Disease ecology

Threshold theorem

For a disease to spread, on average it must be successfully transmitted to a new host before its current host dies or recovers. This observation lies at the core of the most important idea in epidemiology: the threshold theorem. The threshold theorem states that if the density of susceptible hosts is below some critical value, then on average the transmission of a disease will not occur rapidly enough to cause the number of infected individuals to increase. In other words, the reproductive rate of a disease must be greater than 1 for there to be an epidemic, with the reproductive rate being defined as the average number of new infections created per infected individual. Human immunization programs are based on applying the threshold theorem of epidemiology to public health; specifically, if enough individuals in a population can be vaccinated, then the density of susceptible individuals will be sufficiently lowered that epidemics are prevented. See Epidemiology, Vaccination

In general, the rate of reproduction for diseases is proportional to their transmissibility and to the length of time that an individual is infectious. For this reason, extremely deadly diseases that kill their hosts too rapidly may require extremely high densities of hosts before they can spread. All diseases do not behave as simply as hypothesized by the threshold theorem, the most notable exceptions being sexually transmitted diseases. Because organisms actively seek reproduction, the rate at which a sexually transmitted disease is passed among hosts is generally much less dependent on host density.

Population effects

Cycles in many animal populations are thought to be driven by diseases. For example, the fluctuations of larch bud moths in Europe are hypothesized to be driven by a virus that infects and kills the caterpillars of this species. Cycles of red grouse in northern England are also thought to be driven by disease, in this case by parasitic nematodes. It is only when grouse are laden with heavy worm burdens that effects are seen, and those effects take the form of reduced breeding success or higher mortality during the winter. This example highlights a common feature of diseases: their effects may be obvious only when their hosts are assaulted by other stresses as well (such as harsh winters and starvation).

The introduction of novel diseases to wild populations has created massive disruptions of natural ecosystems. For example, the introduction of rinderpest virus into African buffalo and wildebeest populations decimated them in the Serengeti. African wild ungulates have recovered in recent years only because a massive vaccination program eliminated rinderpest from the primary reservoir for the disease, domestic cattle. But the consequences of the rinderpest epidemic among wild ungulates extended well beyond the ungulate populations. For example, human sleeping sickness increased following the rinderpest epidemic because the tsetse flies that transmit sleeping sickness suffered a shortage of game animals (the normal hosts for tsetse flies) and increasingly switched to humans to obtain meals.

It is widely appreciated that crop plants are attacked by a tremendous diversity of diseases, some of which may ruin an entire year's production. Diseases are equally prevalent among wild populations of plants, but their toll seems to be reduced because natural plant populations are so genetically variable that it is unlikely that any given pathogen strain can sweep through and kill all of the plants—there are always some resistant genotypes. But when agronomists have bred plants for uniformity, they have often depleted genetic diversity and created a situation in which a plant pathogen that evolves to attack the crop encounters plants with no resistance (all the plants are the same). For example, when leaf blight devastated the United States corn crop, 70% of that crop shared genetically identical cytoplasm, and the genetic uniformity of the host exacerbated the severity of the epidemic. See Plant pathology

Disease emergence

Humans are dramatically altering habitats and ecosystems. Sometimes these changes can influence disease interactions in surprising ways. Lyme disease in the eastern United States provides a good example of the interplay of human habitat modifications and diseases. Lyme disease involves a spirochete bacterium transmitted to humans by ticks. However, humans are not the normal hosts for this disease; instead, both the ticks and the bacterium are maintained primarily on deer and mouse populations. Human activities influence both deer and mice populations, and in turn tick populations, affecting potential exposure of humans to the disease. Much less certain are the impacts of anticipated global warming on diseases. There is some cause for concern about the expansion of tropical diseases into what are now temperate regions in those cases where temperature sets limits to the activity or distribution of major disease vectors. See Lyme disease, Population ecology