334 



SARCOCYSTIS, TOXOPLASMA AND RELATED PROTOZOA 



lesions of necrotizing pneumonitis, peri- 

 and myocarditis, necrotizing hepatitis, 

 focal necrotizing encephalitis and ulcera- 

 tive gastroenteritis. 



Altho natural infections occur in the 

 chicken, Jones el al. (1959) found that 

 this bird is remarkably tolerant to the 

 parasite. Disease can be produced exper- 

 imentally only by large inocula in mature 

 birds, and even very young chicks can 

 survive inoculation of enough parasites to 

 kill rabbits, guinea pigs and hamsters. 

 Parasitemia appears in 2 to 3 days after 

 inoculation and disappears spontaneously, 

 seldom persisting longer than 2 weeks. 

 Even when enormous numbers of para- 

 sites were injected into large birds, Toxo- 

 plas»ia was rarely found in the tissues 

 more than 40 days later. 



The histopathology of toxoplasmosis 

 has been reviewed by Frenkei (1956a) and 

 Smith and Jones (1957). In the brain, 

 ToxoplasDia multiplies in the neurons and 

 other cells and may cause cellular and 

 interstitial necrosis. Sometimes infarc- 

 tion necrosis causes extensive lesions. 

 Whenever aqueductal obstruction and in- 

 ternal hydrocephalus are present, peri- 

 ventricular vasculitis and necrosis are 

 generally observed; these constitute a 

 lesion unique for toxoplasmosis. 



Koestner and Cole (1960) studied the 

 neuropathology of canine toxoplasmosis 

 in detail. They found lesions attributed to 

 Toxoplasma in the central nervous systems 

 of 47 out of 63 experimentally or naturally 

 infected dogs with confirmed toxoplasmo- 

 sis, and they found Toxoplasma itself 

 microscopically in the central nervous 

 systems of 25 of the animals. The para- 

 sites themselves were found in the cere- 

 bral cortex and basal ganglia of 17 dogs, 

 in the midbrain of 12, the cerebellum of 

 9, the pons of 8, the medulla of 13 and the 

 spinal cord of 4. Lesions were found in 

 the cerebral cortex and basal ganglia of 

 47, the midbrain of 28, the cerebellum 

 of 21, the pons of 20, the medulla of 29 

 and the spinal cord of 9. In acute cases, 

 the lesions consisted of vascular damage 

 and focal necrosis; extracellular troph- 

 ozoites were found associated with the 

 necrotic foci. In chronic cases, glial 



nodules and repair were seen, and intra- 

 cellular parasites and cysts were present. 

 In reactivated latent toxoplasmosis, rup- 

 tured cysts and a hyperergic response 

 were present. 



The lesions in the liver consist of 

 small, sharply delimited areas of coagu- 

 lation necrosis in any part of the hepatic 

 lobules. The hepatic cells surrounding 

 them are apparently normal, and there is 

 little or no cellular reaction. The lungs 

 contain small, grey, tumor-like nodules 

 scattered thru 1 or all the lobes. These 

 consist of alveoli filled with large mono- 

 nuclear cells and leucocytes; the cells of 

 the alveolar walls are cuboid or columnar 

 and contain aggregations of Toxoplasma. 

 The lymph nodes are usually involved. 

 They are enlarged to several times their 

 normal size and contain extensive areas 

 of coagulation necrosis. These areas are 

 irregular in outline, with sharply demar- 

 cated boundaries and slight leucocytic in- 

 filtration around their margins. Toxo- 

 plasma is present around these areas, in 

 the endothelial cells of the veins, in mono- 

 cytes or free in the tissues. There may 

 be ulcers in the intestine. These may in- 

 vade the muscularis, producing chronic, 

 necrotizing lesions followed by granula- 

 tion. Granulomatous chorioretinitis is 

 sometimes seen in man, but ocular infec- 

 tions are apparently rare in animals. 



Weinman and Klatchko (1950) found 

 that a toxin which they called toxotoxin is 

 produced in the peritoneal fluid of animals 

 infected with ToxoplasDia. It is heat sta- 

 ble and usually kills mice in 1 or 2 min- 

 utes following intravenous injection. Cook 

 and Jacobs (1958), however, found no 

 evidence of toxin production in tissue cul- 

 tures of the organism. 



Immunity : There is a definite age 

 immunity against toxoplasmosis. Con- 

 genital infections are the most common, 

 and the mothers usually do not show signs 

 of disease themselves. Young animals 

 are more susceptible than adults. 



In infections acquired after birth, 

 humoral antibodies appear at the time that 

 the parasitemia disappears and are prob- 

 ably responsible in part for clearing the 



