No. 3059.

APRIL 15, 1882.

ABSTRACT OF THE

Troonian LecturesON THE

CLIMATE AND FEVERS OF INDIA.Delivered before the Royal College of Physicians,

March, 1882,

BY SIR JOSEPH FAYRER, K.C.S.I., M.D., F.R.S.,FELLOW OF THE ROYAL COLLEGE OF PHYSICIANS, LONDON.

LECTURE III.THIS lecture was devoted to a description of fever due to

ordinary causes, and also those types designated as febriculaor ephemeral fever, by some ascribed to malaria alone. Thelecturer proposed to add to the list that of endemic, enteric,or continued fever, and urged that the adoption of the fol-lowing classification would be useful in registration, andwould lead to more definite conclusions as to disease, at

present much confounded : - (a) Ephemeral or febricula.,(b) Ardent or thermic, (e) Endemic, enteric, or continuedfever. (d) Specific enteric fever. Sufficient allowance wasnot always made for the modification of disease in India, ascompared with temperate climates.Ephemeral Fever, or Febricula, is a mild simple fever

common in India, due to ordinary causes, as changes oftemperature, excesses in eating or drinking, fatigue, excite-

ment, disordered secretion, functional derangement of abdo-minal viscera, and most frequent in hot seasons. Most

-people newly arrived have it, and then it is probably notdue to malaria; whilst in natives and old residents suchattacks are probably malarial. The symptoms are. malaise,headache, foul tongue (which is white with red edges), dis-ordered bowels, nausea or sickness; temperature 104° to1060, preceded by chills, malaise, muscular pains, followedby diaphoresis. In plethoric or intemperate people the re-action may be severe, with high fever and delirium, conges-tion of liver and of gastro-intestinal tract. It is, however,mostly simple, and readily yields to treatment-viz., freerelief of the bowels or an emetic, diaphoretics, tepid.sponging, restricted diet, and rest. Most people newlyarrived in India incur an attack, which to Europeans is anacclimatising process.Ardent or 2’her7a;c Fever is more serious, and varies from

simple to intense fever, attaining its maximum in sunstroke.Dr. Wood, in his recent monograph on Fever, gives resultsof experiments confirming what others have shown thatexternal heat, by inducing vaso-motor paralysis, causes

intense pyrexia, which, if not mitigated, rapidly de-stroys life by causing failure of the respiratory centre,the high temperature causing fatal nutritive disturb-ances.l The causes predisposing to this influence ofheat are-previous illness, debility, intemperance, consti-pation, bilious derangement, imperfect breathing in crowdedrooms and barracks, ill ventilation, and defective perspira-tion. The vitiated and over-heated blood paralyses theheat-controlling mechanism ; there is great rise in tempera-ture, and death if the patient be not relieved. Exhaustionand syncope may occur during exposure to a high tempera-ture, as in the case of engine-room men in the tropics, ormen who are exposed to the sun’s rays. The skinis pale, cold, and moist, and the pulse feeble. Death mayoccur from failure of the heart, and asphyxia and apnoeamay supervene after premonitory depression and weakness,during such exposure, when the nervous energy is loweredby fatigue, illness, or dissipation. The respiratory centresare overwhelmed by the sudden rise of temperature, and,as Professor Claude Bernard and Dr. Lauder Bruntonhave shown, the heart’s action is first accelerated andfinally arrested in a state of tetanic contraction. In othercases there is ardent fever, which may occur apartfrom direct exposure to the sun in predisposed subjects.

1 "External heat applied to the body of a normal animal (or mtm) soas to elevate the temperature produces derangement of the functions ofinnervation, of circulation, of nutrition and secretion, similar to thoseseen in natural fever, the intensity of the disturbances being directlyproportionate to the rise of temperature."-WOOD on Fever.

