The epidemiology of R. equi remains ill-defined and continues to evolve. Two epidemiologic questions of clinical importance regarding Rhodococcus equi foal pneumonia are "Why are some foals affected while others in the same environment remain unaffected?", and "Why does the
disease occur recurrently at some farms but not at others?". To answer these questions, studies performed at the level of
the foal and farm, respectively, are needed. The evidence from foal-level and farm-level studies will be reviewed in this presentation.
Rhodococcus equi is widespread in the environment of mares and foals. This is reflected by high seroprevalence, and the fact that R. equi can be isolated from feces, soil, air, and feed at horse breeding farms. Consequently, most (if not all) foals are exposed
to virulent organisms, yet only some foals develop disease. These findings imply that some foals are more susceptible to
infection than others, are exposed to higher concentrations of virulent organisms, or both. One study has examined fecal
concentrations of virulent R. equi of dams in relation to subsequent disease in their foals. Although the fecal concentrations of individual mares did not
explain the occurrence of disease in their particular foals, the finding that all mares at a breeding farm were shedding virulent
R. equi in their feces during the periparturient period indicates that mares are a source of virulent R. equi for the environment into which foals are born. A subsequent study has demonstrated that the high prevalence of fecal shedding
of virulent R. equi can be generalized to other breeding farms in central Kentucky. To date, only 1 study has specifically attempted to address
the association between signalment, history, and management factors for foals and R. equi pneumonia. That study identified significant differences in disease incidence between farms and between years, but no foal-level
factors were significantly associated with the disease.
Anecdotally, some mares are described as being more likely to have affected foals. These anecdotes along with aforementioned
evidence that some foals are predisposed to developing disease suggest the possibility of genetic contributions to susceptibility
to R. equi pneumonia. Polymorphisms in microsatellites, and the transferrin, IL1-receptor, and NRAMP1 genes have been associated with susceptibility to R. equi pneumonia, but the strength of these associations have not been compellingly strong. Mice lacking the galectin-3 gene are
more resistant to R. equi infection than mice with that gene. Thus, genetic factors influence host susceptibility to R. equi, but the trait is likely complex and polygenic in nature, and is undoubtedly modulated by environmental factors such as the
density of mares and foals at farms.
Both innate and adaptive immune responses of the host play a critical role in the pathogenesis of R. equi pneumonia. The concentrations of neutrophils (cells that play a key role in innate immune responses) and the ratio of CD4+:CD8+
lymphocytes (reflective of adaptive immunity) were significantly lower at 2 weeks of age among foals that subsequently developed
R. equi pneumonia than among age-matched controls from the same environment that failed to develop the disease.
In summary, few studies have examined foal-level risk factors, and these studies have not yielded strong evidence for
any particular causal factor(s).