362 POST GRADUATE MEDICAL JOURNAL July 1948

Serous Meningitis or Aseptic MeningitisThis is the name given to the syndrome in which

a meningeal reaction occurs as the result of aninfective focus adjacent to the meninges, e.g.mastoiditis, lateral sinus thrombosis, extraduralabscess, intra-cerebral abscess, etc. The pressureof the C.S.F. is increased, and there is an increasein cells, generally polymorphs, but sometimeslymphocytes predominate. The protein is slightlyincreased, but the sugar and chlorides are normal.The cell count is usually in the neighbourhood of200-300, but occasionally it is as high as I,ooo per

c.cm. Organisms are not present. In some casesan actual meningitis may supervene.A lymphocytic meningitis is not an infrequent

occurrence in the early stages of Weil's disease andan example came under my own observationrecently. The lymphocytes were several hundredsper c.cm. and took two-three weeks to return tonormal. There was no jaundice in this patientand the diagnosis was made by finding a highagglutination titre in the blood.

BIBLIOGRAPHYALEXANDER, H. E., 'Treatment of Haemophilus Influenzae In-

fections, and of Meningococci and Pneumococci Meningitis,'Amer. Jour. Dis. Child., Aug., 1943, lxvi, x60.

DINGLE, J. N., FINLAND, M. (1942), War Med., 2, I.

MENINGITIS: RATIONALE OF DIAGNOSISBy JOHN APLEY, M.D., M.R.C.P.

Department of Child Health, Bristol University

Increased power entails increased responsibility.With the advent of chemotherapy delay in thediagnosis of purulent meningitis can no longer beexcused, for diagnosis at leisure is condonableonly when dealing with an incurable or benigndisease. Virtually all the common varieties ofpurulent meningitis are now curable, yet even nowmany patients die, or survive only with distressingresidua. Inadequacy of laboratory facilities andimproper selection of therapeutic agents are con-tributory factors in the production of thesefailures; but the most important single factor isdelay in diagnosis.

It is axiomatic in medicine that urgent diagnosisdepends on leisurely preparation. The diagnos-tician who has failed to discipline himself by re-peated observation, analysis and synthesis willfail also to attain that maturity of judgment whichpermits diagnosis to be made rapidly yet withoutthe sacrifice of accuracy. The study of meningitisprovides an example of the preliminary, catholicpreparation which is essential for urgent diagnosis.Though the present discussion is centred onpurulent meningitis the logical approach must bethrough the subject of lepto-meningitis in itswider aspects.Features of Meningeal IrritationThe essential feature common to the many

forms of meningitis is meningeal irritation. Thisphenomenon may occur even in the absence ofinfection of the meninges; but, whatever thecause of the irritation, the clinical features whichmay be observed result in all cases from stimula-

tion of the meningeal nerves and those portions ofthe cranial and spinal nerves which traverse thetheca. The mechanism is identical with thatobtaining in peritonitis, and the results are similar.The three characteristic features of meningeal

irritation are :--() pain, (2) hyperaesthesia, and(3) muscular rigidity. The first two of these arisefrom irritation of sensory components, and thethird through the mechanism of a meningeal-motor reflex.The various signs, such as those of Kernig and

Brudzinski, and the demonstration of neck rigidity,which are employed in the diagnosis of meningitis,depend for their effects upon increasing theirritability of the meninges by mechanical stretch-ing.Correlation of Symptomatology with Siteof Meningeal IrritationThe production of the three characteristic

features of meningeal irritation can be clearlyillustrated by contrasting anterior poliomyelitiswith meningococcal meningitis. At the same timethe discussion can be taken a stage further toprovide evidence on which to attempt localizationof the site of meningeal involvement.

