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Cerebro-Spinal Fever
1911 Encyclopedia Britannica
or "CEREBRO-SPINAL FEVER 18.130). - Although serious outbreaks of cerebro-spinal fever had occurred in Belfast in 1907, and in Glasgow and Edinburgh in 1906 and 1907, and although the deaths from cerebro-spinal fever in Scotland in 1907 reached 1,087, yet no considerable outbreak of the disease occurred in England or Wales until the first winter of the World War.
Cerebro-spinal fever had been made compulsorily notifiable in England in 1912, and in that year, in 1913, and in 1914, approximately 300 cases were notified in England and Wales each year. In 1915 the disease increased more than elevenfold, there being 2 ,343 civilian and 1,136 military cases. In Feb. 1915 the outbreak indeed assumed very menacing proportions, and in a single week 228 cases were notified. Considerable alarm was aroused as the mortality was exceedingly high, and the serum treatment which had been so successful in the New York and Belfast epidemics appeared at this time to have little effect upon the mortality rate. Special investigations were therefore commenced by the responsible authorities (especially by the army with the assistance of the Medical Research Committee), which were continued during the war, and added greatly to the knowledge of the bacteriology and epidemiology of the disease. Diminishing somewhat in 1916 the disease broke out with fresh vigour in 1917, military and civil cases being now about equal in numbers.
Aetiologically, there can be little doubt that the outbreak in England which followed the birth of the new armies was principally due to the overcrowding of young recruits in depots, camps, and billets. It is also probable, although this has been warmly controverted, that fresh and highly virulent strains of the meningococcus were brought to England by the Canadian contingents arriving in the late autumn of 1914 after having had several cases of cerebro-spinal fever in their home camps before embarkation and during the voyage east on their crowded transports, and a sharp outbreak on arrival on Salisbury Plain several weeks before British troops were affected. These virulent Canadian strains may have aggravated the outbreak.
At Portsmouth, for example, the disease began on Jan. 15 1915, at Eastney barracks among men who came in contact with a Canadian football team which visited there on Jan. 9, and the first case of the disease at Caterham depot occurred in a man who travelled up from Scotland by night with three Canadian soldiers in the same compartment.
The aetiology of cerebro-spinal fever is peculiarly instructive from the fact that, in at least 95% of all cases, the disease results not from infection derived from another patient suffering from the disease but from infection derived from an apparently healthy carrier, that is a person who harbours the meningococcus in his nasopharyngeal secretion without contracting the disease, and who is usually unaware of having ever been in contact with a patient suffering from the disease. Infection is most often transmitted in sleeping quarters.
Carriers are of two kinds: temporary carriers who harbour the meningococcus for only two or three weeks and who then become free spontaneously; and chronic carriers who harbour the germ for many months and even years.
Cleminson has shown that almost all chronic carriers have marked nasopharyngeal defects, the commonest type being that in which there is an obstinate mucous contact between a deflected and thickened nasal septum and the middle turbinate.
Chronic carriers are responsible for carrying on the disease from epidemic to epidemic and also for the sporadic cases which occur between epidemic times. Recovered patients are often chronic carriers, the meningococcus having been recovered after two years from the nasopharyngeal secretion in several instances.
In ordinary times the population probably contains some 2% of carriers, but at the height of an epidemic in a crowded community, such as that on a ship or in a crowded depot, the carrier-rate may rise to 75%, the vast majority of the carriers being temporary.
At the outbreak of war the necessity for rapidly raising enormous forces at once led to very serious overcrowding of the available barracks and depots, and the hastily erected camps and hutments were overcrowded as soon as they were erected. Military necessity was urgent and imperative.
In Jan. 1915, all the known requisite factors for an outbreak of cerebro-spinal fever were present: severe overcrowding, cold weather, and a population rendered susceptible by youth, by the fatigue of rapid training, by nostalgia, and by entry into a new method of life. Recruits have always shared with infants a peculiar susceptibility to cerebro-spinal fever. The armies in the field despite far greater hardship suffered much less than the recruits training at home. The incidence of cerebro-spinal fever in the U. S. training camps following their entry into the war was 45 times as great as that in corresponding male age groups in civil life.
