Pneumonia Caused by Rhodococcus equi Infection in Foals

CHAPTER 31 Pneumonia Caused by Rhodococcus equi Infection in Foals



Nathan M. Slovis


Pneumonia caused by Rhodococcus equi infection in foals is a well-known, worldwide problem. Other less common clinical manifestations of R. equi infection 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 organism is another important route of exposure and immunization but might not lead to hematogenously derived pneumonia unless the foal has multiple exposures to a 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, although clinical signs do not develop until foals are 30 to 60 days of age or older (see Chapter 29, Epidemiology of Rhodococcus equi Pneumonia in Foals).


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Figure 31-1 Grade 0: No evidence of pulmonary disease. Note the vertical hyperechoic lines that are reverberation artifacts in the ventral tip of the lung.


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Figure 31-2 Grade 1 pulmonary abscess measuring 7.4 mm in diameter.


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Figure 31-3 Grade 3 pulmonary abscess measuring 2.1 cm in diameter.


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Figure 31-4 Grade 4 pulmonary abscess measuring 3.3 cm in diameter. Notice the hypoechoic center in the lesion.



PATHOGENESIS


R. equi is a facultative intracellular pathogen with infectivity limited to cells of the monocyte-macrophage lineage. The virulence mechanisms of R. equi are associated with the virulence plasmid. These 80- to 90-kb plasmids, which encode a family of seven closely related virulence-associated proteins, designated VapA and VapC to VapH, are responsible for the bacterium’s ability to persist in and eventually destroy alveolar macrophages. Plasmid-cured derivatives of virulent R. equi strains lose the ability to replicate and survive in macrophages and fail to induce pneumonia in foals, confirming the importance of these plasmids for 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 had multiple affected foals, whereas 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 are a potential source of R. equi exposure for the environment and possibly a direct source of infection for foals. A study of 171 mares in central Kentucky investigated 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 one sampling period for every mare examined, and more than 33% had positive results of fecal culture 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 with dams of unaffected foals. It was concluded that dams of affected foals do not shed more R. equi in feces than dams of unaffected foals and that heavier fecal shedding in given 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 one sampling period indicates that mares are likely an important source of R. equi for the surrounding environment.


What host factors determine the outcome of exposure is not known, but it is clear that cell-mediated immunity plays a critical role in resistance to R. equi infection. Clearance of virulent strains of R. equi from the lungs of adult horses is associated with production of interferon-gamma (IFN-γ) by CD4+ and CD8+ T cells. In a study of experimental R. equi infection in foals, CD4+ T cells collected from foals infected with the virulent strain failed to produce IFN-γ mRNA and instead produced significantly more interleukin (IL)-4 mRNA, indicating a Th2-type immune response. Recent data indicate that the low numbers of peripheral CD4+ T cells in foals may contribute to their increased susceptibility to infection, although the precise contribution of these cells to resistance was not determined.



CLINICAL MANIFESTATIONS


The most common manifestation of R. equi infection in foals is a suppurative bronchopneumonia with extensive abscess formation 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 include only a slight increase in respiratory rate and mild fever. These signs are often missed, allowing the disease to progress. This results in the signs of respiratory distress appearing to be acute in onset. A small percentage of affected foals may simply be found dead. More commonly, foals are noticed to be in a state of acute respiratory distress and have high fevers (105 to 106° F [40 to 41° C]), even when there were no previous signs or history of respiratory tract disease. Approximately 50% of foals with R. equi

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May 28, 2016 | Posted by in EQUINE MEDICINE | Comments Off on Pneumonia Caused by Rhodococcus equi Infection in Foals

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