In anterior poliomyelitis, when the' site of pre-dilection is in the lumbar region of the cord, themanifestations of meningeal irritation appear firstin the back and the legs; from these regions theymay spread or remain localized, according as thedisease process spreads or is halted. In menin-gococcal meningitis, when, as commonly occurs, thesite of predilection is at the base of the brain, the

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July 1948 APLEY: Meningitis: Rationale of Diagnosis 363

results of meningeal irritation are manifest first inthe head and neck, to become widespread only asthe infective process extends. Since the anteriorand middle cranial fossae are supplied by thetrigeminal nerve, the results of irritation in theseareas will be manifest in the frontal, facial andtemporal regions; the posterior fossa is suppliedby the upper cervical nerve roots, so that dis-turbances originating in stimulation of these nerveswill be referred to the occipital and post-nuchalregions. In practice the three fossae are, however,generally involved concurrently, so that clinicallocalization of the infection to one or other of themis usually not possible.As between the different types of infective

meningitis, the variations in symptomatology maybe explained, at least in part, by what is known oftheir applied pathology. In the meningococcalvariety, as also in tuberculous meningitis, the in-flammatory exudate tends to be concentrated atthe base of the brain. It fills the interpeduncularspace, spreading thence with the flow of cerebro-spinal fluid down into the spinal theca, forwardalong the optic nerves, backward into the cisterns,or upward along the middle and anterior cerebralarteries to the vertex. In the natural history ofthese diseases neck rigidity and occipital pain

tend, therefore, to occur at an early stage. Inpneumococcal meningitis, on the contrary, theyellow-green exudate may predominate at thevertex of the brain. As a result, though headacheis severe, neck rigidity is minimal or absent. Ininfluenzal and in streptococcal meningitis the dis-tribution of the exudate is capricious, following noset pattern, and the symptomatology is corres-pondingly unpredictable. Post-basic meningitis ofinfants, a chronic 'variety of meningococcalmeningitis, derives its unique features from thespecial conditions pertaining in infancy. Becauseof the comparative softness of the infantile brainthe sulci become closed at an early stage in thedisease process, so that the exudate is confinedalmost exclusively to the basal cisterns.

Mechanisms of Production of MeningealIrritationComprehension of the widely different mechan-

isms by which meningeal irritation may be pro-duced is of more than academic interest; withoutit differential diagnosis remains as unsatisfying asit is superficial. The conditions which give rise tomeningeal irritation will be described in fivegroups, a division which appears natural andcontributes to clarity of diagnosis (see Table i),

PATHOGENESIS OFFIG. MENINGEAL REACTIONS

arachnoid villi

/ /venous

blood / / //--// - MENINGEAL INFECTION

/

nervous CEREBROSPINALnervous /, CEREBROSPINAL C.N.S. INFECTION WITH SUBSIDIARYtissue // ) FLUID / MENINGITIS

lepto- /meninges /NON-INFECTIVE MENINGEAL

/ / - // IRRITATION

//// ASEPTIC MENINGEAL REACTION TO/ / / EXTRA-MENINGEAL SEPSIS

////arterial // / / V

blood / / / MENINGISM: INCREASE IN C.S.F. FROM// / / / / / / / // / BLOOD OSMOTIC DISTURBANCES ·

choroid plexusReproduced by permission from ' The Clinical Apprentice,' by J. M. Naish and J. Apley, published by J. Wright, Bristol

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POST GRADUATE MEDICAL JOURNAL

TABLE i

CAUSES OF MENINGEAL IRRITATION

GROUP I.-Predominantly Meningeal Infections(commonly bacterial).

Cocci: meningo-, strepto-, pneumo-, staphylo-.Others : B. tuberculosis, H. influenzae,

B. coli, B. proteus, Brucellosis, B. typhosus.Virus: benign lymphocytic meningitis.

GROUP 2.-C.N.S. Infection with SubsidiaryMeningitis (commonly virus).

Anterior poliomyelitis, polioencephalomyelitis,encephalitis (especially in association with specificfevers), infectious mononucleosis.

Syphilis, Weil's disease, actinomycosis and otherfungus infections, infections with yeast-like organisms(e.g. torula, coccidioides).

