Interactive influence of infectious disease and genetic diversity in natural populations

Abstract

The importance of infectious disease in the survival and adaptation of animal populations is rapidly becoming apparent. Throughout evolution, animal species have been continually afflicted with devastating disease outbreaks which have influenced the demographic and genetic status of the populations. Some general population consequences of such epidemics include selection for disease resistance, the occasional alteration of host gene frequencies by a genetic 'founder effect' after an outbreak, and genetic adaptation of parasites to abrogate host defense mechanisms. A wide variety of host cellular genes which are polymorphic within species and which confer a regulatory effect on the outcome of infectious diseases has recently been discovered. The critical importance of maintaining genetic diversity with respect to disease defense genes in natural populations is indicated by certain populations which have reduced genetic variability and apparent increased vulnerability to infectious disease.

Population genetics of the olive‐winged bulbul (Pycnonotus plumosus) in a tropical urban‐fragmented landscape

“…These effects have been found to affect even avian species with high dispersal propensities (Segelbacher and Storch 2002; Caizergues et al. 2003), thereby highlighting the importance of population genetic research and of maintaining genetic diversity and connectivity between fragmented populations (O'Brien and Evermann 1988). …”

Extrinsic Factors Significantly Affect Patterns of Disease in Free-Ranging and Captive Cheetah (Acinonyx Jubatus) Populations

“…Although most terrestrial carnivores lack the diversity of other mammals, cheetahs (Acinonyx jubatus) are unique in the extent to which they have lost polymorphism , and this homogeneity has been suspected as the cause of poor health and reproductive failure in captivity (O'Brien et al, 1985;O'Brien and Evermann, 1988;Marker-Kraus, 1997). High neonatal mortality rates in cheetahs have been cited as further evidence of genetic impoverishment (O'Brien et al, 1985).…”

“…The occurrence of catastrophic feline infectious peritonitis (FIP) epidemics in captive cheetahs was cited as support for this hypothesis (Evermann et al, 1983). The propensity for cheetahs to maintain persistent viral infections and develop atypical immune responses to common pathogens (Evermann et al, 1988;Junge et al, 1991;Eaton et al, 1993;Steinel et al, 2000;Munson et al, 2003) may also have a genetic basis, although modulation of the immune response by chronic stress has also been proposed .…”

“…The occurrence of catastrophic feline infectious peritonitis (FIP) epidemics in captive cheetahs was cited as support for this hypothesis (Evermann et al, 1983). The propensity for cheetahs to maintain persistent viral infections and develop atypical immune responses to common pathogens (Evermann et al, 1988;Junge et al, 1991;Eaton et al, 1993;Steinel et al, 2000;Munson et al, 2003) may also have a genetic basis, although modulation of the immune response by chronic stress has also been proposed . In light of these suspected inherent vulnerabilities to viral agents, we were surprised to find that morbidity and mortality in North American (NA) cheetahs were principally due to chronic degenerative diseases, such as veno-occlusive disease, glomerulosclerosis, and amyloidosis, rather than infectious disease (Munson, 1993;Papendick et al, 1997;Bolton and Munson, 1999).…”

Condition, innate immunity and disease mortality of inbred crows

“…within the first 34 months of life) would have been in poor condition as nestlings relative to birds with other fates; and (iii) these condition indices would predict the probability of disease mortality. Furthermore, based on both theoretical expectations (Obrien & Evermann 1988;Coltman et al 1999) and empirical observations in other taxa (Reid et al 2007), we hypothesized that inbreeding would depress immune response, predicting that inbred individuals would have lower innate immunity scores than relatively outbred individuals. We ran two assays to characterize individual innate immune response: (i) a bacterial killing assay, which is a general assay of constitutive innate immunity that reflects the ability of the whole blood to stop a potential pathogen (Millet et al 2007), and (ii) an assay for natural antibody (NAb)-mediated complement activation (Matson et al 2005).…”