Integration of epidemiology into the genetic analysis of mastitis in Swedish Holstein

Heritability of mastitis (and diseases in general) tends to be low. One possible cause is that no clear distinction can be made between resistant and nonresistant animals, because healthy animals include animals that have not been exposed to pathogens and resistant animals. To account for this, we quantified the prevalence of clinical mastitis (CM) and subclinical mastitis (SCM) in 2,069 Swedish Holstein herds as a measure of exposure. Herd prevalence averaged 26.5% for SCM and 6.4% for CM; 61% of the first lactations of 177,309 cows were classified as having at least one case of SCM and 10% as having CM. In a reaction norm approach, heritability of (S)CM was quantified as a function of herd prevalence of (S)CM. The best-fitting model was a second-order polynomial of first-lactation cow SCM as a function of herd prevalence SCM, and a first-order (linear) polynomial of first-lactation cow CM as a function of CM herd prevalence. Heritability for SCM ranged from 0.069 to 0.105 and for CM from 0.016 to 0.032. For both, we found no clear effect of herd prevalence on their heritability. Genetic correlations within traits across herd prevalences were all greater than 0.92. Whether relationships among prevalence, exposure, disease, and genetics were as expected is a matter of discussion, but reaction norm analyses may be a valuable tool for epidemiological genetics.