
 clear, vesicular, and contain larger and smaller masses of 
 chromatin. Around these large nuclei there is a faintly 
 stained, very much branched, irregular mass of granular 
 protoplasm. This presents some similarity to a branched 
 connective tissue corpuscle, but can be distinguished from it 
 by the more faintly stained and more granular character of 
 the protoplasm. The shape of the cells varied ; some were 
 branched in all directions, while others were more spindle- 
 shaped, with short secondary protoplasmic prolongations from 
 the main branches. Many of the cells contained two nuclei, 
 and in places there were groups of four or more nuclei 
 closely clustered together with a considerable amount of proto- 
 plasm around them (Plate VII., Fig. 4). In all these places, in 
 favorable tissues, varying numbers of nuclear figures were found 
 (Plate VI., Figs. 2 and 3). They presented the same forms 
 as other multiplying nuclei, and in some cases the spindles 
 and centresomes were distinct. Apparently for the recognition 
 of these nuclear figures much depends either upon the condition 
 of the tissue or the period of the disease. They were numerous 
 in one specimen, while in others, in which there was evident 
 proliferation, they could be found only after prolonged search. 
 In some of the places where the proliferation was most 
 marked there was some infiltration of the tissue with pus 
 cells ; in others the nuclear figures were found at a distance 
 from such infiltration and in apparently normal tissues. The 
 same change in the neuroglia was found deeper down in the 
 cortex among the ganglion cells. The number of nuclei 
 around the ganglion cells was increased, and in several instances 
 nuclear figures were found in these places. The greatest increase 
 in the neuroglia was found around the foci of haBmorrhage and 
 
108 
 
 cellular infiltration in the white matter. The haemorrhagic area 
 was often surrounded by an area made up of proliferating 
 neuroglia cells, and areas composed of them were often found 
 apart from such haemorrhages ; but these seemed probably to be 
 the peripheries of haemorrhages which did not appear in the 
 section. In all of these places there were numerous nuclear 
 figures. The same proliferation in the neuroglia with the 
 presence of nuclear figures was also found in the acute areas 
 of softening in the cerebellum and in the neuroglia of the optic 
 and olfactory nerves. 
 
 In every case proliferative changes in the neuroglia were found 
 in the tissue of the ventricles. Where the ependymal lining 
 was preserved the cells were closely packed together, the nuclei 
 were large and proliferation had evidently taken place, but no 
 definite nuclear figures were found. Beneath this the tissue 
 was loose and reticular, and contained large numbers of single 
 cells and cell groups. The first nuclear figures were found 
 in the neuroglia cells here, but they were not as numerous as 
 in the cortex and in the white matter. In the more chronic 
 cases the changes in the neuroglia of the cortex were not so 
 marked as in the acute. There was some increase in the cells, 
 most of which assumed a normal appearance, the tissue was 
 denser and the fibres more evident. These more chronic changes 
 in the neuroglia were best studied in the ventricles. In these 
 there was a dense lining of neuroglia with rather coarse fibres, 
 and with a greatly increased number of cells immediately beneath 
 the ependyma and extending into the tissue. In those cases 
 in which there were granulations on the surface they were com- 
 posed of neuroglia alone. 
 
 Marked changes in the neuroglia of the cord were found in 
 but one case. In this the central canal was dilated and around 
 it were cell aggregations. The blood vessels were dilated, and 
 their sheath and the tissue around them infiltrated with pus cells. 
 This was most marked in the gray matter. The neuroglia 
 cells were greatly increased in number in the gray matter of 
 the cord, and to a less extent in the white, and there were 
 numerous nuclear figures within them. In some of the chronic 
 
109 
 
 cases there was thickening of the neuroglia around the periphery 
 of the cord. 
 
 These neuroglia changes were accompanied by changes in the 
 connective tissue. The cells of the blood vessels were swollen, 
 increased in number and nuclear figures found in them. In the 
 same field nuclear figures were often found in the neuroglia cells 
 and in the blood vessels. In the smaller hsemorrhagic foci 
 the walls of the vessels were often found infiltrated with large 
 epithelioid cells, together with lymphoid and plasma cells. This 
 cellular infiltration was most marked around the blood vessels 
 beneath the surface of the ependyma. A definite formation of 
 connective tissue proceeding from this vascular proliferation was 
 not found save in the chronic case referred to, and in this the 
 process had advanced so far that the steps in the formation of 
 the connective tissue could not be followed. In this same case 
 sections through the indurated areas in the optic thalamus 
 showed masses of fibrin in the tissue with dense cellular aggre- 
 gations. These cell masses were almost entirely composed of 
 plasma cells, with a few lymphoid cells between them. 
 
 The examination of the ganglion cells for degenerative lesions 
 was the least satisfactory part of the work. The tissue was 
 examined in all the usual methods after hardening in alcohol and 
 formaline. In many of the cases the tissues undoubtedly re- 
 mained too long in the hardening fluid before examination. 
 Changes were undoubtedly present, especially in the most 
 chronic cases. The changes found consisted in an alteration 
 in the cell granules, combined with irregularity in shape and 
 often atrophy of the body of the cell. The granules in some 
 cases were absent, in others in place of the large angular 
 granules there was an indistinct fine granulation. In some of 
 the sections which were hardened in Flemming's solution and 
 in some hardened in Miiller's fluid and subsequently treated by 
 Marchi's method for degeneration, fatty degeneration was found 
 in the cell protoplasm. These fat granules resulting from degen- 
 eration could be distinguished from the pigment granules of the 
 cells, which also stain with osmic acid, by their greater intensity in 
 staining, their irregular size and irregular distribution in the cells. 
 
110 
 
 In addition to the nerves, portions of both brain and cord were 
 treated by Marchi's method for degeneration in the nerve fibres. 
 Degeneration to some degree was present in all the cases ex- 
 amined. In sections of the cortex embracing the white matter 
 it was present to some degree but was not marked. Here and 
 there in the white matter small areas of degeneration could be 
 seen. In those sections of the brain which embrace the internal 
 capsule the degeneration was more conspicuous. The degenera- 
 tion was much more marked in the cord. In this, it was most 
 conspicuous in the posterior column of the cord. Under a low 
 power these columns were often almost black from the extent of 
 the degeneration. A certain amount was evident in the pyramidal 
 tracts of the cord and in the antero-lateral tract. The stain for 
 degeneration was of importance in another way, — in bringing out 
 a degeneration of the swollen cells of the vessels, which was often 
 of high degree. 
 
 Diplococci were found in variable numbers in the meninges and 
 in the brain (Plate III., Fig. 1). They were always most numer- 
 ous in the acute cases, where the exudation was composed almost 
 wholly of pus cells. Variable numbers were found in the single 
 cells, but the cells wholly filled with them which were so common 
 in the alveoli of the lungs were rarely found. In the chronic 
 cases prolonged search was often necessary to find them ; in the 
 acute cases numbers of cells containing them were often found 
 in a single field. In the meninges of the cord they seemed to 
 be less numerous than in the brain. In the brain they seemed 
 more numerous close to the inner surface. They were also found 
 in the tissue of the brain in those acute cases in which there 
 was considerable purulent infiltration of the tissue. Here they 
 were found not only in the pus cells around the vessels, but in 
 the single cells in the interior of the tissue. 
 
 Lesions in the Nerves and Ganglia. 
 
 The importance of the study of the nerve lesions was only 
 
 appreciated in the latter part of the epidemic, so that in the 
 
 earlier cases the nerves were not examined. In six cases the 
 
 cranial nerves, including the Gasserian ganglia, were examined, 
 
Ill 
 
 and in two cases the spinal ganglia. In one case, in addition 
 to the cranial nerves a number of peripheral nerves were 
 examined for degeneration. The nerve roots of the spinal 
 nerves were examined in the sections of the cord in every case. 
 Lesions of greater or less degree were found in every case 
 examined, and seem sufficiently constant to justify the conclusion 
 that they are present certainly in all the severe cases. 
 
 The most marked lesions were found in the second, the fifth 
 and eighth nerves. The lesions in the optic nerves represent an 
 extension of the inflammatory process from the meninges. The 
 nerve was examined in cross and longitudinal sections from the 
 brain to its entrance into the eye. The dural covering of the 
 nerve in the orbit showed little change save dilatation of vessels. 
 The sub-dural space was dilated, but usually contained no cellular 
 exudation. Just as in the brain, the purulent exudation was 
 found in the pia-arachnoid of the nerve. The connective tissue 
 of this was infiltrated with pus, and there were masses of pus cells 
 in the membrane and in spaces chiefly around the retinal artery after 
 this had entered into the sheath (Plate IV., Fig. 1). The blood 
 vessels of the nerve itself were dilated, the space between the 
 bundles of fibres increased, and around the periphery were lines 
 of cellular infiltration which extended from the outside between 
 the bundles of fibres. In a longitudinal section of the nerve, 
 involving a part of the retina, the infiltration could be followed 
 from the meninges of the nerve into the eye. Another longitu- 
 dinal section of the nerve in one case showed a small mass of pus 
 cells lying in the sub-dural space and the dura immediately over 
 this was infiltrated with cells. In the acute cases the cells in the 
 meninges of the nerve extending between the nerve bundles were 
 polynuclear leucocytes. The degree of the infiltration varied. 
 In one case considerable numbers of leucocytes were found 
 extending almost to the centre of the nerve. In more chronic 
 cases along with the pus cells there were numerous large epithelioid 
 cells similar to those found in the meninges of the brain. Around 
 the vessels there were very few lymphoid and plasma cells. 
 Changes similar to those in the optic nerve were found in the 
 olfactory nerve and the bulb, but the cellular infiltration between 
 
112 
 
 the nerve bundles was not so marked. It was very interesting to 
 find in both the optic and olfactory nerve proliferative changes in 
 the neuroglia cells similar to those described in the brain. In one 
 case of five days' duration nuclear figures in great variety and 
 beauty, showing centresomes and spindles, were found in the 
 neuroglia cells (Plate VII., Figs. 2 and 3). Two such figures 
 were sometimes seen in the same field. Cells with granular proto- 
 plasm and two or more nuclei were also seen. 
 
 Sections of the eighth nerve (Plate V., Fig. 1) in acute cases 
 showed the nerve embedded in a mass of pus, the nerve sheath 
 softened, broken up and in places entirely lost. The nerve itself 
 was infiltrated with enormous numbers of pus cells, partly in the 
 form of lines running through it, partly as a more diffuse 
 infiltration. In some sections the nerve was broken up, greatly 
 swollen and the single bundles of fibres separated by large 
 accumulations of cells. Here also in acute cases only pus cells 
 were found around the invading nerve, and in the more chronic 
 cases there were fewer pus cells, and in the place of them lines of 
 epithelioid and plasma cells. The seventh nerve frequently showed 
 as great degree of infiltration as the eighth. Some infiltration 
 was also found along the third and sixth nerves, but it was not so 
 marked. In one case longitudinal sections of the fourth nerve 
 were made, and showed no infiltration. 
 
 Longitudinal sections of the fifth nerve, involving the ganglion 
 and some of the peripheral branches, showed an intense neuritis 
 on the cerebral side of the ganglia. The single bundles of fibres 
 were widely separated from one another, and between them there 
 was considerable exudation, in which there were numbers of pus 
 cells and epithelioid cells. The cellular infiltration did not seem 
 to extend so diffusely into the nerve bundles as it did in the case 
 of the eighth nerve. These exudative changes were accompanied 
 in the fifth nerve, as in the spinal nerve, by a considerable degree 
 of cellular proliferation. 
 
 Sections of the nerve roots (Plate IV., Fig. 2) of the spinal cord 
 showed that these were affected in every case, but there was a great 
 deal of difference in the extent of the lesions. As a rule, the 
 greatest degree of affection of the nerve roots was found in that 
 
113 
 
 part of the cord where the cellular infiltration was greatest, 
 although in some cases a considerable degree of involvement of 
 the nerve roots was found, with very little infiltration of the 
 meninges. In most of the acute cases the lesions in the nerve 
 roots, as shown on cross and oblique sections, were of the same 
 character as those seen in the cranial nerves. There was a marked 
 degree of dilatation of the blood vessels, the peri-neurium was 
 infiltrated with pus cells, the nerve was swollen, the separate 
 bundles of fibres separated from one another by spaces in which 
 there was considerable cellular infiltration. Even in the most 
 acute cases these changes were accompanied b}^ proliferative 
 changes in the peri- and endo- neurium. The cells of the blood 
 vessels were swollen, increased in number, and around the blood 
 vessels along with the pus cells there were numbers of large 
 epithelioid and plasma cells. The lymphoid cells were compara- 
 tively few in number. Nuclear figures were often found in the 
 epithelioid and plasma cells. Not only were these changes found 
 in the peri-neurium and in the small bundles of connective tissue 
 separating the larger bands of nerve fibres, but small collections 
 of plasma and lymphoid cells were occasionally found within the 
 nerve bundles and between the fibres (Plate VII., Fig. 1). All 
 of these changes were more marked in the posterior than in the 
 anterior roots. 
 
 In some of the more chronic cases lesions in the spinal nerve 
 roots were more marked than in the acute. Around all of the 
 blood vessels, even the smallest, there was an intense prolifera- 
 tion of cells, which so extended between the single nerve fibres 
 that in places these seemed to be entirely destroyed. The cells 
 belonged principally to the type of plasma cells. The greatest 
 amount of nerve degeneration, as shown by the Marchi method, 
 was found in the optic nerve in one case (Plate VII., Fig. 2), 
 and in the eighth nerve in another. Sections of the optic nerve 
 under the low power were very dark from the masses of fatty 
 degenerated myelin stained black with osmic acid. With a high 
 power in some of the bundles a large number of the single nerve 
 fibres were found to be affected. The degeneration was almost 
 as marked in the seventh nerve. In a longitudinal section of 
 
IM 
 
 the nerve, in which the degeneration of the single fibres could 
 easily be followed, a count showed in one place three-fourths of 
 the fibres to be affected. In most of the nerves in which the 
 myelin was swollen and broken up the axis cylinder was swollen, 
 transparent or entirely absent. 
 
 Longitudinal section of the optic nerve from the same case did 
 not show so great degree of involvement. In every case degen- 
 eration was found in the spinal nerve roots, and was more marked 
 in the posterior than in the anterior roots (Plate VIII., Fig. 1). 
 Only in one case was there an extensive examination of the 
 peripheral nerves for degeneration. A minor degree of degen- 
 eration was found in the nerves of the cauda equina and in 
 the popliteal nerves. A considerable degree was found in the 
 same case in the seventh nerve. The fifth nei've was only 
 examined in one case, in which there had been great involve- 
 ment of the ganglia, and in this extensive degeneration was found. 
 
 In one of the cases a section treated for degeneration was 
 taken through all the nerves and muscles of the orbit. All 
 of the nerves showed more or less marked degenerative changes, 
 but the optic nerve, and next to this the branches of the sixth, 
 seemed to be most affected. The muscles of the section showed 
 advanced fatty degeneration. Sections of the spinal cord stained 
 by Weigert's method show equally the destruction of the nerve 
 roots. In one chronic case comparatively few intact nerve 
 fibres were found. 
 