GROUP 3. Non-infective Mechanical Irritationof Meninges.

Intra-thecal therapeutic agents, e.g. anaesthetics,sera, penicillin, streptomycin.

Blood: Sub-arachnoid or cerebral haemorrhage.Neoplasm: medulloblastoma, cholesteatoma, oligo-

dendrogliosis, leukaemia.Chemical: lead encephalopathv.Cyst fluid.

GROUP 4. Aseptic Meningeal Reaction toExtra-Meningeal Sepsis.

Skull sepsis, extra-dural abscess, venous sinusthrombosis, brain abscess.

(Otitis media, mastoiditis and sinusitis are thecommon predisposing causes.)GROUP 5. Meningism.

I. Infection predominatly meningealIn this group are included those conditions in

which meningeal irritation is produced by infectionconfined to, or predominating in the meninges. Ithas been stated that no organism evokes ex-clusively a meningitic or an encephalitic reaction,but clinically one or the other almost invariablypredominates. In contrast with virus infections,bacterial infections are characterized by a selectiveaffinity for the lepto-meninges, and they producetheir effects by direct irritation. It is unnecessaryto enumerate all the bacteria which give rise to

meningitis; those which have not done so onsome occasion must be rare. The bacteria most

commonly encountered are shown in Table I,and comprise the common agents of purulentmeningitis.Some virus infections break the general rule,

in that the site of maximal infection is in themeninges. Benign lymphocytic meningitis is acommon example; anterior poliomyelitis is also

frequently characterized, in its early stages, by ameningeal reaction which is transient.

2. Infection of C.N.S. with subsidiary meningitisIn accordance with the general statement pre-

viously made, the majority of virus infections ofthe central nervous system fall into this group.The more important of these are shown in Table i.

Conversely, suppurative encephalitis, though ofbacterial origin, is invariably preceded bymeningeal inflammation.Some diseases due to organisms other than

viruses also fall into this group. Of these, the onlycommon one is syphilis. Extremely rarely Weil'sdisease, actinomycosis and some fungus andsimilar diseases are similarly concerned.

3. Non-infective mechanical irritation of meningesVarious non-infective causes may give rise to

direct irritation of the meninges. Even normalsaline produces a meningeal reaction when intro-duced into the theca, so that the effects of thera-peutic agents similarly introduced can readily beunderstood. Thus, streptomycin frequently evokesa well-marked pleocytosis (predominantly poly-morphonuclear) which may be accompanied byclinical signs of meningeal irritation (M.R.C.,1948).4. Aseptic meningeal reaction to extra-meningealsepsis

This reaction has been given many names,such as ' aseptic meningitis' and ' sympatheticmeningitis '; under the term ' serous meningitis 'it is frequently confused with disease-processeswhich fall more naturally into groups 3 or 5.The effects produced arise from irritation by a

septic focus which is adjacent, but external to themeninges. In the production of the asepticmeningeal reaction the type of organism does notappear to be of importance. An increase inpressure and of cells in the cerebro-spinal fluidoccurs, but the meninges continue to function asa barrier which prevents the passage of organisms.After removal or sterilization of the septic focusthe cerebro-spinal fluid reverts to normal. Thedanger inherent in the situation is that, with failureto recognize and ablate the source of sepsis, themeningeal barrier may be broken down andpurulent meningitis result.

5. MeningismThe clinical distinction between meningism and

meningitis was, according to Walshe, first made bySir William Jenner. In meningism headacheceases when delirium begins; in meningitis itcontinues.

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APLEY: Meningitis: Rationale of Diagnosis

The syndrome of meningism has in the pastbeen attributed to many causes, all equallynebulous, of which the most popular was'toxaemia.' It now appears clear (FremontSmith, et al., I928-29) that meningism is pro-duced, for the major part at least, by disturbancesin equilibrium between the blood and the cerebro-spinal fluid. The characteristic changes in thecerebro-spinal fluid may occur at the onset of anyfebrile illness, though only in childhood do signsand symptoms commonly result. When they dooccur they are those typical of meningeal irrita-tion, presumably as a direct effect of mechanicalstretching of the meninges.

