Equine Lyme Disease

Lyme disease in North America is caused by the bacteria Borrelia burgdorferi sensu stricto.  Borrelia burgdorferi survives in a small rodent and Ixodes spp. tick cycle.  Horses and many other mammals may become infected during tick feeding.  Generally, 24 to 48 hours of attachment are required to transfer B. burgdorferi from the tick to the mammalian host.  Female adult Ixodes spp. ticks are believed to be primarily responsible for transmitting B. burgdorferi to horses, while in humans the smaller and harder to see nymphs are responsible for more infections.  Several strains of B. burgdorferi exist and prior infection may not provide cross-protective immunity against other strains.  Ixodes ticks may simultaneously harbor other pathogens, e.g., Anaplasma phagocytophilia, causing co-infections in many horses.

B. burgdorferi infection in horses is common in several areas of North America.  Horses in the mid-Atlantic and northeastern states have a high seroprevalence for B. burgdorferi, as do horses in areas of Minnesota, Wisconsin, and extending into southern Canada.  Infected horses also are reported in regions of California and sporadically through other areas of North America.  Both human and equine B. burgdorferi infections are expanding geographically.

A wide variety of clinical signs have been attributed to B. burgdorferi infection in horses, but cause and effect have been difficult to document in most cases.  Clinical signs most often attributed to equine Lyme disease include stiffness and lameness (generally in multiple limbs), muscle tenderness, increased sensitivity to touch and sensation (hyperesthesia), lethargy, and behavioral changes.  Muscle wasting, pain upon palpation of the topline and occasionally ataxia may occur.  Infection of the nervous system (neuroborreliosis), uveitis, dermal inflammation mimicking lymphoma, and synovitis are documented; all occur with a characteristic lymphohistiocytic inflammatory response.

Current serologic tests are sensitive and specific for detecting B. burgdorferi antibodies, but these may not distinguish between prior and current infections.  The clinical diagnosis of Lyme disease is difficult and might best be based upon the following parameters: geographic location, known exposure to B. burgdorferi by serologic testing, probability of the clinical signs being due to B. burgdorferi infection based on where the organism can reside (synovial membranes, skin, fascia, meninges, nerves, and sometimes vitreous eye fluid), laboratory testing of tissue or fluid by polymerase chain reaction and/or histopathology, and most importantly ruling out other diseases.  Response to treatment and change in antibody levels are of modest benefit in confirming a diagnosis due to the anti-inflammatory properties of tetracyclines and the prolonged antibody response that can occur even after seemingly appropriate antimicrobial therapy.

Tetracyclines are the most frequently used drugs for treatment of equine Lyme disease.  In an experimental pony infection model, intravenously administered tetracycline was highly effective in eliminating B. burgdorferi while an intramuscularly administered cephalosporin and orally administered doxycycline were somewhat effective.  Because of ease of treatment, doxycycline and minocycline are the two most commonly used drugs for Lyme disease treatment in horses.

Horse owners in high risk areas of Lyme disease, and those who are traveling with horses to these areas should consult their veterinarians about appropriate protective measures.

Article courtesy of Equine Disease Quarterly


Dr. Thomas Divers (607) 253-3226 tjd8@cornell.edu

Dr. Linda Mittel (607) 253-3633 ldm65@cornell.edu

Cornell University College of Veterinary Medicine, Ithaca, New York

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