 In five cases sections were made of the Gasserian ganglia, 
 and in two of the spinal ganglia. The Gasserian ganglia 
 in the acute cases were infiltrated with pus, and masses of gan- 
 glion cells were often separated from their connection (Plate V., 
 Fig. 2). Even single ganglion cells were often found lying 
 free in the exudation. Along with the purulent exudation 
 there was more or less haemorrhage . Many of the ganglion 
 cells, especially those most distant from the exudation, seemed to 
 be normal. Others were small, their outline exceedingly irreg- 
 ular, the nucleus pale or in some cases absent altogether. Small 
 irregular masses, representing completely necrotic ganglion cells, 
 were often found. In the most marked cases the granulation 
 
115 
 
 of all of the cells was iudistinct. The cells also often con- 
 tained large vacuolar spaces. The diplococci were found in the 
 pus cells infiltrating the optic nerve and in the infiltration of 
 the pia-arachnoid around it. In several cases they were found 
 in the sections of the Gasserian ganglia, but were not found in 
 the sections of the spinal ganglia. In one case they were found 
 in the olfactory nerve and in the auditory in one. They were 
 not found in the other nerves or in the nerve roots of the 
 spinal cord. No leucocj-tes were found in the necrotic ganglion 
 cells. In the more chronic cases the amount of leucocytic in- 
 filtration was less, and throughout the ganglia there were large 
 numbers of cells which came from proliferation of the connective 
 tissue. In one case the ganglion appeared to be oedematous. 
 The tissue was loose and the single cells widely separated from 
 one another both by cellular infiltration and by the oedema. 
 Immense numbers of newly formed cells were found around 
 the ganglion cells. The cellular investment of the single cells 
 was in most cases much thicker, and the cells were swollen and 
 many took on an epithelioid character. Nuclear figures were 
 found in the surrounding cells. The cells lying in the tissue 
 between these ganglion cells often had the character of plasma 
 cells. There were also considerable numbers of lymphoid cells. 
 The same condition of atrophy of the cells, often going into 
 complete necrosis, was found here as in the acute cases. The 
 spinal ganglia were not equally affected. This was apparent 
 on macroscopic examination. All seemed to be somewhat 
 swollen and oedematous, but in some this condition was much 
 more marked than in others. On microscopic examination much 
 the same changes were found in these as in the Gasserian 
 ganglia. The blood vessels were injected and the ganglion 
 infiltrated with pus. There was proliferation of the cells about 
 the blood vessels and of the cells about the ganglion cells. 
 The ganglion cells were often separated from their connection 
 and lying in the exudation. These were irregular in shape 
 and the nucleus stained imperfectly or not at all. Others showed 
 the same degenerative lesions as have been described in the 
 Gasserian ganglion (Plate VI., Fig. 1). Sections of the gan- 
 
116 
 
 glion, including longitudinal section of the nerve roots in con- 
 nection with it, showed these infiltrated with pus. The rapidity 
 with which these changes can take place was shown in a sec- 
 tion of the ganglia in the goat which died not later than twelve 
 hours after inoculation in the spinal canal with a pure culture 
 of the diplococcus. In one of the ganglia there was beginning 
 purulent infiltration. There seems little doubt that in both 
 the spinal and Gasserian ganglia the condition is due to direct 
 extension along the nerves. There were no lesions in a small 
 sympathetic ganglion found in one of the sections through the 
 orbit. In one case, in which sections of the Gasserian gan- 
 glion and the nerves showed a very extensive neuritis, sections 
 were made through the olfactory bulb. This was swollen and 
 in places intensely infiltrated with cells among which were many 
 pus cells, but the cells seemed to come principally from pro- 
 liferation. The tissue was (Edematous and the large triangular 
 nerve cells often appeared atrophied. Sections passing through 
 the olfactory nerve from the same case showed a considerable 
 degree of degeneration. 
 
 Sections of the eye were examined in two cases, in one of which 
 choroiditis, cloudiness of cornea and conjunctivitis were ascer- 
 tained during life. The sections embraced in this case the fundus 
 of the eye through the entrance of the optic nerve, the 
 ciliary region and the cornea. The sections through the optic 
 nerve and fundus showed a marked infiltration of the nerve 
 sheath up to its entrance into the eye. Where the nerve sheath 
 was lost in the eye there was a considerable accumulation of 
 pus cells, with proliferation of the adjoining tissue cells. From 
 this point an infiltration with leucocytes extended directly into 
 the eye. The optic nerve was swollen, the spaces between the 
 fibres increased, and in these spaces an occasional pus cell 
 and cells of new formation were found. All of the vessels of 
 the choroid were intensely injected, but there were few haemor- 
 rhages and no infiltration with pus cells in this. The retina 
 on either side of the entrance of the optic nerve was broken 
 up and infiltrated with pus. Further up the retina was in places 
 very well preserved, but generally nothing could be seen of the 
 
117 
 
 layer of rods and cones. The tissue was infiltrated with pus 
 cells and haemorrhage, and in places the entire retina, with the 
 exception of the granular layer immediately beneath the rods 
 and cones, was destroyed. All the blood vessels of the retina 
 were intensely injected, and in places there was a considerable 
 amount of fibrin around them. Notwithstanding the enormous 
 congestion of the blood vessels of the choroid, no diapedesis 
 seemed to take place from them and in none of them was there 
 an accumulation of leucocytes. Only in a few places scattered 
 leucocytes were found in the tissue of the choroid. The tissue 
 appeared to be looser than normal, and in the loose meshes of 
 the tissue epithelioid cells with nuclear figures were found. The 
 vitreus was filled with a large amount of pus made up entirely 
 of polynuclear leucocytes, none of them containing eosinophile 
 granules. The largest mass of this pus was adherent to the 
 retina and to the iris. The anterior chamber contained a large 
 amount of pus. The tissue of the iris was oedematous and 
 infiltrated with pus cells. The blood vessels were injected. 
 The pigment cells were broken up, the pigment scattered in the 
 tissue, and the pus cells in the iris and in the anterior chamber 
 were loaded with pigment derived from this destruction of cells. 
 A considerable amount of reticular fibrin and numbers of red 
 blood corpuscles were found among the pus cells in the anterior 
 chamber. No evidences of proliferation were seen in any of 
 the pigment cells of the iris or ciliary region. In the ciliary 
 region the blood vessels were injected, the tissue was swollen, 
 oedematous and infiltrated both with pus cells and with cells arising 
 from proliferation. The sclera was normal, except at the corneal 
 attachment. There all of the blood vessels were injected, and 
 it contained large numbers of pus cells and epithelioid cells. 
 The cells of the vessels were swollen, and nuclear figures were 
 found in them. The section passing through the cornea showed 
 the fibres of this separated, and the tissue contained a great 
 many pus cells lying in the corneal spaces. At its commence- 
 ment the cornea was almost homogeneously infiltrated, further 
 along toward the middle a few pus cells were found in the 
 posterior portion of the cornea and they seemed most abundant 
 
118 
 
 in the middle. The epithelium was almost entirely lost over 
 the posterior surface of the cornea, and over the anterior sur- 
 face it was for the most part reduced to single cells. In this 
 case the duration of the disease was seven days. In the other 
 eye examined, coming from a case of three days' duration, the 
 lesions were not so marked. The vessels of the choroid were 
 intensely injected, and here and there a slight amount of 
 haemorrhage and cellular infiltration was found. The retina 
 was separated, the vessels were intensely injected, and a few 
 slight haemorrhages were found. The different layers of the 
 retina were usually made out, and appeared to be but little 
 changed. 
 
 In the eye first described a portion of the conjunctiva was cut 
 at the same time with the eye. All of the blood vessels in this 
 were intensely injected and there was a great deal of hsemorrhage 
 in the tissue which seemingly came from the small vessels. The 
 tissue was infiltrated with pus cells which extended up into the 
 epithelium. The spaces in the tissue beneath were increased, and 
 it was evidently oedematous. About the vessels in the spaces in 
 the tissue there were large numbers of plasma cells and occasional 
 groups of epithelioid cells. Nuclear figures were found in both 
 in small numbers. Diplococci were found in considerable numbers 
 in the pus cells in the vitreous and in the anterior chamber. In 
 one section a few were found in the retina. None were found in 
 the cornea or in the iris. In the acute case it was easy to trace 
 the organisms from the brain along the optic sheaths to the eye. 
 
 Pituitary Body. 
 In two cases the pituitary body was examined. Sections pass- 
 ing through the pedicle showed a purulent infiltration extending 
 around this and down into the gland. At the periphery of the 
 gland in one place the exudation extended down into the tissue 
 and there was necrosis and atrophy of the glandular elements. 
 
 Nose. 
 In three cases sections of the mucous membrane of the upper 
 air passages were examined. Two were normal and in one there 
 
119 
 
 was a purulent infiltration of the mucous membrane and of the 
 sub-mucous tissue with intense hypersemia of the blood vessels. 
 A few single pairs of diplococci were found in the pus cells. In 
 this case microscopic examinations of the nasal secretion from the 
 nose during life were positive, showing diplococci in the pus cells. 
 
 Lungs. 
 
 The condition of the lungs is interesting, on account of the 
 relation which has very generally been supposed to exist between 
 acute epidemic cerebro-spinal meningitis and pneumonia. In 
 thirteen cases there was merely congestion, with more or less 
 oedema. In a few of the cases the oedema was well marked. In 
 seven cases there was broncho-pneumonia, most marked in the 
 lower posterior portions of the lung, with more or less bronchitis. 
 In two cases there was characteristic croupous pneumonia, one in 
 the stage of red hepitazation bordering on gray. There was a 
 fibrinous pleurisy over the consolidated lung. Pneumococci were 
 found in cultures and on microscopic examination. In eight cases 
 a pneumonia due to the diplococcus was found. Nearly all of 
 these cases come from the last part of the epidemic. It is very 
 possible that in some of the earlier cases in which the lesions were 
 described simply as broncho-pneumonia, they were really due to the 
 diplococcus. The lung lesions in cases which are described as 
 broncho-pneumonia with bronchi-ectatic cavities, and foci of con- 
 solidation with necrosis and breaking down, may also have been 
 due to the diplococcus. The lesions macroscopically consisted 
 of areas of consolidation in various parts of the lung, more par- 
 ticularly in the lower lobe and they were most numerous beneath 
 the pleural surface. The foci varied in size from a pin's head 
 up to that of a bean, and on section some of them resembled 
 small hsemorrhages in the tissue. In other cases the periphery 
 of the area was distinctly haemorrhagic and the centre opaque 
 and yellowish. The number of these areas varied. In some 
 of the cases but few were found, in others they were numerous. 
 In one case the consolidation in the lung was so extensive that 
 it might easily have been regarded as croupous pneumonia, par- 
 ticularly as the pleura over it was covered with a definite fibrinous 
 
120 
 
 exudation. On section the large area was composed of a number 
 of irregular grayish foci with softened centres and with haemor- 
 rhagic and oedematous tissue between them. 
 
 The lung tissue in the yellowish centres was frequently broken 
 down, and pus oozed from this. The bronchi in these places 
 contained more or less muco-purulent material, but there did not 
 seem to be that relation between the bronchi and the areas of 
 consolidation which is found in broncho-pneumonia. 
 
 On microscopic examination the central areas showed in most 
 cases a purulent infiltration of the tissue, breaking down and 
 beginning abscess formation. In the centres there were large 
 numbers of pus cells in the alveoli. The walls of the alveoli were 
 thin, infiltrated with pus and in places entirely broken down. 
 Surrounding this the purulent infiltration was not so intense and 
 around the outside there was often oedema with a slight amount of 
 hsemorrhage. Some of the foci were distinctly hasmorrhagic, with 
 areas here and there of purulent infiltration. The exudation in 
 the alveoli in the centres contained nothing but pus cells. 
 Further out mixed with the pus cells there were numbers of large 
 cells similar to those in the brain, and they often enclosed the pua 
 cells. These large cells were also found in the more oedematous 
 portions. In addition to the exudation, at the periphery there 
 was some cellular proliferation of the tissue of the lung. There 
 were plasma and epithelioid cells about the blood vessels, and the 
 cells lining the walls of the alveoli were swollen. In one case 
 nuclear figures in small numbers were found in these cells. The 
 exudation in the lung, as in the brain, was characterized by the 
 absence of eosinophile cells. On microscopic examination the 
 foci of consolidation did not appear to be bronchial in origin. 
 The bronchi in the vicinity often contained pus cells, but their 
 walls were not infiltrated. The duration of the disease in the 
 cases in which diplococcus pneumonia was found was : in twa 
 cases, three days ; in one case, two days ; in one, five days; in 
 one, nine days ; in one, twenty-three, one seventy-four and one 
 five days. The average duration was fifteen and one-half days. 
 It will be seen from these figures that the lung complications due 
 to the diplococcus can take place in almost any period of the 
 
121 
 
 disease. In the case of seventy-four days' duration the lesions in 
 the brain and cord could be regarded as almost completely healed, 
 and the lesions in the lung were acute. In one case, in which the 
 apparent history of the disease was only of two days' duration, 
 the lung lesions were so advanced that they seemed possibly to 
 antedate those of the brain, providing the history as given by the 
 patient's relatives was accurate. 
 
 Immense numbers of diplococci were found in the pus cells in 
 these places (Plate III., Fig. 2). They were most numerous in 
 the cells in the centres of the foci, where the softening of the 
 tissues was taking place. Sometimes in an alveolus every pus 
 cell was almost filled with them. With low power the places 
 containing them in greatest abundance could be easily recognized 
 by the dark color which their presence gave to the cells. They 
 were found exclusively in the cells. Although most numerous in 
 these places, they were also found in the pus cells in considerable 
 numbers around the periphery of the central area and in the 
 scattered pus cells of the oedematous portion. None were found 
 in any of the large cells, but occasionally a few swollen and 
 imperfectly stained forms were found in the pus cells enclosed in 
 these. In the centre of one of the foci a small branch of the 
 pulmonary artery occluded by a thrombus formed of pus cells 
 enclosing large numbers of diplococci was found. It seemed 
 probable that this thrombus may have come as an embolus from 
 the meninges and may have produced the infection of the 
 surrounding tissue. The organisms were also found in the pus 
 cells in some of the bronchi within the consolidated areas, but 
 they were not found in the bronchi at a distance. The peri- 
 vascular lymphatics were dilated and contained coagulated 
 material, pus and fibrin. 
 
 Spleen. 
 There is a great variation in the size of the spleen. In 
 general it is not much enlarged, and is probably smaller than 
 in most of the acute infectious diseases. In only three cases 
 was it found considerably enlarged ; in one of these it weighed 
 four hundred and ten gms., in one three hundred and seven 
 
122 
 
 and in one three hundred and two gms. The average weight 
 of the adnlt cases was one hundred and sixty-three gms. It 
 is rather remarkable that in the two acute cases complicated 
 with croupous pneumonia the spleen should have weighed in 
 one eighty gms. and in the other eighty-five gms. The small 
 spleen was normal on histological examination. In the largest 
 spleen, which was macroscopically rather soft, there was no en- 
 largement, but rather a diminution in the size of the malpighian 
 bodies, with considerable diminution in the lymphoid cells. In- 
 creased size of the spleen was due chiefly to acute hypersemia. 
 At the beginning of our study of the disease we were of the 
 opinion that the smallness of the spleen could serve clinically 
 as a differential mark in distinguishing this form of meningitis 
 from the pneumococcus form, but a small size is not suflSciently 
 constant to be of service clinically. In some of the more chronic 
 cases the capsule of the spleen was wrinkled, showing that the 
 spleen had been larger. The average duration of disease in 
 the three cases of enlarged spleen was five days. 
 
 Lymphatic Glands. 
 The lymphatic glands in the uncomplicated cases were never 
 found enlarged. Microscopically the blood vessels were injected, 
 but there was no alteration in the histological structure of the 
 gland and no dilatation of the lymph spaces. 
 
 Liver. 
 The liver presented but little abnormal. It was generally 
 rather pale and cloudy on section. In three cases microscop- 
 ically there was slight increase in the fibrous tissue, with cellular 
 infiltration. In one case, where it was enlarged, the cells were 
 swollen, granular and fatty, and there were numbers of leucocytes 
 in the capillaries. In one case there were foci of purulent infiltra- 
 tion in the enlarged portal spaces. There were no foci of necrosis 
 such as are sometimes found in some of the infectious diseases. 
 
 Kidneys. 
 In two cases acute lesions were found in the kidney. In one of 
 these the kidney lesion had nothing to do with the meningitis, the 
 
128 
 
 boy having become infected with diphtheria, of which he died, 
 after having practically recovered from the meningitis. The 
 kidneys in this case were swollen, the glomeruli enlarged and 
 opaque, showing as yellowish points. Under a low power the 
 glomeruli were prominent. About most of them there was a darkly 
 stained mass, composed of fibrin and blood. The interstitial 
 tissue was dilated. With high power the convoluted tubules were 
 everywhere swollen, in some places entirely filling up the lumen, 
 and the cells in some places were filled with hyaline granules. 
 In a large number of tubules there was haemorrhage, and in places 
 they were filled with masses of definite fibrin. In a few places 
 in the intermediate zone of the kidney there were found both 
 in the vessels and in the interstitial tissue the large cells 
 characteristic of acute interstitial nephritis. Around most of 
 the glomeruli there was a mass of fibrin, partly reticular, partly 
 converted into hyaline masses. In places in the glomeruli groups 
 of vessels were necrotic and here and there were haemorrhage 
 and leucocytes with broken-down nuclei in the tissue. Some 
 of the glomeruli were completely necrotic. The haemorrhage and 
 fibrinous material in the capsules of the glomeruli extended into 
 the tubules leading off from them. The kidney lesions in this 
 case should be attributed not to the meningitis but to the diph- 
 theria, although such glomeruli lesions are extremely uncommon in 
 diphtheria. In this case there was complete anuria for two days 
 before death. 
 