It is important to appreciate the mechanism ofproduction of meningism. It is analogous withthe experimental injection of hypotonic solutionsinto the veins, whereby the osmotic pressure ofthe serum is reduced, with a resultant increase inthe rate of formation of the cerebro-spinal fluid anda rise in its pressure. With the onset of an acutefebrile illness the osmotic pressure of the bloodfalls, and the serum becomes temporarily hypo-tonic compared with the cerebro-spinal fluid. Asa result, there is an increased flow through thechoroid plexus, and the cerebro-spinal pressurerises accordingly. The symptomatology is pro-duced by the increase in amount and pressure ofthe cerebro-spinal fluid; when equilibrium isrestored the signs and symptoms disappear.The common causes of meningism are the

common febrile illnesses which have an abruptonset. It may occur as a transient phenomenonat the commencement of many diseases, but ismost marked, and therefore most frequentlyrecognized, in pneumonia, tonsillitis and pyelitis.Natural History of Purulent MeningitisThe different mechanisms by which meningeal

irritation may be produced, whether in thepresence or absence of meningeal infection, have sofar been discussed. The complete syndrome ofmenin-geal infection comprises additional components,which can be deduced from general principles.

Purulent meningitis, like tuberculous meningitis,is commonly secondary to infection elsewhere inthe body. Before the local effects of infection ofthe meninges become appreciable the causativeagent may produce other disturbances. Usuallythey are generalized and predominate only at theoutset, but this predominance may persist, as notinfrequently occurs in infants. They may evenprove fatal before meningeal irritation is recog-nized; an example is the Waterhouse-Friederich-sen syndrome, in which the septicaemic stage offulminating meningococcal infection may causedeath through acute adrenal failure beforemeningitis becomes clinically manifest.

In its later stages, after the stage of meningealirritation, with the natural progress of meningealinfection certain mechanical factors may come intooperation. As the exudate increases and extendswidespread irritative phenomena may occur.Later, organization takes place; obstruction tothe flow of the cerebro-spinal fluid may arise,either inside or outside the ventricular system;and the final picture is that of increased intra-cranial tension, with depression and failure offunction.The stages through which a typical meningeal

infection passes are most easily distinguishable intuberculous meningitis. With purulent meningitisthe stages are less clearly demarcated; thesequence may be modified or distorted accordingto many factors-the characteristics of thecausative agent, the rapidity of development ofthe disease process, the extent and site of maximalinfection, the resistance of the subject, and theeffects of treatment. The natural history ofpurulent meningitis, despite these limitations, mayhowever be usefully described according to threestages :

(I) The stage of invasion.(2) The stage of meningeal irritation.(3) The stage of raised intra-cranial tension.

I. Stage of invasionChanges in mentality are often the first to be

observed; they may be extremely pronounced orso trifling as to escape notice. The sudden oc-currence of delirium accompanied by a rise intemperature is not uncommonly the first mani-festation. Irritability alternating with drowsinessis not infrequent. Malaise, discomfort andlanguor may precede the onset of more definitesymptoms by a variable period. Headache, feverand a rise in pulse rate are the rule. Petechialeruptions in the skin are characteristically presentin the early stage of meningococcal infection.The occurrence of vomiting at this early stage is

difficult to explain, but it is a common event inpyogenic and, more especially, in tuberculousmeningitis.2. Stage of meningeal irritationThe three cardinal features already described

are almost always evident. The site at which theyappear depends on factors which have been dis-cussed; but it may be repeated that these mani-festations tend to be localized in the early stages,and to become widespread as the infection extends.