Overcrowding has at least a threefold importance as a factor in the production of cerebro-spinal fever epidemics: First, the atmosphere of an overcrowded and ill-ventilated room or hut, by lowering the individual resistance, tends to favour the chances of the meningococcus attacking the meninges with success. Secondly, by shortening the distance between man and man, overcrowding facilitates the transmission of infections of the upper respiratory passages, since these are present in droplets of secretion which are liable to be sprayed out into the surrounding air, in the acts of coughing, sneezing and loud speaking. For this reason, overcrowding favours the occurrence of catarrhal diseases, which so frequently precede and accompany an outbreak of cerebro-spinal fever. Thirdly, for a similar reason, overcrowding tends to produce a high carrier-rate of the meningococcus in a community; thus ensuring to any susceptible individual, freshly introduced, a massive dosage of the organism.
In addition, the rapid transmission from one temporary carrier to another which a high carrier-rate implies may very probably tend to increase the virulence of a strain of meningococcus previously of low virulence.
Glover's work on carrier-rates demonstrated that the meningococcus carrier-rate is a direct index of the degree of overcrowding, and that, when this overcrowding is remedied by increasing the distance between the beds, a high carrier-rate rapidly falls to a normal rate. There is a sharp rise in the carrier-rate of a community before an epidemic, that is to say, a " carrier epidemic " precedes and accompanies the " case epidemic." For practical purposes, a carrier-rate of 20% has been regarded as the danger line.
Cerebro-spinal fever is an acute infectious disease, due to the meningococcus. It occurs sporadically and in epidemics, and has usually as its chief manifestation an acute meningitis affecting both brain and spinal cord. The causal organism is undoubtedly the diplococcus intracellularis of Weichselbaum, a gram-negative coccus of characteristic kidney shape, almost invariably seen in pairs, and having no well-defined capsule. In the body fluids, and especially in the cerebro-spinal fluid, it is usually seen inside a polymorphonuclear white corpuscle. Often, however, the diplococcus is seen to be extracellular. Prognosis in a case is usually considered to be better when a slide of the cerebro-spinal fluid shows the majority of the diplococci intracellular rather than extracellular.
The meningococcus stains well, and is invariably gram-negative. An excellent culture medium is Gordon's trypagar enriched for primary culture with a solution of laked rabbit blood or fresh human blood. The optimum temperature is 37° C. The meningococcus ferments glucose and maltose, but not levulose or saccharose. Whilst it can be distinguished from other gram-negative diplococci by cultural tests, the best criterion for identification is serological, that is by agglutination tests with the sera of animals, immunized by repeated injections of killed meningococci obtained by culture from the cerebro-spinal fluid of patients suffering from the disease.
By the use of this method of agglutination and the allied method of absorption, Gordon divided the meningococci found in military cases of the disease in 1915 into four types. Dopter had previously differentiated two types, which he termed meningococcus and parameningococcus respectively, and the first two types of Gordon, which together account for 80% of the cases, correspond to Dopter's groups, Gordon's type i being Dopter's meningococcus and his type 2 Dopter's parameningococcus. Gordon's type 3, which is more closely allied to type 1 than to type 2, gave rise to some 15% of the cases, whilst Gordon's type 4 was of rare occurrence except in one outbreak at Chatham.
A patient suffering from cerebro-spinal fever harbours only a single type of meningococcus in his cerebro-spinal fluid and it is almost invariably present in his nasopharyngeal secretion.
Determination of the type of the invading meningococcus is of great practical importance, as the serum of an animal immunized against one type has little or no therapeutic or protective value in a patient suffering from an invasion of a different type of meningococcus. A therapeutic serum must therefore either be polyvalent or if monovalent, be used only for its appropriate type when the type has been determined. For general use a polyvalent serum has the merit of simplicity and with potent serum the results are extraordinarily good.
Tullock has shown that type 2 is a complex type divisible into three sub-groups, and the much greater difficulty in producing a good anti-type 2 serum is probably owing to this fact.
Criticism of Gordon's types has concentrated mainly on his types 3 and 4, but there can be no doubt that Gordon's types were of the utmost value for the epidemic of 1915-8. In a series of 526 strains of meningococci from the cerebro-spinal fluid of patients, 98% were identifiable with one or other of the four types, and one-fifth belonged to types 3 and 4.
Infection of the nasopharynx probably always takes place first. In most cases a blood infection appears to precede the meningeal invasion, but the actual channel of infection between the nasopharyngeal secretion and the meninges is uncertain; it may be either through the blood stream, or by the sheaths of the olfactory nerves passing through the cribriform portion of the ethmoid, or by the sphenoidal sinuses.
