214 



THE TELOSPORASIDA AND THE COCCIDIA PROPER 



of imbalance between infection rate and 

 resistance. Actually, the best type of en- 

 vironment to control coccidiosis is one in 

 which the chickens become infected lightly 

 enough to develop an immunity without 

 suffering any disease. 



Many workers have studied the devel- 

 opment of immunity to coccidiosis (Walet- 

 zky and Hughes, 1949; Brackett and 

 Bliznick, 1950). Most of this research 

 has been done with E. lenella. Farr (1943) 

 immunized chickens with 1000 oocysts 

 daily for 15 days or with 3 doses of 1000, 

 5000 and 9000 oocysts given 5 days apart. 

 She also carried out 5 similar experiments 

 with differing numbers of oocysts, all of 

 which showed that repeated small doses of 

 E. lenella oocysts would produce immun- 

 ity. Horton-Smith (1949), Waletzky and 

 Hughes (1949) and Gordeuk, Dressier and 

 Glantz (1951) found that single doses of 

 oocysts would also produce immunity, and 

 that the degree of protection was propor- 

 tional to the intensity of the initial infec- 

 tion. Babcock and Dickinson (1954) found 

 that a total of 1600 sporulated oocysts, 

 given either in one or several doses, 

 would produce practical immunity that 

 withstood severe challenge. The number 

 of individual doses required to make the 

 total did not materially affect the immun- 

 ity produced. It took 4 days longer for 

 immunity to result following exposure to 

 1050 sporulated oocysts than to 2125. 

 Gordeuk, Bressler and Glantz (1951) found 

 that day-old chicks could develop a certain 

 degree of immunity. They found, too, that 

 feeding the oocysts in the mash resulted 

 in higher mortality than when a similar 

 dose was given by mouth. 



Many workers have shown that immun- 

 ity will develop against coccidiosis in birds 

 on suppressive therapy (Waletzky and 

 Hughes, 1949; Johnson, Mussell and Diet- 

 zler, 1949, 1949a; Grumbles el at. , 

 1949; Bankowski, 1950; Kendall and McCul- 

 lough, 1952). The drugs are ineffective 

 against the sporozoites or first generation 

 schizonts, at least in the concentrations 

 used, but they do kill the merozoites or 

 later stages. The coccidia are thus able 

 to invade the host tissues and stimulate 

 the development of immunity, but are 



killed before they can multiply enough 

 to harm the host. 



A number of workers have attempted 

 to produce immunity by infecting birds 

 with oocysts attenuated in different ways. 

 Jankiewicz and Scofield (1934) heated the 

 oocysts to 46" C for 15 minutes before 

 sporulation, and found that when they were 

 then sporulated and fed to chickens, they 

 stimulated the production of immunity 

 with a minimum of injury. Waxier (1941) 

 produced mild infections with oocysts 

 irradiated with 9000 r of x-rays. Follow- 

 ing recovery, the chicks were almost as 

 resistant as those which had had a severe 

 attack after infection with normal oocysts. 

 Uricchio (1953) produced marked immunity 

 by feeding chicks 100, 000 oocysts which 

 had been held at -5^ C for 5 days, and a 

 lesser degree of immunity with oocysts 

 which had been heated at 45'' C for 12 

 hou rs . 



It is well known that cultures slowly 

 lose their infectivity upon storage. Bab- 

 cock and Dickinson (1954), for example, 

 observed reduced pathogenicity in a culture 

 of E. tenella after storage for 236 days, 

 and reduced immunogenicity at 344 days. 

 Using a standard immunizing procedure 

 in which 600 oocysts were fed the first 

 day and 1000 the second, they found that 

 it took 3 days to produce immunity with a 

 culture less than 150 days old and 6 days 

 with a culture more than 300 days old. 



There is an unanswered question 

 whether such treatments produce true at- 

 tenuation or whether the observed results 

 are due simply to the death of some of the 

 oocysts. Invasion must take place for im- 

 munity to result, and attempts to immu- 

 nize birds with killed antigens have not 

 succeeded. 



Most attempts to find circulating anti- 

 bodies have failed. However, McDermott 

 and Stauber (1954) found agglutinins 

 against merozoites in the serum of exper- 

 imentally infected chickens and also pro- 

 duced them in rabbits and roosters by in- 

 jecting formalinized merozoite suspensions. 

 Becker and Zimmermann (1953) found that 

 infected chicks injected intravenously with 



