HAEMOSPORIDIA 605 



after the bites of infected mosquitoes, but in one case as long as 304 

 days; in P. malariae, 4-5 weeks, with the onset of fever lagging 3-12 

 days behind; and in two strains of P. falciparum, one, 6-25 days and 

 the other, 9-13 days; in another observation, P. falciparum was 

 observable in the peripheral blood in 5-9 days and the onset of fever 

 in 7-12 days. 



The paroxysm of malaria is usually divisible into three stages: chill 

 or rigor stage, high temperature or febrile stage (104° F. or over) 

 and sweating or defervescent stage. The time of paroxysm corre- 

 sponds, as was stated already, with the time of liberation of mero- 

 zoites from erythrocytes, and is believed to be due to extrusion of 

 certain substance into the blood plasma. The nature of this ma- 

 terial is however unknown at present. In the grown schizonts as well 

 as in gametocytes of Plasmodium, are fcund invariably yellowish 

 brown to black pigment granules which vary in form, size and num- 

 ber among different species. They are usually called haemozoin gran- 

 ules and are apparently the catabolic products formed within the 

 parasites. The pigment of P. gallinaceum and P. cynomolgi has been 

 identified with haematin (ferri protoporphyrin) (Rimington and 

 Fulton, 1947). The pigment possesses certain taxonomic significance, 

 as will be described below. The infected erythrocytes, if stained 

 deeply, may show a punctate appearance. These dots are small and 

 numerous in the erythrocytes infected by P. vivax and P. ovale, and 

 are known as Schiiffner's (1899) dots, while those in the host cells in- 

 fected by P. falciparum are few and coarse and are referred to as 

 Maurer's (1902) dots. No clots occur in the erythrocytes infected by 

 P. malariae. Pathology (Maegraith, 1948); splenomegaly (Darling, 

 1924, 1926; Russell, 1935, 1952a; Hackett, 1944); histopathology 

 (Taliaferro and Mulligan, 1937); character of paroxysm (Kitchen 

 and Putnam, 1946) ; blood proteins during infection (Boyd and 

 Proske, 1941); stippling of erythrocytes (Thomson, 1928). 



The condition which brings about the formation of gametocytes 

 is not known at present. The gametocytes appear in the peripheral 

 blood at various intervals after onset of fever, and remain inactive 

 while in the human blood. The assumption that the macrogameto- 

 cytes undergo parthenogenesis under certain conditions and develop 

 into schizonts as advocated by Grassi, Schaudinn and others, does 

 not seem to be supported by factual evidence. The initiation of 

 further development appears to be correlated with a lower tempera- 

 ture and also a change in pH of the medium (Man well). If living 

 mature microgametocytes of human Plasmodium taken from an in- 

 fected person are examined microscopically under a sealed cover glass 



