Monkeypox, hantavirus pulmonary syndrome (HPS), Lassa fever, Argentine and Bolivian hemorrhagic fevers, Lyme disease, granulocytic ehrlichiosis, leishmaniasis, Bubonic plague, scrub typhus, tick-borne encephalitis, Crimean-Congo hemorrhagic fever - for these diseases and many more, we are the unwitting victims of pathogens that cycle, often cryptically, within rodent populations.
It seems likely that disease transmission will be reduced when rodent populations occur both at chronically low densities and away from human habitation. Conversely, disease risk will increase with increasing rodent density, magnitude of fluctuations, and tendency to invade human dwellings.
In a literature review combined with new theory, we (Ostfeld and Holt 2004) recently found that rodent predators have a strong potential to protect human health. Generalist or highly mobile predators seem likely to be most effective at regulating rodent numbers at low levels, whereas specialist predators of limited mobility appear responsible for dramatically fluctuating rodent populations. Medium-sized mammalian predators and raptors illustrate the type of predators most likely to play a strong role in regulating rodents.
Habitat destruction and degradation generally affect predatory vertebrates more strongly than more herbivorous ones. As a consequence of predator loss, which we term "missing weapons of mouse destruction," we expect many rodent populations, and the pathogens they transmit, to perform well in fragmented landscapes. Although some studies support his expectation, further research is needed. Research frontiers include: correlations between rodent population density and human disease incidence (as opposed to behavior or age structure effects); the roles of different predators in determining both population dynamics and rodent density per se; and the effects of human-caused environmental change on predators and their rodent prey.