Integrating genetics and genomics to identify new leads for the control ofEimeriaspp.
SHIRLEY MW., BLAKE D., WHITE SE., SHERIFF R., SMITH AL.
Eimerian parasites display a biologically interesting range of phenotypic variation. In addition to a wide spectrum of drug-resistance phenotypes that are expressed similarly by many other parasites, theEimeriaspp. present some unique phenotypes. For example, unique lines ofEimeriaspp. include those selected for growth in the chorioallantoic membrane of the embryonating hens egg or for faster growth (precocious development) in the mature host. The many laboratory-derived egg-adapted or precocious lines also share a phenotype of a marked attenuation of virulence, the basis of which is different as a consequence of thein ovoorin vivoselection procedures used. Of current interest is the fact that some wild-type populations ofEimeria maximaare characterized by an ability to induce protective immunity that is strain-specific. The molecular basis of phenotypes that defineEimeriaspp. is now increasingly amenable to investigation, both through technical improvements in genetic linkage studies and the availability of a comprehensive genome sequence for the caecal parasiteE. tenella. The most exciting phenotype in the context of vaccination and the development of new vaccines is the trait of strain-specific immunity associated withE. maxima. Recent work in this laboratory has shown that infection of two inbred lines of White Leghorn chickens with the W strain ofE. maximaleads to complete protection to challenge with the homologous parasite, but to complete escape of the heterologous H strain, i.e. the W strain induces an exquisitely strain-specific protective immune response with respect to the H strain. This dichotomy of survival in the face of immune-mediated killing has been examined further and, notably, mating between a drug-resistant W strain and a drug-sensitive H strain leads to recombination between the genetic loci responsible for the specificity of protective immunity and resistance to the anticoccidial drug robenidine. Such a finding opens the way forward for genetic mapping of the loci responsible for the induction of protective immunity and integration with the genome sequencing efforts.