Acute cachexia occurs almost only in severe malarial regions, as Senegal, Guadeloupe, the west coast of Africa, Madagascar, India, and Tongking. A few cases have been observed in Holland'and in Italy.

Roux is of the opinion that the constitution of the patient and the hygienic conditions under which he lives exercise the greatest influence on the rapidity with which the cachexia develops. He believes that the intensity of the attack has nothing to do with it. Moreover, Haspel and Kelsch and Kiener stated previously that acute cachexia usually occurred in individuals weakened by hardship or excesses. Still, exceptional cases have been seen in persons who were, previous to the attack, apparently strong and healthy.

The statement that the severity of the attack is of no importance in the production of the cachexia strikes me as questionable. Generally speaking, it is very difficult to make a criterion for severity. Yet it cannot be denied that it is usually the estivo autumnal fevers that lead to cachexia. The cases consequently occur in greatest numbers during autumn and winter. Though the parasites of the second group are the principal causal agents, those of the first group sometimes play the role. This is especially true in case of obstinately relapsing quartan fever.

The question at issue has not yet been sufficiently investigated to speak conclusively about it. Researches in regard to the etiology of cachexia from a parasitic point of view are, therefore, desirable.

The symptoms of cachexia are as follows:


This is a very special characteristic. To it is owing the color of the skin, which often shows an excessive degree of pallor, in spite of the brownish discoloration contributed by the melanosis and a frequently associated light yellow. It explains, too, a series of subjective symptoms, as vertigo, ringing in the ears, malaise, disinclination for work, headache. It may be made responsible for the diminution in intellectual activity, the languid mumbling or indifferent voice, the sleeplessness.

Further attributable to the anemia are some of the vascular symptoms, as dilatation of the heart, tachycardia, accidental systolic murmurs, venous murmurs, etc.; likewise the dyspnea associated with any physical exertion.

Finally, we place at its door the cold sensations, the cold skin, and the subnormal temperature, which fluctuates usually under 37°.

The blood examination shows the number of red blood corpuscles to be greatly decreased-often under 1,000,000.

The leukocytes are sometimes diminished in number, though again there is a pronounced leukocytosis. L. Colin found, among 65 cases, a more or less considerable increase in leukocytes in 50, while Ascoli claims a striking leukopenia.

The hydremia constitutes the second cardinal symptom. There are no actual specific gravity estimations, yet the very low hemoglobin percentage, the hypalbuminosis, as demonstrated by Castan, Leonard, and Foley, and the edema leave no doubt as to its existence.

Edema as a direct result of the hydremia is never entirely wanting and is usually marked. Contrary to the conclusions of Cohn heim and Lichtheim, it has been experimentally proved by Strieker and Gartner that edema may be produced by hydremia.

In regard to its distribution, the edema shows the same character as that of nephritis. The pale face is frequently bloated; the eyelids are swollen, and swellings are also encountered on the extremities and other situations of the body. Effusions into the serous cavities, like ascites, hydrothorax, hydropericardium, are frequent. Symptoms pointing to edema of the brain are sometimes observed, and edema of the glottis or of the lungs may become actually threatening. Still, not every edema in the course of a malaria is to be regarded as an expression of cachexia. This is even less true than that an anemia or a splenic tumor should make a cachexia. It is not rare to see a more or less marked edema follow a series of paroxysms and disappear within a few days after the cessation of the fever. I have observed this especially in children, though occasionally in adults.

In the second place, edema and transudates may occur and be attributable not to the hydremia, but to other causes, like local stasis, inflammation, and nephritis.

In this regard we may call attention to the stasis edema of venous thromboses which are the result of the deteriorated condition of the blood. From experience we know that under the influence of edema and hydremia, as in severe chlorosis, leukemia, the cachexia of carcinoma, etc., the blood has a tendency to coagulate in the vessels, with the production of thrombi. This same tendency also exists in malarial cachexia. These thrombi may form in any part of the vascular system, the heart itself, as well as peripheral veins, the portal vein, etc. The dangers which they give rise to are beyond our scope, though we may see that sometimes, as a result of arterial thrombi, more frequently of emboli, gangrene of the extremities occurs as a complication.

Among the other symptoms produced, at least in part, by the deteriorated condition of the blood, are frequent hemorrhages. Epis taxis may be a daily occurrence, and not infrequently we see larger or smaller hemorrhages into the skin, hemorrhages from the gums, into the muscles, from the bladder, from the female genitals, into the serous membranes, into the brain, into the spleen and liver, into the retina, in the form of hemoptysis, hematemesis, etc. The thought of scorbutus frequently arises, and undoubtedly it often occurs as a mixed infection-but about this later. Intermittent hemorrhages have been reported (Verneuil), though on scarcely sufficient evidence. It has also been asserted that slight wounds, like the sting of insects, the bite of leeches, give rise to severe hemorrhages, but this is not generally true. Operations on cachectics usually proceed without marked loss of blood (MacNamara, Duka).