THE PIROPLASMASIDA 



289 



In the life cycles described above, 

 the adult tick picks up the infection, but 

 does not transmit it. This is done by the 

 next generation. Babesia can also be 

 transmitted by different stages in the 

 same generation; it can be picked up by a 

 larval tick and transmitted by the nymph, 

 or it can be picked up by the nymph and 

 transmitted by the adult. The occurrence 

 of this stage-to-stage transmission de- 

 pends upon both the species of Babesia and 

 the species of tick. Neitz (1956) has as- 

 sembled information on this subject, and 

 it is given below in the discussion of the 

 individual species. 



The life cycle in the tick in stage-to- 

 stage transmission was studied carefully 

 by Shortt (1936) for B. vogeli {B. canis) 

 of the dog in Rliipiceplialus sanguineus in 

 India. He saw no evidence of sexual stages. 

 After the nymph has taken a blood meal, 

 the parasites do not multiply in the gut 

 epithelium, but in the phagocytes next to 

 the hypodermis in the body cavity. Here 

 they reproduce by multiple fission to form 

 what Shortt called pseudocysts- -clumps of 

 up to 200 organisms contained within the 

 envelope of the parasitized host cell. 

 These are fully developed about 7 days 

 after the nymph has left its host. They 

 are 14 to 35 )i in diameter. The stages 

 within these pseudocysts are at first more 

 or less spherical and 1 . 7 to 3. 3 fi in di- 

 ameter. They become club-shaped in 4 to 

 8 more days, at which time they measure 

 about 9 by 2|i . The club-shaped stages 

 then break out of the host cell and migrate 

 to the muscles and muscle-sheaths. They 

 penetrate the cells, round up, and divide 

 by repeated binary fissions to form a 

 large number of relatively small, ovoid 

 or slightly elongate parasites about 1.2(i 

 long. This stage is reached about 20 days 

 or more after the nymph has fed. This 

 phase of the life cycle corresponds to that 

 which takes place in the eggs of the adult. 



The muscles remain unchanged during 

 metamorphosis. When the adults begin to 

 feed on a dog, the parasites migrate to the 

 salivary glands and enter their cells. De- 

 velopment then continues as described by 

 Reichenow and Regendanz (1933) for B. 

 canis. The parasites multiply by repeated 



binary fissions to form large numbers of 

 spherical or ovoid infective stages about 

 1.9ji or less in diameter. 



Pathogenesis: Babesiosis is a highly 

 pathogenic disease in most hosts. It is 

 unusual in that the death rate is much 

 higher in adults than in young animals. 



The various species of Babesia cause 

 a similar disease in different hosts. In 

 most cases there are fever, malaise and 

 listlessness. Affected animals do not eat, 

 or eat little. There is severe anemia, 

 and destruction of the erythrocytes is ac- 

 companied by hemoglobinuria. The mu- 

 cous membranes become pale, and icterus 

 develops. The spleen is greatly enlarged, 

 with soft, dark red pulp and prominent 

 splenic corpuscles. The liver is enlarged 

 and yellowish brown. The lungs may be 

 slightly edematous. There may be diarrhea 

 or constipation, and the feces are yellow 

 except in very early or peracute cases. 

 Affected animals lose condition, become 

 emaciated, and often die. 



The signs of babesiosis may vary 

 markedly from this typical picture, how- 

 ever. As Malherbe (1956) said, "Anybody 

 with extensive experience of these dis- 

 eases. . .is forcibly struck by the deviate 

 and protean manifestations of the disease 

 picture as it is encountered from time to 

 time. There is almost no guise under 

 which the disease does not masquerade at 

 some time or another, and it is therefore 

 no accident that the majority of South Af- 

 rican veterinarians have a pronounced 

 attachment to their microscopes." Mal- 

 herbe remarked on the similarity of the 

 clinical and pathological manifestations of 

 babesiosis to those of malaria, stating 

 that "in spite of the differences in the life 

 cycle of the parasites, their effect on the 

 body is capable of exactly similar poten- 

 tialities. " 



Death, if it occurs, is due to organic 

 failure which, in turn, is due not only to 

 the destruction of erythrocytes with re- 

 sultant anemia, edema and icterus, but 

 also to the clogging of the capillaries of 

 various organs by parasitized cells and 

 free parasites (Malherbe and Parkin, 1951; 



