Further Evidence of Hereditary Resistance and Susceptibility to Cecal Coccidiosis in Chickens

Rosenberg, M. M.; Alicata, Joseph E.; Palafox, A. L.

doi:10.3382/ps.0330972

Cited by 29 publications

(10 citation statements)

References 8 publications

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“…ii) We excluded the possibility that our chicks harbored residual coccidiostats, which are frequently included in chicken feed to prevent devastating outbreaks of the related apicomplexan parasite Eimeria tenella (Takaya et al, 1999;Pines et al, 2000), which could have affected the exoerythrocytic stages of P. gallinaceum. iii) One remaining possibility is that White Leghorns have gained resistance to tissue stages of P. gallinaceum, because modern commercial chicken breeds have been selected for increased resistance to disease, including E. tenella infection (Edgar et al, 1951;Champion, 1954;Rosenberg et al, 1954;Johnson and Edgar, 1982;Caron et al, 1997). 4) Finally, the quinine used in the 1940s may have been of lesser purity thus permitting the generation of secondary exoerythrocytic stages from a low level parasitemia.…”

Section: Discussionmentioning

confidence: 99%

Exoerythrocytic development of Plasmodium gallinaceum in the White Leghorn chicken

Frevert¹,

Späth²,

Yee³

2008

International Journal for Parasitology

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Plasmodium gallinaceum typically causes sub-clinical disease with low mortality in its primary host, the Indian jungle fowl Gallus sonnerati. Domestic chickens of European origin, however, are highly susceptible to this avian malaria parasite. Here we describe the development of P. gallinaceum in young White Leghorn chicks with emphasis on the primary exoerythrocytic phase of the infection. Using various regimens for infection, we found that P. gallinaceum induced a transient primary exoerythrocytic infection followed by a fulminant lethal erythrocytic phase. Prerequisite for the appearance of secondary exoerythrocytic stages was the development of a certain level of parasitemia. Once established, secondary exoerythrocytic stages could be propagated from bird to bird for several generations without causing fatalities. Infected brains contained large secondary exoerythrocytic stages in capillary endothelia, while in the liver primary and secondary erythrocytic stages developed primarily in Kupffer cells and remained smaller. At later stages, livers exhibited focal hepatocyte necrosis, Kupffer cell hyperplasia, stellate cell proliferation, inflammatory cell infiltration and granuloma formation. Because P. gallinaceum selectively infected Kupffer cells in the liver and caused a histopathology strikingly similar to mammalian species, this avian Plasmodium species represents an evolutionarily closely related model for studies on the hepatic phase of mammalian malaria.

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Section: Discussionmentioning

confidence: 99%

Exoerythrocytic development of Plasmodium gallinaceum in the White Leghorn chicken

Frevert¹,

Späth²,

Yee³

2008

International Journal for Parasitology

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“…Finding genes associated with coccidiosis resistance will be useful to efficient genetic selection for disease-resistant lines and understanding mechanisms underlying disease resistance in chickens (Lamont et al, 2002;Zhu et al, 2003). There were evidences that resistance and susceptibility to avian coccidiosis are associated with inheritance (Rosenberg et al, 1953) and eventually chicken lines resistant to avian coccidiosis could be established by genetic selection (Johnson and Edgar, 1982). The resistance to avian coccidiosis QTL has been identified near 2 microsatellite markers LEI0071 and LEI0101 on chromosome 1 (Zhu et al, 2003;Kim et al, 2006).…”

Section: Introductionmentioning

confidence: 97%

Genetic effects analysis of myeloid leukemia factor 2 and T cell receptor-β on resistance to coccidiosis in chickens

Kim¹,

Hong

Lillehoj³

2010

Poultry Science

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Associations between the parameters of resistance to coccidiosis and SNP in 3 candidate genes located on chromosome 1 [T cell receptor-beta (TCR-beta), myeloid leukemia factor 2 (MLF2), and lymphotactin] were determined. Single nucleotide polymorphisms were genotyped in 24 F1 generation and 290 F2 generation birds. Four SNP were identified in the lymphotactin gene, 12 were located in the TCR-beta gene, and 4 in the MLF2 gene. At various times after experimental infection of the F2 generation with Eimeria maxima, BW, fecal oocyst shedding, and biochemical parameters were measured as parameters of coccidiosis resistance. Single marker association test was applied to determine the associations between the 20 SNP and the parameters of coccidiosis resistance. The maximum additive genetic effect on disease resistance of an SNP in MLF2 was explained by BW (P = 0.0002). The SNP in MLF2 significantly associated with BW was also associated with fecal oocyst shedding (P = 0.001). Four SNP associated with oocyst shedding were found within the coding region of TCR-beta (P < 0.05). Although none of the lymphotactin SNP were associated with oocyst shedding, interferon-gamma level was associated with 2 SNP in lymphotactin. These results suggest that the SNP in the MLF2 gene can be one of the markers to select coccidiosis resistance in chickens.

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“…Other diseases for which susceptible and (resistant lines have been specifically developed by family selection are cocoiidiosis (Rosenberg et al, 1954;Champion, 1954;Challey, 1966;Klimes and Orel, 1969), and, less successfully, Newcastle disease (Gordon et al, 1971). These studies involved the use of standardized challenges, and in the later examples, progeny tests.…”

Section: Determination Of a Selection Methodsmentioning

confidence: 99%

Genetics and control of avian diseases

Payne

1973

Avian Pathology

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This paper discusses the main principles involved in applying genetic resistance to the control of avian infectious diseases, and the actual and potential importance of this approach to disease control. The principles are considered, with illustrative examples, under the following headings: (1) mechanisms of resistance, including virus receptors, interferon, macrophages, immune responses, hormones and body temperature, (2) recognition of resistance, (3) inheritance of resistance, including simple and polygenic control, (4) selection for resistance, including testing for genetic variability, comparison of exposure methods, selection methods and correlations between resistance and other traits.

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Further Evidence of Hereditary Resistance and Susceptibility to Cecal Coccidiosis in Chickens

Cited by 29 publications

References 8 publications

Exoerythrocytic development of Plasmodium gallinaceum in the White Leghorn chicken

Exoerythrocytic development of Plasmodium gallinaceum in the White Leghorn chicken

Genetic effects analysis of myeloid leukemia factor 2 and T cell receptor-β on resistance to coccidiosis in chickens

Genetics and control of avian diseases

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