Pneumonia in foals, caused by Rhodococcus equi (R. equi) is a well-known worldwide problem. Other less common clinical manifestations of R. equi infections in foals include ulcerative enterocolitis, colonic/mesenteric lymphadenopathy, immune mediated synovitis and uveitis,
osteomyelitis, pyogranulomatous dermatitis, brain abscess, immune mediated anemia and septic arthritis. Inhalation of contaminated
dust particles is thought to be an important route for pneumonic infection of foals. Ingestion of the organisms is a significant
route of exposure and immunization but may not lead to hematogenous pneumonia unless the foal has multiple exposures to very
large number of bacteria. Recent epidemiologic evidence indicates that foals that develop R. equi pneumonia are most commonly infected during the first few days of life, but clinical signs do not develop until foals are
30 to 60 days of age or older.
R. equi is a facultative intracellular pathogen and its infectivity is limited to cells of the monocyte-macrophage lineage. The
virulence mechanisms of R. equi are associated with the virulence plasmid. These 80-90 kb plasmids encoding a family of seven closely related virulence-associated
proteins designated VapA and VapC to Vap H, are responsible for the ability of R. equi to persist in, and eventually destroy alveolar macrophages. Plasmid-cured derivatives of virulent R. equi strains lose their ability to replicate and survive in macrophages and fail to induce pneumonia in foals, confirming the
importance of these plasmids for the virulence of R. equi.
Foal pneumonia caused by R. equi is endemic on some farms, intermittent on others, and absent on most farms. Anecdotally, some mares have reportedly had
multiple affected foals, while foals of other mares from the same environment are consistently unaffected. The source of
infection for foals remains unknown. Results of previous studies indicate that the feces of mares is a potential source of
R. equi for the environment and possibly a direct source of infection for foals. A study looking at 171 mares in central Kentucky
looked at the association between R. equi pneumonia status of the foal and shedding of virulent R. equi by its dam. Shedding of virulent R. equi was observed in at least 1 sampling period for every mare examined, and >33% were culture-positive during all sampling periods.
However, significant differences were not observed in either the fecal concentrations of total or virulent R. equi from dams of affected foals compared to dams of unaffected foals. In conclusion dams of affected foals do not shed more
R. equi in feces than do dams of unaffected foals, indicating that heavier shedding by particular mares does not explain infection
in their foals. However, the finding that virulent R. equi in the feces of all sampled mares during at least 1 sampling period indicates that mares are likely an important source of
R. equi for their surrounding environment.
It remains unknown as to what host factors determine the outcome of exposure, however it is clear that cell-mediated immunity
plays a critical role in resistance to R. equi. The clearance of virulent strains of R. equi from the lungs of adult horses is associated with the production of interferon-gamma (IFN-γ) by CD4+ and CD8+ T cells. In a study of experimental R. equi infection of foals, CD4+ T cells collected from those foals infected with the virulent strain failed to produce IFN-γ mRNA and instead produced significantly
elevated amounts of interleukin (IL)-4 mRNA, indicating a Th2-type immune response. . Recent data indicate that decreased
numbers of peripheral CD4+ T cells in foals may contribute to their increased susceptibility to infection, though the precise contribution of these
cells to resistance was not determined
The most common manifestation of R. equi in foals is a suppurative bronchopneumonia with extensive abscessation and suppurative lymphadenitis. The slow spread of
the lung infection coupled with the remarkable ability of foals to compensate for the progressive loss of functional lung
makes early diagnosis difficult. Early clinical signs may only include a slight increase in respiratory rate and mild fever.
These clinical signs are often missed, allowing the disease to progress. Therefore the respiratory signs are often apparently
acute in onset. A smaller percentage of these foals may be found dead or more commonly present in acute respiratory distress
with high fevers (105-106 F) and no previous history of clinical respiratory disease. Approximately 50% of R. equi pneumonic foals presented to necropsy also had intestinal manifestations characterized by granulomatous or suppurative inflammation
of the Peyer's patches and the mesenteric and/or colonic lymph nodes. Interestingly, the majority of the foals with R. equi pneumonia do not show clinical signs of the intestinal disease. It has been speculated however, that foals with subclinical
intestinal manifestations may not gain body weight as readily as they should have. In the same study, only 4% of the foals
with intestinal R. equi lesions did not have pneumonia. Immune-mediated polysynovitis, particularly the tibiotarsal and stifle joints can be seen
in 30% of cases with R. equi pneumonia.