SARCOCYSTIS, TOXOPLASMA AND RELATED PROTOZOA 



321 



gradually disperses. Cell division now 

 begins, starting from the conoid at the 

 anterior end and proceeding posteriorly. 

 The nuclei round up, their nucleoplasm 

 becomes thicker, and they move toward 

 the posterior part of the newly forming 

 cells. New central granules appear in the 

 cytoplasm in front of the nuclei. The 

 daughter cells remain attached at their 

 posterior ends for a time and then separ- 

 ate entirely. 



Finally, as the cyst itself becomes 

 older, the trophozoites in the central com- 

 partments degenerate and disappear. 

 After the cyst becomes mature, its wall 

 breaks down and the trophozoites are re- 

 leased. They enter the blood stream, 

 reach the digestive tract, and pass out in 

 the feces. They have also been found in 

 the nasal secretions of sheep (Scott, 1943). 



Quite a different account has been 

 given by Spindler and his associates, who 

 believe Sarcocystis to be a fungus rather 

 than a protozoon. Spindler and Zimmer- 

 man (1945) reported that they had isolated 

 an Aspergillus -like fungus from sarco- 

 cysts from pig muscles, and that 25 out of 

 50 pigs injected with or fed material from 

 the cultures had sarcocysts in their mus- 

 cles 4 to 6 months later, while the control 

 pigs were negative. They also said that 

 pigs, rats and mice fed the cysts passed 

 yeast-like bodies in their urine or feces 

 which produced a similar fungus upon cul- 

 ture, and they found these bodies in the 

 kidneys of infected mice and in clumps 

 attached to the walls of the ileum and ce- 

 cum of infected rats and mice. 



Spindler, Zimmerman and Jaquette 

 (1946) were unable to infect pigs directly 

 with sarcocysts in pig muscles, but they 

 observed that the pigs became infected if 

 they ate their own feces. They fed pork 

 containing sarcocysts to pigs, dogs, cats, 

 rats, mice and chickens. These subse- 

 quently passed a stage in their feces and/or 

 urine which was infective for swine. Their 

 observation, incidentally, may perhaps ex- 

 plain the remark of Scott (1943) that feed- 

 ing experiments in sheep indicate that the 

 trophozoites of S. tenella must undergo 

 some change before they can infect other 

 sheep. 



Spindler (1947) described a network of 

 jointed, hypha-like structures in cysts 

 from a sheep and a duck, and said that the 

 trophozoites appeared to be exogenous 

 growths on these structures. However, 

 Grass^ (1953) commented that his illustra- 

 tions were not convincing, and that the 

 structures he described appeared to be the 

 result of marked alterations in the true 

 ones. Frenkel (1956a), too, disagreed 

 with Spindler. He found no fungal charac- 

 teristics in morphological studies of or- 

 ganisms from man, the sheep, mouse, 

 rabbit, squirrels and the duck. Unlike 

 fungi, the trophozoites and cyst walls did 

 not give a positive reaction with the per- 

 iodic acid-Schiff stain. Sarcocystis from 

 cottontail rabbits and house mice failed to 

 grow on the media customarily used for 

 fungi. Frenkel concluded that these or- 

 ganisms neither look nor behave like fungi. 



Scott (1943), too, and others cited by 

 him were unable to cultivate organisms 

 from the cysts. Only Ciesla (1950) has 

 reported positive results. He observed 

 "sporozoites" in cultures from cysts from 

 cattle, and said that these eventually turned 

 into round corpuscles with a quick, convul- 

 sive type of movement which budded into 

 branched chains of mycelia. 



The weight of the evidence thus indi- 

 cates that Sarcocystis is a protozoon and 

 not a fungus. 



Pathogenesis : Sarcocystis is not 

 generally considered very pathogenic. 

 However, Scott (1943a) believed that it is 

 of greater economic importance than is 

 usually supposed. 



Light or moderate infections produce 

 no noticeable signs, but in very heavy in- 

 fections there may be lameness, weakness, 

 emaciation, paralysis and even death. 



The sarcocyst destroys that part of 

 the muscle fiber which it occupies, and as 

 it grows it may cause pressure atrophy of 

 adjacent cells. Calcification may also 

 occur. There is ordinarily little if any 

 cellular reaction around the cysts. Focal 

 myocarditis and myositis develop when the 

 cysts break down. Destombes (1957) des- 

 cribed a marked inflammatory reaction 



