Tropical Diseases/Chapter 5

From Wikisource
Jump to navigation Jump to search
Tropical Diseases
by Patrick Manson
Chapter 5 : Malaria : Malarial Cachexia, etc.
3219310Tropical DiseasesChapter 5 : Malaria : Malarial Cachexia, etc.Patrick Manson

CHAPTER V

MALARIA : MALARIAL CACHEXIA, ETC.

MALARIAL cachexia is the term applied to a group of conditions, more or less chronic, believed to be the result of an antecedent attack of severe malarial fever, or of a succession of such attacks, or of prolonged exposure to malarial influences.

Undoubtedly many of the more or less chronic morbid conditions which were formerly attributed to the malaria parasites are the outcome of infections by trypanosomes, by the Leishman body, by spirochætes, or by some as yet unidentified protozoal organisms.

Symptoms.—— The leading symptoms are those of a special kind of anæmia, characterized objectively by a peculiar earthy sallowness of skin, somewhat yellow sclerotics, enlargement of the spleen and—— in the early stages at all events—— of the liver. Usually the subject of this cachexia is liable to frequent attacks of an irregular type of fever, particularly after exposure, or fatigue, or, in fact, after any unusual physiological strain.

Malarial cachexia without fever.—— It should be mentioned that fever is not a necessary antecedent or accompaniment of malarial cachexia. In highly malarious countries it is not unusual to see typical examples in which fever had never been a feature, or, at all events, had been of so mild a character as not to have seriously attracted attention, or had occurred in childhood and been forgotten.

Enlarged spleen.—— In such countries a large proportion of the population have enormously enlarged spleens. The traveller cannot fail to be struck by the number of people he sees with big bellies and spindle shanks; by their languid and depressed air; their sallow, dry, rough, unhealthy-looking skins. In many malarial cachectics the skin pigmentation is remarkably dark; patches of almost black pigmentation are also sometimes discoverable on the tongue and palate.*[1] It is said that in some intensely malarial places children are occasionally born with enlarged spleens, as if the malarial poison had already affected them in utero. I cannot personally vouch for this, but I have often seen very young children with bellies enormously protuberant from distended spleen. According to Scheube, De Freytag and Van der Elst observed in 1873 and 1878 in Atchin that all the children born were affected at the time of birth with malarial cachexia, and that most of them died in a few months. Bein and Kohlstock found malaria parasites in the blood of the four-months-old child of a malarial mother, born some time after the arrival of the latter in a non-malarial district. Bignami failed to find malarial parasites, malarial pigmentation, or other sign of paludism in the fœtus of a woman who died of a pernicious malarial attack an observation which has been repeated and confirmed by other pathologists. Although unusual, more recent observations have shown that infection of the fœtus in utero through the maternal circulation does occasionally occur, presumably through rupture of the placental attachments.

Clark's observations on placental blood films in subtertian malaria suggest that the malaria parasite does not enter the fœtal circulation unless through an accidental rupture of placental vessels during pregnancy. Films made from the maternal face of the placenta showed parasites in 19 cases, whereas films made from blood from the umbilical cord of the same cases showed parasites in one instance only, and in this case there was a history of accident during the pregnancy. Clark found that the maternal placental blood was much richer in parasites than finger blood from the same cases, and in a considerable proportion of instances (11 in his 19 cases) showed infection in which examination of finger blood proved negative.

Delayed development.—— In some instances of malarial cachexia of early development the general growth of the body is stunted and puberty retarded. I have seen a malarial cachectic who, although 25 or 26 years of age, had the stature and sexual development of a child of 11 or 12. Abortion and sterility are common effects of malarial cachexia, which, in this as well as in other and more directways, becomes a potent agent in the repression of population.

Acquired tolerance of the malarial toxin.—— In many instances, although the state of cachexia may have attained an excessive degree, ague, or, in fact, fever of any kind, has never been a prominent symptom. It would seem that the body can become accustomed to the fever-producing toxin of the malarial parasite, much in the same way that it may become accustomed to opium and many other organic poisons. I have watched for three weeks the rhythmical development of a tertian parasite in a sailor who, although previously the subject of frequent attacks of ague, was yet quite free from fever during the period that I had him under close observation. Just as in those habituated to the use of opium a full dose of the drug, which in the unhabituated would produce profound or even fatal narcosis, acts merely as a gentle stimulant, so in those constantly exposed to, and actually infected with, malaria from infancy, the poison sometimes fails to act as a febrogene. And, to continue the comparison, just as the habitual use of opium produces a species of chronic poisoning or cachexia without narcosis, so the habitual presence of the malaria toxin may produce its peculiar cachexia without giving rise to fever. As a rule, however, particularly in the case of Europeans forced to reside in highly malarious countries, attacks of fever are of frequent occurrence in malarial cachectics.

