Epidemiology of Rhodococcus equi foal pneumonia and control of disease on endemic farms (Proceedings)


Epidemiology of Rhodococcus equi foal pneumonia and control of disease on endemic farms (Proceedings)

Oct 01, 2008

Rhodococcus equi, formerly called Corynebacterium equi, is the etiology of one of the most severe and devastating forms of pneumonia in foals. R.. equi is a Gram-positive, soil-borne, facultative, pleomorphic coccobacillus, and has been recognized as a pulmonary pathogen of foals for over 80 years, causing significant morbidity and mortality in foals, typically between the ages of 3 to 20 weeks of age. Pneumonia caused by R.. equi results in animal distress and economic losses to the equine breeding industry. Prevalence is high on some equine breeding farms. Case fatality rates can be high as well. Diagnosis is challenging, particularly during the early stages of infection. Treatment is generally prolonged, expensive, associated with adverse effects, and not always successful. Breeding farms reputed to have endemic pneumonia attributable to R.. equi are likely to lose clients.

Foals affected with pneumonia caused by R.. equi develop pyogranulomatous lesions in the lungs and mediastinal lymph nodes. Clinical signs include fever, cough, lethargy, tachypnea, and progressive respiratory distress. Although pneumonia is the most common manifestation of infection, R..equi can invade other organs and cause extrapulmonary disorders, such as osteomyelitis, abdominal lymphadenitis, and enterocolitis.(Chaffin 1997) Also, immune-mediated disorders, such as uveitis and polysynovitis, can result from R.equi infections.

Although R.equi can be cultured from the feces of foals and older horses, and may be a normal commensal of the GI tract, it does not cause disease in horses > 6 months of age, unless they are severely immunocompromised. There are only a handful of case reports of adult horses with R.equi infections, and some involved horses with documented immunosuppression. Similarly, in humans, the disease occurs typically in immunocompromised patients (ie, infected with the HIV virus or immunocompromised by chemotherapeutic or other immunosuppressive agents).

Age of foals at time of infection

Clinical signs of R.equi–induced pneumonia do not typically become apparent until foals are 30 to 100 days old; however, there is a growing body of evidence that most affected foals become infected early during the neonatal period. Foals < 2 weeks old are more susceptible to experimental infection with R.equi, compared with the susceptibility of older foals. (Martens, 1989). Epidemiologic data, using Sartwell's model, are consistent with the hypothesis that most foals with naturally developing disease become infected near the time of birth (Horowitz 2001). Researchers recognize controversy over the age when foals become infected, and it has been suggested that although many foals become infected very early in life, it has been proposed that infection is not limited to this time period (Hooper-McGrevy 2001).

The reasons for increased susceptibility of neonatal foals remain unknown. Foals from farms with endemic R.equi infections that subsequently develop pneumonia caused by R.equi have lower CD4+ T-lymphocyte concentrations at 2 and 4 weeks of age than do unaffected foals.(Chaffin 2004). Also, they have lower CD4+:CD8+ T-lymphocyte ratios during the first 2 weeks after birth than do foals that do not subsequently develop R .equi–induced pneumonia (Chaffin 2004). As foals increase in age, the immunophenotypic differences between affected and unaffected foals become smaller in magnitude until they are no longer apparent.

Also, foals are born with an inherent inability to mount a Thelper-1–based cell-mediated immune response and to generate ?-interferon (Breathnatch 2006, Boyd 2003). Newborn foals exhibit a marked inability to express the IFN-gamma gene and produce IFN-gamma protein. This deficiency occurs in both circulating and pulmonary lymphocytes. However, IFN-gamma gene expression and protein production increases steadily throughout the first 6 months of life (Breathnatch 2006).

These mechanisms represent critical components of the host protective immune response against R.equi infections. Analysis of these findings suggests that affected foals probably have relatively ineffective or immature immune responses to R.equi during the early neonatal period and are thereby less prepared to develop an adequate antimicrobial defense against R.equi infections.