The body temperature may rise to 108° or more; there aredyspnoea, restlessness, and pungent skin. The pulse insome is full and labouring, in others quick and jerking; theface and neck are livid and congested; the carotid pulsatiorvery perceptible; pupils, at first contracted, dilate widelybefore death. Stertor, coma, delirium, or convulsions,frequently epileptiform in character, with relaxation of

sphincters, and suppression of urine, are the precursors ofdeath, and there may be cerebral hsemorrhage. Many fatalcases among Europeans are so caused. The premonitorysymptoms appear some hours or even days before the dan-gerous conditions

supervene. There are malaise, disordered

secretions, profuse and requent micturition, restlessness,insomnia, apprehension of impending evil, hurried andshallow breathing, prsecordial anxiety, giddiness, headache,occasionally nausea or vomiting, thirst, anorexia, fever,which, soon becomes intense. These conditions frequentlyare worst at night, and the patient may pass into a state ofunconsciousness and die. Ardent fever may supervene’onordinary fever, especially when the atmosphere is loadedwith moisture, so as to prevent evaporation from the person;hence the dry atmosphere of Upper India is better toleratedthan the damp atmosphere of Lower Bengal or parts ofSouthern India, though the temperature is lower. Vigorous,healthy persons, of moderately spare frame, with soundviscera, and temperate habits, can sustain great heat if theatmosphere be pure and moderately dry. Fresh arrivals inIndia are more prone to suffer until they have accustomedthemselves to the climate; but when the temperature risesabove a certain standard all succumb, and natives sufferand die like others. Much depends upon the actual state ofhealth, and free perspiration in the tolerance cef heat. Ofthose who recover, or rather who do not die; many remaininvalids for life, which is often shortened by obscure cerebralor meningeal changes. Irritability, impaired memory,epilepsy or epileptiform attacks, headache, mania, partialor complete paraplegia, or blindness, extreme intolerance ofheat, especially of the sun’s rays, rendering the personincapable of serving in hot climates or of ’ enduringany exposure to the sun; or, it may be, graduallyending in complete fatuity, dementia;- or epilepsy;chronic meningitis, with thickening of. calvaria, -,whichmay account for the intense cephalalgia; or in a lesserdegree in disordered innervation and general functionalderangement, which seriously compromise health. Whendeath occurs suddenly there is no remarkable morbidchange. The heart may be flaccid or contracted, the lungsand brain congested or not, the venous system full of darkgrumous partly fluid blood effused in patches of ecchy8f0sts.In death from thermic fever there is similar venous engorge-ment and ecchymosis ; the blood is more fluid than natural,and acid in reaction. The body for some time retains ahigh temperature, and rigor mortis comes on very rapidly.In some cases there is cerebral bsemorrhage and ventriculareffusion. The treatment consists in removing the patient to acooler place, giving the cold douche, removing tight clothing,applying ammonia to the nostrils, &c. Rest and avoidanceof exposure and fatigue must be enjoined. Future exposureto the sun should be carefully guarded against, and greatcare taken to avoid excitement, and errors or excesses

of diet and stimulants. The object in treatment is toreduce temperature as speedily as possible. Hypodermicinjections of quinine (first used for this purpose, I believe,by Mr. Waller of Calcutta) has been employed. Bleeding hasbeen abandoned ; for although it may produce temporaryrelief relapse follows. Cold affusion and ice generally answer,and the bowels should be relieved. On the subsidence ofsevere symptoms the febrile condition is treated on ordinaryprinciples. ’

Continued Fever.-Writers on Indian and tropical diseaseshave described a form of continued fever liable to be modi.fied by visceral complications, and, in a fatal termination,post-mortem examination revealing pathological changes ofvarious importance. It is attributed to such circumstancesas heat, atmospheric vicissitudes, terrestrial emanations,personal habits; whilst no very distinct characters differen-tiate it from remittent which has assumed a continuedform. Twining, Annesley, Martin, and others regarded it asa variety of- malarial fever, in which perhaps there is littledifference of opinion. But it is necessary to distinguish itfrom specific continued feveJJ&bgr;, with which it may be con.founded. From typical cases of remittent the distinction isclear enough, but in many cases it is difficult, if not im.possible, for the characters of the temperature curve vary

