180 



THE TELOSPORASIDA AND THE COCCIDIA PROPER 



The intestines of infected lambs had thick- 

 ened, somewhat edematous areas in the 

 upper part. The Peyer's patches and the 

 last 8 to 10 inches of the small intestine 

 above the ileocecal valve were inflamed. 



EIMERIA ARLOINGI 

 (MAROTEL, 1905) 

 MARTIN, 1909 



Hosts : Sheep, goat. Rocky Mountain 

 bighorn sheep, Ovis »iusl)>ioii, O. polii. 

 Copra ibex, Hemmilragus jenilaicus, roe 

 deer. 



Location : Small intestine. 



Geographic Distribution : Worldwide. 



Prevalence: This is probably the 

 most common coccidium in sheep. Chris- 

 tensen (1938a) found it in 90% of 100 sheep 

 from Idaho, Maryland, New York and 

 Wyoming. Balozet (1932) found it in 52% 

 of 63 sheep and 56% of 41 goats in Tunisia. 

 Jacob (1943) found it in 58% of 100 sheep 

 and 18% of 11 goats in Germany. Svanbaev 

 (1957) found it in 52% of 302 sheep and 52% 

 of 48 goats in Kazakhstan. 



Morphology : The oocysts are usually 

 elongate ellipsoidal, but are sometimes 

 asymmetrical, with one side curved more 

 than the other, or slightly ovoid. They 

 are 17 to 42 by 13 to 27 /i with a mean of 

 27 by 18/i; their length-width ratio is 1. 1 

 to 1.9 with a mean of 1.49 (Christensen, 

 1938a). The oocyst wall is 1.0 to 1. 5 fi 

 thick, transparent, almost colorless to 

 yellowish-brown, and composed of 2 

 layers, the outer one being half as thick 

 as the inner, according to Christensen 

 (1938a). The oocyst wall is apparently 

 lined by a membrane. A micropyle 2 to 

 3(1 in diameter is present. A micropylar 

 cap is present; it varies from an incon- 

 spicuous, flat structure to a prominent, 

 transparent, pale yellow to yellowish- 

 green rounded cone or crescent, 0.2 to 

 2[x high by 3 to 8 fi wide with a mean of 

 1.2 by 5/i. This cap is a tough, lid-like 

 structure which is easily dislodged and 

 may be lost in some specimens. An 

 oocyst residuum is absent. An oocyst 



polar granule is present according to 

 Balozet (1932). The sporocysts are ovoid, 

 13 by 6/1. A sporocyst residuum is pres- 

 ent. The sporulation time is 1 to 2 days 

 (Christensen, 1938a) to 3 to 4 days (Balo- 

 zet, 1932). 



Life Cycle : Lotze (1953a) studied the 

 life cycle of E. arloiiigi in experimentally 

 infected lambs. The sporozoites emerge 

 from the oocysts in the small intestine, 

 enter the crypts of Lieberkuehn, and pene- 

 trate thru the tunica propria into the in- 

 terior of the villi. Here they enter the 

 endothelial cells lining the central lacteals 

 and grow. The host cell also grows, and 

 its nucleus becomes very large. There is 

 apparently only 1 generation of schizonts 

 and merozoites. The schizonts become 

 mature 13 to 21 days after infection. At 

 this time they are about 122 to 146 /i in 

 diameter and contain a large number 

 (probably millions) of merozoites about 

 9/i long and 2 /i wide. 



The merozoites break out of the schi- 

 zonts and enter the epithelial cells of the 

 small intestine. Sometimes only a small 

 group of cells at the bottom of the crypts 

 is parasitized, but in heavy infections 

 practically all the epithelial cells of the 

 villi are invaded. The infected villi are 

 enlarged and greyish. Some of these 

 merozoites become microgametocytes; 

 these form many microgametes, leaving 

 a large mass of residual material. Most 

 of the merozoites become macrogametes, 

 which contain large plastic granules when 

 mature. 



Following fertilization, the macro- 

 gametes turn into oocysts, which break 

 out of the host cells and are first seen in 

 the feces on the 20th day after infection. 

 Their numbers increase for about 5 days 

 and then decrease at about the same rate 

 for the next 5 days. Thus the prepatent 

 period is 19 days and the patent period 

 about 10 days following a single exposure. 



Pathogenesis : Lotze (1952) studied 

 the pathogenicity of E. arloiiigi in 3- 

 month-old lambs experimentally infected 

 with 200,000 to 60 million oocysts. No 

 visible signs were produced by infections 