The incubation period is usually three to four days. The onset is sudden and contrasts with the usually more gradual onset of tuberculous meningitis. In no disease is early diagnosis of more urgent importance. Intense headache, vomiting, a moderate degree of pyrexia with a comparatively slow pulse, stiffness of the muscles of the neck and a positive Kernig's sign are the primary symptoms. The disease is usually well defined; these five symptoms being all present in 85% of cases, and only some io % of cases are atypical, the most common deviation being a long initial pyrexia.
If there be any suspicion of the disease lumbar puncture should be performed at the earliest possible opportunity for the purposes of both diagnosis and treatment. Retraction of the head is a later symptom and should never be waited for.
The characteristic " spotted " rash is present in a percentage of cases, which varies considerably in different epidemics. Rashes appear more constant in American experience. In 1917 in London it was present in about 25% of patients: it is a macular rash appearing first on the skin and the dorsum of the foot, then upon pressure points, elbows, buttocks and back. Large purpuric patches are characteristic of fulminating cases, which form about 5% of the cases. Petechial maculae, erythema, rose spots, and blotches often occur in cases of ordinary severity.
Labial herpes is a later symptom than the rashes, and is of favourable import. Inequality of the pupils is less common than in tuberculous meningitis. Squint is seen in a smaller proportion of cases (6%) than in tuberculous meningitis. Hemiplegia, usually transient, and nerve deafness, usually permanent, each occur in about 5% of cases. Albuminuria is common, but usually transient; haematuria occurs in a small proportion, and, to a less extent, glycosuria. Constipation is almost invariable and with the incessant vomiting may lead to the diagnosis of an acute abdominal condition.
In children the disease is often ushered in by convulsions. Retraction occurs at an earlier stage than in adults. Persistent tetany of hands and feet is common and rapid emaciation occurs.
Three main clinical types of the disease are described, fulminant, severe and atypical. A fulminant case is one in which the initial systemic invasion results in so profound a toxaemia that the death or early collapse of the patient may obscure the meningeal condition. Death may take place in a few hours after onset. Fulminant cases amount to some 5% and are more common at the height of an epidemic. Typical severe cases form some 85% of all cases and in them cerebro-spinal fever forms as clear a clinical feature as does any disease. Atypical cases form some 10% and the most usual form is one with a long preliminary pyrexia which may be diagnosed as enteric or trench fever. Ambulant or slight attacks do not occur. The essentials of the treatment of cerebro-spinal fever are three :- First, early and repeated relief of pressure by lumbar puncture; this procedure alone will considerably reduce the case mortality rate in adults. Secondly, the early and repeated intrathecal administration of. a potent antimeningococcal serum (intravenous administration may also be beneficial if the systemic invasion be marked). Thirdly, the relief of pain.
Serum treatment depends for its success upon early administration, upon sufficient dosage and upon the therapeutic potency of the serum itself. The serum treatment of cerebro-spinal fever was introduced by Flexner and Jobling in the New York epidemic of 1905 with great success, and reduced the " untreated case " death-rate of over 70% to a " treated case " death-rate of under 20% in those patients who received serum in the first week of illness.
Unfortunately, at the beginning of the 1915 epidemic in England the only serum available proved very disappointing. It had been made from laboratory strains from previous epidemics, and had very little therapeutic effect. Subsequently it was found to fail to agglutinate types 1 and 2 at a dilution of I in 50. Following the collection of fresh strains from the current epidemic by Arkwright, Gordon, and others, however, a very potent serum was produced from them by McConkey at the Lister Institute in 1916, which again fully vindicated the value of serum treatment, reducing the mortality rate in cases where it was used in the first week to 14%. Gordon has shown that the therapeutic value of serum appears to depend chiefly upon its capacity of neutralizing the toxin of the meningococcus. There is great variation in therapeutic value even in batches produced by the same laboratory, although Gordon's modification of Besredka's method for determining anti-endotoxic content promises well as a method whereby a standardization of anti-meningococcal serum could be reached.
Owing to the complex character of type 2, it is harder to produce a serum satisfactory for all cases infected with this type than to produce potent serum for the other types. The monovalent type 1 serum produced by Griffith for the Medical Research Committee was extraordinarily effective for type I cases, but his type 2 serum was much less efficacious for type 2 cases.
