Genetic management of infectious diseases: a heterogeneous epidemio-genetic model illustrated with S. aureus mastitis

Abstract

-Given that individuals are genetically heterogeneous in their degree of resistance to infection, a model is proposed to formulate appropriate choices that will limit the spread of an infectious disease. The model is illustrated with data on S. aureus mastitis and is based on parameters characterizing the spread of the disease (contact rate, probability of infection after contact, and rate of recovery after infection), the demography (replacement and culling rates) and the genetic composition (degree of relationship and heritability of the disease trait) of the animal population. To decrease infection pressure, it is possible to apply non-genetic procedures that increase the culling (e.g., culling of chronically infected cows) and recovery (e.g., antibiotic therapy) rates of infected cows. But the contribution of the paper is to show that genetic management of infectious disease is also theoretically possible as a control measure complementary to non-genetic actions. Indeed, the probability for an uninfected individual to become infected after contact with an infected one is partially related to their degree of kinship: the more closely they are related, the more likely they are to share identical genes like those associated to the non-resistance to infection. Different prospective genetic management procedures are proposed to decrease the contact rate between infected and uninfected relatives and keep the number of secondary cases generated by one infected animal below 1. infectious disease resistance / heterogeneous SIS model / genetic management / mastitis

Genetic control of interactions among individuals: contrasting outcomes of indirect genetic effects arising from neighbour disease infection and competition in a forest tree

“…Interactions between host individuals contribute to disease transmission in many host-pathogen systems (Detilleux, 2005;Lively, 2010;Lipschutz-Powell et al, 2012). Teratosphaeria nubilosa is mainly spread by wind-dispersed ascospores (Park, 1988).…”

“…Thus, in contrast to resource-limited traits, the rapid evolution of host defence traits may be favoured by the positive covariance between direct and indirect genetic effects on disease damage. With IGEs for disease transmission, the relative importance of local to global host dispersal and disease transmission can significantly alter the evolution of host defences (Agrawal et al, 2001;Detilleux, 2005;Debarre et al, 2012). In the presence of IGEs and spatial genetic structure resulting from genetically related neighbours, such evolution can involve traits that not only reduce disease susceptibility of the focal individual (Roy & Kirchner, 2000;Medzhitov et al, 2012) but also reduce transmission to related neighbours (Detilleux, 2005).…”

“…With IGEs for disease transmission, the relative importance of local to global host dispersal and disease transmission can significantly alter the evolution of host defences (Agrawal et al, 2001;Detilleux, 2005;Debarre et al, 2012). In the presence of IGEs and spatial genetic structure resulting from genetically related neighbours, such evolution can involve traits that not only reduce disease susceptibility of the focal individual (Roy & Kirchner, 2000;Medzhitov et al, 2012) but also reduce transmission to related neighbours (Detilleux, 2005). Indeed, it is only in the presence of local spatial structure that kin selection can act, and that traits are expected to evolve which reduce transmission, including the altruistic strategy of suicide upon infection (Hamilton, 1964;Debarre et al, 2012).…”

Can oysters Crassostrea virginica develop resistance to dermo disease in the field: The impediment posed by climate cycles

“…Thus, initial allele frequency for alleles conferring disease resistance, all given the A genotype, approximated 10%. This low allele frequency invokes the assumption that such alleles are rare in naïve populations, possibly due to the likelihood that such alleles are inherently deleterious if the disease is not present (e.g., Cotter et al, 2004;Detilleux, 2005;Zbinden et al, 2008;Hasu et al, 2009;Duffy and Forde, 2009). Guo (unpubl.…”

Genetic factors affecting susceptibility to udder pathogens

“…Such evolutionary models can be used to suggest measures to A c c e p t e d M a n u s c r i p t control mastitis (Dieckmann et al, 2002). Assuming that genetically related cows share genes conferring resistance to mastitis, a genetic-epidemiologic model was proposed to determine the genetic contribution to the spread of S. aureus mastitis among heifers (Detilleux et al, 2005). Using data from Lam et al (1996) and Zadoks and al.…”