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HOW-TO SESSION: LIFE STAGE MANAGEMENT


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 mul- tiple exposures to very large number of bacteria. Epidemiologic evidence suggests that foals that de- velop R. equi pneumonia are most commonly in- fected during the first few days of life, but clinical signs do not develop until foals are 30–60 days of age or older.4


Pathogenesis


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 desig- nated VapA and VapC to VapH, are responsible for the ability of R. equi to persist in, and eventually destroy alveolar macrophages. Plasmid-cured de- rivatives of virulent R. equi strains lose their ability to replicate and survive in macrophages and fail to induce pneumonia in foals, confirming the impor- tance of these plasmids for the virulence of R. equi.5 Foal pneumonia caused by R. equi is endemic on


some farms, intermittent on others, and absent on most farms. Anecdotally, some mares have report- edly had multiple affected foals, whereas foals of other mares from the same environment are consis- tently unaffected. The source of infection for foals remains unknown. Results of a previous study sug- gest that the feces of mares is a potential source of R. equi for the environment and possibly a direct source of infection for foals.6 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.6 Shedding of virulent R. equi was observed in at least one sampling period for every mare examined, and 33% were culture positive during all sampling pe- riods. However, significant differences were not observed in either the fecal concentrations of total or virulent R. equi from dams of affected foals com- pared with dams of unaffected foals. The study concluded that dams of affected foals do not shed more R. equi in feces than do dams of unaffected foals, suggesting that heavier shedding by particu- lar 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 sam- pling period suggests that mares are likely an im- portant source of R. equi for their surrounding environment. The association between the exposure to airborne virulent R. equi and the incidence of R. equi pneu- monia among individual foals was recently as- sessed.4 In that study it was noted that airborne concentrations of virulent R. equi were significantly higher in stalls than in paddocks and virulent R.


438 2016  Vol. 62  AAEP PROCEEDINGS


equi were more frequently isolated from air samples obtained from stalls than from paddocks. Among the foals that later developed R. equi pneumonia, it was more likely that virulent airborne R. equi was present in the stalls at approximately 1 week of age than for foals that remained free of this disease. These findings suggest that environments contain- ing airborne virulent R. equi during the first week of life may influence the risk of subsequent disease of the foal.4


Diagnosis


The insidious course of infection makes early diag- nosis difficult. Recognition of foals with R. equi pneumonia prior to the development of clinical signs would likely reduce losses and limit costs associated with long-term treatment of affected foals. Many diagnostic tests including complete blood cell count, fibrinogen level, thoracic ultrasound, radiographs, and serology have all been used to help distinguish R. equi pneumonia from that caused by other patho- gens. However, bacteriologic culture or PCR am- plification combined with cytological examination of a TTW are still the gold standards used to arrive at a definitive diagnosis. Foals with a white blood cell count greater than


14,000 cells/L with no clinical signs of disease and normal lung sounds should be considered for additional diagnostic tests such as thoracic ultra- sonography.7 Ultrasonography may reveal abnor- malities of the peripheral pulmonary parenchyma. If these abnormalities are detected, a TTW and/or antibiotic treatment should be initiated. Farms with endemic R. equi that have suffered significant morbidity and/or mortality rates should be monitor- ing rectal temperatures twice daily, with febrile foals selected for further testing (thoracic ultra- sonography) or treatment. In the author’s experi- ence performing twice-monthly thoracic ultraso- nography (starting at 3–4 wk of age until 3 mo of age) has proven to be very effective for early disease recognition and reduction of mortality attributed to R. equi pneumonia on several endemic farms.3 Diagnostic thoracic ultrasonography has been shown to be an accurate alternative imaging modal- ity for detection of pulmonary pathology attributed to R. equi pneumonia in foals when thoracic radiog- raphy is not available. Pulmonary lesions were as- signed a grade according to the severity (Table 1). The grading scale ranged from 0 (normal) to 10 (the entire lung surface is affected). A grading scale was implemented to aid in the documentation of lesions to determine whether treatment was suc- cessful, and to help with the description of pneumo- nia. The foal’s grade was determined not by the total number of lesions that were visualized but by the highest grade visualized. For example, a foal with multiple one’s of the left hemithorax as well as one grade 3 would be identified as a grade 3 in the left thorax. The rationale for this early screening is the belief that earlier initiation of specific treatment


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