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so little that it is not a sure guide. Other fevers inIndia may assume this condition, especially if not dealtwith properly at first, and visceral complications are

usually the precursors and concomitants of the change of"type.*-enteric Fe’ver.-Since Annesley recorded his belief thatall the fevers of India depended on climatic conditions,and that there were no specific fevers, great advances:: have been made in our knowledge of the nature offevers, and now it appears as the chief fever death causeamong our young soldiers. Its distinction from remittentwas first pointed out by Mr. Seriven in 1853,2 although

Annesley, Twining, Martin, and others had drawn attentionto the occurrence of diarrhosa, enteric ulceration, and otherphenomena characterising the adynamic types of climaticfever. Annesley describes the ulcers as largely seated inthe lower end of the dieum. Sir R. Martin says he foundulceration very prevalent in congestive continued feveramong the labouring classes of nations. Twining, in 1842,describing "congestive fever," speaks of congestion of themesentery and ulceration of intestines as generally existing,and was aware of its resemblance to European typhus.Dr. Morehead gave a guarded assent to the fever being thesame as typhoid. About 1851 Assistant-Surgeon Lee ob-served ulceration of Peyer’s patches in cases of fever chieflyamong European seamen ; and Dr. Macpherson did notrthink that these fevers differed in cause from those hithertoattributed to exposure, climate, and season. In 1854 thelecturer saw a case at Lucknow in a young Frenchman,aged twenty-eight, who died after a fever of more

than three weeks’ duration, attended with diarrhcea,haemorrhage from the bowels, iliac gurgling, tympanites,stupor, and finally death, collapse evidently super-.vening on perforation. The fever was regarded as

,climatic; and there was no reason to suppose that he had;been exposed to the influence of fseca.1 poisoning ; and thecase suggested the possibility of malarial fever assuming anenteric torm. Dr. Maclean, C.B., says that so far back as’1838 he treated fevers of long duration with bowel compli-cations and lesions, now known to be characteristic of entericfever. Dr. Gordon, C.B., also noted the frequent occurrenceof intestinal ulceration, especially in young subjects; and;although he does not deny the existence of the specific,typhoid in India, he insists on the need of sifting all cases,-with a view of ascertaining whether cases recorded as

,specific fsecal enteric fever may not have been of malarialor climatic origin. Dr. Chevers points out that the recogni-tion of enteric fever should not lead to the withholding of free,and steady use of quinine. Dr. Wall demurs to too extreme,an application of the term typhoid fever. Dr. Don and Dr.MacConnell point out that in not a few cases it seems tohave an etiology different from that usually assigned to it inEurope. Dr. Alfred Clarke also,believes that in some casesclimatic influences may initiate the disease, having seengenuine enteric fever in India when all filth causes, in theordinary sense of the term, were absent ; and refers to theoutbreak in Natal, Jan. 1882, as an example. Dr. Woodward(U.S.A.) has applied the term "’typho-malarial" to indicatethat form of fever which appears to be the result of the com-bined influence of malarial poisoning and the cause of typhoidfever ; and was quite unable to draw a line between the post-mortem conditions met within such cases and those of typhoid.In India localities notoriously malarious are not remarkablefor the prevalence of typhoid, but no part of India, exceptthe hill stations, can be regarded as exempt from malarialinfluences ; and that no station where Europeans are

located is exempt from typhoid ; but there appears to benothing in India to support the theory of antagonism be-tween malarial and typhoid fever ; that if, as is thought bysome, fever with enteric ulceration is of miasmatic origin,the question of relative prevalence and mortality provesnothing more than that the fever had assumed one typerather than the other; very careful analysis of the historyof individual cases and outbreaks should be made, especiallyin such developments of fever as have occurred in regionslike Burdwan, the Doab, and other districts where low andcontinuous forms of fever, ascribed to miasmatic influences,have prevailed. Some interesting reports have been pub-lished on the Burdwan fever by Drs. French and Roy, ofthe Bengal service; they attribute it, as do others, to

