The mucous membrane of the mouth, and especially of the gums, sometimes undergoes marked changes in chronic malaria . Loosening of the teeth, hemorrhage, and gangrene may occur. These complications are seen particularly in persons enfeebled by insufficient nourishment or overwork, though they sometimes belong to the epidemic of a definite year and accompany it as a complication.
Under the same conditions the parotid gland may be the seat of a suppurative inflammation. Lancis.i reports a malarial epidemic, tertian in type, at the beginning of the eighteenth century (1709-1710), which manifested the following symptoms: after the third or fourth paroxysm, intense headache, followed by jactitation, coma, a hemorrhagic exanthem on the skin, severe epistaxis, and parotitis, the last often producing death by suffocation.
Since then parotitis has been repeatedly described as a serious complication in severe malarial epidemics.
We have discussed, in numerous places on the preceding pages, how frequently the functions of the stomach and intestines are disturbed in the course of acute and chronic malaria , and especially cachexia.
Here we will only add that when the original infection was prolonged, these functional disturbances often persist for a long time after it has passed.
These disturbances are of various kinds. On the part of the stomach, there is frequently a want of appetite, a feeling of weight after eating, pyrosis, and a distaste for certain foods, especially fat. These symptoms, according to their combination, indicate atony of the stomach, chronic gastric catarrh, or atrophy of the gastric mucous membrane.
The intestinal disturbances express themselves in an inclination to meteorism, constipation, or more rarely diarrhea. They may torment the patient for years after the malarial infection has terminated. In all cases we should endeavor to find out whether they are expressions of a local functional or anatomic disease of the gastrointestinal tract, or are secondary symptoms from disease of the portal system. This last is not rare after malaria , or even during its course, and is, therefore, always to be kept in mind.
A rare occurrence is intermittent hemorrhage from the intestine or intestinal hemorrhage at all during the acute infection (see p. 300). Cases of this kind were observed, among others, by Frerichs and Bohn. They become of importance on account of the diagnosis (possible confusion with typhoid fever) or treatment. Quinin does wonders in these cases.
Acute ascites is even more rare. It develops either in cachectics, as the result of a pyelothrombosis, or in acute cases, possibly as the result of occlusion of the portal capillaries by melaniferous cells. De Brun assumes for these cases a congestion of the peritoneum.
After the thorough investigations of Bertrand and Fontan, it has been determined that the so called Cochin China diarrhea has nothing to do with malaria .
It is undoubted that in a number of cases malaria lays the foundation for progressive disease of the liver. I have repeatedly observed enlargement of the organ, with a painful feeling of tension, in acute and especially chronic infections. These symptoms are due to hyperemia of and a deposit of pigment in the organ. They disappear in the majority of cases and leave no trace after the pigment has been excreted.
According to Kelsch and Kiener, the hepatomegaly of cachectics, the result of the overloading with pigment, may remain for a long time, even persistently, on account of the functional activity of the organism being so depressed that elimination of the pigment does not take place, or at least not to any great extent. We frequently see, therefore, in cachectics a large liver, producing a feeling of weight and tension in the right hypochondrium.
Disturbances on the part of the gastro intestinal canal are, as a rule, simultaneously present, as loss of appetite, nausea, feeling of weight in the stomach after eating, irregularities in bowel movements, etc.
Another frequent condition of the liver seen after long infections is atrophy. This has been described by Haspel, Frerichs, Kelsch and Kiener, and others. We shall see later that this atrophy in malaria is not always attributable to the same causes, and that the structure of the organ does not always show the same changes. It follows, therefore, that the symptoms of atrophy of the liver are not always the same, and that it is difficult to give a general description appropriate to all conditions.
The proof of atrophy by physical signs is always unsatisfactory, on account of the more or less marked ascites usually present. This is frequently so profuse and develops so quickly that puncture after puncture is necessary. If, after its evacuation, the diminished size of the liver is recognized, the question still remains whether this is the result of simple atrophy or of cirrhosis. Only under especially favorable conditions, and with very thin abdominal walls, is it possible to decide whether the surface of the liver is smooth or finely granulated. In the first case we would likely have to do with a simple atrophy.
In atrophy icterus is wanting, though it may precede the beginning of the condition. The stools are usually diarrheic, and manifest but little color. The urine, too, lacks bile coloring matter.
The appetite is, as a rule, severely depressed; the food eaten is badly borne and sometimes vomited. Hematemesis and melena are occasionally observed. The general appearance is that of marked marasmus. In the minority of cases there may be slight symptoms of portal obstruction, though usually these are wanting.
The smallness of the liver, as evidenced by percussion, together with the general appearance and the absence of icterus, usually indicates the diagnosis of atrophy, or, at least, permits it to be conjectured.
The majority of observers agree that malaria may be the exciting cause of cirrhosis of the liver. There are differences of opinion only in regard to the frequency of the condition, and in regard to whether or not the cirrhosis thus provoked has particular characteristics.