 In one other case there was acute haemorrhagic nephritis. 
 In this case there was an accompanying acute pericarditis, the 
 organisms causing which could not be ascertained. In two 
 cases there was a minor degree of chronic interstitial nephritis. 
 The only lesions found in the kidneys which could be properly 
 attributed to the meningitis were acute degenerative lesions, 
 which were always present. In one case there was an abcess 
 in the seminal vesicles. The case was accompanied by croupous 
 pneumonia, and on both cover-slip examination of the contents, 
 and in the cultures only pneumococci were found. On micro- 
 scopic examination, in addition to the numerous pneumococci a 
 small number of swollen and degenerated diplococci were found 
 in the pus cells. 
 
124 
 
 Intestinal Canal. 
 
 The intestinal canal was found normal in every case save in 
 the case accompanied by diphtheria, and in this the usual 
 swelling of the follicles was found. This is interesting in view 
 of the fact that swelling of the follicles and even ulceration have 
 been described in the disease. 
 
 In one case an abscess of the tonsil was found, in which 
 characteristic diplococci were found on cover-slip examination 
 and cultures. No sections of this were examined. 
 
 Heart. 
 The heart was not examined microscopically as a matter of 
 routine. In several cases in which sections were made of it 
 it was found normal. In two cases there was an acute peri- 
 carditis, combined in one case with foci of necrosis and purulent 
 infiltration in the myocardium. No diplococci were found in 
 connection with these lesions. 
 
 Skin Lesions. 
 Lesions of the skin were found in but one of the cases which 
 came to autopsy. In this case over upper and lower extrem- 
 ities, chest and abdomen there were numerous small, dark 
 purplish spots in the skin, varying in size from a pin's head 
 up to that of a pea. The smaller ones were not elevated 
 above the surface. In many of the larger ones the centres were 
 more opaque and slightly elevated. They could not be made 
 to disappear on pressure, but remained more sharply marked, 
 the blood being pressed from the surrounding hypersemic vessels. 
 On microscopic examination of these areas there was intense 
 congestion and dilatation of the blood vessels of the skin in 
 the area and in the surrounding skin. Immediately beneath 
 the epithelium there were small and diffuse haemorrhages. In 
 the deeper tissue about the sweat glands and extending down 
 into the fat the haemorrhages were more diffuse and more 
 extensive. The largest hsemorrhages were found in the sub- 
 cutaneous fat. The deep vessels of the skin and the vessels 
 
125 
 
 of the fat were intensely congested. There was some prolif- 
 eration around the superficial blood vessels throughout the entire 
 area. In the centre corresponding to the area of haemorrhagic 
 infiltration beneath the epithelium there was some infiltration 
 with pus cells. In the larger areas with a yellowish centre the 
 epithelium was infiltrated with pus, and one of the specimens 
 showed the upper layers of the epithelium slightly elevated by 
 the accumulation of pus cells beneath. No diplococci were 
 found in the pus cells in these areas. In one case the herpetic 
 vesicles on the lip were examined. In them there was an intense 
 infiltration with pus cells in the tissue around the vessels with 
 proliferation of the fixed cells of the tissue. Here also no 
 diplococci were found in the pus cells. 
 
 CLASSIFICATION OF THE DISEASE. 
 
 Hirsch^^ divides the disease into the following form : — 
 
 1. Meningitis cerebro-spinalis epidemica siderans. 
 
 2. Meningitis cerebro-spinalis epidemica abortiva. 
 
 3. Meningitis cerebro-spinalis epidemica intermittens. 
 
 4. Meningitis cerebro-spinalis epidemica typhoides. 
 Striimpel,^" while in the main adopting the classification of 
 
 Hirsch, thinks that the so-called abortive form should include 
 the mild cases which begin with the phenomena of the disease 
 in an intense form and which rapidly recover. 
 
 While recognizing the futility of attempts to classify a dis- 
 ease, it would probably be well for practical purposes to recog- 
 nize certain types, the differences between which depend on the 
 intensity and duration of the disease. There were no cases 
 seen of what might be regarded as the abortive form of the 
 disease. Cases of this have been reported in early epidemics 
 in which patients would be suddenly attacked with the phe- 
 nomena of the disease in an intense form, and in a short while, 
 often in twenty-four hours, all the symptoms would disappear.* 
 These cases were most frequently seen in children, and occurred 
 
 * Such cases would be seen more likely in private practice than in hospitals. 
 
126 
 
 in the course of severe epidemics. It is very possible that in 
 many cases these sudden symptoms may have had some other 
 origin, and only the presence of an epidemic caused them to 
 be referred to meningitis. Until the diagnosis in these cases 
 shall be confirmed by spinal puncture they must always remain 
 in doubt. 
 
 We can distinguish an acute type which will include the 
 fulminating type. In the acute should be reckoned those cases 
 in which the active symptoms last not more than fifteen days. 
 In these acute cases the term of the patient in the hospital is 
 much longer, but he is then recovering from the conditions which 
 the disease has left. In the fulminating type those cases should 
 be included which are fatal within forty-eight hours from the 
 onset. The chronic form includes those cases in which the 
 symptoms from the beginning are not so active, and in which 
 during the course of the disease there are remissions and exacer- 
 bations. 
 
 The intermittent form is founded mainly, on the character of 
 the temperature. In this there may be complete intermissions 
 of the temperature with or without abatement of the other phenom- 
 ena. It would seem probable, from some results which have 
 been obtained from spinal puncture, that the exacerbations in 
 this type correspond to multiplication and fresh invasions of 
 the organisms causing the disease, they having previously been 
 quiescent. 
 
 Acute Type, including Fulminating Cases. 
 The very acute type of the disease appears to have been more 
 common in the early epidemics than in the late. In Jackson's 
 report to the Massachusetts Medical Society^*^ he says many of the 
 cases died suddenly in ten to twelve hours, others in twenty-four, 
 thirty-six, or forty-eight hours after the first symptoms. Some 
 physicians who had much experience with the disease considered 
 the patients safe if they passed the first twenty-four hours without 
 mortal symptoms. North^^ says that patients may die in the first 
 twelve to twenty-four hours. Woodward'^*^ says death often ap- 
 
127 
 
 peared in ten to twelve hours after the first attack. Lowy/^ in 
 the epidemic in Papa, had one case in which death took place in 
 twelve hours ; in another, in three days. 
 
 Frew" gives the following history of a fulminating case. Girl, 
 aged eight and a half years, in good health up to the evening of 
 February 28, when she went to bed complaining of headache. 
 She afterwards arose and stood by the fire for some time, and 
 was found in the morning at 4 a.m., almost comatose. She com- 
 plained of thirst, and asked for water. She drank greedily, but 
 vomited it immediately afterwards, mixed with greenish matter. 
 Previously she had vomited in bed. At 6 a.m. she got out of 
 bed, partially unconscious, and walked across the room to procure 
 more water, which she immediately vomited. She seemed to be 
 shaking all over, and died at 9 a.m. 
 
 Giuliui'" reports such a case in a child five and a half years old. 
 At 5 P.M. she was suddenly attacked with pain in head, weakness, 
 pain in bones and chill ; at 6 p.m. vomiting and diarrhoea came 
 on, which continued during the night, together with great rest- 
 lessness, fever and thirst. In the morning at 6 o'clock general 
 convulsions occurred, varying with spasmodic cramps of both 
 upper and lower extremities. These convulsive movements ap- 
 peared whenever the skin was touched. At 9.30 consciousness 
 was lost. Urine and fgeces were passed unconsciously. Tem- 
 perature of skin increased, pulse hardly perceptible ; abdomen 
 retracted ; death took place shortly afterwards. 
 
 Haiiser'^ reports a case in which death took place five hours 
 after the initial symptoms. Many of Eichter's^^ cases were ful- 
 minating, death taking place in twelve to fourteen hours. In 
 Klarner's" cases death took place in one in ten and another in 
 twelve hours. 
 
 Bauer^*^ thinks that in the beginning of epidemics these very 
 acute cases are more common than towards the end. There have 
 been very few post-mortem examinations on these fulminating 
 cases reported, and there are no reports of microscopic exami- 
 nations. In the post-mortem examinations which have been 
 made, no exudation was apparent to the naked eye. There was 
 
128 
 
 intense hyperaemia, with cloudiness of the meninges. In an au- 
 topsy by Haiiser on his first case, which died in six hours, there 
 was no pus, but simply cloudiness of the meninges. 
 
 That extensive lesions both in the meninges and brain can be 
 produced in a short time is seen in the case of experimental 
 meningitis in a goat. The duration of the disease in this case 
 could not have been more than twelve hours. 
 
 Eight of our cases were extremely acute. In five of these the 
 time from onset to death was three days, in one two days and in 
 two about thirty-six hours. Certainly in one of these cases the 
 history seemed to have been at fault, for at the autopsy there was 
 extensive diplococcus pneumonia. 
 
 Chronic Type. 
 
 The chronic form has been seen in all of the epidemics. 
 Woodward'''^ says that some patients survive the acute symptoms 
 and afterwards die, seeming to sink away under the load of the 
 disease. They become cold and die comatose, with all the marks 
 of general mortification. ClozeP gives a peculiar case of the 
 chronic form. A soldier was carried in a delirious condition into 
 the hospital on the 21st of May. On the 29th all the symptoms 
 of excitation had disappeared. The patient fell into a coma and 
 remained in this condition for two months. He speaks of another 
 case, which lasted from the 16th of February until the 6th of May. 
 Daga^* gives a typical history of a chronic case which lasted from 
 the 19th of March until the 27th of May, and which eventually 
 recovered. 
 
 Osier®* reported a case of blindness following chronic meningitis 
 in which there was gradual restoration of sight. The child had a 
 typical acute attack five months previously. This may have been 
 the remittent form, for the report says she recovered and was 
 sitting up in bed, then had a second attack with high fever and 
 stiffness of the extremities. 
 
 Martin and Levall (Daga") give an admirable account of this 
 chronic form. They say that there is as much danger at the end 
 as at the beginning of the disease. Recovery takes place with 
 difficulty, and it is impossible to say when it begins. There may 
 
129 
 
 be weakness of the limbs, paralysis of various muscles, and after 
 the paralysis disappears the limbs may remain feeble. 
 
 Long-continued diseased conditions which may be due to faulty 
 enervation are not uncommon. The wretched patients may be 
 reduced to skeletons. The skin is dry, the face without 
 expression, they lie on their beds heavily covered, silent, 
 indifferent to what is taking place around them. They answer 
 with difficulty questions addressed to them. They have no 
 appetite for food, and the stomach often rejects the food which is 
 taken. The temperature is diminished (in one case Daga saw 
 it descend to 34^° C), the marasmus continues, and they 
 eventually die. 
 
 Leyden® says that if the first attack does not kill there may be 
 a return of the process, and the patients may eventually die in the 
 long convalescence. 
 
 The cases reported by Hart^ in Birmingham seem nearly all to 
 have been of the chronic form. The shortest case lasted three 
 weeks, the longest fourteen weeks. In the long-standing cases 
 there was great emaciation. In thirteen of the fatal cases in this 
 epidemic the average duration of the disease was forty-three days. 
 In one case, in which a post-mortem examination was made, the 
 duration was seventy-four days, and in another the time given was 
 thirty days, and may have been much longer. In two of the cases 
 which recovered, and in which the disease ran a typical chronic 
 course, with numerous complications, remissions and exacerba- 
 tions, the duration was five months. The cases described by 
 Hirsch^ as the typhoid form come under the chronic type. 
 
 The symptoms in these chronic cases may be due to the 
 persistence of conditions left by the acute attack. The exudation 
 may not be absorbed completely and a slow form of inflammation 
 may be developed. It is probable also that an extensive and 
 general neuritis may follow. 
 
 The iNTERJVnXTENT AND REMITTENT TtPES. 
 
 These types are common. The disease is characterized by 
 decided remissions, or in some cases actual intermissions, in 
 which not only the fever but all of the other symptoms of the 
 
130 
 
 disease abate. The remissions may be followed by exacerbation 
 of all the symptoms. These cases are probably due either to the 
 successive involvement of parts of the meninges which have been 
 hitherto free from inflammation or to a fresh growth of the 
 organisms. A case seen at the Children's Hospital would point to 
 this. In this case two spinal punctures made at periods of 
 remission showed an almost clear fluid, with absence of organisms 
 microscopically or in culture. A spinal puncture made during one 
 of the exacei-bations gave a cloudy fluid, containing numerous pus 
 cells and diplococci. In the present epidemic there have been 
 numerous cases of this form. Cases 11, 50, 70, 72 and 108, 
 with temperature charts, show the characteristics of this form. 
 Leyden®- gives a case which was marked by complete intermission 
 of all symptoms. Child aged sixteen years was taken ill on the 
 19th of April with headache, pain in the neck and vomiting. On 
 the 24th of April she returned to school, and remained well until 
 May 1. She was again taken with vomiting and intense pain in 
 the head. From the 7th to the 11th of May she was again in 
 school. On the 11th there was a chill, headache, intense pain in 
 the neck, piercing pain in the eyes, continued vomiting and 
 delirium. Throughout this attack vomiting was seen to be one of 
 the most dangerous symptoms, as it prevented the patient from 
 taking any nourishment. There was slow recovery by June 19. 
 Lowy saw one case in which there was a relapse three weeks after 
 the disease was apparently recovered from. The second attack 
 began with vomiting, intense headache, etc., just as the first 
 attack did. Meschede™ reports a case which showed an intermit- 
 tent type during the fourteen weeks of the disease. It began 
 with chills, vomiting, painful stiffness of the neck and neuralgic 
 pains. Henoch'^ speaks of the frequent intermittent course of the 
 disease. Most of his cases were in children. The disease began 
 with the usual acute symptoms, then the fever diminished and the 
 symptoms disappeared. After a short interval of twenty-four 
 hours or several days all of the symptoms again appeared and the 
 general condition became worse. In these cases there was a 
 general absence of the phenomena which point to the involvement 
 of the spinal cord. 
 
131 
 
 SYMPTOMS. 
 
 Wunderlich^*' divides the symptoms of the disease into two 
 groups : in the first group, he includes those which depend 
 upon the local disturbances of the cerebro-spinal organs ; and in 
 the second, those which must be regarded as evidence of a general 
 disturbance of the organism. Among the constitutional symptoms 
 he speaks of the enlargement of the spleen, the eruption of the 
 skin, haemorrhages, and secondary inflammations, especially of 
 the lungs. In the most severe and rapidly fatal cases the 
 symptoms of both groups seemed to be united. In the least 
 severe cases the nervous symptoms are more predominant and are 
 more important for diagnosis. 
 
 Berg" divides the symptoms into three classes : — 
 
 1. Those produced by the poison of the disease, chills, con- 
 vulsions, fever, vomiting, nasal catarrh, constipation, skin erup- 
 tions, emaciation and affections of the joints. 
 
 2. Symptoms produced by inflammation of the cord, stiffness 
 of the neck, opisthotonos, pain along spine, hemiplegia, difficulty 
 in micturition, incontinence of fjeces and urine. 
 
 3. Symptoms produced by inflammation of the brain, headache, 
 slow pulse, hydrocephalic cry, vertigo, convulsions, delirium, 
 stupor, coma or coma vigil, Cheyne-Stokes respiration, eye symp- 
 toms, ptosis, strabismus, internal inflammation of the eye, con- 
 junctivitis, corneitis, paralysis, hemiplegia and paraplegia. 
 
 "We have not made any attempt at such a classification of the 
 symptoms nor is it possible with our present knowledge to do so. 
 
 Vomiting. 
 Leyden®- regards vomiting as one of the most common symptoms 
 of the disease. It may become a complication which seriously in- 
 terferes with recovery. In one of the cases reported by Leyden 
 there was constant vomiting, which prevented the patient from 
 taking food, and which constituted one of the most dangerous 
 symptoms of the case. In our one hundred and eleven cases 
 vomiting was absent in but forty-one, and in nearly all of these 
 stupor and unconsciousness or delirium was marked from the 
 
132 
 
 beginning. Vomiting may appear among the initial symptoms, 
 or later in the course of the disease. It is generally regarded 
 as cerebral in origin, and due to direct or reflex stimulation of the 
 vomiting centre.^ 
 
 Delirium. 
 
 In all of the accounts of epidemics which we have gone over 
 delirium is mentioned as among the most common symptoms. 
 North says that violent mania may come on in a few hours after 
 the onset, especially in sanguine young men. It was present in 
 sixty of the cases reported by us. The character of the delirium 
 varied greatly, sometimes being so violent that the patient had to 
 be forcibly restrained ; in other patients it was of the low mutter- 
 ing variety. In many cases it developed very early, and in others 
 at a late period of the disease. It was not more frequently present 
 in the cases which died than in those which recovered. Some 
 patients were delirious from the time they entered the hospital 
 until death ; in others there were periods of delirium, alternating 
 with periods of consciousness. The attacks of delirium were not 
 always coincident with increase of temperature and aggravation of 
 the other symptoms. 
 
 Pain. 
 