Lumbar puncture, preferably under an anaesthetic, should be done at the earliest possible occasion. As much cerebro-spinal fluid, usually about 60 c.c., as will flow should be allowed to run from the needle into sterilized test tubes for culture and examination, until the fluid comes one drop at a time with each respiration. If the cerebro-spinal fluid be cloudy or purulent, 30 c.c. of serum warmed to blood-heat is then run in through the needle by gravitation with a rubber tube. The foot of the bed is raised after administration.
This procedure is repeated at intervals of 24 hours until four doses have been given, which are usually sufficient with a potent serum. The cerebro-spinal fluid becomes clear and free from meningococci. Often two or three doses are sufficient. It is often wise to conclude the series with a lumbar puncture without the use of serum for the relief of pressure only. Curative vaccines have been used in prolonged cases, where serum appears to be losing its effect. An autogenous sensitized vaccine should be used.
Another method of treatment used in cases where the patient does not react well to the curative horse serum, or where no curative serum is available, is to inject intrathecally 30 to 50 c.c. of the patient's own serum, separated under strictly aseptic conditions from blood drawn from his basilic vein.
This procedure, based upon the fact that anti-bodies are developed in greater extent in the blood than in the cerebro-spinal fluid, has in some instances appeared to do much good.
Serum sickness on the 8th to the 10th day is often observed, but is not usually serious. Anaphalaxis is very occasionally seen. It is more liable to occur with intravenous than with intrathecal injection. The principal complications met with are pneumonia, the supervention of a pneumococcal meningitis, arthritis, cystitis due to the meningococcus, hydrocephalus, panophthalmitis.
In patients who recover, complete nerve deafness is the most common (3 to 5%) of the serious sequelae. Permanent mental change is unusual. A prolonged convalescence is essential.
The chief post-mortem findings in the majority of fatal cases are confined to the central and nervous system. Their macroscopic appearance is similar to those found in cases of other forms of meningitis. Fulminant cases may show little save injection of the dura mater, a lustreless arachnoid, a soft and swollen appearance of the brain together with a pink congestion of the pia mater. The cerebro-spinal fluid may only be slightly turbid in these fulminant cases.
The ordinary acute case shows a thick yellow purulent exudate mostly at the base of the brain extending along the main fissures, and down the cord. The bulb and the posterior surface of the cord are usually covered with marked accumulations of the exudate. Flaky and turbid fluid is found in the distended ventricles.
In chronic cases there is marked hydrocephalus. The convolutions are pale and flattened; localized adhesions and thickenings are marked between the membranes, thus forming pockets in the cranium and theca. The various foramina, particularly that of Majendie, may be obliterated, interfering with the circulation of the cerebro-spinal fluid. Marked emaciation is usual.
The post-mortem appearances in other organs are not usually striking. Embleton has shown the frequency of empyema of the sphenoidal sinus. A broncho-pneumonia is almost invariable. Purpuric and other haemorrhages are common in many organs, and have been especially described by some observers in the suprarenal capsules in fulminant cases. Arthritis, orchitis and pericarditis are described and a meningococcal cystitis may be found.
The chief point in the prophylaxis against cerebro-spinal fever is, of course, the prevention of overcrowding; this is of paramount importance. Ventilation and distance between the beds in sleeping quarters are of much greater importance than mere floor or cubic space. " Wall space " is essential.
The early isolation of cases of catarrhal disease is of great importance in preventing the increase in the carrier-rate for the reason that a carrier with a catarrhal sneeze or a cough will spray the meningococcus in a much more effective manner than the same carrier without a catarrh. As a rule the meningococcus itself does not give rise to catarrhal symptoms in the carrier.
Where overcrowding is unavoidable and spacing-out impracticable, steam spray treatment, using a 2% solution of zinc sulphate, may be given for 10 minutes daily to the overcrowded community. In several instances this procedure appeared to check the incidence of cases during an actual outbreak of cerebro-spinal fever. This method of treatment should, however, never be used as a substitute for spacing-out and improved ventilation.
Prophylactic vaccination cannot be regarded as having been proved to afford protection, though at Salisbury and at Camp Funston it appeared to give promising results. (J. A. G.)
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Chisholm, Hugh, General Editor. Entry for 'Cerebro-Spinal Fever'. 1911 Encyclopedia Britanica. https://www.studylight.org/encyclopedias/eng/bri/c/cerebro-spinal-fever.html. 1910.
