Since it was first identified in 1915 in California, pigeon fever has spread throughout the country. Here is more information about pigeon fever from the University of Kentucky College of Agriculture’s Equine Disease Quarterly by Sharon Spier, DVM, PhD, DACVIM, of the University of California, Davis. Earlier this year the American Association of Equine Practitioners (AAEP) released guidelines for better understanding, diagnosis, treatment and control of pigeon fever (see StableManagement.com article here). The full AAEP guidelines can be found on the AAEP website.
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, California, in 1915. Since that time, the disease commonly referred to as “pigeon fever” can be 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 Texas, Louisiana, Colorado, New Mexico, Utah, Wyoming, Kentucky, Missouri, Oregon, Washington, Idaho, and British Columbia, Canada, involving 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, Musca domestica and Stomoxys calcitrans 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 may not be present at the time of maturation of the abscesses.
Antimicrobials are indicated for horses with ulcerative lymphangitis and for horses with internal abscesses. The use of antimicrobials for external abscesses is not necessary in most horses. Antimicrobial therapy may be justified when signs of systemic illness are present, such as fever, depression, and anorexia, and when extensive cellulitis or lameness is present.
Corynebacterium pseudotuberculosis is susceptible in vitro to most commonly used antibiotics in horses. The average duration of antimicrobial therapy for internal infection is four to six weeks and is best determined by repeat abdominal ultrasound and clinicopathologic results. Horses with ulcerative lymphangitis or cellulitis should be treated early with antimicrobials, or residual lameness or limb swelling may occur.
Until a protective bacterin or toxoid is developed for horses, we can only suggest that horse owners practice good sanitation and fly control and avoid unnecessary environmental contamination from diseased horses. Presently there is no evidence that diseased horses within a stable should be quarantined other than by paying strict attention to insect control. The feed-through products containing cyromazine are safer than organophosphate products and may reduce the incidence of disease by controlling vector populations. Fastidious wound care and prevention of ventral midline dermatitis is also important in preventing infection from a contaminated environment.