 Pain, sometimes limited to the head, sometimes extending all 
 over the body is also a common symptom of the disease. North 
 says that in the acute forms of the disease the pain is often 
 agonizing ; in the more common form the pain in the head and 
 limbs is less severe. Fiske"' gives the following graphic descrip- 
 tion of the character of the pain: "In some cases a pain 
 resembling the sensation felt from the sting of a bee extends 
 from the extremities of the fingers or toes, it darts from the 
 foot or hand to some other part of the limbs. After traversing 
 the extremities, generally on one side only, it seizes the head 
 and flies with the rapidity and sensation of electricity over the 
 whole body, occasioning blindness, fainting, nausea, with inde- 
 scribable distress about the precordia." 
 
 Almost all the patients in the epidemic reported by Gahlberg-'' 
 complained of severe pain in the head. The pain was so severe 
 
133 
 
 that the patients often tore the hair or struck the head against 
 the wall. The pain often showed an intermittent character, 
 coming on from day to day at the same time. 
 
 Levy*'" says that hypersesthesia of the skin was constant in his 
 cases, and could be made out even in a comatose condition of 
 the patients. It might extend over the entire body, or it 
 might affect only certain portions. The patients begged not to 
 be touched. There was often spasm of the muscles of the skin. 
 Almost without exception pain was a constant phenomenon in 
 the cases observed in this epidemic. The headache was often 
 agonizing, and was felt either generally or to a greater degree 
 in certain portions of the head. Patients often complained of 
 headache in the occipital region, extending down the back ; 
 in other cases the headache was frontal, and often assumed 
 the character of an intense neuralgia. In a few cases, mostly 
 in children, the first symptoms of the disease were colicky pains 
 in the abdomen, and in some cases pains in the extremities. 
 Patients often buried the head in the pillow to shut out light 
 and sound. In the course of the disease the pain varied in 
 character and intensity. There were periods in which the 
 patient was free from pain, alternating with periods in which 
 the pain would become more intense. These severe attacks of 
 pain were often followed by periods of unconsciousness. Pain 
 was more constant in the head than in any other part. The 
 pain suffered can easily be accounted for. The general pain 
 in the head is due to the inflammation of the meninges. The 
 neuralgic character of the pain may in some instances be referred 
 to the extension of the process from the meninges to the Gasse- 
 rian Ganglia ; the pain in the cervical region and back may 
 be referred to pressure exerted by the exudation on or inflam- 
 mation of the posterior nerve roots. 
 
 Neck Symptoms. 
 Symptoms referred to the neck were found in all but twenty- 
 eight cases. In many cases there was pain in the neck, with or 
 without pressure. In many there was simple stiffness in the 
 muscles, without contraction or retraction of the head. In all 
 
134 
 
 these cases any attempts to move the head or neck increased 
 the pain. The muscle contractions were sometimes limited to the 
 neck ; in some cases the muscles of the back were also affected, 
 producing opisthotonos. In one case in which the neck symptoms 
 were absent the post-mortem examination showed that the cervical 
 cord was very slightly affected. It is obvious that all these 
 symptoms can be referred to the effect of pressure on or inflamma- 
 tion of the spinal nerve roots. 
 
 Coma, etc. 
 Various disturbances of consciousness, which varied from stupor 
 and drowsiness to deep coma, were noted. In some cases coma 
 came on in the beginning, and the patients remained in a comatose 
 condition until death ; in other cases it was among the later 
 symptoms. StriimpeP^^ finds the same variations in the cerebral 
 symptoms a in the temperature. Variations may appear not 
 only from day to day but from hour to hour. Insensibility will 
 suddenly give place to consciousness, intense pain in the head may 
 cease, and a marked opisthotonos may suddenly relax. 
 
 Paralysis. 
 
 Paralysis is not uncommonly observed. It may develop during 
 the disease and disappear shortly, or it may persist for some time. 
 We have not found any cases recorded in which the paralysis was 
 permanent. 
 
 Gahlberg^ reports paralysis of the bladder in one case ; in 
 another, paralysis of the right side of the face and of the right 
 upper and lower extremity. In one case there was paresis of 
 the tongue, which disappeared in eight weeks after recovery. 
 Mosler^' reports, in one case which recovered, paresis of the 
 lower extremities. Baxa- found that the disease was often 
 accompanied and sometimes followed by paralysis. In three 
 out of twenty-nine cases reported by Leichtenstern*^"^ there was 
 complete hemiplegia, including the facial nerve, and in one case 
 paralysis of all the extremities, including the rectum and blad- 
 der. In one of Ziemmsen's cases, reported by Sittman, there 
 
135 
 
 were left hemiplegia and facial paralysis which passed off in a 
 few days after recovery. Striirapel observed in one case 
 unilateral facial paralysis ; in another, well-marked paralysis of 
 the lower extremities, and in this case the cerebral symptoms 
 were not so marked as the spinal. In our cases paralysis was 
 rare. In two cases there was unilateral facial paralysis ; in 
 one, bilateral ; in one paralysis of the right leg ; and in two, 
 complete hemiplegia. In one of the cases of hemiplegia in 
 which a post-mortem examination was made the exudation in 
 the meninges was much more abundant on the side opposite 
 the paralyzed side, and there was marked purulent infiltration of 
 the cortex. Minute foci of haemorrhage with surrounding puru- 
 lent infiltration were found in the internal capsule. 
 
 SKIX. 
 
 Lesions of the skin seem to have played a greater part in the 
 descriptions of the early epidemics than in the more recent. In 
 the early epidemics these lesions gave the commonly accepted 
 name of spotted fever to the disease. Jackson says the skin 
 lesions may occur in any stage of the disease. A rash or miliary 
 eruption may appear. This may itch and the skin be torn by 
 scratching, resulting in the formation of ulcers. He describes 
 particularly the appearance of large blisters, often from two to 
 five inches in length, which seem to have been more common in 
 the reports of the disease from "Worcester than elsewhere 
 (Woodward™) . It is more than probable that these large blisters 
 were due rather to the treatment than to the disease. Sweating 
 was induced by placing billets of wood, which had been immersed 
 in boiling water, in bed with the patient. Such a billet of wood 
 in bed with an unconscious patient is capable of producing such 
 blisters very easily. Every one is acquainted with similar con- 
 ditions which have been produced by hot water bottles. 
 
 The frequency of the skin affections in the first epidemics 
 varied much, according to the different observers. One found 
 that in eighty cases only four had any affection of the skin. 
 Another estimates them as appearing in one-half of all his cases. 
 
136 
 
 Jackson did not regard these lesions of the skin as the seat of the 
 disease, but as being merely symptomatic. 
 
 Vieusseaux does not mention these lesions of the skin. North 
 gives a very good description of the eruption. He says "they 
 take the form of blind haemorrhages, where the blood flowing from 
 the vessels of the skin is detained beneath the cuticle, forming 
 petechial spots. So frequent was this species of haemorrhage in 
 the early part of the epidemic that it was considered one of the 
 most striking characteristics, and gave rise to the name petechial 
 or spotted fever, which has been very generally but inaccurately 
 given to the disease. These spots appear commonly on the face, 
 neck and extremities, frequently over the whole body. They were 
 generally observed in the early stages of the disease ; in size the 
 head of a pin, and a six-cent piece would mark the two extremes. 
 They were evidently formed of extraversated blood. They do not 
 arise above the surface and do not recede upon pressure. In 
 color they vary from a common to a very dark purple, and the 
 darker the shade the more fatal the prognosis. These spots, 
 which in 1806-1807 marked almost every case, in 1808-1809 were 
 rarely observed." 
 
 Woodward'^^ says there was soreness of the flesh, and spots 
 appeared on the skin the size of half a common duck shot, 
 resembling blood blisters. 
 
 North, in a letter to the Philadelphia Medical Museum, says 
 further that some of the patients have in the true skin spots which 
 resemble flea bites. One patient was covered all over with such 
 spots for a number of days, but more commonly there were a few 
 scattered ones on different parts of the body. They are of 
 different grades of color, from red to dark, some resembling 
 bruises. Fiske says an eruption of the skin is not a constant 
 attendant on the disease. It generally comes on in some form or 
 other, according to the violence of the disorder ; sometimes 
 appearing as a miliary eruption over the entire body. It may 
 appear in patches in the bend of the arm or the breast or neck, 
 without any discoloration at first. These skin eruptions seem to 
 have been especially abundant in the epidemics in Ireland in 1866 
 and 1867 . 
 
137 
 
 Gordoa^"^ observed ia one case an eruption something like 
 measles, but the patches were irregular in size and shape. They 
 were dark colored, rough looking on the surface and thickly 
 interspersed with petechias. In another place he describes a 
 definite eruption, which conies out with great rapidity and is 
 found on all parts of the body, but chiefly on the lower extrem- 
 ities. It is of a very dark color, sometimes deep brown or 
 purple, or even black. In some cases it is studded with black 
 spots, appearing on the nose or face of the patient as though 
 a quantity of black ink were scattered over his face. 
 
 Marston found in very few cases an intense eruption of 
 petechiee, which was followed by rapid coma and collapse. The 
 rapidity with which this very dark eruption appeared, its great 
 extension and the deep collapse which accompanied it gave to 
 the cases a frightful appearance, and caused the people to describe 
 it as the black death. 
 
 In all of the investigations on this epidemic in Ireland it 
 was seen that the nervous symptoms preceded the affection of 
 the skin even in the most rapid cases. 
 
 In Upham's cases, in Newbern, petechias often identical with 
 those of true typhus were seen in all parts of the body except 
 the face. 
 
 In the epidemic reported by Hermann and Kober^ petechise on 
 the skin or conjunctiva were frequently seen. Many of the 
 cases reported by Richter^^ had petechise and ecchymoses. 
 Gahlberg says that the skin eruptions may vary, and he has 
 seen one case in which it was ver}^ similar to measles. In the 
 report by Tipton"^ purpuric spots occurred in some cases, but 
 they were generally absent. 
 
 Herpes is far more common than any other form of eruption. 
 It is more common on the lips and nose, but may appear on 
 other parts of the face and even elsewhere on the body. 
 
 Klemperer''' speaks of the frequency of herpes in meningitis, 
 and says it is more common in the epidemic than in any other 
 form. 
 
 Leichtenstern found herpes in twenty-six out of twenty-nine 
 cases examined. 
 
138 
 
 Frey^ describes herpes as very common in the epidemic re- 
 ported by him. 
 
 Hallenstein says that herpes is the most common of the skin 
 affections of the disease. It is most common on the nose and 
 mouth, then on the cheek, forehead, eyes and ears. More 
 rarely there is an eruption of the vesicles on the neck and ex- 
 tremities. RoUet^^® did not find herpes common in the cases 
 examined by him, although he says it was present in Strassburg 
 in nearly all the cases. Friis in the epidemic in Copenhagen 
 found herpes of the lips in seventeen cases. Decloux^^ found 
 herpes and other skin eruptions in all of the cases which recovered. 
 
 In this series of one hundred and eleven cases herpes was 
 mentioned as occurring in thirty-five cases. It is possible that 
 its presence was not always noted. The amount of it varied 
 from an eruption of a few fine vesicles to an abundant eruption 
 of large vesicles. Cultures were not made from the contents 
 of the vesicles. 
 
 Petechise or larger hsemorrhagic foci in the skin were found 
 in eleven eases. They were most abundant in two fatal cases, 
 the duration in one case being two days, in the other seven 
 days. In the two-day case, that Of a child, there was present 
 all over the body an abundant eruption, which developed with 
 great rapidity. The spots were more commonly found over the 
 elbows and knees. Circumscribed areas of hypersemia which dis- 
 appeared on pressure were mentioned in a few cases. Hgemor- 
 rhages in the skin were found in but one of the cases in which 
 a post-mortem examination was made. In the centres of some 
 of these there was a beginning formation of pustules. 
 
 PNEUMONIA. 
 
 The relation between pneumonia and the epidemic meningitis 
 has been complicated by confusing other forms of meningitis with 
 this. Meningitis is sometimes seen in connection with acute 
 croupous pneumonia, and is due to a metastasis from the lungs. 
 And from this it has become a common belief that pneumonia 
 is a frequent complication even of epidemic meningitis. In most 
 
139 
 
 cases the character of the pneumonia is not defined, but it is 
 apparent that croupous pneumonia is referred to. 
 
 It has been frequently stated that epidemics of pneumonia 
 have occurred at the same time with epidemics of cerebro-spinal 
 meningitis, and this statement has been used by those who 
 sought in the pneumococcus the cause of epidemic meningitis. 
 We have not been able to find the authority for such a state- 
 ment. It is very possible that the opinion of the relation 
 between the two may be due to the fact that both diseases are 
 more common at the same time, — that is, in the late winter 
 and spring. Practically all of these accounts of the relation 
 between the two diseases come from clinical sources. 
 
 Levy^ remarks on the frequency with which congestion of 
 the lungs is found as a complication. He thinks this condition is 
 rather a consequence than a complication of the disease, and is 
 due to the hebitude of the patient and the dorsal decubitus. 
 
 Jaffe^*^'', who reported the epidemic in Hamburg, found but one 
 case of typical fibrinous pneumonia with meningitis, and the 
 clinical history of this case would rather show that the 
 meningitis followed the pneumonia and was probably due to 
 the pneumococcus. 
 
 Immerman and Heller*^ speak of the frequency of complica- 
 tions of croupous pneumonia with purulent meningitis at the 
 close of the epidemic in Erlangen in 1866. They say that after 
 a pause of several months, from August, 1866, up to January, 
 1868, thirty cases of pneumonia were seen, nine of which were 
 complicated with meningitis. This appeared at the end of the 
 epidemic, and they think there is no relation between the two, 
 but that the epidemic meningitis paves the way for the pneu- 
 monia. 
 
 Leichtenstern, in his admirable account of the epidemic in 
 Cologne, takes up the question, and does not believe that there 
 is any relation between the two. 
 
 Croupous pneumonia was found at the post-mortem examina- 
 tions of two of our cases. In these the pneumonia was the result 
 of infection with the pneumococcus which was found in the lungs, 
 while the diplococcus intracellularis was found in the lesions in the 
 
140 
 
 brain. In several of our cases there were small foci of broncho- 
 pneumonia and small areas of congestion in the lungs from which 
 the pneumococcus along with other organisms was obtained. 
 
 It is very possible that many of the cases of pneumonia which 
 have been reported in connection with epidemic meningitis were 
 not cases of genuine croupous pneumonia, but cases of diplo- 
 coccus pneumonia. This was found in eight cases and in one 
 the amount of lung involved was so extensive that it could have 
 been mistaken both clinically and anatomically for a case of 
 croupous pneumonia. Leichtenstern found no cases of croupous 
 pneumonia in the epidemic reported by him, and opposes the 
 prevalent view that the pneumococcus is the cause of epidemic 
 meningitis. He says " pneumonia is a disease spread over the 
 entire earth, and appears at all times, there being no land 
 immune from it. Epidemic meningitis is very rare, and in many 
 countries is still unknown. Croupous pneumonia attacks every 
 age, the disposition increasing somewhat with increasing age. 
 Epidemic meningitis is a disease which affects children and 
 young people ; beyond thirty-five there is slight disposition 
 towards it. Croupous pneumonia has a typical course and a 
 crisis ; epidemic meningitis has no crisis. The complications of 
 the two diseases are different. Epidemic meningitis frequently 
 shows multiple synovitis as a complication ; this is extraordi- 
 narily rare in croupous pneumonia. The affections of the eye, 
 etc., which are seen in meningitis, are extremely rare in pneu- 
 monia. The character of the exudation in the two diseases is 
 different, being more fibrinous in croupous pneumonia. It is 
 often difficult to make a differential diagnosis between menin- 
 gitis and severe pneumonia with predominant brain symptoms." 
 
 In these cases, according to Leichtenstern, at the time of the 
 crisis, the brain symptoms drop just as the other symptoms. He 
 thinks it is also possible to distinguish clinically between menin- 
 gitis arising as a complication of pneumonia and epidemic 
 meningitis. In meningitis following pneumonia contraction of the 
 muscles of the neck is often absent, while in epidemic meningitis 
 it is almo'st invariably present. Pneumonia-meningitis soon leads 
 to delirium and coma, while in the epidemic form the sensorium 
 
141 
 
 may be normal throughout the entire course. Pneumonia- 
 meningitis, moreover, is rapidly fatal, while the epidemic form is 
 frequently recovered from. The remissions and exacerbations, 
 the varying course and relapses, the following hydrocephalus, the 
 uncertain gait, the eye and ear affections, — are all exclusive 
 attributes of the epidemic form. 
 
