Adaptation of gastrointestinal nematode parasites to host genotype: single locus simulation models

Kemper, Kathryn E., Goddard, Michael E. and Bishop, Stephen C. (2013) Adaptation of gastrointestinal nematode parasites to host genotype: single locus simulation models. Genetics Selection Evolution, 45 . doi:10.1186/1297-9686-45-14


Author Kemper, Kathryn E.
Goddard, Michael E.
Bishop, Stephen C.
Title Adaptation of gastrointestinal nematode parasites to host genotype: single locus simulation models
Journal name Genetics Selection Evolution   Check publisher's open access policy
ISSN 0999-193X
1297-9686
Publication date 2013-05-28
Sub-type Article (original research)
DOI 10.1186/1297-9686-45-14
Open Access Status DOI
Volume 45
Total pages 14
Place of publication London, United Kingdom
Publisher BioMed Central
Language eng
Formatted abstract
Background: Breeding livestock for improved resistance to disease is an increasingly important selection goal. However, the risk of pathogens adapting to livestock bred for improved disease resistance is difficult to quantify. Here, we explore the possibility of gastrointestinal worms adapting to sheep bred for low faecal worm egg count using computer simulation. Our model assumes sheep and worm genotypes interact at a single locus, such that the effect of an A allele in sheep is dependent on worm genotype, and the B allele in worms is favourable for parasitizing the A allele sheep but may increase mortality on pasture. We describe the requirements for adaptation and test if worm adaptation (1) is slowed by non-genetic features of worm infections and (2) can occur with little observable change in faecal worm egg count.

Results: Adaptation in worms was found to be primarily influenced by overall worm fitness, viz. the balance between the advantage of the B allele during the parasitic stage in sheep and its disadvantage on pasture. Genetic variation at the interacting locus in worms could be from de novo or segregating mutations, but de novo mutations are rare and segregating mutations are likely constrained to have (near) neutral effects on worm fitness. Most other aspects of the worm infection we modelled did not affect the outcomes. However, the host-controlled mechanism to reduce faecal worm egg count by lowering worm fecundity reduced the selection pressure on worms to adapt compared to other mechanisms, such as increasing worm mortality. Temporal changes in worm egg count were unreliable for detecting adaptation, despite the steady environment assumed in the simulations.

Conclusions: Adaptation of worms to sheep selected for low faecal worm egg count requires an allele segregating in worms that is favourable in animals with improved resistance but less favourable in other animals. Obtaining alleles with this specific property seems unlikely. With support from experimental data, we conclude that selection for low faecal worm egg count should be stable over a short time frame (e.g. 20 years). We are further exploring model outcomes with multiple loci and comparing outcomes to other control strategies.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: Institute for Molecular Bioscience - Publications
 
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