This section is from the book "Malaria, Influenza And Dengue", by Julius Mennaberg and O. Leichtenstern. Also available from Amazon: Malaria, influenza and dengue.
The term malarial cachexia is given different meanings by different writers. Some understand by it a condition of the organism, the principal characteristic of which consists in the impossibility of eliminating the injurious influences put into play by the malarial infection. This impossibility being final, the organism is doomed to destruction. Others make the definition broader and include certain transitory disturbances. The former take certain anatomic, irremediable alterations in the tissues as the basis of the cachexia; the latter, either persistent or transitory disturbances, due to functional as well as pathologico anatomic processes. A common bond between both definitions is made by the similarity of the clinical symptoms. It is only in their prognosis that they are diametrically opposed, in that in one case it is absolutely unfavorable; in the other, only dubious.
Since we are discussing malaria principally from its clinical aspect, and are looking to the requirements of the physician, we will pay no further attention to the former definition, but will include under our term every condition characterized by a persistent or transitory loss of power on the part of the tissues coming into consideration, namely, the bone marrow, liver, and spleen.
We would understand the pathogenesis very inadequately if we were to attribute these disturbances, even principally, to the processes in the blood.
The red blood corpuscles are the first to meet the attack of the malarial parasites. These are destroyed by billions and billions, but it is the blood making organs that must make good this loss. Moreover, this is only half of what they must do, for theirs is the work of removing the debris of the hemoglobin consumed by the parasites (the melanin). This work falls principally on the liver, but also on the spleen, the lymph glands, the kidneys, and the intestinal mucous membrane. As long as the bone marrow and these organs are equal to the demands made by the organism on account of this devastation of the parasites, so long will there be no question of cachexia; but as soon as a disturbance of activity occurs in these organs, whether this is only functional and, therefore, temporary, or organic, and in this case unalterable, there arises the condition which we call cachexia.
Kelsch and Kiener very appropriately compare the condition of the organism in the course of a malaria to that of the heart during a valvular affection. So long as the reserve power and the hypertrophy of the heart muscle are sufficient to compensate for the disturbance, so long the organism shows none at all or only slight symptoms of the valvular disease, but as soon as the activity of the heart is interfered with, all kinds of compensatory disturbances occur. In the same way in malarial infection when the tissues in consideration become functionally insufficient, the symptoms of cachexia appear.
From this it is evident that the cachexia consists principally of the anemic and hydremic symptoms, associated with those due to overloading of the organism with pigment. Since the functions of the organism are depressed and no rapid compensation is possible, we find grouped about these other symptoms of the most varied kind.
Considering the number of disturbances that anemia and hydremia alone may produce; recalling the lessened resisting power of an organism paralyzed in its most important functions to different injuries; remembering that the malarial pigment when it cannot be removed by way of the bile and of the urine remains lying in the parenchyma as an irritating foreign body, and adding to this that, in the majority of cases of cachexia, the malarial parasites are still capable of continuing their depredations on the erythrocytes and of producing toxin, we must realize the endless perspective of symptoms that can arise in malarial cachexia.
Cachexia occurs most frequently in individuals exposed uninterruptedly for years to the influence of the malarial virus. It is, therefore, most common among the inhabitants of severe malarial regions. Moreover, it is almost always the poor and miserable, who live under bad hygienic conditions, that become its victims. They draw in, as it were, the malarial poison with their mother's milk, spend their youth in the midst of the pest, and get no opportunity to change their residence so as to recuperate. Cachexia is seldom seen in immigrants, first, because they are usually at an age when the organism is more resistant; secondly, and this is the principal reason, because the strangers are usually in a position to seek, at least now and then, a more salubrious climate in which to recuperate. In malarial regions soldiers in garrisons are commonly returned home after a series of malarial paroxysms, and office holders and merchants confine their stay to the shortest possible time.
Some cachectics assert that they have never suffered from fever, though I put little faith in these statements. We have mentioned in several places how frequently patients are unconscious of the fever, and when this is the case in well educated men accustomed to observe themselves, how much more would it be so in people who, in their arduous struggle for existence, find little time to devote to general health. Leon Colin, together with Nepple, Bailly, Monfalcon, Boudin, Catteloup, and others, claims that cachexia does occur in the natives without preceding fever, and he refers to the cachexia of lead poisoning, which sometimes sets in without colic, paralysis, arthropathy, etc., as an analogy.
In the majority of cases the cachexia is preceded by numerous infections or relapses and so develops gradually. We speak of such a cachexia as chronic.
Sometimes the symptoms come on rapidly at the close or in the course of an infection; in this case we speak of acute or galloping cachexia. It is very rare to see the acute cachexia set in after a single infection (cases of Jacquot, L. Colin).
 
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