 Runeberg^^ reports a case of pneumonia with following menin- 
 gitis which recovered, but in this case the symptoms of meningitis 
 were not definite. In one of Weichselbaum's cases there was 
 lobar pneumonia in connection with the meningitis. He found the 
 pneumococcus in the lobar pneumonia and the diplococcus in the 
 meninges. 
 
 Striimpel does not mention croupous pneumonia as a complica- 
 tion in his cases. 
 
 THE EYES. 
 
 Symptoms relating to the eyes have a prominent place in the 
 descriptions of epidemics of meningitis. North describes dila- 
 tation and in some cases contraction of the pupils, redness and 
 suffusion of the conjunctiva, double or triple vision, and in a 
 few cases there was total blindness. Woodward says that the* 
 eyes are red and watery. The pupils are dilated in some cases, 
 in others they are small, like those of dying persons. Bestor'^® 
 says the eyes are often red and suffused, and the pupils are 
 enlarged. There may be double or triple vision, and in some 
 cases there was partial or total blindness after the first twenty- 
 four hours. Baxa- says blindness is often seen in cases which 
 recover. Friis-^ examined the eyes in thirteen out of thirty 
 cases, and in three of these cases he found congestion of the 
 optic papilla. Tourdes^^' found ophthalmia in six of his cases ; 
 in three cases it occurred during convalescence, and was not 
 severe. Daga,^^ in the epidemic in Metz, found purulent oph- 
 thalmia in a number of cases, but he considers this to be an 
 accidental complication which is not usually dangerous. Wilson^^ 
 says the eyelids may be enormously swollen, and present the 
 appearance of purulent ophthalmia or suppurative inflammation 
 of the eye-ball. He thinks this may result from lack of sensa- 
 
142 
 
 tion and exposure of the eye. The anterior chamber often 
 contains pus and the choroid and iris are often affected. 
 Blindness may occur either as the result of clouding of the lens, 
 with adhesions and infiltration of the iris, or of atrophy of the 
 optic nerves. Knapp^*^ found eye symptoms in four or five per 
 cent, in all cases of meningitis. They appeared ordinarily during 
 the second or third week of the disease. The eye symptoms 
 often took the form of more or less intense choroido-iritis, which 
 could lead to blindness in three or four days. This condition 
 was often accompanied by injection of the conjunctivae and 
 infiltration of the cornea, with adhesions and discoloration. 
 There was complete blindness in ten of the cases observed by 
 Mm. He does not think that the eye lesions can be regarded 
 as an extension of the inflammation from the meninges along the 
 optic nerves, but regards it as an acute idiopathic iritis. 
 Collins^^ observed, relatively frequently, serious affections of the 
 eyes, among which he especially speaks of irido-choroiditis with 
 separation of the retina, purulent infiltration of the eye and 
 atrophy. Hirsch describes conjunctivitis as an almost constant 
 symptom. 
 
 In the epidemic reported by Frey^ there was injection of the 
 conjunctiva, strabismus, turgescence of the eyeball and more or 
 less serious disturbances of sight. 
 
 In the epidemic described by Bllimm* both subjective and 
 objective eye symptoms were prominent. The patients com- 
 plained of light. In one case there was destruction of the cornea. 
 He thinks that softening of the cornea may be due to tropho- 
 neurosis. 
 
 Hallenstein^^ says the most frequent lesion of the eye is 
 paralysis of the oculo-motor nerves, producing dilatation of the 
 pupil, divergent strabismus and ptosis. Next to this comes 
 paralysis of the abducens with convergent strabismus. The con- 
 junctiva at the height of the disease is injected, reddened and 
 swollen. There are also affections of the cornea, appearing as 
 clouding and ulceration, paralysis and spasms of the eye muscles, 
 abnormal narrowness or dilatation of the pupils, and even com- 
 plete blindness. The blindness may result either from a purulent 
 
143 
 
 inflammation of the eye with separation of the retina and 
 destruction of the bulb, or from an optic neuritis. 
 
 Niemeyer^™ thinks that the affections of the eye arise from 
 imperfect nutrition of the tissue, due to inflammation of the 
 trigeminus. He founds his views on the fact that in meningitis 
 the same conditions of the eye are seen which come from the 
 destruction of the Gasserian ganglion. 
 
 Rudnew concludes that inflammation of the eyes is not sec- 
 ondary to the meningitis, and does not arise by an extension of 
 the process from the membranes of the brain to the eye. It 
 comes simultaneously with the affection of the meninges, and is 
 due to the same cause. Disturbances of innervation of the eye 
 were seen in almost all of Striimpel's cases. He says the 
 ophthalmoscopic investigation of the eye may show changes 
 without the sick person being aware of any disturbance of sight. 
 
 Randolph*^, in the epidemic in Lahaconing, examined the eyes 
 in thirty-five cases, twenty of which were fatal. He reports the 
 different cases in detail, and from this some idea of the character 
 and frequency of the lesions may be gained. In the thirty-five 
 cases examined the fundus was normal in but seven. Of these 
 seven cases one had divergent strabismus and dilated pupils. 
 The right eye was more often affected than the left. Every case 
 of strabismus was of the divergent variety. He found congestion 
 of the optic disc in many cases, and thinks this marks the begin- 
 ning of optic neuritis. There was atrophy of the optic nerves in 
 one case which recovered. Osler*^ has reported a case similar to 
 the one described by Jack (page 144), in which there was total 
 blindness following a case of meningitis with gradual recovery of 
 sight after months. Omerod''- found in one case internal 
 strabismus of the right eye, but the fundus of each was normal. 
 In one case there were purpuric spots on the conjunctiva. One of 
 the cases reported by Mills and CahalP was blind and deaf three 
 weeks before death. In the cases reported by us no systematic 
 examination of the eyes was made in all cases. 
 
 Various abnormal conditions of the eyes were noted in sixty- 
 seven cases. Strabismus, usually affecting both eyes, was noted 
 in twenty-eight cases. It was convergent in thirteen, divergent 
 
144 
 
 in eight, and in the remainder its character was not noted. 
 Conjunctivitis was not commonly present ; it was noted in but 
 ten cases, and in these the condition varied from injection of 
 the conjunctiva up to a purulent discharge. In one case the 
 purulent secretion of the conjunctiva was examined for bacteria, 
 but no diplococci were found. In many cases irregularity in 
 the pupils was noted. In one case there was slight bulging of 
 the eyes. No post-mortem examination of this case was made, 
 so that it cannot be known whether this condition was due to 
 purulent infiltration of the orbit. Nystagmus was seen in but 
 ten cases. In none of the cases which recovered was there 
 complete blindness. 
 
 We are indebted to Dr. Edwin E. Jack for the following de- 
 scription of the eye lesions observed by him in the cases seen 
 at the Children's Hospital : — 
 
 The conditions found were conjunctivitis, dessicating keratitis, stra- 
 bismus, contraction and dilatation of the pupil with little or no reflex 
 action, inequality of pupils, neuritis of various grades, from redden- 
 ing of the disc to violent inflammation of the choked-disc variety, post- 
 neuritic atrophy and purulent choroiditis. No cases of loss of vision 
 without ophthalmoscopic appearances such as might occur from trouble 
 at the convexity were observed, though one case in which no ophthal- 
 moscopic examination was made must remain in doubt. Visual aeute- 
 ness and fields of vision could naturally not be taken. There was no 
 implication of the orbital tissue in any case and no oedema of the conjunc- 
 tiva. Conjunctivitis was frequent. The dessicating keratitis seen was 
 due to the imperfect closure of the lids and secondaiy necrosis of 
 the cornea. Strabismus caused by paralysis or irritation of the ocular 
 nerves by exudation at the base was present in many instances, and 
 in those personally observed was always convergent. It is doubtful 
 if there was any paralysis of the third nerve except so far as the 
 pupillary branch was concerned. Strabismus seemed to have no con- 
 nection with the severity, length or outcome of the disease. Of all 
 the children still alive who had this symptom I have found but one 
 in whom the squint persists, though diplopia is not apparent. No 
 instances of conjugate deviation were noted. 
 
 Neuritis, present or past, as shown by atrophy of post-neui'itic character, 
 was present in at least six cases, and probably in more ; for, in addition 
 to the cases not seen, no case was recorded as having neuritis without 
 having definite signs in the way of cloudiness of the disc or distended or 
 tortuous vessels. It was suspected in others from the appearances, so 
 that the number is probably larger than stated. It is often hard, even 
 under the most favorable circumstances, to decide whether a disc is 
 
. 145 
 
 abnormal or not; but in these children, the struggles and movements of 
 the eyes making only a fleeting glance possible, mucus on the cornea and 
 in some instances an uneven surface, made the task still more difficult. 
 Neuritis was apparently no more common in the fatal cases than in those 
 who recovered, and was most marked in two childi-en who still live. 
 One of these had violent neuritis with htemorrhages, which had not then 
 gone on to atrophy, and the sight was apparently jDerfectly good. I have 
 recently seen this child. The vision is as good as ever, the discs are 
 normal, showing no traces whatever of the previous inflammation. 
 The other is a remarkable instance of restored vision after weeks of 
 blindness. The child was ill a very long time, was extremely emaciated 
 and had decidedly atrophic discs. Much to my surprise, two weeks ao-o 
 I found a vision which enabled the child to go about readily ; the disc 
 was more pink in color and the vessels were actually larger. Her 
 mother stated, perhaps with exaggeration, that the chikl could recoo-nize 
 her at a distance from the yard to the second or third story Avindow In 
 this case there was total deafness, which has persisted. 
 
 There were two eases of purulent choroiditis. This condition closely 
 resembles glioma of the retina. One of the children died, the other 
 lived, and is to-day perfectly well, with the exception of a useless rio-ht 
 eye. The fatal case was a very marked one, with a historj- of some 
 weeks' illness before entrance. It was said by the parents that the right 
 eye, meaning probably the lids, was swollen one week before, and that 
 after that the eye began to look small. When seen, the eye was much 
 smaller than the other, soft, had considerable ciliary injection, pupils mod- 
 erately dilated (atropin had been used), iris discolored, its pupillary edo-es 
 frayed and uneven, and from behind the lens was seen a yellow reflex 
 tinged with red, the whole making a typical picture of what is known 
 as metastatic choroiditis. This child was very ill, and in marked con- 
 trast with the other one, who came into the hospital looking perfectly 
 well, and indeed nothing out of the way could be found. The day pre- 
 vious he had had vomiting and slight fever. On the second day the eyes 
 were looked at and the fundus was normal. On the third day there was 
 vomiting, jjallor, coldness, weak pulse and the child seemed partially 
 unconscious, but was better in the evening. Strabismus was apparent. 
 Next day it was noticed that the right eye was red. In tAvo or three 
 days the child was all right again, the strabismus had disappeared, 
 and from that time he seemed well. At the first appearance of the in- 
 flammation in the eye, on account of great difliculty in examination, the 
 child screaming loudly even when approached, nothing was made out 
 except iritis and a deposit of lymph in the pupil. Later the typical yel- 
 low reflex was visible, making the diagnosis cei"tain,the general apjjear- 
 ance resembling that already described in the first ease, though the eye 
 was not so shrunken at that time. 
 
 This case is intei'esting for several reasons : first, the coincidence in 
 point of time of the only cerebral symptoms, and the beginning of the 
 process in the eye ; second, the fact that the lumbar jjuncture was neg- 
 ative. With reference to this, on account of the possible doubt it might 
 throw on the diagnosis, it should be stated that the patient's sister died 
 
146 . 
 
 at this same time, after less than a week's illness, of undoubted cerebro- 
 spinal meningitis. In her case lumbar jjuncture was positive and optic 
 neuritis was present. Third, it shows that this complication is not 
 limited to severe or fatal cases. 
 
 Notwithstanding the frequency of the eye complications in 
 cerebro-spinal meningitis, there have been but few anatomical 
 investigations of the eyes after death. Rudnew and Burzew 
 examined the eye in one case. Pus was found in the ciliary 
 region and in the vitreous. They regarded the lesions in the 
 eye as probably embolic. 
 
 Hoffman*^ reports an interesting condition of the eye following 
 meningitis. There was complete blindness in one eye in a case 
 which recovered, with ptosis, dilated pupils, immobility of the 
 eye-balls and swelling of the lids. This condition remained for 
 some time. He then operated, and found the sheath of the 
 optic nerves dilated into an ampular form and evacuated con- 
 siderable pus. 
 
 Saltini^^ investigated the eye in two cases of meningitis. One 
 eye was removed three and one-half minutes and the other four 
 or five minutes after death. He found total separation of the 
 retina and extensive inflammatory destruction especially of the 
 anterior equatorial parts of the uvea and retina. There was 
 also atrophy of the optic nerve, with cellular infiltration of the 
 sheath and of the septum. 
 
 Leichtenstern reports that at one autopsy all the cranial 
 nerves were bathed in the exudation, and the oculomotor nerve 
 was rosy red. There were no cases seen of involvement of the 
 optic nerve, and no cases of pan-ophthalmitis. 
 
 Confusion has also arisen, in that this form of meningitis 
 has not been distinguished from the pneumococcus and other 
 forms. Axenfeld^ reports four cases of metastatic inflammation 
 of the eye, due to the pneumococcus, and two of these were 
 from meningitis. One of his meningitis cases was secondary 
 to an acute endocarditis. He found no continuity between the 
 organisms in the sheath of the optic nerve and those in the 
 interior of the eye. There were fresh capillary emboli in the 
 retina, which he regarded as the source of the eye lesions. He 
 
147 
 
 does not think that it has been shown in a single undoubted 
 case that there is a continuity between the inflammation in the 
 eye and that in the meninges. In one of the autopsies reported 
 by Klebs^^ there was purulent infiltration of the tissues of the 
 orbit. 
 
 When we review the eye lesions of this disease, it can easily be 
 seen that they are due to three causes. In the first place, there 
 may be neuritis or degeneration of the nerves of the eye, due to 
 their involvement in the exudation at the base of the brain without 
 any extension of the inflammatory process to either the orbit or 
 the eye. This condition seems to affect the oculomotor more 
 than the other motor nerves. The optic nerves may also be 
 involved in this exudation. Secondly, the inflammation from the 
 meninges may extend directly from the brain into the eye, the 
 route most frequently chosen being the pia arachnoid of this 
 nerve. All of the cases of purulent choroido-iritis, and the very 
 rare cases of suppuration in the orbit, are probably due to such an 
 extension. Most of the ophthalmologists seem to have a deeply 
 rooted belief that these conditions are due to metastasis, but it is 
 plainly not a metastasis but a direct extension. Undoubtedly 
 there are cases of metastatic choroido-iritis seen in connection 
 with other forms of meningitis, but in these cases both the menin- 
 gitis and the eye lesions are due to metastasis. Such are the 
 cases of meningitis accompanying acute endocarditis, croupous 
 pneumonia and certain other infectious inflammations. The 
 lesions of the cornea may be due to an extension of the inflamma- 
 tion to this from the iris and ciliary region, which was 
 undoubtedly true in one case examined. The third cause of the 
 eye lesions, and that to which most of the cases of keratitis in 
 meningitis are due, is neuritis of the fifth nerve, with destruction 
 of the Gasserian ganglion and loss of sensation. There are no 
 lesions" due to tropho-neurosis. Purulent conjunctivitis, which is 
 frequently found, may also be due to this lack of sensation. We 
 have but one record of the examination of the pus from the con- 
 junctiva, and in this case no diplococci were found in the pus. 
 
148 
 
 EAR COMPLICATIONS IN MENINGITIS. 
 
 The symptoms relating to the ears play an important part in 
 all the descriptions of meningitis. That there should be dis- 
 orders of hearing is apparent from the study of the lesions. 
 In all the post-mortem examinations made by us in which the 
 auditory nerves were examined there was a greater or less degree 
 of involvement. The nerve was generally swollen and surrounded 
 by exudation. Microscopic examination showed in some cases 
 purulent exudation along the nerve sheath, with more or less 
 complete destruction and infiltration of the nerve. The studies 
 of nerve degeneration showed extensive degeneration of the 
 nerve fibres in all cases examined, the degeneration being most 
 marked in the more chronic cases. The bony ear was saved for 
 examination in a number of cases, but it has not been possible 
 to complete the microscopic examination. This has been done 
 by others, however, in a number of cases, and the anatomical 
 foundation of the ear symptoms has been established. 
 
