This article is part of the supplement: Second International Symposium on Candidate Genes for Animal Health. 16-18 August 2002, Montpelier - France
Research
Selection assisted by a BoLA-DR/DQ haplotype against susceptibility to bovine dermatophilosis
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* Corresponding author: Jean-Charles Maillard maillard@cirad.fr
1 Cirad – Département d'Élevage et de Médecine Vétérinaire Tropicale, Animal Health Program, Montpellier, France
2 Cirdes, Unité de Recherches Biologiques, Bobo-Dioulasso, Burkina Faso
3 Fofifa – Département de Recherches Zootechniques et Vétérinaires, Antananarivo, Madagascar
4 Inra – Station d'Amélioration Génétique Animale, Castanet-Tolosan, France
Genetics Selection Evolution 2003, 35(Suppl 1):S193-S200 doi:10.1186/1297-9686-35-S1-S193
Published: 15 June 2003Abstract
Bovine dermatophilosis is a severe skin infection of tropical ruminants inducing a severe loss in productivity and a 15% mortality rate. This disease is caused by the actinomycete bacterium Dermatophilus congolensis associated with the tick Amblyomma variegatum. Currently there are no prospects for a vaccine, and acaricide or antibiotic control is hampered by the development of chemoresistance. Animal breeders have observed that dermatophilosis susceptibility seems to be determined genetically, and we previously identified a BoLA-DRB3-DQB class II haplotype marker for high (R2 = 0.96) susceptibility to the disease. With this marker, we developed a successful eugenic selection procedure for zebu Brahman cattle in Martinique (FWI). Over a period of five years, a marked reduction in disease prevalence, from 0.76 to 0.02 was achieved, and this low level has been maintained over the last two years. The selection procedure, based on a genetic marker system targeting the highly polymorphic BoLA locus, eliminates only those individuals which are at the highest risk of contracting the disease. In the present work, we discuss the properties of this system, including the "heterozygote advantage" and the "frequency dependence" theories, and examine their involvement in the biological mechanisms at the host/pathogen interface. We speculate on the exact role of the MHC molecules in the control of the disease, how the natural selection pressure imposed by the pathogens selectively maintains MHC diversity, and how our results can be practically applied for integrated control of dermatophilosis in developing countries.