Although natural selection has been genetically improving disease resistance in pigs for millennia, pathological organisms are also evolving to survive in an ever changing environment and host organism. Humans confound the situation by constantly changing the environment and managerial practices used to raise pigs. Alterations in animal density, vaccinations, and antibiotics have significantly modified this ecosystem and have made the relationship between hosts' genetics and susceptibility to acquired diseases extremely complex.
A few general theories from quantitative genetics form the basis of these genetic mechanisms (Falconer 1981). First, an animal's phenotype is the result of its genotype and the environment in which it developed. Animal breeders usually partition phenotypic variation into its causal components and describe it with the following equation:
phenotypic variation (P) = genetic variation (G) + environmental variation (E) + interaction between G and E
Second, genetic variation is partitioned into the components of additive variation, dominance variation, and epistatic variation. An important concept to remember is that selection, whether natural or imposed by humans, utilizes only additive genetic variation. Heritability is the proportion of phenotypic variation that is due to additive genetic variation and is defined as
heritability (h2) = additive genetic variation/ phenotypic variation
An analogous definition of heritability, and the one most used by producers, is the response to selection relative to the superiority of the selected parents. If a population of pigs has an average tenth-rib fat measurement of 2.5 cm (h = 0.40) and the average of the selected parents is 2.0 cm, then we would expect the progeny to have an average tenth-rib fat measurement of 2.3 cm; that is, 0.40(2.0 - 2.5) + 2.5 = 2.3. Even though the selection differential of the parents was 0.5 cm, only 40% of that difference is expected to be passed on, because the heritability of the trait is 0.40. Heritabilities less than 0.20 are considered low, those between 0.20 and 0.40 moderate, and those above 0.40 high.
A trait with low heritability should not be assumed to be unaffected by genetics. In fact, any trait that differs between breeds or responds to heterosis has a significant genetic component. Heterosis is the difference in performance of crossbred animals from the average performance of purebred animals and is attributed to genes with dominant and epistatic action. Traits most affected by heterosis are those pertaining to fitness (longevity, reproduction rate, etc.). It is quite common to observe that F1 females will have litters approximately 10% larger than the average litter size of the two breeds used to produce the crossbred gilt. This larger litter size is because of the heterosis (or hybrid vigor) present in crossbred animals.
Producers would like to be able to breed pigs resistant or resilient to invasion of all pathogens (general disease resistance). However, the etiologies of diseases can be quite different and the host has different mechanisms which it uses to prevent pathogens from causing disease. The two basic lines of a pig's defense are antibody-mediated and cell-mediated immunity. The defense mechanism utilized depends on the pathogen. It also appears that these mechanisms are controlled by different genes located throughout the genome. The situation is further complicated by clear evidence that resistance to certain pathogens can be largely controlled by nonimmunological factors. Identification of the genetic mechanisms that affect susceptibility should be easier for diseases with simple etiologies than for diseases with complex etiologies. When resistance/susceptibility is clearly defined and controlled by a single gene, scientists can use the recently developed swine genetic map (Rohrer et al. 1996) to identify the chromosomal region of the genome which possesses the gene. Genetic improvement of disease resistance in pigs requires identifying heritable phenotypes (measurements) of resistance which are well defined, accurately measured, and highly correlated with incidence of disease (marker traits). If we focus selection on resistance to a single pathogen, we may produce animals that are only resistant to a specific disease. Selection of animals less susceptible to many pathogens requires measurements of marker traits for antibody-mediated immunity (AMI) and for cell-mediated immunity (CMI) and that the phenotypes be incorporated into a selection index (general disease resistance).