Rodents are the most abundant and diversified order of living mammals in the world. Already since the Middle Ages we know that they can contribute to human disease, as black rats were associated with distribution of plague. However, also in modern times rodents form a threat for public health. In this review article a large number of pathogens that are directly or indirectly transmitted by rodents are described. Moreover, a simplified rodent disease model is discussed.

The sublethal effects of high predation risk on both prey behavior and physiology may have long‐term consequences for prey population dynamics. We tested the hypothesis that snowshoe hares during the population decline are chronically stressed because of high predation risk whereas those during the population low are not, and that this has negative effects on both their physiology and demography. Snowshoe hares exhibit 10‐yr population cycles; during declines, virtually every hare that dies is killed by a predator. We assessed the physiological responsiveness of the stress axis and of energy mobilization by subjecting hares during the population decline and low to a hormonal‐challenge protocol. We monitored the population demography through live‐trapping and assessed reproduction through a maternal‐cage technique. During the 1990s' decline in the Yukon, Canada, hares were chronically stressed—as indicated by higher levels of free cortisol, reduced maximum corticosteroid‐binding capacity, reduced testosterone response, reduced index of body condition, reduced leucocyte counts, increased overwinter body‐mass loss, and increased glucose mobilization, relative to hares during the population low. This evidence is consistent with the explanation that predation risk, not high hare density or poor nutritional condition, accounted for the chronic stress and for the marked deterioration of reproduction during the decline. Reproduction and indices of stress physiology did not improve until predation risk declined. These findings may also account for the lag in recovery of hare reproduction after predator densities have declined and thus may implicate the long‐term consequences of predation risk on prey populations beyond the immediate effects of predators on prey behavior and physiology.

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Estimates of body condition in mammals may be constructed from measures of skeletal size and body mass. We illustrate the methodology for doing this using data from two populations of feral house mice (Mus domesticus) in Australia, and point out an erroneous method that has commonly been used in the literature. Indices of condition for individual house mice were not correlated with the fat content of their carcasses. Indices of condition for house mice have a relatively low repeatability because of variation from day to day in body mass and because of variation in length measurements taken by different observers. Bias in measurements among observers must be eliminated to make indices of condition from live animals useful.

House mice (Mus domesticus) in the Victorian mallee region of southeastern Australia show irregular outbreaks. Changes in reproductive output that could potentially drive changes in mouse numbers were assessed from 1982 to 2000. Litter size in females is positively correlated with body size. When standardized to an average size female, litter size changes seasonally from highest in spring to lowest in autumn and winter. Litter size is depressed throughout breeding seasons that begin when the abundance of mice is high, but is similar in breeding seasons over which the abundance of mice increases rapidly or remains low. Breeding begins early and is extended on average by about ¢ve weeks during seasons when mouse abundance increases rapidly. The size at which females begin to reproduce is larger during breeding seasons that begin when mouse abundance is high. An extended breeding season that begins early in spring is necessary for the generation of a house mouse plague, but it is not in itself su¤cient. Reproductive changes in outbreaks of house mice in Australia are similar but not identical to reproductive changes that accompany rodent population increases in the Northern Hemisphere. We conclude that food quality, particularly protein, is a probable mechanism driving these reproductive changes, but experimental evidence for ¢eld populations is con£icting.