 The first investigation on the condition of the internal ear in 
 epidemic cerebro-spinal meningitis comes from Heller,^"- who 
 examined the ears in two cases in the epidemic in Erlangen in 
 1865. In both he found acute purulent inflammation of the 
 labyrinth, which he thought was due to the extension of the 
 inflammation from the brain along the nerve. Schwabach^**^ 
 gives a more detailed account of the examination of the ears 
 in a case of otitis, which developed in the course of an attack 
 of meningitis. The symptoms of ear trouble developed seven 
 days after the beginning of the attack, and consisted in throbbing, 
 drumming, difficulty of hearing and unbearable pain. Death 
 took plac3 five weeks after the beginning of the disease. He 
 found great hypersemia of the vessels in the course of the 
 acoustic nerves and in all parts of the labyrinth, purulent 
 inflammation of the sheath of the acoustic and ecchymoses 
 between the fibres. There was abundant formation of granula- 
 tion tissue in some of the branches of the nerves and in the 
 ganglia, combined with suppuration and haemorrhage. Pus was 
 found in the peri-lymphatic spaces of the scala and other parts. 
 
149 
 
 There was slight purulent infiltration of the sheath of the 
 facial nerve on the right side. In the pus taken from the 
 middle ear by puncture of the drum he found enclosed in the 
 cells diplococci which he says resembled the pneumococci. (It is 
 most probable that this was the diplococcus intracellularis.) 
 Lucae^'^ examined the ears in a case of cerebro-spinal menin- 
 gitis which was fatal in twenty-four hours. At the post-mortem 
 examination he found a purulent infiltration of the meninges 
 which extended along the facial and acoustic nerves. The exu- 
 dation extended along the acoustic to the cochlea and vestibule, 
 and into the semi-circular cauaL There was no alteration of 
 the middle ear or of the drum membrane. 
 
 An interesting case is that reported by Schultze,™ who ex- 
 amined the ears of a deaf-mute, five years after an attack of 
 meningitis, to which the condition was due. There was atrophy 
 of both auditory nerves and formation of granulation tissue in 
 the labyrinth. Nothing remained of the organ of Corti. The 
 cavity of the cochlea was filled with osteoid tissue and round 
 cells. 
 
 Kochner says in the disease of the ear which follows menin- 
 gitis there may be ecchymoses with thickening and softening of 
 the membranous part of the labyrinth. Moos''^ says the inflam- 
 mation extends along the perivascular and perineural lymphatics 
 from the brain to the ear. From the perineurium of the acoustic 
 nerve the disease extends to the labyrinth. Merkel has found 
 destruction of the semi-circular canals in one ear. 
 
 In all these investigations it has generally been seen that the 
 disease of the ear was secondary to the meningitis, and due to 
 extension of the inflammation from the brain to the ear along 
 the nerves ; or, as Mosler''-^ has suggested, to an involvement of 
 the strise acoustics in the fourth ventricle. There was nothing 
 found in our cases which spoke in favor of this view of Mosler. 
 
 Some confusion has existed in the minds of writers as to the 
 relation between otitis and meningitis, some regarding the ear 
 affections as primary, others as secondary to the meningitis. 
 There are forms of meningitis which are secondary to ear dis- 
 ease, and result from the extension of the inflammation in the 
 
150 
 
 ear to the brain. The infection in these cases, according to 
 Korner,^'^ may take place by contact with the diseased bone 
 or by extension of the suppuration. In all the cases which 
 we have seen of this, the infectious organism was either the 
 pneumococcus or the streptococcus. The ear lesions of epidemic 
 cerebro-spinal meningitis are always secondary. 
 
 Voltoline^'^^ described as an independent disease inflammation 
 of the labyrinth, beginning with intense pain in the head, 
 vomiting, high fever and convulsions. It lasts for some days, 
 and usually ends in recovery. It often leaves deafness and 
 uncertain, trembling gait. One of the chief points which makes 
 Voltoline regard this as an independent disease, and not as a 
 complication of meningitis, is that it only affects children, and 
 in a short time tends to recovery. He finds that herpes of the 
 lips, so common in meningitis, is rare in the labyrinth disease. 
 In the ear disease vomiting is constant and may be absent in 
 meningitis. This view has been shown to be erroneous by Moos 
 and by Leichtenstern. Leichtenstern says there are slight abortive 
 cases of epidemic cerebro-spinal meningitis which lead to deafness 
 in consequence of a simultaneous affection of the labyrinth, so 
 that the affection of the labyrinth may seem to be the most 
 important or primary. 
 
 These ear lesions are the most common of the complications 
 of meningitis. Schwabach^**^ found that one-half the cases of 
 deaf -mutism were the result of disease of the central nervous 
 system. Moos'"' found that of sixty-four cases of meningitis 
 which recovered fifty-nine per cent, were deaf, thirty-one per 
 cent, had normal hearing and in seven the hearing was im- 
 paired. Out of forty-three cases deafness appeared in two on 
 the first day, in six on the second, in three on the third, in 
 seventeen between the fourth and tenth and in fifteen between 
 the fourteenth day and the fourth month. He thinks that it is 
 possible that the abortive form of epidemic cerebro-spinal men- 
 ingitis is the cause of many cases of early acquired deafness. 
 Erhardt observed twenty-seven cases of deafness after cerebro- 
 spinal meningitis, and comes to the conclusion that the severity 
 of the disease stands in no relation to the deafness. The deaf- 
 
151 
 
 ness appears suddenly, without pain, and, as a rule, in the be- 
 ginning of the disease. Jackson^' found purulent discharge 
 from the ears in a number of cases, and in a few there was 
 deafness on recovery. Friis^ found seven cases of ear disease 
 in thirty cases investigated by him. Of those that recovered, 
 two had otitis media, one otitis interna and one was partially 
 deaf without discoverable cause. Kuapp^*^ reports a case of 
 unilateral deafness. The character of the disorders of hearing 
 has been investigated. Kochner found, in the cases studied by 
 him in Wurzburg, many variations in the character of sound 
 perception. There were transitions from more or less difficult 
 hearing to absolute deafness. When deaf to ordinary sounds, 
 patients could often distinctly hear scratching noises. Bliimm^ 
 describes buzzing and hammering in the ears and hallucinations 
 of hearing. Mosler'^ gives the history of a case with slow re- 
 covery. At first there was total deafness, after a time loud 
 sounds could be distinguished ; there was ringing in the ears 
 during the entire time. The walk was at first trembling and 
 uncertaio, but gradually became better. Gahlberg^ reports the 
 case of a child three years old which recovered, having a totter- 
 ing, swaying motion and a tendency to turn in a circle. The 
 disease of the internal ear may or may not extend to the 
 middle ear. 
 
 In the notes on our cases pathological conditions relating to the 
 ears are mentioned sixteen times. The conditions found varied 
 from pain and mastoid tenderness to deafness with or without 
 otitis media. One case was operated on for mastoiditis, and pus 
 was found in the sinuses. Otitis media developed in five cases, 
 and in three of these the pus was examined for diplococci. The 
 organisms were found enclosed in pus cells in all three of the 
 cases examined. These cases of secondary otitis media with 
 diplococci in the pus cells are important, from the possibility of 
 further infection which they offer. They also furnish proof of the 
 extension of the infection from the brain. 
 
152 
 
 NOSE AND THROAT. 
 
 Acute Coryza. 
 
 There is but little mention of acute coryza as a complication. 
 Richter reports that in all his cases there was coryza in the 
 beginning, and nasal catarrh was sometimes seen among the 
 prodromata. Strlimpel says that in a number of his cases menin- 
 gitis was preceded by nasal catarrh, and in one case there was 
 marked disturbance of smell. This matter is of interest, in view 
 of the opinion which was first advanced by Weigert, that in 
 meningitis the nose forms the portal of entry for the infectious 
 organisms. In our cases acute coryza is mentioned but once. 
 There were three cases of epistaxis, and in one this was among the 
 first symptoms noted. 
 
 Scherrer examined the noses in eighteen cases, and in the 
 secretion of all found pus cells with diplococci. He believes that 
 this examination of the nose is one of the most important points 
 in the diagnosis of the disease. 
 
 The nasal secretion of nineteen of our cases was examined by 
 means of cover-glass preparations. The preparations were stained 
 first by Gram's method and afterwards with a solution of Bismarck 
 brown, as in the method for the examination of urethral pus for 
 gonococci. 
 
 The material for examination was obtained in most instances 
 from the higher portions of the nasal cavities, with the aid of the 
 platinum "loop." 
 
 Of the 'fifteen cases, ten showed the presence in the nasal 
 secretion of diplococci, decolorizing by Gram's method, and iden- 
 tical in morphology with the diplococcus intracellularis menin- 
 gitidis. They occurred as a rule in small numbers, and were very 
 frequently observed inside of polynuclear leucocytes. 
 
 Similar Gram decolorizing diplococci were also found within 
 leucocytes in the nasal secretions of two cases of convalescent 
 meningitis. Attempts were made to isolate this diplococcus by 
 cultures in ten cases in which the microscopical examination 
 showed it to be present, but without success. This was probably 
 
153 
 
 due to the large number of colonies of other bacteria which 
 developed and to the relatively small number of the diplococci. 
 
 With reference to the occurrence of this organism in the nasal 
 secretions of patients not affected with meningitis, twelve hospital 
 patients, chosen at random, were examined. In the nasal 
 secretions of two among these twelve diplococci- like the 
 preceding were found by cover-glass examination. They were 
 not cultivated. 
 
 From the results of these examinations it would seem either 
 that the diplococcus intracellularis may be met with in the nasal 
 secretion of patients who have not meningitis, or that other 
 species of diplococci identical with this morphologically and in 
 staining peculiarities may be found there. It is greatly to be 
 regretted that it was not possible to obtain cultures of the 
 organisms from this locality, for only by that method combined 
 with inoculations can the identity be established. At any rate, it 
 is impossible to regard the presence of diplococci decolorized by 
 the Gram stain in the nose as of much diagnostic value, as has 
 been claimed by Scherrer. 
 
 The mucous membrane was examined microscopically four 
 times, and in one case pus cells and small numbers of diplococci 
 were found. In three other cases in which the membrane was 
 examined at autopsy no inflammatory condition was found. The 
 relation of acute coryza to meningitis is of great importance, and 
 it is one point which must be cleared up in the future investigation 
 of the disease. Even assuming that the organisms found in the 
 nose were certainly the diplococcus intracellularis meningitidis it 
 would seem that the presence of an acute Coryza with organisms 
 in the pus cells is not a conclusive proof that the nose forms the 
 portal of entry for the organisms. The acute coryza can be just 
 as well a secondary complication, and due to the entry of the 
 organism into the nose from the brain. 
 
 Inflammation of the throat is frequently mentioned in the earlier 
 accounts of the epidemics, but not in the latter. Jackson says 
 that patients often complain of sore throat, and the fauces were 
 often found red and inflamed. North says that aphthous patches 
 were often seen in the throat. In one of Daga's cases there were 
 
154 
 
 small abcesses in the tonsils. Lavaran says that the tonsils are 
 frequently the seat of small abcesses. Faure-Villar ^^ mentions a 
 case in which there was gangrenous pharyngitis complicating the 
 disease. In one case reported by Senator ^"^ there were drops of 
 pus in the tonsils. Swelling and abscess of the tonsil were found 
 in one of our cases at autopsy, and a culture from the abscess 
 material showed the presence of diplococci. The tissue was not 
 examined microscopically. 
 
 JOINTS. 
 
 Acute inflammation of the joints is frequent in meningitis. 
 Jackson says in some cases the joints and limbs were swollen, and 
 resembled gout. North describes swelling of the joints, resem- 
 bling acute rheumatism. Lavaran says that acute articular rheum- 
 atism was very common at the same time with the epidemic of 
 meningitis, and was found as a complication in one of the cases of 
 meningitis. In three of the cases reported by Richter^^ there was 
 acute inflammation of the joints. In one it appeared on the sixth 
 day. Kotsonopulos,^"^ in the epidemic observed by him at Naup- 
 lia, Greece, found acute inflammation of the joints in a large 
 proportion of his cases. He gives no anatomical description of the 
 lesions. Striimpel found multiple swelling of the joints in several 
 cases. In one of the cases reported by Friis there was an inflam- 
 matory exudation in the knee joint, but no organisms were found 
 in the synovia examined. Berg says that in the epidemic in New 
 York, in 1895, affections of the joints were present in most of the 
 cases which he saw. The knees were most commonly affected ; 
 and the condition varied from pain to swelling, redness, and con- 
 ditions simulating acute articular rheumatism. Levy found pus in 
 the joints twice. In one case there was phlegmonous pus in almost 
 all the joints, extending into the sheaths of the tendons. There 
 are no records of any microscopic examination of these joints, and 
 the only record of an examination of the pus for organisms is that 
 given by Friis. In six of our cases acute inflammation of the joints 
 was found. Five of these cases recovered. At all of the post- 
 mortem examinations the articulations were examined with great 
 
155 
 
 care, bnt no lesions were fouud in them. It is greatly to be re- 
 gretted that the opportunity was not given for careful bacterio- 
 logical and histological examination of this interesting condition, 
 to ascertain its cause and its relation with the other lesions of the 
 disease. 
 
 BLOOD. 
 
 Blood counts were made in thirty-three cases. In many 
 of these a number of counts were made at varying intervals 
 throughout the disease. Leucocytosis was always present. The 
 highest number of leucocytes in any case was 31,000 ; the smallest 
 number was 9,350. In general, when several blood counts were 
 made during the course of the disease it was found that the 
 leucocytes gradually diminished towards the end of the disease 
 in those cases which recovered. Differential counts showed that 
 the increase was due to the polynuclear leucocytes. 
 
 PULSE AND TEMPERATURE. 
 
 There was no careful study of the temperature of the disease 
 until the epidemic in Leipzig in 1863 and 1864, in which the pulse 
 and temperature were carefully studied by Wunderlich. Jackson 
 says that there seemed to be a great deal of variation in the bodily 
 temperature. North says but little on the presence and character 
 of the fever. Wunderlich^* found in his studies of the tempera- 
 ture that the fever has nothing characteristic, and shows a marked 
 degree of difference, according to the development and the dura- 
 tion of the disease. He thinks that marked differences in the 
 course of the fever may be due to complications of the disease. 
 Exacerbations of the nervous symptoms are not always coincident 
 with a rise of temperature. The fever can have the course and 
 the exacerbations and may attain the height of a typhoid tempera- 
 ture, but the curve varies materially from this. It is more similar 
 to the fever in tuberculosis, and in no place shows the regularity, 
 of the typhoid curve. The most marked characteristic of the dis- 
 ease is the inequality between the pulse and temperature. The 
 fever is of short duration, and, while the temperature may reach 
 
156 
 
 a considerable height, the pulse often remains normal. In the 
 article by Striimpel there is also an interesting study of tempera- 
 tures. He finds no relation between the height of the fever and 
 the severity of the other symptoms. He gives a temperature 
 chart, in what he speaks of as the abortive type, in which there is 
 a temperature up to 1054° on the third day, and on the sixth, 
 normal temperature. 
 
 5a->iS 
 
 CHAKTI' 
 
 oj^ ^<Lsa4*t X Zi 3 4 5 6 
 
 ^ n 
 
 
 A 
 
 ■■ 
 
 i ^^ 
 
 
 i i 
 
 
 iq" i 
 
 t 
 
 
 t 
 
 
 
 3 -- 
 
 
 / 
 
 
 •^3 . \ 
 
 
 / 
 
 -^C 
 
 ^tt- 
 
 -4X K- 
 
 ^f^i, 
 
 t c 
 
 
 t t 
 
 
 X _ 
 
 26 ■"""■ ■"■ 
 
 4 
 
 . 
 
 - 4 
 
 n _ 
 
 d 
 
 zt. 
 
 V.-. 
 
 
 
 3T ^- 
 
 
 i 
 
 ;d 
 
 
 H?^ 
 
 C. 
 
 
 105-8 
 
 104- 
 
 102-2 
 
 100-4 
 
 98 6 
 
 F. 
 
 He says, on the one hand, that severe cases may have a 
 rapid course with but little fever ; and, on the other hand, very 
 mild cases may have high fever. In a number of cases there 
 was no relation between the degree of fever and the other 
 symptoms. The accompanying curve, which is taken from 
 Striimpel, gives an example of a very severe case, ending fatally 
 with but slight fever. It is possible for the most severe cases 
 to run their course without any or very slight increase of tem- 
 
157 
 
 perature. The fever may suddenly drop, but the symptoms do 
 not abate ; for weeks there may be severe disturbances of con- 
 sciousness, delirium, opisthotonos and headache, while the fever 
 has long ceased or the temperature has even become sub-normal. 
 In one of his cases which ended fatally, there was a sub- 
 normal temperature throughout. The autopsy in this case showed 
 a very marked purulent infiltration of the meninges everywhere, 
 and he thinks that the absence of fever may be explained by a 
 direct influence of the lesions on the heat-regulating centre. A 
 large number of severe and medium cases shows the type of 
 
 CHART H 
 
 Dniii^H. 12. IS, H. 15. 16. it 18. 19. 
 
