Resistance of birds to challenge with Eimeria tenella

Burns, Wm. C.; Challey, John R.

doi:10.1016/s0014-4894(59)80001-1

Cited by 17 publications

(6 citation statements)

References 5 publications

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“…Another aspect of interest is that an infection confined primarily to a small portion of the large intestine was apparently able to produce immunity in the entire large intestine. This finding is similar to those of Horton-Smith, Beattie, and Long (1961) and of Burns and Challey (1959) showing that immunity to E. tenella may be transferred to one cecum from the other. …”

Section: Discussionsupporting

confidence: 91%

Response of Immunized and Nonimmunized Calves to Cecal Inoculation of First-Generation Merozoites of Eimeria bovis

Hammond¹,

Andersen²,

Miner³

1964

The Journal of Parasitology

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Section: Discussionsupporting

confidence: 91%

Response of Immunized and Nonimmunized Calves to Cecal Inoculation of First-Generation Merozoites of Eimeria bovis

Hammond¹,

Andersen²,

Miner³

1964

The Journal of Parasitology

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“…A connection between the flagellum and microtubules was not Microtubules in trypanosomatids were first reported by Kleinschmidt and Kinder (17) from dried and shadowed pellicles of Trypanosoma lewisi and by Lofgren (23) from lysed cells of Leishmania tropica. They were found in sections by Anderson et al ( 1 ) . Their presence has been confirmed in electron micrographs of all trypanosomatids.…”

Section: Discussionmentioning

confidence: 83%

“…been incubated in serum from immune chickens fail to initiate infections when inoculated into susceptible chickens ( 5 ) . Burns and Challey (1) found that if an initial infection is confined to a ligated cecum, the other, uninfected cecum becomes resistant to a challenge infection.…”

mentioning

confidence: 99%

Cellular Aspects of the Resistance of Chickens to Eimeria tenella Infections*

Huff

Clark

1970

The Journal of Protozoology

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SYNOPSIS. Sporozoites of Eimeria tenella were injected into the peritoneal cavity of normal chickens and chickens immunized against E. tenella. In some experiments normal scrum and serum from resistant chickens were injected prior to the injection of sporozoites. After 15 or 30 minute periods of intraperitoneal incubation, exudates were harvested and the occurrence of intracellular sporozoites was determined. Only macrophages and degranulated granulocytes were observed to contain sporozoites. There was no significant difference between the number of macrophages obtained from normal chickens (normal macrophages) which contained sporozoites and the number of macrophages obtained from immune chickens (immune macrophages) which contained sporozoites. Significantly fewer immune macrophages treated with immune serum contained sporozoites than untreated normal or immune cells, normal macrophages treated with either serum, or immune macrophages treated with normal scrum. Sporozoites in untreated normal macrophages did not appear to be harmed by the intracellular environment, based on structural observations. The majority of sporozoites in macrophages from all other groups were difficult to distinguish within the cytoplasm and were visibly distorted. It is hypothesized that the presence of fewer infected macrophages in exudates of immune chickens and serum‐treated normal chickens was caused by an enhanced ability of these cells to destroy the parasite. Similar observations were noted in the case of sporozoites within degranulated granulocytes of experimental groups. The lack of understanding of the degranulation phenomenon makes it difficult to interpret these findings.

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“…Whether immune phagocytosis plays a role in immunity to infection is not known but it would be reasonable to assume that it could do so provided that the conditions were suitable. Obviously, contact between cells and parasite is a prerequisite; the intestinal epithelium is fairly well supplied with macrophages and, in the case of E. tenella, E. necatrix, and E. acervulina, there is some evidence that sporozoites may be transported within macrophages to their developmental sites (3,5,7,15,24); therefore, contact between cells and parasite could occur readily in vivo. Sensitization of cells and/or parasites could be by circulating or by locally produced antibodies; local vascular permeability is increased at the time of infection, especially in immunized birds (11,20).…”

Section: Discussionmentioning

confidence: 99%

Immune Responses in Infections with Coccidia: Macrophage Activity

Rose

1974

Infect Immun

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Peritoneal exudate cells from chickens immunized with two species of coccidia, Eimeria tenella or Eimeria maxima, were examined for their capacity to phagocytose stages of the parasite in vitro. True phagocytosis of the sporozoite stage is difficult to estimate because of its ability to invade cells, but may be evaluated by comparison with control suspensions. Peak activity (compared with cells from coccidia-free chickens) was found 3 to 5 weeks after the first inoulum of oocysts of E. tenella, and 1 week after the first inoculum of E. maxima-times which correspond to the onset of complete immunity to infection. Cells from coccidia-free chickens, in the presence of serum from birds immunized with E. tenella, phagocytosed sporozoites of E. tenella in a similar manner to cells from immunized birds. The immune serum had both cytophilic and opsonic adherence properties and the latter was species specific (for the two species tested).

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Resistance of birds to challenge with Eimeria tenella

Cited by 17 publications

References 5 publications

Response of Immunized and Nonimmunized Calves to Cecal Inoculation of First-Generation Merozoites of Eimeria bovis

Response of Immunized and Nonimmunized Calves to Cecal Inoculation of First-Generation Merozoites of Eimeria bovis

Cellular Aspects of the Resistance of Chickens to Eimeria tenella Infections*

Immune Responses in Infections with Coccidia: Macrophage Activity

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