290 



THE PIROPD^SM^SIDA 



Malherbe, 1956). The stasis resulting 

 from this sludging (Knisely el al. . 1947) 

 causes degeneration of the endothelial 

 cells of the small blood vessels, anoxia, 

 accumulation of toxic metabolic products, 

 capillary fragility, and eventually peri- 

 vascular escape of erythrocytes and ma- 

 croscopic hemorrhage. Purpura may 

 result, the great majority of such cases 

 in dogs being due to babesiosis. The 

 signs of the disease depend in part on the 

 location where the most serious stasis 

 takes place. Cerebral babesiosis similar 

 to cerebral falciparum malaria may occur. 

 Gilles, Maegraith and Andrews (1953) 

 described liver damage in B. canis infec- 

 tions, beginning with early damming of 

 the blood in the sinusoids around the cen- 

 tral vein, thru centrilobular atrophy and 

 degeneration of the hepatic cells, to ne- 

 crosis of the cells. Kidney damage is 

 also present. 



ported animals usually die. The native 

 cattle were infected as calves and are 

 premunized. Lambs and puppies, how- 

 ever, are highly susceptible. 



There is no cross-immunity between 

 the different species of Babesia. 



Treatment : The treatment of babesi- 

 osis has been reviewed by Goodwin and 

 Rollo (1955), Carmichael (1956) and 

 Richardson and Kendall (1957), among 

 others. There is an interesting relation- 

 ship between the chemotherapy of babesi- 

 osis and that of trypanosomosis. Many of 

 the compounds effective against Try/jan- 

 osoDia are also effective against Babesia. 

 This may perhaps indicate a phylogenetic 

 relationship, but I hasten to warn that a 

 similar line of reasoning was once used to 

 suggest a relationship between the trypano- 

 somes and the spirochetes. 



Immunity : Cattle which have recov- 

 ered from an attack of babesiosis due to 

 B. bigeuiiiia remain infected for life, and 

 are immune to reinfection. This type of 

 immunity, due to continuing low-grade 

 infection, is known as premunition. Pre- 

 munition in cattle due to species other 

 than B. bigeniiiia, and in sheep, swine 

 and dogs, lasts up to 2 years. Premu- 

 nized animals do not show signs of dis- 

 ease except under stress of one sort or 

 another. For instance, an attack of foot 

 and mouth disease may reactivate babesi- 

 osis in cattle, and distemper may do the 

 same in dogs. 



The spleen plays an important role 

 in maintaining immunity, and it is a com- 

 mon observation that splenectomy is often 

 followed by a severe or fatal relapse in 

 premunized animals. In addition, sple- 

 nectomized animals are much more sus- 

 ceptible to infection with Babesia and 

 much more seriously affected than nor- 

 mal ones. 



Calves, foals, young pigs and kids 

 are much less seriously affected by 

 babesiosis than are adult animals. This 

 is the reason that cattle can often be 

 raised in highly endemic areas without 

 being seriously affected, whereas im- 



Nuttall and Hadwen (1909) introduced 

 the first effective drugs, the azo-naphtha- 

 lene dyes, trypan red and trypan blue. 

 The latter is still used in some areas. It 

 is the sodium salt of ditolyl diazo-bis-8- 

 amino-l-naphthol-3, 6-disulfonic acid. It 

 must be given intravenously, since absces- 

 sation and sloughing follow subcutaneous 

 injection. It stains the tissues blue-green 

 for several months after injection. It does 

 not eliminate all parasites, so that recov- 

 ered animals are premunized. 



The acridine derivative, acriflavine 

 (trypaflavine, gonacrine, flavin, euflavin) 

 was introduced by Stephan and Esquibel 

 (1929). It is a mixture of 2,8-diamino- 

 10-methylacridinium chloride with a small 

 amount of 2, 8-diaminoacridinium chloride. 

 It, too, is still being used, especially 

 against B. eqiii in South Africa and in 

 cattle in North Africa. It does not elim- 

 inate all parasites, and recovered, 

 treated animals are premunized. 



The quinoline derivative, acaprin 

 (Acapron, Pirevan, Babesan, Piroparv, 

 Zothelone, Piroplasmin) was introduced 

 by Kikuth (1935) and also bv Carmichael 

 (1935). It is 6,6'-di-(N-methylquinolyl) 

 urea dimethosulfate„ It is administered 

 subcutaneously. In large doses it elim- 



