Environmental Change

Pollutants, malnutrition, and thermal stress due to climate change are all examples of stressors hypothesized to increase individual susceptibility to infectious diseases. This line of thought suggests that parasites should increase in response to environmental stress. For example, intensities or prevalences of ciliates on fish gills increase with oil pollution, pulp mill effluent, industrial effluent, and thermal effluent. This appears to be due to an increase in host susceptibility because toxic conditions impair mucus production which is a fish's main defense against gill parasites.

An opposing prediction generally emerges from considering the population dynamic context of infection. Outside stressors that depress host population density should reduce the chance of an epidemic, or even the ability of a parasite to persist at all, because factors that reduce host density also reduce contact rates between infected and uninfected individuals. Threats to biodiversity, which are generally mediated through reductions in abundance, should indirectly reduce risk to host-specific parasites. By this same reasoning, direct reduction of host density should reduce disease. Culling of seal populations reduces intestinal nematode parasites by reducing host density below transmission thresholds. Fishing can similarly reduce parasites in fish populations and may be responsible for long-term declines in fish parasites in the ocean. For instance, a species of swim bladder nematode was apparently extirpated from native trout in the Great Lakes after a variety of stressors reduced trout populations to very low levels. Alternatively, some stressors may increase parasitism by increasing host density. In particular, the addition of nutrients to aquatic systems increases primary productivity that indirectly increases some grazers and predators. This is probably why the stress most commonly observed to be associated with increased parasitism in fishes and invertebrates is eutrophication.

Stressors may more negatively influence parasites than their hosts. Toxic chemicals and metals have a relatively consistent negative effect across studies of intestinal helminths. Selenium, for example, is more toxic to tapeworms than to their fish hosts. A pollutant may also kill sensitive free-living stages of the parasite. For example, trace metals in sewage-sludge reduce the survival of free-living cercariae and miracidia, leading to a lower trematode prevalence in intermediate-host snails. It is also possible for parasitic infection to make the host more susceptible to toxins. For instance, cadmium is much more toxic to amphipods infected with larval acanthocephalans than uninfected amphipods. While this latter effect decreases the spread of an epidemic through a population, it also increases the impact of disease on infected individuals.

This heterogeneous array of potential effects of stress on infectious disease makes it unclear how a particular stressor should affect the overall course of an epidemic in a host population, or endemic levels of a disease. Although stressed individuals should be more susceptible to infection if exposed, the stressor could simultaneously reduce opportunities for infection because the contact rate between infected and uninfected individuals will decline with the extent that the stressor reduces host density. In addition, populations of some parasites that are directly susceptible to the stressor may not be able to persist at all. It would also appear, a priori, that stress can either aggravate or diminish the population-level impact of a host-specific infectious disease organism upon its host.

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