2 Dr. J. Ewart was the first, I believe, to describe specific entericfever in natives of India. This discovery was made independently ofScriven’s on the Europeans in India

paludal influences ; in their account of the cases there ismuch that is suggestive of enteric fever. That fever withulceration occurs in India among the native population isbeyond dispute ; but how much of it depends on specificpoisoning ; how much on general causes ; and what are thedistinctive phenomena in life and lesions after death-aresubjects that require further inquiry. I repeat myconviction that there is much fever of climatic originwhich is as like specific typhoid as one case of typhoidmay be like another, and that is of the same characteras that called by Americans "typho-malarial," and bythe French "typhoide palustre." After many years’experience, such is the conclusion I have arrived at,and I find that similar views are entertained by others.Dr. J. Wise of Dacca believes also that enteric fever inIndia may arise from malarial causes, so that in spite ofthe irresistible mass of facts collected by Murchison, Budd, andothers, proving that entericfeverin Europe is truly pythogenic,in India we cannot accept that as the sole, or perhaps chief,existing cause. Dr. Parkes also entertained doubts whetherthe generally accepted cause is the only one to whichenteric fever is to be referred. Dr. Bryden has also per-sistently and ably argued in the same sense. Afterquoting other authorities the lecturer mentioned that Dr.Kynsey of Ceylon had sent him a note on the fevers in thatisland, in which he says there is no doubt as to theexistence of genuine enteric fever, but also of another feverindistinguishable during life from it, but without itscharacteristic lesions. Dr. P. Manson of Amoy has describedan epidemic of anomalous continued fever in China,3 whichin some respects resembled enteric, in others malarial, fever.Quinine was of benefit in some cases only. Dr. Grabbamof Madeira has met with typhoid fever there, apart fromany source of filth contamination. Surgeon-General Irvinereports an outbreak of enteric fever among our troops inSouth Africa attributed to the fouling of the streams bydead cattle and filth of all sorts. I believe a considerableamount of climatic fever occurs in the tropics, inwhich the symptoms and phenomena so closely re-

semble those of true enteric fever, that they may be,and are, mistaken for them, and that the post-mortemdiscovery of ulceration attests the severity of the disease.I would ask all medical officers in India to study eachcase in all its aspects most critically, for no one willdeny that we have still much to learn about fever in- tropical climates. If it be admitted that specific entericfever may originate in organic effluvia and emanationsgenerally, and is not restricted to a specific contagiumdeveloped only in human excrement, it is probable thatin this source we may find its origin, for there are fewlocalities in which organic exhalations do not taint the airor pollute the soil or water. Still the fact that theseconditions are often so rife, and yet this form of fever so in-frequent, and that the effects of season, locality, age, and wantof acclimatisation play so important a part in developing it,seems to indicate that climatic conditions are largely con-cerned. Dr. J. Marston says :—" I think, as a tentative andworking hypothesis, that there are two forms of it in India,which cannot, however, be clinically or pathologically differen-tiated : one (the larger class) which does not depend onthe contagion of any specific poison generated in the in-testine of one person and conveyed to another through somevehicle, nor indeed on any fsecal poisoning, or poisoning ofany kind, unless it be that the patient is anti’geneticallypoisoned by his own fsecal matter, the other occurring inoutbreaks (not singly in isolated cases) and with a historyby which the cases can be traced to some common cause,such as infection, fouled air or water, diseased or highmeat, &c. In the first variety, however, I am disposed tothink climate-meaning by it to include the whole com-

, bination of changed physiological conditions environing the: young and newly arrived soldier in this country-plays a

very important if not the main part. It is a notable fact, that of a number of fatal cases returned as remittent fever,

where the - -mortem appearances rlisclosed an absenceof any intestinal glandular lesion, the subjects are oldermen and longer resident in the country ; whereas whereulceration of Peyer’s patches was found, but th" fever hasbeen diagnosed as remittent or enteric fever, subjectsare, as a-rule, younger and less lorg res<1en’ sc’die.’ Thesymptoms generally are much the same in Indi) "" elsewhere,modtned, perhaps, by malarial influences. At the outset the

