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Lyme Disease

Lyme Disease or (Borreliosis) is a tickborne, bacterial disease of domestic animals and humans. Areas of greatest incidence in the USA include the Atlantic seaboard, upper midwest, and Pacific coast. Borreliosis also is seen in Europe, Asia, Australia, and elsewhere. The importance of borreliosis as a zoonotic disease is increasing; although the incidence of disease in a geographic area is similar in animals and humans, animals, especially dogs, are at significantly higher risk.

Etiology and Transmission:
In the USA, proven tick vectors of Borreliaburgdorferi , the causative agent of borreliosis, are Ixodespacificus on the west coast and Iscapularis elsewhere. The Ixodes tick vectors are 3-host ticks that hatch from eggs as uninfected larvae. Both larvae and nymphs may acquire infections by feeding on infected reservoir hosts and, after molting, can transmit infection to their host. Small mammals, especially rodents, play a major role as reservoir hosts, although experimental findings have shown that dogs can also serve as a reservoir. Risk of transmission is highest during periods when the nymphs (spring) and adults (spring and fall) are actively seeking hosts.

Clinical Findings and Diagnosis:
Numerous clinical syndromes have been seen in domestic animals, including limb and joint disease and neurologic, cardiac, and renal abnormalities. In dogs, lameness, fever, anorexia, lethargy, and lymphadenopathy with or without swollen, painful joints constitute the most common clinical syndrome. Renal, cardiac, and neurologic forms of the disease are characterized by clinical and laboratory abnormalities in the affected systems. Renal borreliosis is the second most common canine syndrome and is generally fatal. It is characterized by uremia, hyperphosphatemia, and severe protein-losing nephropathy, often accompanied by peripheral edema. Conduction abnormality with bradycardia is typical of the rare cardiac form. Facial paralysis and seizure disorders have been reported in the neurologic form.

Diagnosis is based on history, clinical signs, elimination of other diagnoses, laboratory data, epidemiologic considerations, and response to antibiotic therapy. Clinical signs are appropriate for the affected organ system, while autoimmune panels, CBC, blood chemistry, radiographs, and other laboratory data are generally normal, except for results pertaining directly to the affected system (eg, uremia in renal disease, heart block on ECG in cardiac disease, and soft-tissue swelling in limb and joint disease).

Serologic testing for antibodies to Bburgdorferi is an adjunct to clinical diagnosis. Presence of antibodies detected by ELISA, immunofluorescent antibody (IFA), or protein immunoelectrophoresis (Western blot) assays indicates exposure. However, long incubation periods, persistence of antibodies for months to years, and the disassociation of the antibody response from the clinical stage of disease make diagnosis by blood testing alone impossible. Recent studies of Western blot data indicate that the immune response to tickborne spirochetes is notably deficient in production of antibodies against the outer surface proteins A and B (Osp A and Osp B) of Bburgdorferi . This is significant because antibodies directed against these, as well as other Borrelia proteins, are protective against infection and disease in several animal models. High ELISA and IFA titers in borreliosis may be attributed to rapid sequestration of spirochetes in fibroblasts and endothelial cells and to production of antigen by these spirochetes. Persistence of antibodies after therapy and similarity of Western blot profiles in all stages of disease and convalescence further demonstrate the limitations of serology in diagnosis. More recently, a membrane ELISA bench test has been introduced. It measures antibody to the C-6 Bburgdorferi protein. The test is convenient and eliminates antibody responses to Lyme vaccines. However, 10% false-positive reactions were recently reported in field samples.

Isolation or detection by PCR of Bburgdorferi from joints, periarticular tissue, blood, or other sources may also be helpful in diagnosis. Interpretation of culture results must include consideration of incubation period, the possibility of asymptomatic infection, and the technical difficulty of culturing these organisms.

Treatment and Control:
Antibiotic therapy is indicated in all cases. Antimicrobials in the penicillin and tetracycline groups are effective, and rapid response is seen in limb and joint disease in most cases, although incomplete or transient resolution of signs is seen in a significant number of affected animals. Clinical and research data indicate that infection in animals, including humans, may persist in spite of antibiotic therapy. In dogs, standard antibiotic doses and treatment for 2 wk have been evaluated and demonstrated to be as effective as higher doses and longer durations. Symptomatic therapy directed toward the affected organ system and clinicopathologic abnormalities is also important, especially in renal, cardiac, and neurologic disease. In limb and joint disease, the use of NSAID concurrent with antibiotic therapy may lead to confusion over the source of clinical improvement and make diagnosis based on therapeutic response difficult. Corticosteroid treatment causes a clinical relapse in persistently infected dogs.

Tick avoidance plays a role in disease control. While highly effective products (permethrin spray, amitraz collar, and fipronil spot-on) are available for use on dogs, lack of owner compliance in application is often a barrier to effective, longterm tick avoidance. Furthermore, tick control products are evaluated by the EPA (USA) for their efficacy against the vectors (ticks), not for their ability to prevent disease transmission. Killed, whole-cell bacterins for the prevention of borreliosis in dogs have been in use since June 1990. Immunized dogs have strong antibody titers to Osp A and Osp B and produce antibodies that kill Bburgdorferi in vitro. In one field efficacy study, dogs vaccinated with a commercially available bacterin before tick exposure had the highest degree of protection against disease. Analysis of postvaccination Western blots indicated that these dogs lacked the response to antigens typically seen in natural infections. In 1996, a canine vaccine containing only Osp A was introduced in the USA. While it was once believed that Osp A was the first Bburgdorferi protein to which the immune system of the infected dog was exposed, it has been demonstrated that when a tick attaches to a warm-blooded animal, the Bburgdorferi in that tick stop producing Osp A and begin producing a new protein, Osp C. However, antibodies to Osp A block transmission of Bburgdorferi from the midgut of infected, engorging ticks and prevent infection. Development of vaccines that contain multiple Bburgdorferi antigens is being pursued.

Strategically, in endemic areas, young dogs should be vaccinated before natural exposure to ticks to attain the highest percentages of protection. Prevaccination infection, long incubation, and persistence of infection after antibiotic therapy, rather than vaccine failure, may lead to disease in immunized dogs. In newly emerging areas of canine borreliosis, vaccination programs should be started before large numbers of dogs are exposed to infected ticks. Two doses of either type of vaccine are administered SC to dogs ≥ 9 wk old at 3-wk intervals, and annual revaccination is recommended.

Information obtained from Merck Veterinary Manual website: http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/50600.htm&word=lyme

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