Pain is usually described as headache, thoughthere may also be pain down the spine. Theheadache previously attributable to toxaemia isreplaced by one which is more intense. It isdescribed as continous, though fluctuations in

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severity occur; it may be deep-seated or referredto the surface, usually to the back of the neck andoccipital area; it is aggravated by any movementor manoeuvre which stretches the meninges or in-creases the intra-cranial pressure. The shrill' meningitic cry' may be explained teleologicallyby a combination of some of these factors; severeheadache compels the patient to cry out, but thecry is restrained in an attempt to limit muscularmovement and the consequent rise in intra-cranial tension which would aggravate the pain.

Local and general hyperaesthesia may be evidentearly. Muscle rigidity is nearly always demon-strable. In the early stages it may be localizedand, since meningitis is commonly maximal at thebase of the brain, neck rigidity is an early mani-festation, frequently demonstrable when Kernig's,Brudzinski's and other signs are equivocal. Later,the whole back may become rigid, the head re-tracted, and the thighs flexed on to the abdomen.

3. Stage of raised intra-cranial tensionAt this stage the classical signs of raised intra-

cranial tension, whatever its origin, may be mani-fest. Often they occur in an exaggerated form,because of the rapidity with which the tension isincreasing; some, however, may be lacking be-cause of the time factor or for other naturalreasons. Headache, for example, may not beregistered because the patient is stuporose.Vomiting commonly occurs. Papilloedema is rareexcept in the late stages of tuberculous meningitis.Drowsiness develops into stupor. The pulse andrespiration may become slow and are commonlyirregular.With the spread of the inflammatory process

irritative phenomena, such as fits and myoclonicor choreiform movements, may appear, to besucceeded by paralyses. These motor signs tendto develop with involvement of the cerebralvertex. With basal lesions the cranial nerves aremore liable to disturbance; there may be strabis-mus, pupillary inequality, ptosis, trismus andteeth-grinding.The terminal phase is one of depression of

function leading inexorably to death.

Meningitis in InfancyThe manifestations of meningitis, producing

together so clear-cut a picture in children andadults, are greatly modified in infancy. They mayin early life be so atypical as to be misleadingunless the great differences are borne in mind.The symptomatology of adult meningitis occurs ininfants only at an advanced stage of the disease.Again, the analogy with peritonitis, as contrastedin adults and infants, may be drawn.

In infants in whom the anterior fontanelle re-

mains patent, and in the absence of dehydration,palpation reveals an increase of pressure in thefontanelle. This important sign may precede theonset even of neck rigidity by several days. Inolder children, in whom the fontanelle is nolonger patent, there may be no clinical evidence ofmeningitis beyond fever, failure to thrive, drowsi-ness alternating with irritability, and in some casesa' meningitic cry.'The Cerebro-Spinal Fluid

Examination of the cerebro-spinal fluid playsan essential part in the diagnosis of meningitis;it completes, and is complementary to, clinicalexamination, but cannot be substituted for it.Clinical examination may occasionally afford acomplete diagnosis, as in the case of meningococcalmeningitis in the presence of meningeal irritationand a petechial rash. As a rule, however, it is con-cerned in the main with detecting the evidence ofmeningeal irritation, perhaps among a host ofother and confusing data, and with the eliminationor disclosure of antecedent conditions. Examina-tion of the cerebro-spinal fluid provides informa-tion regarding the nature of any meningeal re-action, and may in some instances furnish animmediate diagnosis. Since the clinical manifesta-tions of purulent meningitis are, as a rule, non-specific, a specific diagnosis, on which appropriatetreatment should be based, must await examinationof the fluid.