3 China Imperial Maritime Customs’ Report, No. 2, 1881.

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disease may be insidious, and for the first few days there areonly malaise, chill., perhaps diarrhoea, loss of appetite,’weariness, aching of the limbs, and headache. The patientat length lays up, the pulse quickens, the temperature rises,the skin becomes hot and dry, there are thirst, heaviness,and dulness; whilst the thermometer indicates a graduallyrising temperature,’ until it reaches 104&deg; or naore,, witha remission towards morning. The abdomen becomes dis-tended, and there is tenderness on pressure, especially in theright iliac region, with gurgling. The diarrhoea probablyincreases, and becomes of a yellowish colour; it may betinged with blood. The tongue is red at the tip and edges,dry, cracked, and tender. The teeth begin to be coveredwith sordes. During the second week the characteristicspots make their appearance, but are often absent, and onthe dark skin of the coloured races are difficult to detect.As the disease progresses the patient becomes delirious ; thedelirium is at first wandering, but it gradually becomes in-coherent, and may be noisy or muttering, with completeprostration. The diarrhoea increases, the tongue is dry andglazed, the teeth covered with sordes. There may be epi-staxis, or haemorrhage fromthe bowels, and the patient becomequite unconscious. The temperature rises to 106&deg;, or evenhigher. He has subsultus of the tendons, muscular twitch-ings, picking of bedclothes. Death supervenes from

exhaustion, or from peritonitis caused by perforation of theulcerated bowel. The ordinary duration is three weeks,often more; in severe cases it may terminate fatally muchearlier, probably before the intestinal ulceration has takenplace, by the intense action of the poison on the nerve

centres ; but in milder cases it may terminate earlier. Aboutthe fourteenth day the symptoms sometimes improve, thetemperature begins to fall, the general symptoms abate, anddiarrheca decreases, and the appetite and sleep improve.The diagnosis between specific enteric and climatic enteric isvery difficult. The close resemblance between some remittentsand the specific forms is very great. In the specific form theinvasion is gradual, and it is not for some days, during whichthe temperature rises, until about the fourth evening, thatit attains 104&deg;. In the climatic or malarial forms the pre-

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monitory symptoms are more sudden. There is more markedchill or rigor, the malaise is greater, the temperature risingto 104&deg; to 1060 as early as the evening of the first or secondday, though these distinctions are not always well marked.There is diarrhoea in both and all the other symptoms;ulceration being established, the phenomena become iden-tical. The rose-coloured spots are by some regarded aspathognomonic, but they are often not observed in casesof specific enteric, and it is very difficult to detect, or to

distinguish them on the dark skins of natives; it is pos-sible that they may, standing in relation to the bowel ulce- Iration, occur, however, before that condition is established.It would unduly prolong the subject to enter into furtherdetails; nor is it necessary to say much on treatment, for,in fact, it is exactly that which is adopted here, and consistsmainly in the careful administration of fluid nutrients,avoiding all that could excite or irritate the disordered bowel;diarrhoea should be controlled, not unduly checked ; tempe-rature should be reduced by apyretics and baths, or diapho-retics, and by the use of quinine in moderate doses-usefulin pyrexia, however caused; whilst as to the mode andextent of its administration, the circumstances of each parti-cular case will be the proper guide. As regards wine orother form of alcohol, I have administered it according tothe effect it produced. As to nourishment, animal broths andmilk--perhaps diluted with some alkaline water-have beenthe most appropriate, avoiding any possible source of gastro-intestinal irritation, even after convalescence was well estab-lished. Relapses occasionally occur, and a nearly fatal onein an officer of long service, who in the fourth or fifth weeksuffered from a recurrence of dangerous symptoms, simplyas the result of eating a few raisins given him by the nurse,left a strong impression on my mind as to the importance ofcaution as to diet. The temperature cliarts will show thevaried character of the pyrexia, and how little there is thatcan be said to draw a distinct line of demarcation betweenthe different forms of fever. I regret that I am unable toanalyse them at length, but will only ask you to look atthem and the specimens and drawings which represententeric ulceration from fever patients in India, for whichI am indebted to Professor Aitken, of Netley, and ProfessorMcConnell, of Calcutta, to whom, as to many of my brotherofficers in India and at home, I am so much indebted, asmy frequent allusions to their contributions attest.

