292 



THE PIRO°LASM\SlDA 



BABESIA BIGEMISA 



(SMITH AND KILBORNE, 1893) 



Synonyms : Pyrosoma bigeminum, 

 Apiosoma bige»iinu»i , Piroplasma 

 bigeni ilium, Piroplasnia auslrale, Babesia 

 hudsonius bovis. 



Disease : Bovine babesiosis, piro- 

 plasmosis, redwater, Texas fever. 



Hosts : Ox, zebu, water buffalo, 

 deer (Mazania ainericana reperlicia) 

 (syn.,Ay. sarlprii reperlicia), white- 

 tailed deer (Odocoelius virginianus chir- 

 iquensis (syn. , O. chiriquensis). 



Location : Erythrocytes. 



Geographic Distribution : Central 

 America, South America, Europe, North, 

 Central and South Africa, Australia, for- 

 merly North America (U.S. ). 



Prevalence : This species causes one 

 of the most important diseases of cattle 

 in the tropics and subtropics. 



Morphology : The trophozoites in the 

 erythrocytes are piriform, round, oval or 

 irregularly shaped. The piriform tropho- 

 zoites occur characteristically in pairs, 

 a feature which gives the species its name. 

 B. bigemina is relatively large. The 

 round forms are 2 to 3 /i in diameter and 

 the elongate ones 4 to Sjn long. 



Life Cycle : This has been described 

 above (p. 287). The tick vectors are 

 Boopliilus aiumlalus in North America, 

 B. microplus in South and Central Amer- 

 ica, B. auslralis in Australia, B. cal- 

 carahis in North Africa and the USSR, B. 

 decoloralus in South Africa, Hae»iapliy- 

 salis punctata in Europe, Rhipicephaliis 

 appendiculatus and R. everlsi in South 

 Africa, and R. bursa in North Africa. 

 Transmission takes place thru the egg in 

 all species; stage-to-stage transmission 

 also takes place in Haeniapliysalis and 

 Rhipiceplmlus. 



Intrauterine transmission may also 

 take place (Enigk, 1942). 



Pathogenesis : B. bigemina is highly 

 pathogenic for adult animals but much less 

 so for calves. The incubation period is 8 

 to 15 days or less. The first sign of dis- 

 ease is a rise in temperature to 106 to 

 108° F. The temperature persists for a 

 week or more. Affected animals are dull, 

 listless, fail to eat and stop ruminating. 

 The feces are yellowish brown. Severe 

 anemia is caused by the invasion and des- 

 truction of the erythrocytes; up to 75' ( of 

 them may be destroyed. Hemoglobinuria 

 is ordinarily present, but may be absent. 

 Affected animals become thin, emaciated 

 and icteric. In chronic cases the temper- 

 ature is not very high and there is usually 

 no hemoglobinuria, but diarrhea or con- 

 stipation with hard, yellowish feces is 

 present. 



The initial febrile response is asso- 

 ciated with the appearance of parasites in 

 the peripheral blood. 



Death may occur in 4 to 8 days in 

 acute cases. The mortality is as high as 

 50 to 90% in untreated cases, but treat- 

 ment reduces it markedly. Calves less 

 than a year old are seldom seriously af- 

 fected. 



Chronically affected animals lose con- 

 dition quite rapidly and remain thin, weak 

 and emaciated for weeks before finally 

 recovering. 



The principal lesions are splenomegaly 

 with soft, dark red splenic pulp and prom- 

 inent splenic corpuscles. The liver is en- 

 larged and yellowish brown. The gall 

 bladder is distended with thick, dark bile. 

 The mucosa of the abomasum and intestine 

 is edematous and icteric, with patches of 

 hemorrhage. The subcutaneous, subser- 

 ous and intramuscular connective tissues 

 are edematous and icteric, and the fat is 

 yellow and gelatinous. The blood is thin 

 and watery, the plasma may be tinged with 

 red, and the urine in the bladder is usually 

 red. 



Immunity : As mentioned in the gen- 

 eral discussion of immunity, recovered 

 cattle are premunized, and premunition 

 due to latent infection persists for life. 



