This section is from the book "Malaria, Influenza And Dengue", by Julius Mennaberg and O. Leichtenstern. Also available from Amazon: Malaria, influenza and dengue.
It is an old, well known fact that malaria frequently recovers even when quinin is not employed-in other words, in response to expectant treatment. These spontaneous cures have been observed, especially in hospital patients. Osier, in Johns Hopkins Hospital, left 58 cases to themselves and saw all of them recover spontaneously.
Spontaneous recovery takes place in infections with parasites of the second, as well as of the first, group; even pernicious cases may, under circumstances, cure spontaneously. Several such cases have been reported by Torti. The following are examples of spontaneous cure:
J. L., aged nineteen, says he has had a paroxysm daily for fourteen days; never had fever before. He is a robust youth, quite pale, sub icteric in color. The spleen is evidently palpable. He complains of splenic pain and overfatigued limbs.
October 6, 1892: 10 a. m.: Temperature, 36.5°.
Blood examination: (1) Large pigmented parasites, almost the size of the blood corpuscles, showing actively swarming pigment; (2) pretty numerous, likewise markedly pigmented parasites, filling half of the corpuscle. The infected blood corpuscles are frequently swollen and decolorized.
Diagnosis: Double tertian.
3 p.m.: Temperature, 37°.
6 p. m. : Temperature, 37.5°. The expected paroxysm failed to occur. During the night, no sweating.
October 7: 10 a. m. : Temperature, 36.2°.
Blood examination: The same as yesterday afternoon, with, in addition, numerous melaniferous leukocytes.
4 p. m. : Temperature, 37.5°.
Blood examination: A very few large parasites.
6 p.m.: Temperature, 38°.
October 8: 10 a. m. : Temperature, 36.3°.
Blood examination: After a long search a large free parasite was found with actively swarming pigment. The patient manifested no further paroxysm, and nothing further was found in the blood.
P., aged forty seven, asserts that he has had violent typical paroxysms daily for four days.
September 21: 3.30 p. m.: Temperature, 40.3°; pulse, 120; tension subnormal. Slight icterus; the spleen extends beyond the border of the ribs about two fingerbreadths.
Blood examination: A few non pigmented ameboid parasites.
September 22: During the night, a profuse sweat.
9 a. m. : Temperature, 35.8°.
Blood examination: Isolated, small, immovable parasites in ring form; no pigment.
4.30 p.m.: Chill; temperature, 39°.
5.30 p. m. : Temperature, 40°; chill still continues.
8 p. m. : Temperature, 40.2°.
September 23: 9 a. m. : Temperature, 36.7°. Patient very much exhausted; the spleen has greatly increased in size since yesterday.
Blood examination: A very few small parasites, immovable, in ring form.
6 p. m. : Apyretic.
September 24: Apyretic.
Blood examination: Two melaniferous leukocytes; no parasites. September 28: The patient has remained apyretic. Blood examination: Crescents.
In both these cases the treatment was expectant. As is evident, the first was a case of infection with the common tertian parasite; the second, with the genuine quotidian parasite.
The problem as to how the organism gets rid of the parasites may be regarded as partially solved. It is likely that the quiet, the nursing, and the malaria free air of the hospital strengthen the organism in its struggle against the parasites, at least against new infections; though the significance of this is not great on account of the eight to fourteen days' incubation of malaria.
Further, Metschnikoff has shown that the macrophages of the spleen and bone marrow develop an energetic phagocytic activity. Bignami, as we have seen in the section on Pathologic Anatomy, devoted special attention to this. He found that the macrophages of the spleen and of the bone marrow took up large numbers of parasites in every stage of development. The endothelium of the splenic, hepatic, and cerebral vessels, likewise, manifest this phagocytic power, though in a slighter degree. Still, occasionally the endothelial cells seem to participate more actively-for instance, Barker reports a case in which the endothelium of the liver capillaries and Kupffer's cells were packed with parasites.
In addition to the macrophages, the vascular endothelium, and Kupffer's cells, the circulating leukocytes play a role in phagocytosis. True, we never find leukocytes inclosing recognizable parasites either in freshly made natural preparations or in dry stained ones; yet after observing a natural preparation protected from evaporation for some time it is not rare to see a polynuclear leukocyte gradually approach a parasite, even one with flagella, and take it up. The movement of the pigment in the parasite continues for a short time in the body of the leukocyte and then ceases. The contour of the parasite gradually disappears until nothing but the pigment remains as a recognizable remnant. It is much more rare to see the parasites taken up by lymphocytes, and the greatest rarity by eosinophiles.
It has not been absolutely determined that the leukocytes possess this phagocytic power in the circulating blood, and the fact that in fresh preparations there is no suggestion of it seems to speak against it. We do not know even how much of the phagocytic action on the part of the macrophages and endothelial cells is postmortem and how much intra vitam.
Moreover, it is worth recalling that the number of leukocytes is usually decreased in malaria . Billings (quoted by Barker), as well as Bastianelli, found that during a paroxysm there was a decrease in the polynuclear and an increase in the large mononuclear cells, while the small mononuclear and eosinophile cells showed no regular deviations from the normal.
Vincent found similar results; namely, immediately after the beginning of the paroxysm a very transitory, more or less considerable leukocytosis, due especially to lymphocytes, less so to eosinophile and large mononuclear cells, while the polynuclear cells did not participate at all. This leukocytosis disappeared within a few minutes, and on the development of the hot stage a leukopenia took place. This alteration in the number of leukocytes is by no means characteristic of the malarial paroxysm, since it has also been observed in other infections.
 
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