The present study reported bartonella infection in deer mice at a high prevalence (>80%). The results are in accordance with reports from other studies (4
). Genetic analysis demonstrated that all bartonella isolates from deer mice were of B. vinsonii
, with six genetic variants identified. Our findings support the fact that there is specificity of Bartonella
spp. for their rodent hosts, at least in North America and some other regions (22
How bartonella infections are maintained at such high prevalences in rodent populations is puzzling. Our longitudinal study provides an explanation for such an observation. In this study, bartonellae were successively detected by mark-recapture techniques in repeatedly captured deer mice, consecutively or intermittently, for more than 1 year. Although deer mice can live up to 5 years in captivity, they survive for only a mean of about a year in the wild due to predation by foxes, coyotes, snakes, and birds of many species. As a consequence of successive infections, most deer mice likely become infected during their lifetimes. Over time, a very high prevalence of infection develops in the population of surviving deer mice. Nonconsecutive infection may suggest that a mouse could clear the infection, perhaps through an immune mechanism. Nevertheless, it looks like the immunity does not last long, as many mice later became infected again, even with bartonellae of the same genotype.
Similar observations were reported earlier. Cotton rats can be infected with a bartonella strain that is different from the bartonella strain with which it had been infected, perhaps due to poor cross-protection against the related organism (25
). This does not explain the findings from the present study. Although Bartonella
variants may replace other variants, all Bartonella
variants that we found in deer mice were of the same species and had very high similarities. In fact, an intermittent bartonella infection in deer mice may not be the case at all. It is possible that many mice have chronic, persistent infections, from which bartonellae were never completely cleared. A plausible explanation is that the deer mice were not free of infection but that their bacteremia levels were too low to be cultured and may be detected only by a more sensitive approach, such as PCR. An alternative explanation is that these bacteria can persist in a “hidden niche” in their latent form and can be reactivated and amplified from sequestration under specific conditions, such as sudden changes in surroundings. The ages of rodents, often assessed by their weights, have been found to be an important factor in assessing infection rates in a population. An inverse correlation of bartonella prevalence and ages of the rodent hosts has been reported in several studies (2
). Acquiring immunity was hypothesized to explain such a correlation (2
). In the present study, we were not able to detect bartonella prevalence differences between age groups, and we did not observe a weight-dependent prevalence pattern. This might explain why deer mice may be found to be infected with bartonellae on different capture occasions, regardless of age. Moreover, the same very high prevalence of bartonellae in very young deer mice may suggest that vertical transmission of bartonellae has occurred. However, it is possible that the mice were quickly infected postpartum due to intimate contact with infected mice and by sharing bartonella-infected arthropods. Deer mice are well known to be involved in the natural cycles of Borrelia burgdorferi
and other borreliae causing Lyme disease, as well as in the transmission of Sin Nombre virus, an etiologic agent of hantavirus pulmonary syndrome. The present study suggests that deer mice are the, or a, primary reservoir of Bartonella vinsonii
, a species that has been associated with human bartonellosis (12
). The work reported here extends our understanding of the epidemiologic significance of deer mice and their public health importance as reservoirs of pathogenic agents.