 38. 
 
 37. 
 
 38. 
 
 — JU- ^ 
 
 : EEEEEE==z-S-« 
 
 ra^ Mfi 
 
 
 Sb- 
 
 d^ztt^-t-ztm-t-iti 
 
 100-4= 
 
 - 98-6 
 
 9S-8 
 
 remittent fever. The temperature rarely reaches the height of 
 104° and varies between 102.2° and 100.4°. Sometimes this 
 course is interrupted by deep remissions. In these cases the 
 curve has a certain similarity with the curve in mild cases of 
 typhoid. The fever ceases gradually, and the fall is interrupted 
 by irregular rises and falls. Striimpel has seen cases of typical 
 intermittent character, and the intermissions took place in the 
 morning and forenoon. He gives two cases showing typical 
 intermissions. Both recovered. A terminal rise of temperature 
 was seen in a number of his cases, and he gives the curve of 
 one case in which there was a rise to 107f°. (Chart III.) 
 
158 
 
 Grimsbaw,"^ in his study of the temperature in the disease, 
 concludes that there is no typical temperature chart. In mild 
 
 cases the fever seldom exceeds 
 
 
 c. 
 
 CHA-RT n- 
 
 4 5 
 
 .105-: 
 
 104- 
 
 100-4 
 
 100°. In some rapidly fatal 
 cases 103° was found, and in 
 none was there a temperature 
 of over 104°. The degree of the 
 temperature and the rapidity of 
 the pulse have not that accord 
 usually found in acute diseases. 
 Variations in temperature sel- 
 dom precede but usually ac- 
 company variations in other 
 symptoms. Low temperatures 
 »rtn n" frequently indicate severe cases, 
 as do temperatures over 104°, 
 and frequent variations of tem- 
 operature indicate a severe and 
 prolonged case with doubtful 
 result. 
 „ Hermann and Kober^ say that 
 98' 6 the temperature is never typical. 
 Some cases begin with chill and 
 high temperature, others with 
 sub-normal temperature. The curve of the temperature in the 
 course of the disease is always irregular. There are remissions 
 and exacerbations, sometimes continuous sub-normal tempera- 
 tures, and at others the curve shows the type of continued fever, 
 with a temperature of 102.2° to 104°. Levy® says the disease 
 frequently begins with chill ; the temperature in general is not 
 high and the pulse is slow. 
 
 Gahlberg, in the epidemic of Mailburg, found the temperature 
 low, usually not exceeding 102.2°. Hermann^^ reports one case 
 in which the temperature was very high, reaching 113°. In the 
 cases reported by Berg^ in New York, in 1893, he found in some 
 rapid rise and fall of temperature. As a rule the temperature 
 was not high, but cases dying in a comatose condition as a 
 
 41 
 
 4C 
 
 3d 
 
 38 
 
 31 
 
 
 
 
 ■ ■ * 
 
 
 Y 
 
 
 
 
 
 
 
 
 
 
 
 
 ■ 
 
 
 
 
 
 
 
 
 
 , 
 
 
 ,«.L.., 
 
 
 
 
 
 
 
 
 
 
 
 I N 
 
 
 \ 
 
 
 1 
 
 ■L_ 
 
 
 tv- 
 
 
 -feX 
 
 
 J 
 
 
 1 
 
 _ 
 
159 
 
 rule have high temperatures, up to 106° or over. Most of 
 Berg's observations were made on children. 
 
 Bungeroth says many cases begin with chill and sudden increase 
 of temperature, while in others the temperature is scarcely raised 
 above normal, and it gradually increases, sometimes to a consider- 
 able degree. In the first report by Leichtenstern of the cases in 
 Cologne he says that the fever is exceedingly irregular and atypical, 
 and not always proportionate to the severity of the case. Severe 
 and fatal cases may show for some time a sub-normal temperature, 
 which increases rapidly at the end. In some of his cases there was 
 agonal and post-mortem elevations of temperature. Sub-febrile 
 temperatures were often interrupted by a rapid rise, which could 
 take place at any time of the day or night. Sometimes there were 
 marked daily variations at irregular intervals. 
 
 The pulse shows the same irregularity as the temperature, and 
 in all the epidemics observers have agreed that there is no relation 
 between the pulse and temperature, such as is seen in acute febrile 
 diseases. North says the pulse is often soft and weak, slow or 
 slower than in health, often intermittent and fluttering. Jackson 
 says there is great irregularity in the pulse, and its character and 
 rapidity vary at short intervals. Wunderlich says that, while the 
 temperature may reach a considerable height, the pulse often re- 
 mains normal or even under normal, and this relation is not met 
 with in any other disease. Bungeroth says it was constantly 
 observed that the pulse was soft and small in the beginning of the 
 disease. In severe cases it was thread-like and could scarcely be 
 felt. In fatal cases the pulse generally becomes rapid and inter- 
 mittent, or it changes suddenly from very slow to very rapid, so 
 that in a minute it varied from 70 to 130. 
 
 Mankopf observed in a series of cases that the rate of the 
 pulse in the beginning of the disease was diminished, so that even 
 in high temperatures at the beginning of the disease the pulse 
 scarcely reached normal, and might be below it. In almost all 
 of the fatal cases the rate of the pulse went up to over 120, 
 while at the same time the temperature fell. Leichtenstern found 
 that the pulse varied enormously. Changes from 80 to 100 in the 
 following minute were seen. Absolute slowness of the pulse was 
 
160 
 
 not common. Eelative slowness in relation to the temperature 
 was found often, especially in children. In two cases reported by 
 Presse ^^ there was strong pulsating movement of the entire head, 
 and in a child seen by Danielson and Mann there was such strong 
 pulsation that the fontanells bulged. 
 
 The slight variations in these descriptions of the pulse and 
 temperature are probably due to the small number of cases 
 seen by some observers. In going over the histories of the 
 cases we have carefully studied the attached charts, and the 
 extraordinary irregularity of the temperature is most striking. 
 Single charts might be selected which for a week or more show 
 a curve very similar to that of typical cases of typhoid fever. 
 We have appended a number of charts of pulse and tempera- 
 ture to the description of the individual cases, which will give 
 a fair idea of the great variability of both pulse and tempera- 
 ture. These record the morning and evening temperatures, 
 and the four-hour charts show the same irregularity. In one 
 case there was a rise of 5° during the visit of the attending 
 physician. None of these curves shows the temperature for the 
 whole period of the disease. A variable length of time, from 
 one day to several weeks, elapsed from the onset of the dis- 
 ease until the patient entered the hospital. It would be very 
 important to have a few observations of temperature from the 
 onset. All the observations on temperature which have been 
 recorded were made on hospital patients in all of whom the 
 beginning of the fever would be lost. These variations in tem- 
 perature do not seem to have been dependent upon complications 
 of the disease. In one case the onset of acute croupous pneu- 
 monia was marked by a sudden rise in the temperature. While 
 we believe that it would not be possible from a single temperature 
 to diagnose the character of the disease, the observation of a num- 
 ber of charts in an epidemic would enable us to be certain of its 
 character. 
 
 MENTAL CONDITION ON RECOVERY. 
 
 The influence of epidemic meningitis in producing a permanent 
 impairment of the mind has not received the attention it should 
 
161 
 
 have. It is certain that pathological alterations may be pro- 
 duced in the brain which are not easily recovered from. Baxa 
 found that the disease was sometimes followed by idiocy. Ac- 
 cording to Bliimm, the influence of the disease on the intelligence 
 may be marked. In our cases there are four notes on abnormal 
 mental conditions of patients at the time of discharge from the 
 hospital. Marked mental impairment was noted in two cases, 
 a third was irrational and childish and a fourth was stupid and 
 did not recognize his relatives. None of these cases could be fol- 
 lowed up, to see whether the mental disturbance was permanent. 
 
 DIAGNOSIS. 
 
 The diagnosis of typical cases of epidemic meningitis is easy, 
 and other diseases should not be confounded with it. Krannhals^^ 
 says there may be symptoms exactly resembling those of menin- 
 gitis, without the anatomical lesions. He gives the clinical 
 history of seven such cases, with six deaths. It is diflBcult to say 
 on what grounds the diagnosis of meningitis was made in the 
 cases which died. Suddenness of attack, vomiting, pain and 
 stiffness of neck, inequality of the pupils, irregularity of the 
 pulse and temperature were all lacking. There was headache, 
 partial coma, delirium, clonic convulsions, clonic stiffness of the 
 muscles. In every case the spleen was enlarged, and in one case 
 very much so. In the case which recovered the symptoms very 
 much resembled those of cerebro-spinal meningitis. He says that 
 during the epidemic of influenza in Riga, in 1889 and 1890, there 
 were six cases diagnosed as meningitis. One of these cases 
 proved to be endocarditis, one pneumonia and the four others true 
 cases of meningitis. 
 
 Koht"^ speaks of a case of influenza in which there were typical 
 symptoms of meningitis, but the autopsy showed only hypersemia. 
 
 Striimpel says there may be a clinical picture of a primary 
 acute cerebral disease without appreciable cause, so that a 
 diagnosis of acute meningitis is apparently justified, and the 
 autopsy may be entirely negative with the exception of hypersemia 
 or oedema or some such slight alteration. 
 
162 
 
 Hermann thinks that the diagnosis is easy in general, but in 
 children may be confounded with tubercular meningitis ; and some 
 of the cases with abundant skin eruption may be confounded with 
 typhoid. 
 
 It is difficult to make an absolute diagnosis of any disease from 
 the symptoms alone. The surest method of diagnosis, and one 
 which should always be carried out when possible, is by lumbar 
 puncture. The method is easy, and experience has shown it to be 
 devoid of danger. If properly carried out in the early stages of 
 the disease, which is the time when there is most difficulty in 
 diagnosis, it is almost conclusive. It certainly deserves to be 
 ranked as a method of diagnosis with the examination of the 
 sputum. If the patient has meningitis, a more or less cloudy fluid 
 will be withdrawn. If it is the epidemic form, diplococci will be 
 found in it either on microscopic examination or in cultures. It 
 is of the greatest importance, in the study of the epidemics that 
 this method of diagnosis should be carried out especially in the 
 sporadic cases. In some of the chronic cases if seen late there 
 may be a question of diagnosis between meningitis and typhoid 
 fever. 
 
 SUMMARY. 
 
 Epidemic cerebro-spinal meningitis is an acute infectious disease, 
 which is produced by a micrococcus characterized by its growth in 
 pairs and by certain cultural and staining properties. The organ- 
 ism, so far as we can tell by laboratory experiments, is one of 
 feeble vitality, but it must be remembered that we cannot produce 
 in the laboratory exactly the same conditions that the organism 
 might find in nature. The essential seat of the disease is in the 
 meninges of the brain and cord. How the organism gains access 
 to the meninges is not actually known. It is possible that the 
 nose forms the portal of entry, the organism passing from the nose 
 to the meninges by means of the lymphatics connecting this with 
 the subdural spaces. In a number of cases organisms identical 
 with it on microscopical examination, have been found in the nose 
 together with evidences of slight acute inflammation. These or- 
 
163 
 
 ganisms have not been cultivated and have been found in other 
 diseases. The lesions in the meninges are confined to the pia- 
 arachnoid, in which an acute purulent inflammation is produced. 
 From the meninges the process extends into the brain substance. 
 Lesions are found not only in the cortex but in the depth of the 
 tissue and in the ventricles. These lesions consist in part of pur- 
 ulent infiltration of the tissue both around the vessels and else- 
 where, together with proliferative changes in the neuroglia and 
 degenerative changes in the ganglion cells and nerve fibres. The 
 cord is always affected, and to a greater extent than in any of the 
 other forms of meningitis. The organisms are found in consider- 
 able numbers in the most acute cases. In the more chronic cases 
 they may be missed. Probably the surest method of diagnosis in 
 the disease is that by spinal puncture. If the puncture be made in 
 an early stage of the disease, a fluid more or less clouded by the 
 presence of pus cells will be found, and in these pus cells there are 
 variable numbers of the organisms. In many cases the growth of 
 the organism is so feeble that great care must be exercised in mak- 
 ing the cultures, and large amounts of the fluid used. If the spinal 
 puncture be made late in the disease, the results may be negative. 
 The disease, especially in its chronic form, is characterized by 
 remissions and exacerbations. Spinal puncture may be negative 
 if made during a remission, and positive in the exacerbation. 
 
 A marked feature in the pathological lesions of the disease is 
 the tendency for the infection to extend along the nerves, particu- 
 larly along the optic, auditory and fifth nerves. By its extension 
 along the optic nerve it may produce a purulent inflammation of 
 the orbit or a purulent inflammation of the eye. In its extension 
 along the fifth nerve it produces an acute inflammation of the 
 Gasserian ganglion, with destruction and degeneration of the nerve 
 cells composing it. By its extension along the auditory nerve it 
 may lead to destruction of the internal auditory apparatus, with or 
 without acute inflammation of the middle ear. In the acute inflam- 
 mation of the middle ear, which appears not infrequently as a 
 complication of the disease, diplococci are found in the pus cells. 
 It is possible that the presence of the organisms in the nose is to 
 be referred to such an extension, and not to a primary invasion. 
 
164 
 
 The organism does not produce a general septicaemia. There is 
 no general invasion of the other tissues of the body. 
 
 The organism is capable of entering the lung and producing 
 a focal pneumonia characterized by especial anatomical features. 
 In the periphery of the foci there is a hsemorrhagic oedema of 
 the tissue. The foci vary in size from a pea or a bean to an 
 involvement of the lung comparable to an acute croupous pneu- 
 monia. In the large areas of consolidation several centres are 
 usually found. This form of pneumonia was found in eight of 
 our cases. It may appear either in the very acute or in the more 
 chronic cases. It seems probable from the microscopic study 
 of the lesions that the organism enters the lung by means of 
 the blood vessels rather than by the bronchi. The possibilities of 
 bronchial infection are given by the presence of the organism in 
 the nose from which it could easily extend into the bronchi, and 
 by the disease of the middle ear, the organisms from here enter- 
 ing the throat by means of the eustachian tube. 
 
 The symptoms of the disease are those which might be ex- 
 pected from the anatomical lesions. There are no prodromata, 
 and the usual history is that of sudden onset, with vomiting and 
 pain in the head. In most cases there is pain, stiffness and muscu- 
 lar contraction of the neck, which may extend to the muscles of 
 the back and the lumbar region. There is usually delirium, and 
 in many cases unconsciousness passing into complete coma. 
 There are numerous complications in the disease. Those of the 
 eye and ear are easily understood. The joint complications 
 which are seen with greater or less frequency in some epidemics 
 (and they have been very frequent) cannot be explained. No 
 opportunity was given in the study of the epidemic for the micro- 
 scopic and bacteriological examination of these joints. 
 
 Degenerative lesions of the nerves have been found to a greater 
 or less extent in all the cases in which these were looked for. 
 
 The cases reported were seen in the Boston City Hospital, the 
 Children's Hospital and the Massachusetts General Hospital. Few 
 cases seem to have been seen in private practice. The disease 
 was most prevalent among the poor, and the cases were very 
 generally distributed over the city. 
 
165 
 
 Reports as to the contagiousness of the disease vary, but the 
 general opinion is that the disease is not propagated by contagion. 
 In this epidemic there were seen several instances in which two 
 cases came from the same house and family. There were one 
 hundred and eleven cases seen in the epidemic, and of these 
 seventy-six died and thirty-five recovered, making a mortality 
 of sixty-eight per cent. 
 
 There is some ground for the assumption that many of the 
 cases of sporadic meningitis are of the epidemic form. The 
 disease may be present in a community and only show itself in 
 scattered sporadic cases. Then under favorable conditions, the 
 nature of which we do not understand, the number of cases may 
 increase to an epidemic. The epidemics of the disease usually 
 last more than a year and slowly decrease, but the disease does 
 not disappear. The mortality is high and varies much in different 
 epidemics, ranging from twenty to seventy-five per cent. So 
 far as we have been able to learn from a review of the literature 
 methods of treatment have but little influence on the mortality. 
 The disease is most apt to appear in the young, cases being rare 
 in persons over thirty-five j^ears of age. 
 
 Meningitis Due to Various Infectious Organisms. 
 
 With a view of ascertaining the frequency, together with the 
 clinical and anatomical features of cerebro-spinal meningitis due 
 to other organisms than the diplococcus intracellularis, we have 
 collected a number of cases from the reports of the laboratory 
 for the past five years. Most of those cases come from the 
 Boston City Hospital, but a number of them are from private 
 autopsies, and the bacteriological and histological examinations 
 in these cases were made at the Sears Pathological Laboratory 
 of the Harvard Medical School. 
 