Malarial neuroses and skin affections.—— Superadded to the febrile attacks, and to the associated anæmia, we may meet in cachectics with a variety of functional troubles. One characteristic of most of these functional troubles is the periodicity they generally observe. Thus we may have quotidian, tertian, or quartan neuralgias, gastralgias, vomiting, diarrhœa, headaches, attacks of palpitation, of sneezing, and so forth. Besides these, skin eruptions—— such as herpes, erythema nodosum, patches of lichen planus, eczema, urticaria, possibly synovitis—— exhibiting a periodic liability to exacerbations and an amenability to quinine, have been noted in malarial conditions.

Peripheral neuritis.—— I frequently see cases of well-marked peripheral neuritis, especially in patients from the West Coast of Africa, whose symptoms have been attributed to malaria. The degree of paresis varies from total inability to stand to weakness merely. There can be no question about the antecedent malaria, but whether the neuritis in every instance be the direct result of this infection it is hard to say. I have seen a well-marked multiple peripheral neuritis, in which there was slight fever with abundant subtertian parasites, promptly subside on the administration of quinine. In this case the neuritis began with violent cramps in the legs. Loss of memory, partial or complete, appears to be a common accompaniment of this condition.

Herpetic eruptions are very common in malarial attacks. According to Powell, in Assam the appearance of a patch of herpes somewhere about the body, usually the lips, is regarded as an infallible sign that the attack of fever is over for the time being.

Hœmorrhages.—— In high degrees of cachexia, hæmorrhages of various kinds are apt to occur; in such conditions epistaxis, hæmoptysis, hæmatemesis, melaena, retinal hæmorrhages, purpura, occasionally hæmaturia or hæmoglobinuria are not infrequent. In such patients trifling operations——tooth extraction, for example—— may prove a dangerous matter. I have seen in malarial cachectics hæmorrhages from the latter cause which were very difficult to control. Care must therefore be exercised in advising and in performing even the slightest operations on patients of this class.

Intestinal and pulmonary affections.—— In addition to the troubles mentioned, we find that the subjects of malarial cachexia are apt to be dyspeptic; to suffer from irregularities in the action of the bowels; to suffer from morning diarrhœa, at first of dark bilious, and later, perhaps, of pale, copious, and frothy stools. They are also very liable to a low and highly fatal form of pneumonia.

Cachexia associated with functional and with organic lesions.—— There may be said to be two degrees or kinds of malarial cachexia. In one there is merely anæmia with congestion of the portal system; this may be quickly recovered from on the patient being removed from endemic malarial influences and subjected to specific and proper treatment. In the other there is, in addition to anæmia, organic disease of the abdominal viscera—— of the liver, spleen, and kidneys ——the outcome of long-standing congestion of these organs. These tissue changes not only keep up the anæmia, in spite of removal from malarial influences, but, in the long run, inevitably progress to a fatal issue.

Pathology and pathological anatomy.—— The pathology of malarial cachexia is virtually, in the first instance, that of acute malarial disease. There is blood destruction by the direct action of the malaria parasite and of its toxins, eventuating in oligocythæmia and in the deposit of hæmozoin and of hæmosiderin (yellow pigment) in the tissues. The activity and persistence of the process lead to congestion which ultimately determines organic changes in liver, spleen, kidneys, and probably in the bone marrow.

Splenic enlargement.—— The spleen may become so enlarged under repeated attacks of the congestion attending a succession of fever fits, or in consequence of a less active and perhaps feverless hæmolysis, that it may come to weigh many pounds, and so to increase in bulk as to occupy nearly the entire abdomen. The capsule of the gland, particularly on its convex surface, is thickened, and, perhaps, the seat of fibrous patches, or even of adhesions to neighbouring organs. Many of the trabeculæ forming the framework of the gland become greatly hypertrophied. On section, the tissues of such a spleen are found to be moderately firm, and usually of a reddish-brown colour; but when death happens soon after or during a febrile attack, the section of the gland shows a dark surface from deposit of hæmozoin, the pulp at the same time being softened. Perhaps from over-distension some of the vessels in the interior of the gland give way, and then there is a breaking-down of the spleen pulp in patches, the remains of splenic tissue floating about in the extravasated blood. Microscopical inspection of these hypertrophied spleens, especially during fever, shows the black and ochre pigments in the situations already indicated.

"Splenic index"—— There are practical points in connection with malarial spleen which deserve mention. The relative absence, or prevalence, of these enlarged spleens or " ague cakes " in the native population is an excellent rough indication of the salubrity or the reverse, as regards malaria, of any particular district. Wherever they are common the district is malarious, and therefore unhealthy, perhaps to Europeans deadly, and should be looked upon as extremely unfavourable for either camping or residential purposes.

