Experimental Development of Monensin Resistance in Eimeria meleagrimitis

Jeffers, T. K.; Bentley, E. J.

doi:10.3382/ps.0591731

Cited by 21 publications

(5 citation statements)

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“…Whilst it has proved difficult to develop resistance to monensin in the chicken this has not been the case in the turkey: a resistant line of E. meleagrimitis emerged after 10 passages in the presence of drug (Jeffers & Bentley, 1980). This may be due to differences in the effect of the drug upon the parasites involved rather than to differences between the hosts because, according to Smith, Galloway & White (1981), the mode of action of ionophores is directed against extracellular stages of the life-cycle of Eimeria (for example, sporozoites), the host cell not being involved in the expression of anticoccidial activity.…”

Section: Discussionmentioning

confidence: 99%

“…monensin resulted in a slight reduction in pathogenicity and, interestingly, this was also noted with a strain of E. meleagrimitis that had been passaged repeatedly in turkeys medicated with 150 or 180 p.p.m. of monensin (Jeffers & Bentley, 1980). If alteration in the composition of the membrane is dependent upon the presence of the drug, then the partial resistance observed may be readily reversible thus explaining the loss of resistance which occurred after passage of the resistant line in the absence of monensin.…”

Section: Discussionmentioning

confidence: 99%

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Eimeria tenella: experimental development of resistance to monensin in the chicken

Chapman

1984

Parasitology

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The development of resistance by the Houghton strain of Eimeria tenella (H) to monensin has been studied by serially passaging the strain in groups of 30 birds, each inoculated with 10(6) oocysts and given 100 p.p.m. of drug in the food. After 16 passages a line partially resistant to this concentration of monensin was produced. Passage of the line in birds medicated with 200 or 300 p.p.m. of monensin did not result in the acquisition of a greater degree of resistance. A further reduction in sensitivity to 100 p.p.m. monensin was obtained, however, when the line was serially passaged in 15 groups of 6 birds each given 3 X 10(6) oocysts. Five passages in the absence of monensin resulted in restoration of sensitivity, suggesting that the resistance developed was not stable. The pathogenic effects of the line that had been passaged in chickens given 300 p.p.m. of monensin were less than those of the parent line.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Eimeria tenella: experimental development of resistance to monensin in the chicken

Chapman

1984

Parasitology

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“…Resistance to decoquinate was evaluated using a combination of three criteria: the percentage of optimum anticoccidial activity (POAA), the reduction of lesion scores (RLS), and the relative oocyst production (ROP) [22,23,24,25]. POAA was calculated using the following formula: (GSR of treatment group − GSR of INCs) / (GSR of NNCs − GSR of INCs) × 100%, where GSR represents the cage weight at termination divided by the cage weight at initiation.…”

Section: Evaluation Of Decoquinate Resistancementioning

confidence: 99%

Distinct non-synonymous mutations in cytochrome b highly correlate with decoquinate resistance in apicomplexan parasite Eimeria tenella

Hao

Chen

Sun

et al. 2023

Preprint

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Background Protozoan parasites of the genus Eimeria are the causative agents of chicken coccidiosis. Parasite resistance to most anticoccidial drugs is one of the major challenges in controlling this disease. There is an urgent need for a molecular marker to monitor the emergence of resistance against anticoccidial drugs, such as decoquinate. Methods In this study, we developed decoquinate-resistant strains by successively exposing the Houghton (H) and Xinjiang (XJ) strains of E. tenella to incremental concentrations of the drug in chickens. Additionally, we isolated a decoquinate-resistant strain from the field. The resistance of these three strains was tested using the criteria of weight gain (WG), relative oocyst production (ROP), and reduction of lesion scores (RLS). Whole-genome sequencing was used to identify the non-synonymous mutations in coding genes that were highly associated with the decoquinate-resistant phenotype in the two laboratory-induced strains. Subsequently, we further scrutinized the missense mutation in a field-resistant strain for verification. We employed AlphaFold and PyMOL to model the alterations in the binding affinity of the mutants towards the drug molecule. Results We obtained two decoquinate-resistant strains, DecR_H and XJ, originating from the H and XJ strains, respectively, as well as a field-resistant E. tenella strain, DecR_SC. These three strains displayed resistant to 120 mg/kg decoquinate administered through feed. Through whole-genome sequencing analysis, we identified the cytochrome b gene (ETH2_MIT00100) as the sole mutated gene shared between the DecR_H and XJ strains and was also detected in the DecR_SC strain. Distinct non-synonymous mutations, namely Gln131Lys in the DecR_H, Phe263Leu in the DecR_XJ, and Phe283Leu in the DecR_SC were observed in the three resistant strains. Notably, these mutations were located in the extracellular segment of cytochrome b, in close proximity to the ubiquinol oxidation site Qo. Drug molecular docking studies revealed that these mutants exhibited varying degrees of reduced binding ability to decoquinate. Conclusions Our findings emphasize the critical role of cytochrome b mutations in the development of decoquinate resistance in E. tenella. The strong correlation observed between cytochrome b mutant alleles and resistance indicates their potential as valuable molecular markers for the rapid detection of decoquinate resistance.

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“…Most attempts to develop resistance to ionophores in the chicken, however, have been unsuccessful (for example, Jeffers, 1978b;Jeffers, 1981). Surprisingly, in an experiment with Eimeria meleagrimitis, a parasite of the turkey, Jeffers & Bentley (1980a) were able to develop resistance to monensin in as few as four generations of selection. The strain developed was also resistant to other ionophores, illustrating the phenomenon of cross-resistance where drugs with a similar mode of action share resistance (see also Jeffers, 1984).…”

Section: Biographymentioning

confidence: 99%

Thomas K. Jeffers: pioneer of coccidiosis research

Chapman

2012

Avian Pathology

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Thomas K. Jeffers has made many significant contributions to our understanding of the biology of the parasite Eimeria, the cause of coccidiosis in poultry. His work has had direct practical application for the control of this widespread disease. Topics discussed include Jeffers' pioneering work concerned with genetics of the host response to infection, the nature of biological and immunological intraspecific variation, drug resistance and discovery, field surveys of resistance, and his most recognized achievement-the demonstration that the lifecycle of coccidia may be altered by artificial selection. Parasites so modified are attenuated but retain their immunogenicity, a discovery that has led to the development of live vaccines that are inherently non-pathogenic. This article provides a brief biography and describes the contributions that Jeffers has made to our knowledge of coccidiosis.

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Experimental Development of Monensin Resistance in Eimeria meleagrimitis

Cited by 21 publications

References 5 publications

Eimeria tenella: experimental development of resistance to monensin in the chicken

Eimeria tenella: experimental development of resistance to monensin in the chicken

Distinct non-synonymous mutations in cytochrome b highly correlate with decoquinate resistance in apicomplexan parasite Eimeria tenella

Thomas K. Jeffers: pioneer of coccidiosis research

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