Pigeon Fever in Horses: A Re-emerging Disease

High environmental temperatures and drought conditions typically precede pigeon fever outbreaks.
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Infection in horses caused by the Gram-positive bacterium Corynebacterium pseudotuberculosis can assume many forms. Deep intramuscular abscesses in horses caused by C. pseudotuberculosis were first reported in San Mateo County, Calif., in 1915. Since that time, the disease commonly referred to as "pigeon fever" was considered one of the most frequent infectious diseases in the western United States.

Infections tend to occur as sporadic cases on a farm or as outbreaks involving hundreds of horses in a region. Disease incidence is increasing, possibly in association with climate change. Unprecedented epidemics in the past decade have affected tens of thousands of horses in Colorado, Idaho, Kentucky, Louisiana, Missouri, New Mexico, Oregon, Texas, Utah, Washington, Wyoming, and British Columbia, Canada–regions historically low in prevalence. High environmental temperatures and drought conditions preceded all reported outbreaks of this soil-dwelling organism.

The most common clinical form of the disease is characterized by external abscesses in the pectoral or ventral abdomen, hence the term "pigeon fever" due to the swelling of the horse’s pectoral region resembling a pigeon’s breast. Two other clinical forms of the disease include internal organ involvement such as liver, lung, kidney, or spleen abscesses, and infection of the limbs, termed "ulcerative lymphangitis," which appears as a severe cellulitis with multiple draining ulcerative lesions.

The portal of entry for the bacteria is through abrasions or wounds in the skin or mucous membranes. Insects such as Haematobia irritans (horn flies), Musca domestica (house flies), and Stomoxys calcitrans (stable flies) can act as mechanical vectors of this disease. The regional location of abscesses suggests that ventral midline dermatitis is a predisposing cause of infection. Due to the variable incubation period, which is typically three to four weeks or longer, ventral midline dermatitis might not be present at the time of maturation of the abscesses

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