 In the literature of meningitis there are a number of cases 
 reported of infection with various organisms, but there is sel- 
 dom a complete description from both a clinical and anatomical 
 point of view. When the clinical history is good, the bacterio- 
 logical and anatomical investigation has usually been imperfectly 
 carried out, and vice versa. We have found the infection of 
 
166 
 
 the meninges to be most commonly caused by the tubercle 
 bacillus, the pneumococcus and the streptococcus. In one case, 
 the entire history of which is very imperfect, there was a mixed 
 infection with the bacillus pyocyaneous and the staphylococcus 
 aureus, and in another case the infection was due to the anthrax 
 bacillus. 
 
 In most of these cases the meningitis is secondary to infec- 
 tion elsewhere, which fact complicates the clinical history 
 relating to the meningeal symptoms. 
 
 Meningitis Due to the Pneumococcus. 
 Judging from the literature, the pneumococcus appears to be 
 the organism most commonly associated with meningitis. Not 
 only has it been found in most of the sporadic cases, but 
 extensive epidemics are reported as having been caused by this 
 organism. The fact that the pneumococcus organism was the first 
 organism that wS^s described in connection with acute meningitis, 
 and that the first ^ases in which it was found were cases of menin- 
 gitis secondary to pneumonia and acute endocarditis, has led to 
 this organism being generally regarded as the cause even of 
 epidemic meningitis. We have found in our reports ten cases 
 in which the pneumococcus was found, and so associated with 
 the lesions of the disease that it can certainly be regarded as 
 the cause. In eight of these cases the meningitis was secondary. 
 In two there was fracture of the base of the skull, extending 
 across the temporal bone, the organism evidently gaining entrance 
 into the meninges from the middle ear. In one there was otitis 
 media with necrosis of the bone, and the pneumococci were 
 found both in the pus from the ear and in the meninges. In 
 three the meningitis was secondary to acute croupous pneumo- 
 nia, and in one case to acute fibrinous pericarditis. In one case 
 there was broncho-pneumonia and thrombosis of the longitudi- 
 nal sinus. In two the affection of the meninges was primary, 
 no other lesions due to the organism having been found in the 
 body. We regret to say that in none of these cases was the 
 histological examination carried out so thoroughly as in the 
 epidemic meningitis. Only portions of the brain cut from 
 
167 
 
 various places with the meninges attached were examined as a 
 matter of routine, to confirm the anatomical and bacteriological 
 investigation. A thorough and systematic examination of the 
 nerves was not made. In two cases, one of them primary and 
 the other secondary to croupous pneumonia, the sections and 
 portions of tissue were preserved, and from these more detailed 
 examinations have been made. 
 
 The records of the autopsies show some difference in the 
 description of the amount and distribution of the exudation in the 
 meninges. In one case secondary to acute croupous pneumonia 
 there was only a slight fibrino-purulent exudation over the base of 
 the brain extending a short distance over the lateral convexity on 
 each side. In another case there was extensive exudation over 
 the base and over almost the entire surface of the brain. In but 
 one case is it especially mentioned that the exudation extended in 
 lines along the vessels in the sulci, a condition which was so 
 common in the epidemic meningitis. The exudation was usually 
 confined to the meshes of the pia arachnoid, but in one case it is 
 said to have been both in the membranes and on the surface. 
 The microscopic examination showed considerable differences in the 
 lesions here as compared with the epidemic form. Fibrin was 
 present in the exudation in much greater amount. It was found 
 both forming a mesh- work within which pus cells lay, and in 
 separate masses. The fibrin was generally in coarser filaments than 
 in the exudation in the lung alveoli, and in places had undergone 
 hyaline transformation. Some of the smaller veins were thrombosed 
 and surrounded by a reticulum of hyaline fibrin, a condition 
 similar to that often found in the vicinity of diphtheritic mem- 
 brane. In the specimens examined the exudation was confined to 
 the meshes of the pia-arachnoid, the surface of the arachnoid 
 being smooth and free from change. The cells in the exudation 
 were chiefly polynuclear leucocytes. These were most abundant in 
 the meshes of the fibrin, and were to some extent seen in large 
 masses without any fibrin between them. Close to the surface 
 of the brain and beneath the surface of the arachnoid, in addi- 
 tion to the polynuclear leucocytes, there were large numbers of 
 cells somewhat larger than these, with round vesicular nuclei. 
 
168 
 
 None of these contained pus cells in its protoplasm. While it 
 seems probable that these cells came from a proliferation of the 
 connective tissue cells of the meninges, it was not possible to 
 prove this. The large cells enclosing large numbers of leucocytes 
 which were so prominent in the exudation in epidemic meningitis 
 were generally absent. In one of the cases a few were found on 
 the borders of the masses of pus cells. The most marked feature 
 in the process in both the pneumococcus and the streptococcus 
 meningitis was the acute endarteritis. This condition is similar in 
 kind to the vascular lesions which have been described in 
 tuberculosis of the meninges. The condition of the circulation in 
 these vessels could not be ascertained. In many of them there 
 seemed no other change than the acute inflammation of the wall. 
 In some the lumen was filled with cells, chiefly leucocytes, and in 
 others there was a mass of fibrin and red corpuscles. The 
 inflammatory change consisted essentially in an accumulation of 
 cells between the endothelium, which was generally elevated in 
 festoons, and the elastic lamina. In some cases the cell 
 accumulations were so great as to occlude the lumen of the vessels, 
 the endothelial coat lying as an irregular mass in the centre. In 
 others the changes were so slight that they might escape notice. 
 The endothelium in some places was broken through and rolled up, 
 the cells then filling the vessel. The cells were principally poly- 
 nuclear leucocytes, and among them some larger cells of an 
 epithelioid character. It was not possible to ascertain the 
 probable origin of the larger cells in the specimens we have. The 
 muscularis in most cases was unchanged ; in others it was 
 partially invaded by leucocytes. In one case extensive lesions 
 were found in the muscularis. The vessel was greatly dilated, the 
 muscularis in places apparently broken through or destroyed, and 
 in these places the tissue was filled with leucocytes. Outside of 
 the muscularis there was often considerable exudation. In the 
 sections of the meninges of the cord which were examined, the 
 exudation was of the same character as that in the brain, but 
 more limited in amount. There were but slight changes in the 
 tissues of the brain. In one case there seemed to be no involve- 
 ment of the cortex, and in the other there was oedema and slight 
 
169 
 
 softening of the outer layer of the cortex, with some infiltration 
 with pus cells. No lesions were found in the neuroglia. 
 
 The clinical histories in the eight cases in which the meningitis 
 was secondary to other conditions do not throw a great deal of 
 light on the symptoms to be attributed to the meningitis. The 
 symptoms referable to this are complicated with symptoms due to 
 other lesions. In only four cases was vomiting present. Opisthot- 
 onos was found in but one case, and in this it was slight. 
 
 There were few symptoms relating to the eyes. In one case, in 
 which the meningitis was evidently secondary to an acute fibrinous 
 pericarditis, there was a hsemorrhagic eruption on the trunk and 
 limbs which appeared two days before death. Delirium was less 
 common than in the epidemic cases, and in four cases there was 
 unconsciousness. In one of the cases of pneumonia in which there 
 was an extensive exudation in the meninges there was nothing in 
 the symptoms which pointed to this. 
 
 In general it may be said that the differences between the 
 clinical history of pneumococcus meningitis as compared with the 
 epidemic form is in the absence or slight development of symptoms 
 in the pneumococcus form, which point to extensive infection of 
 meninges, of the cord and spinal roots, and extension of the in- 
 fection along the cranial nerves. At the same time it must be 
 remarked that our observations are not sufficiently numerous to 
 enable us to make any extensive generalizations. 
 
 The temperature charts are extremely indefinite. In most cases 
 the patients were in the hospital for such short periods before 
 death that the charts do not show the course of the disease. In 
 two of the cases there w^s a terminal rise to 107° and 108°. The 
 temperature chart which is appended comes from a patient who 
 entered the hospital with well-marked pneumonia and a history of 
 sickness one week before entry. The first drop in the temperature 
 is probably that of the crisis of pneumonia. This was followed by 
 a slight rise, which might be referred to an extension of the 
 pneumonia or to the beginning infection of the meninges. On the 
 16th there was vomiting, and on the 17th active delirium, which 
 continued until unconsciousness came on a few hours before death. 
 At the autopsy there was gray hepatization in the lower lobe of 
 
170 
 
 right lung, red hepatization in the lower lobe of left lung, and 
 fibrino-purulent meningitis. All of the eight cases were in adults, 
 and the average age was thirty-four years. 
 
 Greater interest is attached to the two cases in which the 
 meningitis was primary. In one case, a well-nourished and 
 
171 
 
 well-built child of ten months, there was a history of slight 
 gastro-intestinal disturbances two weeks before onset. The dis- 
 ease began with restlessness, high fever (105° F.) and vomiting, the 
 temperature continuing high until death, three days after onset. 
 The autopsy showed fibrino-purulent exudation in the meninges 
 of the brain, apparently extending down the cord, only the upper 
 portion of which was removed with the brain. Pneumococci with 
 well-marked capsules were found in the meninges, and cultures 
 showed general pneumococcus infection. (We are indebted to 
 Dr. Wentworth for the clinical notes on this case.) 
 
 The other case was that of a child who was taken when six 
 days old with general clonic convulsions, accompanied by a 
 temperature of 104° in the first twelve hours, which afterwards 
 dropped to 102°. The only symptoms were convulsions. Death 
 occurred on the second day. The autopsy showed extensive 
 exudation in the meninges of the brain (cord not examined) . 
 Microscopic examination of the exudation showed numbers of 
 typical pneumococci. (Rotch, "Pediatrics," p. 695.) 
 
 Meningitis Due to Streptococcus. 
 
 There were eight cases of this, and in all the meningitis was 
 secondary to infection elsewhere. In four cases the primary 
 infection was in the ear, and in two of these there was 
 thrombosis of the lateral sinus. In one the meningitis repre- 
 sented an extension to the meninges of an erysipelas of the 
 face and scalp. In one case there was acute endocarditis, and 
 in one the meningitis was secondary to an alveolar abscess. One 
 case was of special interest, in showing an infection which doubt- 
 less took place from the nose. In this case there was fracture 
 of the base of the skull, extending across the cribiform plate of 
 the ethmoid bone. Pus and abundant streptococci were found 
 in the nose. 
 
 In these cases the lesions in the meninges were very similar to 
 those found in the pneumococcus infection. The exudation was 
 purulent, with a variable amount of fibrin, usually not so much 
 as in the pneumococcus cases. The acute endarteritis was well 
 marked, and there was no extension of the process into the brain. 
 
172 
 
 The organisms were found in large numbers in the exudation. 
 The clinical histories of all these cases do not show anything of 
 especial importance. Opisthotonos was found in but one. case, 
 and was not well marked. Pain and stiffness of the neck were 
 found in two cases. Symptoms referable to the eyes were noted 
 in three cases. 
 
 Tubercular Meningitis. 
 
 Twelve cases of tuberculous meningitis were found. Tuber- 
 culosis of the meninges in general presents a different anatomical 
 picture from tuberculosis elsewhere in the body, in the extent 
 of the acute inflammatory lesions with fibrino-purulent exudation, 
 which accompanies the formation of tubercles and tuberculous 
 tissue. This, though present to some extent in tuberculous 
 lesions elsewhere, never reaches the same extent as in the brain. 
 
 We shall not enter into a more detailed description of the 
 clinical and anatomical features of this form of meningitis, 
 which is perhaps the best known of all. 
 
 Anthrax Meningitis. 
 
 The case is that of a man about forty years of age, a 
 teamster, engaged in handling hides. He had a carbuncle in 
 the neck, which was removed by operation. Infection of the 
 alimentary canal probably took place through the instrumentality 
 of his fingers, which he was constantly putting into his mouth 
 to feel an inflamed tooth. At the autopsy there were thirteen 
 carbuncles in various places in the intestinal canal, and an 
 acute hsemorrhagic meningitis with focal haemorrhages through- 
 out the brain. The exudation in the meninges was distinctly 
 hsemorrhagic, and numerous anthrax bacilli were found in the 
 tissues. 
 
 There is no doubt that acute meningitis may be produced by 
 the entrance into the meninges of a number of infectious 
 organisms. These forms are rarely primary. The organisms 
 enter the meninges either by the formation of a communication 
 between the meninges and some cavity where they may be 
 accidentally present (as in the middle ear or nose), or by the ex- 
 
173 
 
 tension to the meninges of an infectious process in the vicinity 
 (mastoiditis, erysipehxs), or they are brought to the meninges by 
 the blood from some other focus in the body (pneumonia, 
 endocarditis). In tuberculous meningitis we have never found 
 a single case in which the lesions in the meninges could be 
 regarded as primary. The only two cases of apparently primary 
 infection were in the two pneumococcus noted, and in one of 
 these the infection may have come from the intestinal canal. 
 We believe that all infections of the meninges other than the 
 diplococcus intracellularis are fatal, but this can only be deter- 
 mined by microscopic and bacteriological examination of the 
 exudation obtained during life by spinal puncture. If tubercle 
 bacilli, pneumococci or streptococci are found with the evidences 
 of meningitis in a case which recovers, it would settle the point ; 
 clinical evidence, without lumbar puncture, will not. 
 
174 
 
 DESCRIPTION OF PLATES. 
 
 Plate 1 : — 
 
 Fig. 1. Forty-eight-hour culture of diplococcus intracellulains on 
 Loefifler's blood-serum mixture. 
 
 Fig. 2. Abundant growth in twenty-four-hour culture on fresh blood- 
 serum. The colonies are minute, very numerous, and 
 somewhat resemble similar cultures of the pneumococcus. 
 
 Plate 2 : — 
 Fig. 1. Portion of the surface of the brain from case of five days 
 duration. 
 
 Fig. 2. Posterior surface of lumbar cord from the same case. 
 
 Fig. 3. Portion of surface of brain from a case of seventy-four days' 
 duration. 
 
 Plate 3: — 
 Fig. 1. Pus cells containing diplococci from the meninges. A few 
 diplococci are in the exudate outside of the pus cells. 
 Between the pus cells there are delicate fibrillse of fibrin. 
 The drawing is an accurate representation of a group of 
 cells in the field of the microscope. 
 
 Fig. 2. Pus cells from an alveolus of the lung in a case of diplococcus 
 pneumonia. The cells are swollen, and contain immense 
 numbers of diplococci. 
 
 Fig. 3. Section passing through a sulcus in brain of goat which died of 
 experimental meningitis. The exudation extends into the 
 cortex, and there are pus cells both around the vessels and 
 infiltrating the tissue. 
 
 Plate 4: — 
 Fig. 1. Cross-section of optic nei've close to eye, showing the purulent 
 infiltration of the inner sheath of the nerve in places ex- 
 tending between the nerve bundles. 
 
 Fig. 2. Cross-section of the posterior root of lower dorsal cord from 
 an acute case, showing hyperaemia and purulent infiltra 
 tion of nerve. 
 
175 
 
 Plate 5 : — 
 
 Fig. 1. Longitudinal section of auditory nerve in acute case, showing 
 purulent infiltration in and around the nerve. 
 
 Fig. 2. Section of edge of Gasserian ganglion from acute ease, show- 
 ing purulent infiltration of nerve and ganglion. 
 
 Plate 6: — 
 
 Fig. 1. Section of posterior root ganglion of cervical cord, showing 
 purulent infiltration with degeneration of ganglion cells. 
 
 Fig. 2. Portion of meninges in acute case, showing the formation of 
 large epithelioid cells. The cells lying free enclose poly- 
 nuclear leucocytes. Immersion, 
 
 Plate 7 : — 
 Fig. 1. Section of posterior root from chronic case, showing perivas- 
 cular infiltration. The plasma and lymphoid cells are the 
 most numerous. The cells with deep-blue protoplasm are 
 plasma cells. Immersion. 
 
 Figs. 2, 3, 4, Sections showing neuroglia proliferation : Fig. 2, neu- 
 roglia cell from olfactory nerve, showing nuclear figure ; 
 Fig. 3, same fi*om optic nerve from acute case; Fig. 4, 
 large neuroglia cells, some with numerous nuclei from 
 beneath lateral ventricle in case of fourteen days' duration. 
 Immersion. 
 
 Plate 8: — 
 Fig. 1. Section of posterior nerve root, showing degeneration. (On 
 the right the nerve has been slightly crushed in cutting.) 
 Marchi method. 
 
 Fig. 2. Section of optic nerve from same case as Plate 4, Fig. 1, show- 
 ins: desreneration. Marchi method. 
 
176 
 
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MASS. STATE BOARD OF HEALTH. 
 
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