The blood of the malaria patient always shows at some time„ the signs of an anemia or of a chloranemia-that is, of a chlorosis with an anemia. The discovery of the parasites demonstrated the reason for this anemia in the destruction of the red blood corpuscles. That some of the blood corpuscles succumb to a soluble parasitic toxin seems to me likewise probable.
In addition, there is frequently a decrease in the color coefficient of the erythrocytes-in other words, a chlorosis. This is probably due to the fact that the bone marrow, as a result of overproduction, sends into the circulation blood corpuscles deficient in hemoglobin. This deficiency is gradually made up with an eventual return to normal; though in chronic malaria with subsequent cachexia the chlor anemia may continue indefinitely.
It has been demonstrated by Kelsch that the greatest destruction of erythrocytes occurs during the first paroxysms, and that after a certain degree of anemia has been reached, this becomes gradually less.
The degree of anemia may be quite marked. Kelsch saw in one case 500,000 erythrocytes to the cubic millimeter*; in another case he observed within four days a reduction of erythrocytes to 2,000,000.
Dionisi saw, after individual pernicious paroxysms, losses of from 500,000 to 1,000,000 red blood corpuscles.
My counts show the same; for instance, in a man with pernicious tertian: On the fourth day of the disease, erythrocytes, 3,131,250; hemoglobin, 60 per cent. One paroxysm. On the seventh day of the disease, erythrocytes, 2,112,500; hemoglobin, 45 per cent.; color index, about 1.1.
In a case of genuine quotidian: On the fourth day of the disease, erythrocytes, 4,978,000; hemoglobin, 100 per cent.
Two paroxysms. On the sixth day of the disease, erythrocytes, 4,012,000; hemoglobin, 85 per cent. No paroxysm. On the eighth day of the disease, erythrocytes, 3,110,000; hemoglobin, 60 per cent.; color index, over 0.9.
Here we see at the beginning of the disease, contrary to Kelsch's rule, no diminution (probably on account of the small number of parasites), yet later, in spite of the cessation of the paroxysms, new losses which were possibly the result of the deleterious effect of the malarial toxin not yet fully excreted.
In a case of quotidian of longer duration: Erythrocytes, 2,544,000; hemoglobin, 65 per cent. No paroxysm. Three days later, erythrocytes, 3,711,000; hemoglobin, 45 per cent.; color index, about 0.67. Here, therefore, there was a chloranemia.
* The following figures, as is evident, relate to the number of erythrocytes in a cubic millimeter. My blood corpuscular counts were done with a Thoma-Zeiss apparatus; the estimation of the hemoglobin, with von Fleischl's hemometer.
In a case with irregular fever: In the third week of the disease, erythrocytes, 2,717,000; hemoglobin, 65 per cent. No paroxysm. Five days after the first examination, erythrocytes, 3,191,000; hemoglobin, 55 per cent.; color index, over 0.9.
In a case of typical tertian: In the third week of the disease, erythrocytes, 2,476,000; hemoglobin, 55 per cent. No paroxysm. Three days later, erythrocytes, 2,650,000; hemoglobin, 40 per cent.; color index, 0.8.
In the last three cases we find that, after the cessation of the fever, in spite of the increase in erythrocytes, the hemoglobin continued to diminish; in other cases the restoration of both went hand in hand.
Among the other appearances in the blood we must mention the great dissimilarity of the erythrocytes observed by Kelsch. In addition to normal sized corpuscles, Kelsch found abnormally large and small forms. Nucleated red blood corpuscles have likewise been observed.
The leukocytes manifest no typical increase or diminution in malaria . In acute cases some leukopenia is usual. This transitory impoverishment of the circulating blood in leukocytes may be due to the accumulation of melaniferous leukocytes in the spleen. According to Vincent, a rapidly evanescent leukocytosis, only evident immediately after the beginning of the paroxysm, precedes the leukopenia. [This has been confirmed by Billet, who has shown that in regular charts of a tertian or quartan type the leukocytic curve bears a close relation to the temperature curve.-Ed.]
Leukocytosis in the course of acute malaria points usually to complications (pneumonia, suppuration, etc.). Leukocytosis (according to Bastianelli, lymphocytosis) appears to be the rule only during paroxysms of blackwater and pernicious fever. In chronic infections it is not uncommon.
[With regard to the relative leukocytic count, many observations show that in malaria there is a marked increase in the percentage of large mononuclear leukocytes present, and this is often so marked, especially during periods of apyrexia, that it is possible, almost solely from this change, to diagnose a malarial infection in cases where parasites are absent, as after quinin or in blackwater fever. An increase to 20 per cent, of large mononuclear leukocytes is so suspicious that prolonged search will not uncommonly reveal a single parasite or so, or, if these be not found, pigmented leukocytes will almost certainly be found. As examples of this change we may quote the following:
(1) Small mononuclear......18.1 per cent.
Large mononuclear and transitional..........31.4 "
Eosinophile............. 0.4 " -(Bastianelli.)
(2) Small mononuclear......19.1 per cent.
Large mononuclear and transitional..........41.0 "
Eosinophile............. 0.6 " -(Bastianelli.)
(3) Small mononuclear......18.1 per cent.
Large mononuclear and transitional..........26.4 "
Polynuclear.............55.3 " -(Pause.)
(4) Small mononuclear......14.8 per cent.
Large mononuclear and transitional..........46.7 "
Polynuclear.............38.5 " -(Stephens and Christophers.)-Ed.]
Melanemia-that is, the occurrence of melanin in the blood-is a condition peculiar to malaria that may be demonstrated in every case, even though only at times. It constitutes, therefore, one of the fundamental characteristics of the disease, and possesses not only a theoretic, but also a practical, importance.
The origin of melanin has, since Laveran's discovery, been eventually explained. As previously stated, it is the product of digestion of the hemoglobin, and is elaborated in the body of the parasite. After destruction of the plasmodium (either by death or multiplication) this pigment is set free, is taken up as lifeless foreign matter by the circulating leukocytes, and is deposited in the different organs.