In the cerebro-spinal fluid the changes as-sociated with meningitis fall into three groups,depending on alteration of function in the meningesand in the vessels of the choroid plexus.i. Changes in pressureThe primary increase in pressure, resulting from

increased formation of fluid, may be accentuatedlater in the disease process by obstruction at thosesites from which absorption normally takes place.With obstruction at any point within the

cerebro-spinal system, on the contrary, an ap-parent diminution in pressure may sometimesresult at points distal to the obstruction. In earlychildhood and in infancy, in particular, obstruc-tion at the base of the brain may result in fluidbeing obtained under low pressure by the commonmethod of lumbar puncture. In more extremecases it may prove difficult or impossible to obtainany fluid by this route, though cisternal orventricular puncture will reveal that the pressureabove the site of obstruction is, in fact, con-siderably raised.As an aid to diagnosis, changes in pressure must

be considered in the light of these findings, andprovided always that an adequate technique isadopted for its estimation. On the whole, changes

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July 1948 APLEY : Meningitis: Rationale of Diagnosis 367

TABIE 2

C.S.F. IN MENINGEAL IRRITATIONI. Pressure 2. Cells 3. Chemistry

(Pressure may be raised in all groups)

Predominant Cell ChemistryGROUP Poly- IDENTIFICATION

morpho- Mono- Sugar andnuclear nuclear Chlorides Protein

I. Bacterial: Mild .. Increased Normal Increased Culture.Severe .. Increased Decreased Increased Gram stain. Direct typing.

Tuberculous .. Increased Decreased Increased Acid-fast film, culture, guinea-piginoculation.

2. Virus . .... Increased Normal Increased Complement fixation. Inoculationin animals.

3. Non-infective Irritation..(e.g. haemorrhage) Increased Normal Increased

4. Aseptic Reaction .. Increased Normal Increased Negative culture.

5. Meningism .... Normal Normal Normal to Normal or Primary cause found.low decreased

in pressure are comparatively valueless in thediagnosis of meningitis. Their occurrence is non-specific, and the highest pressures are frequentlyrecorded in such conditions as meningism or,fallaciously, through faulty positioning or tech-nique in obtaining the specimen of fluid.

2. Changes in cellsIn meningism the cells tend to be diminished in

number by the process of dilution; in all othertypes of meningeal irritation a reactionary increasein cells occurs.The type and number of cells which constitute a

pleocytosis depend not so much on the under-lying cause as on the speed of onset. Thus, theacute purulent meningitides are almost invariablycharacterized by polymorphonuclear leucocytosis,while the chronic forms may show a preponderanceof lymphocytes. On the other hand, though theusual chronic form of tuberculous meningitistypically shows a lymphocytosis, in its occasionalacute form polymorphonuclear cells may pre-dominate. In anterior poliomyelitis a briskmeningeal reaction in the initial stages coincideswith a polymorphonuclear leucocytosis; when thespeed of advance of the disease process slackens alymphocytic reaction occurs.

3. Chemical changesAlteration of the normal chemical composition

of the cerebro-spinal fluid may derive from one oftwo main groups of causes. It may reflect changesin the blood chemistry, even when the meninges

are functioning normally; or it may result fromthe altered permeability of meninges which arefunctionally impaired.Meningism provides an example of the former

group. In this condition the cerebro-spinal fluidchlorides are diminished because of the ante-cedent fall in blood chlorides. The protein inthe fluid obtained by lumbar puncture may, how-ever, also be reduced. This reduction resultsfrom the enhanced circulation of the cerebro-spinal fluid, because with an increased rate of flowthe protein in the fluid obtained by lumbarpuncture approaches the lower level which isnormally to be found only in the ventricles.Examples of the second group are provided

by any infective meningitis. In inflammatorymeningitis, and most markedly in acute infections,because of the increased permeability of theblood-cerebro-spinal fluid barrier, the chemicalcomposition of the cerebro-spinal fluid tends toapproximate to that of the blood plasma (Cohen,1927). Those substances normally present inrelatively greater quantity in the cerebro-spinalfluid than in the plasma (e.g. chlorides) becomereduced in amount; those substances normallypresent in relatively smaller quantity in thecerebro-spinal fluid (e.g. protein, glucose) becomeincreased. Glucose provides an apparent ex-ception; in meningitis its level in the cerebro-spinal fluid may gradually fall, but only because itis utilized in the inflammatory process.