Liability to rupture of splenic tumours.—— Another practical point is that these enlarged spleens are easily ruptured by a blow on the belly. In hot and malarious countries many a coolie goes about doing his work although he has an enormous spleen. This is a fact to be remembered in administering even mild corporal punishment to natives of malarious countries. Europeans have more than once been tried for manslaughter in consequence of neglecting it. Owing to this liability to rupture, the subjects of splenic enlargement must not be allowed to play at violent games, as football or even cricket, or at any game in which the diseased organ is exposed to a blow, Apart from direct violence, an enlarged spleen may rupture spontaneously, owing to sudden accession in size in the course of a fever fit.

Splenic ruptures are, of course, generally fatal. It sometimes happens that the presence of adhesions limits and restrains the hæmorrhage. Localized hæmorrhages of this description may, in time, lead to splenic abscess.

Hepatic enlargement.—— Like the spleen, the liver in malarial cachectics becomes enlarged during accessions of fever. Under the influence of a succession of acute attacks, hepatic congestion may gradually acquire a more or less permanent character. After death from such fevers the capsule of the liver is found to be tense; on section the highly vascular tissue of the organ is seen to be reddish-brown or almost black, according to the degree and kind of pigmentation. If this stage of congestion be long maintained, it tends to bring about various kinds and degrees of chronic hepatitis with hypertrophy of the intralobular connective tissue, and in time leads to hypertrophic or to different forms of atrophic cirrhosis. Thus irremediable organic disease of the liver, portal obstruction, and ascites may ensue.

Siderosis.—— It is in livers of this description that a form of what is called siderosis is produced a condition resulting from chemical changes undergone by the yellow pigment with which the various cells of the organ are charged. It has already been stated that, when first deposited, this pigment gives no ferrous reaction with ammonium sulphide, or with the double cyanide of iron and potassium; and that, as the deposit becomes older, chemical changes ensue, resulting in the elaboration of a form of iron which will then yield the characteristic black colour with the former, and blue colour with the latter reagent. Treated with ammonium sulphide, sections of liver, and also of spleen, kidney, and other hæmosiderin-charged tissues, from chronic malarials, may turn almost black to the naked eye, or, at all events, exhibit under the microscope abundance of blackened pigment. In such sections it is seen that the hæmosiderin is no longer in minute grains, as when first deposited, but in blocks and globules as large as, or even larger than, blood -corpuscles. This pigment is, of course, something quite apart from the parasite-derived hæmozoin deposited in the same organs.

Practical considerations.—— Certain clinical facts about malarial hepatic congestion and malarial hepatitis are of importance. In the first place, such conditions do not tend to terminate in suppuration; in the second, they are almost invariably associated with splenic enlargement. These are important facts to recollect when it becomes a question of the diagnosis of malarial hepatitis from abscess of the liver. Another important fact to remember is that recent malarial enlargement of the liver is usually curable, depending, as a rule, on simple congestion; whereas old-standing malarial hepatic enlargement is usually incurable, depending, as it usually does, on hypertrophy of the connective tissue and a cirrhotic condition of the organ.

Malaria a cause of nephritis.—— Changes similar to those found in the liver in the course of, and in consequence of, malarial disease occur in the kidney; in time they result in confirmed Bright's disease. Hence, probably, the frequency of Bright's disease in some highly malarious climates. In the British Guiana Medical Annual, Daniels mentions that in 926 post-mortem examinations in the hospital at Georgetown, Demerara, a highly malarial district, he found evidence of disease of the kidneys in no fewer than 228.

Cardiac degeneration.—— As a consequence of defective nutrition from prolonged anæmia and recurring fever, the muscular tissue of the heart in chronic malarials may degenerate, the ventricles dilate, and, in time, the lower extremities become œdematous. For the same reason the subjects of valvular affections of the heart, whether compensated or otherwise, must be regarded as unsuitable for residence in malarial countries.

Other sequelœ.—— These include dysenteric conditions, forms of diarrhœa, low forms of pneumonia readily set up by chill and prone to terminate in abscess of the lung or to become associated with empyema, extensive sloughing phagedæna, and other forms of gangrene such as noma; or pernicious fever may supervene at any time and rapidly carry off the subject of advanced malarial cachexia.

Tubercular and syphilitic disease not infrequently concur with malaria; in fact, the latter may powerfully predispose to local manifestations of either of the two former, and vice versa—— a complication as to which the practitioner should always be on his guard.

  1. * Observations in India tend to show that this condition, melanoglossia, is racial and not pathological.