THE TELOSPORASIDA AND THE COCCIDIA PROPER 



163 



The actual numbers of oocysts pro- 

 duced per oocyst fed are usually consider- 

 ably lower than the theoretical ones. K 

 the host is resistant or immune, it des- 

 troys many merozoites, and many others 

 pass out in the feces before they have time 

 to enter host cells. The infecting dose is 

 also an important factor in determining 

 the number of oocysts produced. The 

 greater the infecting dose, the smaller the 

 number of oocysts usually produced per 

 oocyst fed. For example. Hall (1934) ob- 

 tained a yield of 1, 455, 000 oocysts of E. 

 nieschulzi per oocyst fed when the infecting 

 dose was 6 oocysts, 1, 029, 666 when it was 

 150 oocysts, and 144, 150 when it was 2000 

 oocysts. If the infecting dose is too small, 

 however, smaller numbers of oocysts are 

 produced. Hall (1934) found that when only 

 a single oocyst was fed, the yield was 

 62,000. 



Similarly, Brackett and Bliznick 

 (1950, 1952) found that with E. acervuUna 

 of the chicken, 9000 oocysts were produced 

 per oocyst fed when the infecting dose was 

 200 oocysts, 35, 000 to 72, 000 when it was 

 2000 oocysts, 35,000 when it was 10,000 

 oocysts, and 7,600 when it was 20,000 

 oocysts. With E. maxima of the chicken, 

 they found that 11, 500 oocysts were pro- 

 duced per oocyst fed when the infecting 

 dose was 200 oocysts, 2, 250 when it was 

 2000 oocysts, and 940 to 2900 when it was 

 10, 000 oocysts. With E. necatrix of the 

 chicken, they found that 50, 000 oocysts 

 were produced per oocyst fed when the in- 

 fecting dose was 200 oocysts, and 2400 

 when it was 2000 oocysts. With E. tenella 

 of the chicken, they found that the maxi- 

 mum number of oocysts produced per 

 oocyst fed in numerous experiments was 

 400,000. However, in one series of 2- 

 week-old chicks this figure ranged from 

 1200 for chicks fed 40, 000 oocysts to 

 80, 000 when the infecting dose was 50 

 oocysts. 



All the factors responsible for these 

 results are not known. More effective 

 mobilization of the host's defenses is 

 probably important, but lack of enough 

 epithelial cells to parasitize, sloughing of 

 patches of epithelium, increased intes- 

 tinal motility with resultant diarrhea and 



elimination of merozoites before they can 

 reach a cell, and entrapment of merozoites 

 in tissue debris and cecal cores may also 

 play a part. 



Pathogenesis . While many species 

 of coccidia are pathogenic, many others 

 are not. Pathogenicity depends on a num- 

 ber of factors, some of which are probably 

 still unknown. Among those which might 

 be mentioned are the number of host cells 

 destroyed per infecting oocyst (which de- 

 pends upon the number of merozoite gen- 

 erations and the number of merozoites per 

 generation) and the location of the parasite 

 in the host tissues and within the host cells. 

 The size of the infecting dose or doses, 

 the degree of reinfection, and the degree 

 of acquired or natural immunity of the host 

 are also important. 



Even with a pathogenic species, the 

 final effect on the host depends on the in- 

 terplay between many factors; it may range 

 from rapid death in susceptible animals to 

 an imperceptible reaction in immune ones. 



If disease is present, the signs are 

 those of a diarrheal enteritis. There may 

 or may not be blood in the feces, depending 

 on the parasite species and severity of in- 

 fection. Affected animals gain weight 

 poorly, become weak and emaciated, or 

 may even die, depending again on the para- 

 site species and the size of the infecting 

 dose. Young animals are much more com- 

 monly affected than older ones. Those ani- 

 mals which recover develop an immunity 

 to the particular species which infected 

 them. However, this is not an absolute 

 immunity, and recovered adult animals 

 are often continuously reinfected so that 

 they carry light infections which do not 

 harm them but which make them a source 

 of infection for the young. In addition, 

 under conditions of stress their immunity 

 may be broken down and they may suffer 

 from the disease again. 



Differentiation of Species . Both 

 morphological and biological characters 

 are used to separate the species of coc- 

 cidia. Both the endogenous and exogenous 

 stages of the life cycle may differ morpho- 

 logically. However, since the endogenous 