Diagnosis should not rest exclusively on changesin chemical composition, since these changes may

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368 POST GRADUATE MEDICAL JOURNAL July 1948

be considerably delayed. Thus, a normal chloridelevel is not incompatible with the diagnosis oftuberculous meningitis, for the level may becomeappreciably reduced only at an advanced stage inthe disease process.

Table 2 summarizes the important changes inthe cerebro-spinal fluid. It will be seen thatvariations between the cellular and chemicalresponses are of great value in diagnosis, thoughfor ultimate identification additional investigationsusually prove necessary. The differences incellular and chemical responses also serve to em-phasize the classification of the causes of meningealirritation pr-vio,usly advanced on an aetiologicalbasis.

Differentiation of Purulent MeningitidesThe optimal treatment of purulent meningitis

depends on precise identification of the causal or-ganism. The species and type can be determinedonly by accurate bacteriological and, where

necessary, immunological methods. In the largemajority of cases an immediate result can beobtained by staining, either of a direct smear or ofone made after rapid centrifuging of the cerebro-spinal fluid. With skilled technique and ex-perience the culture of organisms from the fluid inpurulent meningitis is more frequently con-firmatory than diagnostic. The severity of the in-fection can rapidly be gauged by a simple quantita-tive test for glucose concentration.The identification of haemophilus influenzae by

the above methods is less frequently successful,since its morphological features are unpredictablyvariable. In difficult cases the capsular swellingphenomenon may be employed.

BIBLIOGRAPHY

COHEN, H. (1927), Brain, L., 6o0.FREMONT-SMITH, F., DAILEY, M. E., and THOMAS,

G. W. (I928-29), J. Clin. Invest., 6, 9.M. R. C. (1948), Streptomycin in Tuberculosis Trials Committee,

Lancet, April 17.

INFANTILE DIARRHOEA AND VOMITINGBy IAN M. ANDERSON, M.D. (Glasgow), M.R.C.P. (London)

Assistant Paediatrician, Westminster Hospital

Infantile diarrhoea is a disease of infancycharacterized by vomiting, frequent waterymotions, rapid dehydration, loss of weight and ahigh mortality rate.

Diarrhoea and vomiting has always been amajor problem to those physicians who have hadto deal with diseases of children. Epidemics havebeen reported since early times. In England aslong ago as the mid I7th century epidemics ofsuch magnitude occurred as to lead to the deathof 2,000 babies during the hot summer weather ofI669-71 (Garrison).' Carter2 in I893 drewattention to the infective nature of the disease andnoted its relationship to impure milk; hesuggested the use of subcutaneous saline. Wilson3(1927) discussed the bacteriology and pointed outthat the disease could be caused by manyorganisms.

Until the second quarter of the present centuryinfantile diarrhoea and vomiting was synonymouswith cholera infantum and the main incidence ofthe disease was in the summer months. Eventuallyhowever, investigations showed that contaminatedmilk and poor hygienic conditions were the most

important factors contributing to the seasonalincidence. With improvement in the milk supply,including the use of pasteurized and dried milksand improvement in sanitation associated with thedisappearance of the horse, the extermination offlies and the establishment of Welfare Centreswhere infant hygiene could be taught to themothers, there was no longer the same seasonalincidence nor mortality. It is probable that acertain amount of infantile diarrhoea and vomitinghas always occurred throughout the year and thatwhen the incidence of summer diarrhoea fell belowthe level of the all-season diarrhoea between 910oand 1930 this latter attracted attention. Marriott4considered that otitis media and mastoiditis com-monly caused infantile diarrhoea and vomitingand following on his papers several others ap-deared claiming success in treatment by mas-toidectomy. Findlay5 (I932) discussed the re-lationship of otitis media to infantile diarrhoea andvomiting and mentioned the social and seasonalincidence. Craig6 (I935) drew attention to thedisease as it occurred in the newborn and apartfrom summer diarrhoea and Dick,7 Barenberg8 and

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