ROLE OF DISEASES IN WILDLIFE POPULATIONS

Disease agents function by reducing the fitness of their hosts in a variety of ways (Scott 1988). In wildlife management, factors that directly reduce wildlife numbers have been termed decimating factors, and diseases are one of many different decimating factors (Leopold 1933).

Historically, a major focus of wildlife man­agers was on the role of diseases as decimating factors, especially among economically impor­tant wildlife such as ungulates, waterfowl, and upland game. These kinds of diseases often are exemplified by microparasites that undergo multiplication within their hosts. Such diseases commonly produce epizootics where waves of infection pass through populations, alternating with periods in which the pathogen disappears following a loss of susceptible hosts as they die or survive and become immune. Examples include avian cholera in wildfowl (Botzler 1991, Samuel et al. 2007), hemorrhagic diseases of deer and other ungulates (Howerth et al. 2001), or tularemia in rabbits (Morner and Addison 2001). The 1988 epizootic of phocine distemper virus in the North Sea population of harbor seals (Phoca vitulina) is a particularly well-documented example of a decimating disease (Hudson et al. 2003). Here the parasite appeared in a series of harbor seal populations around the coasts of northern Europe, and then disappeared following a lack of new susceptible animals (Hudson et al. 2003).

Disease also can serve as a welfare factor by reducing the reproductive success of suscep­tible animals (Gulland 1995). Among bacteria, Salmonella pullorum reduces the egg-laying capacity of ring-necked pheasants (Phasianus colchicus) by 75% or more, and hatched birds often are stunted and less fit (Biester and Schwarte 1965).

Diseases also can reduce the energy resources available for host immunity and lead to greater susceptibility to other parasites. Such parasites benefit when poor nutrition or other environmental conditions reduce the efficiency of the immune system, making their hosts more vulnerable (Chandra and Newberne 1977, Gershwin et al. 1985). For example, normally quiescent but opportunistic bacteria carried in the intestinal tract (e.g., Salmonella spp.) or respiratory tract (e.g., Pasteurella spp.) can cause overt disease in the presence of a com­promised immune system. Also, some species experiencing diseases are more susceptible to other stresses such as cold or food shortage (Sheppe and Adams 1957), thus contributing to diminished well-being of individuals and populations. There also are interactions with malnourishment, infections, and environ­mental chemicals on growth and reproduction (Porter et al. 1984)

Also, macroparasites commonly occur as enzootic infections, more commonly causing host morbidity than mortality. Sick animals may be less cautious and have slower reflexes than healthy animals (Poulin 1994). Such behavioral changes in animals may lead to greater susceptibility to predation or accidents. Likewise, lead poisoning (plumbism) and botulism intoxication may make waterfowl more susceptible to predation. Neurological diseases, such as canine distemper or rabies, may enhance the likelihood of some terrestrial mammals dying from highway mortality or other accidents.

Sexual selection also may be influenced by parasites and diseases. For example, secondary sexual characteristics of male birds, includ­ing brightness or color and vocalizations, may signal a male's overall well-being and freedom from parasites. Males resistant to parasites within a species may be more attractive to breeding females due to their brighter plum­age, more vigorous songs, or other superior mating behaviors, compared to infected males (Hamilton and Zuk 1982, Loye and Zuk 1991, M0ller 1991, Zuk 1991). Linked to these find­ings is evidence that parasitism may be more common among individual animals affected by developmental asymmetry of secondary sexual characteristics (M0ller 1996, M0ller and Swaddle 1997, Thornhill and M0ller 1997). Conversely, higher parasite levels may contribute to greater asymmetry of secondary characteristics. For example, parasite-infected reindeer (Rangifer tarandus) have less sym­metrical antlers (Folstad et al. 1996), and mite- infected barn swallows (Hirundo rustica) have higher levels of asymmetry in wing length and tail feathers compared to uninfected members of their respective species (M0ller 1992). In turn, such levels of asymmetry could influence females seeking males for mating (M0ller and Swaddle 1997) and thereby affect mating success and fitness.

The cost in fitness from an infectious bacte­rium or virus that kills an animal or weakens it to the point where it is susceptible to predation or starvation is self-evident. The fitness costs from arthropods, intestinal nematodes, and some microparasites often are far more subtle (Hart 1997). For example, a light parasite load that may not noticeably impact a healthy, well-fed adult bird may severely affect it in times of nutritional or socially related stress, or in conjunction with the physiological demands of laying and incu­bating eggs, provisioning nestlings, escaping from a predator, or fighting with conspecifics (Hart 1997). In cases where male offspring grow larger and more quickly than female offspring, parasitism can impede the ability of avian moth­ers to raise males, shifting the sex ratio and affecting population viability; removing their parasites allows the mothers to forage longer and rear more sons (Reed et al. 2008). Also, among polygynous species, pathogens are dispersed by infected females after the resident male dies, and the effects of pathogen-mediated dispersal increases as the harem size (number of females) increases (Nunn et al. 2008).