SARCOCYSTIS, TOXOPLASMA AND RELATED PROTOZOA 



331 



but the cysts remain infective in tissue up 

 to 3 hours, while trophozoites liberated 

 by peptic juice from isolated cysts sur- 

 vive 2 hours. Trypsin destroys the cyst 

 wall immediately, but the liberated tropho- 

 zoites survive at least 6 hours; prolifer- 

 ative forms survive at least 3 but less 

 than 6 hours. Thus, parasites encysted 

 in tissues could survive the normal diges- 

 tive period in the stomach and should sur- 

 vive even longer in the duodenum. 



Following experimental inoculation, 

 the protozoa proliferate for a time at the 

 site of injection and then invade the blood 

 stream and cause a generalized infection. 

 Susceptible tissues all over the body are 

 invaded, and the parasites multiply in 

 them, causing local necrosis. The para- 

 sitemia continues for some time, until 

 antibodies appear in the serum, after 

 which the parasites disappear from the 

 blood and more slowly from the tissues. 

 They finally remain only in pseudocysts 

 or cysts, and only in the most receptive 

 tissues. In general, the spleen, lungs 

 and liver are cleared of parasites rela- 

 tively rapidly, the heart somewhat more 

 slowly and the brain much more slowly. 

 These residual infections may persist for 

 a number of years. 



Following experimental infection of 

 rats, Ruchman and Fowler (1951) re- 

 ported that Toxoplasma could be found in 

 the blood regularly for the first week and 

 then occasionally during the next 9 days. 

 It could be found in the spleen for 2 weeks, 

 in the liver and lungs for 10 weeks and in 

 the brain for 2 years after infection. 

 Other workers found it as long as 3 years 

 after infection in the brain of rats, mice 

 and pigeons, and 10 months after infection 

 in that of the dog (Jacobs, 1956). 



Toxoplasma trophozoites have been 

 found in the urine and feces of mice and 

 dogs with acute toxoplasmosis, in the 

 milk of mice, dogs, cows and sows, in a 

 serous exudate from the conjunctiva of a 

 pigeon, and in the saliva of mice, rabbits 

 and man. However, these are the prolifer- 

 ative forms and are very delicate. They 

 are rarely able to infect other animals. 

 Mice can be raised in the same jar with 

 infected mice without becoming infected. 



Olafson and Monlux (1942) reported trans- 

 mission to uninfected puppies caged with 

 a littermate dying of toxoplasmosis, but 

 Jacobs (1957) was unable to repeat this 

 observation under similar circumstances. 

 He was also unable to infect rabbits by 

 spraying large numbers of proliferative 

 forms into a confined space with them. 



Transmission via the placenta occurs 

 in congenital toxoplasmosis. It is gener- 

 ally considered to be an accidental com- 

 plication of an inapparent primary infection 

 of a pregnant female (Feldman and Miller, 

 1956). Foci of infection are set up in the 

 placenta, and the fetus is infected from 

 them. Koestner and Cole (1960) reported 

 the occurrence of congenital toxoplasmosis 

 in 2 consecutive litters whelped by the 

 same bitch. 



Other than placental transmission, as 

 mentioned above, the natural mode of 

 transmission is unknown. Weinman and 

 Chandler (1954) suggested that toxoplas- 

 mosis might be acquired in the same way 

 as trichinosis, by eating infected pork. 

 However, the epidemiological evidence 

 does not appear to support this, altho 

 there is suggestive evidence that dogs 

 might perhaps become infected by eating 

 chronically infected rodents (Jacobs, 1957). 

 Arthropod transmission has been postu- 

 lated without any substantiation. 



One possibility which deserves inves- 

 tigation is that a concurrent disease of 

 some sort may be required for infection 

 to succeed. Campbell, Martin and Gordon 

 (1955) found T. gondii in 6% of 268 dogs in 

 Glasgow, Scotland with clinical evidence 

 of distemper or its neurological sequellae. 

 They found distemper virus inclusion bod- 

 ies in all these dogs, mentioned that the 

 association of distemper with toxoplasmo- 

 sis had been noted by several earlier 

 workers, and remarked that they them- 

 selves had never seen a case of "pure" 

 canine toxoplasmosis or of canine toxo- 

 plasmosis associated with any infection 

 other than distemper. 



Jacobs, Melton and Cook (1955) studied 

 experimental T. gondii infections in dogs 

 and found that only young puppies given 

 relatively large inocula succumbed. Since 



