Synonyms: Eimeria avium, Coccidium tenellum, Coccidium globosum, Eimeria bracheti.
Geographic Distribution: Worldwide.
Prevalence: Very common.
Morphology: The oocysts are broadly ovoid, smooth, 14 to 31 by 9 to 25 u with a mean of 22.9 by 19.1 u. A micropyle is absent. An oocyst polar granule is present. An oocyst residuum is absent. The sporocysts are ovoid, without a sporocyst residuum.
The sporulation time is 1 to 2 days. Edgar (1954) found that the minimum sporulation time is 18 hours at 29°, 21 hours at 26.5 to 28° and 24 hours at 20, 24 and 32°. Maximum sporulation was reached in 22 to 24 hours at 29°, the optimum temperature. Some sporulation took place at 41°. When the oocysts were kept at 8° they failed to sporulate in 8 weeks and most were killed, so that only a few sporulated when they were subsequently held at 28°.
Life Cycle: The life cycle of E. tenella has already been described as an example of coccidian life cycles.
Pathogenesis: This is the most pathogenic of the chicken coccidia and is responsible for heavy losses. Together with the other species, it was estimated by the USDA (1954) to cause an annual loss of $38,229,000 in the United States due to death and disease alone. To this should be added the cost of the medicated feeds which are generally fed to poultry, and various labor and other costs entailed by disease outbreaks.
Cecal coccidiosis is found most frequently in young birds. Chicks are most susceptible at 4 weeks of age, while chicks 1 to 2 weeks old are more resistant (Gardiner, 1955). However, day-old chicks can be infected (Gordeuk, Bressler & Glantz, 1951). Older birds develop immunity as the result of exposure.
Coccidiosis due to E. tenella may vary in severity from an inapparent infection to an acute, highly fatal disease, depending upon the infective dose of oocysts. The pathogenicity of different strains of E. tenella varies, and it is affected also by the breed and age of the chickens and their state of nutrition. Thus, Jankiewicz and Scofield (1934) found that less than 150 sporulated oocysts produced no signs, 150 to 500 oocysts produced slight hemorrhagic diarrhea, 1000 to 3000 oocysts produced moderate hemorrhage and a few deaths, 3000 to 5000 oocysts produced marked hemorrhage and moderate mortality, and more than 5000 oocysts produced severe hemorrhage and high mortality. However, Horton-Smith (1949) found that infections with 15,000 oocysts caused no mortality in week-old birds, 30,000 oocysts caused 32% mortality and 60,000 oocysts caused 45% mortality. Swales (1944) found that in 6-week-old chickens 15,000 oocysts caused 40% mortality, 30,000 oocysts caused 44% mortality and 200,000 oocysts caused 80% mortality, while in 4.5-week-old chicks 120,000 oocysts caused 90% mortality and in 12-week-old chicks 100,000 oocysts caused 50% mortality. Waletzky and Hughes (1949) found that in one experiment 20,000 oocysts produced 18% mortality and 100,000 oocysts 36% mortality in 4-week-old chicks, while in other experiments 50,000 oocysts produced 45% mortality in 7-week-old chicks, 100,000 oocysts produced 67% mortality in 4- to 5-week-old chicks and 500,000 oocysts produced 48% mortality in 3- to 6-week-old chicks. Gardiner (1955) found that 200,000 oocysts were required to produce mortality in 1- to 2-week-old chicks, while 50,000 to 100,000 oocysts produced mortality in older birds.
Cecal coccidiosis is an acute disease characterized by diarrhea and massive cecal hemorrhage. The first signs appear when the second generation schizonts begin to enlarge and produce leakage of blood into the ceca. Blood first appears in the droppings 4 days after infection. At this time the birds appear listless. They may become droopy and inactive, and eat little, altho they still drink. The greatest amount of hemorrhage occurs on the 5th and 6th days after infection. It then declines, and oocysts appear in the feces 7 days after infection if the birds live that long. The oocysts increase to a peak on the 8th or 9th day and then drop off very rapidly. Very few are still being shed by the 11th day. A few oocysts may be found for several months.
Coccidiosis is self-limiting, and if the birds survive to the 8th or 9th day after infection, they generally recover.
The lesions of cecal coccidiosis depend upon the stage of the disease. They have been described by Tyzzer (1929), Tyzzer, Theiler and Jones (1932) and Mayhew (1937). On the fourth day after infection, hemorrhage is present thruout the cecal mucosa. On the fifth day, the cecum is filled with large amounts of unclotted or only partly clotted blood. This increases on the sixth day. Cecal cores of fibrinous and necrotic material begin to form on the 7th day. They adhere tightly to the mucosa at first, but soon come loose and lie free in the lumen.
About 7 days after infection, the wall of the cecum changes color from red to mottled reddish or milky white due to the formation of oocysts. It is greatly thickened. The cecal core, which was at first reddish, becomes yellowish or whitish. If it is small enough, it may be passed intact in the feces, but usually it is broken up into small pieces. In a few days the cecum becomes normal in appearance or at most slightly enlarged and thickened. Occasionally the cecum may rupture or adhesions may form.
About the 4th day, when the second generation schizonts are developing, the lamina propria becomes infiltrated with eosinophiles, there is marked congestion, and the cecal wall is thickened. The epithelium may be torn and coccidia, blood and tissue cells may be released into the lumen in areas where there are large numbers of parasites. On the 5th day, when the second generation merozoites are released, their host cells are ruptured and there is extensive epithelial sloughing. The sloughed material and cecal contents consolidate to form the cecal core, which loosens from the wall as the epithelium is regenerated.
Epithelial regeneration is complete in light infections, but in severe ones it may not be. There is a marked inflammatory reaction, with extensive lymphoid and plasma cell infiltration, and there may be some giant cells. Connective tissue is increased. The epithelium may not be replaced between the glands, and cysts formed by constriction of the glands during the inflammatory stage may persist.
The loss of blood into the ceca causes anemia. Using the microhematocrit technic, Joyner and Davies (1960) found that the packed red cell volume decreased markedly beginning 5 days after experimental infection. From an original level of 26 to 29% it decreased to 18% and 14%, respectively, 7 days after infection with 2000 and 10,000 oocysts. It had returned to normal 5 days later.
Natt (1959) found that E. tenella causes marked changes in the leucocyte picture. He observed lymphopenia and heterophilia on the 5th day, and eosinophilia on the 10th day after infection. A marked leucocytosis began on the 7th day and persisted thru the recovery phase.
Birds which recover from coccidiosis may suffer ill effects for some time or even permanently. Gardiner (1954) found an inverse correlation between growth rate and severity of cecal coccidiosis. Chicks which recovered following severe infection made much poorer weight gains than mildly affected ones. Mayhew (1932, 1932a, 1934) found that it took 10 weeks to 6 months after recovery before infected birds regained the weight they had lost in comparison with uninfected controls. He found, too, that pullets which had been infected when 6 to 8 weeks old laid 19.25% fewer eggs than the controls. In addition, severely affected birds began to lay 6 to 7 weeks later than the controls. Davidson, Thompson and Morre (1936) compared a group of chickens which was passing oocysts with another group which was not. Over a period of 11 months, the positive group had a 12.1% higher mortality, while the negative group averaged 0.44 pounds heavier than the positive one and had a 15.2% higher egg production. Bressler and Gordeuk (1951) found, in a flock of Single Comb White Leghorn chickens which had survived a mortality of 8.3% due to cecal coccidiosis, that weight gains were slightly less than in a "control" group fed 0.0125% sulfaquinoxaline continuously which had not suffered an outbreak of the disease, but that neither egg production nor hatchability were impaired.