Gulstonian LecturesON

PULMONARY CAVITIES ; THEIR ORIGIN,GROWTH, AND REPAIR,

Delivered before the Royal College of Physicians,in March, 1882,

BY WM. EWART, M.D. CANTAB., F.R.C.P.,ASSISTANT-PHYSICIAN AND PATHOLOGIST TO THE BROMPTON HOSPITAL

FOR CONSUMPTION, PHYSICIAN TO THE BELGRAVE HOSPITAL FORCHILDREN, DEMONSTRATOR OF PHYSIOLOGICAL

CHEMISTRY AT ST. GEORGE’S HOSPITAL.

LECTURE III.PAART II.

IN the first part of my lecture I referred at some length tothe external changes which promote the collapse of cavities.Concerning the forces acting from within which conspiretowards the same result my remarks must be brief. Theseforces are mainly-(1) the retraction of the trabecuife, and(2) fibrous shrinking of the bronchi.

(1) In respect of traheculae, it will suffice if I remind youof a statement contained in my last lecture. Owing to theirderivation from collapsed alveolar substance, containing notonly branches of the pulmonary artery and of the pulmonaryvein, but frequently also the blood vessels special to the wallof an adjoining bronchus which has been laid open byulceration, elastic tissue enters largely into their composi-tion. In virtue of this elastic nature, trabecuipe, as long asthey escape ulceration, must tend to approximate their

points of attachment. The same observation applies to thedenuded bloodvessels which stretch across the large vomicaedue to caseous pneumonia. The tension to which I alludeis often demonstrable in the recoil suffered by the segmentsof a trabecuta when the latter is divided. In addition tothis purely elastic force, trabeculae in chronic nbrotic cavitiesare apt to become the seat of a fibrosis analogous to thatoccurring in the cavity wall. The slow contraction peculiarto young fibrous tissue in this case associates itself with theelastic forces inherent to the original tissues, and contributesin no mean degree towards the result which I have indi-cated.

(2) By the side of the influence exercised by trabeeulse inlessening the distance between the opposed surfaces of avomica, another force is exerted by the thickened bronchustending to produce a retraction of the cavity. Bronchi in astate of health are stretched between the root and the peri-phery of the lung, and in virtue of the elasticity which theyshare with other pulmonary constituents, they would retractwhen divided. But this original elasticity, although appre-ciable, is small in comparison with the fibrous retraction ofa more gradual nature induced in the ulcerated air-tubes bychronic irritation. The thickness acquired by bronchi con-nected with the cavities of phthisis is considerable ; it ismainly due to an abundant growth of fibro-cellular materialwithin the peri-bronchial sheath. The bloodvessels richlysupplied to the young tissue undoubtedly possess somedegree of elasticity, which should not be omitted as an

additional agent of retraction, although clearly secondaryin importance to the fibrotic shrinking. The results arestriking : the bronchus terminating in a vomica becomesdistinctly shortened in proportion to its thickening; and bythe shrinking of the bronchus the cavity is drawn towardsthe root of the lung, and additional space is given at theperiphery for the expansion of the alveolar tissue.In the very large and chronic vomicse this special agency is

obscured by the coincidence of many other changes, but in thecase of smaller vomicae which have undergone contractionsand have retreated from the surface it is almost impossible notto recognise the action of a definite and continuous force, thedirection of which lies in the path of the bronchus. My mean-ing will be made clearer by a reference to Fig. 6 (see Lect. III.,Part I.), where the retraction of the cavities has been depicteddiagrammatically it is true, but without exaggeration. I amthe first to admit that this retraction is brought about by acombination of circumstances ; among the latter I hold thecollateral expansions of the surviving tissue to be one ofconsiderable importance. Compensatory hypertrophy, how-