markedly lower bioavailability of orally-administered doxycycline and minocycline in the horse, compared to humans. 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! Because of both the high prevalence of antibodies against B. burgdorferi in horses in some regions of the U.S. and the difficulty in proving clinical disease in most cases, Lyme disease has become the most controversial and possibly over-diagnosed equine disease in those areas. The clinical signs most often attributed to equine Lyme disease include stiffness and lameness generally in multiple limbs, muscle tenderness, hyperesthesia, lethargy, behavioral changes and signs suggestive of neurologic disease. Unlike with human Lyme disease, joint effusion has been minimal in most Lymesuspect horses. Muscle wasting and pain upon palpation of the topline have been present in a few horses with high serum titers and some of these horses have also had ataxia and paresis. In one report, two horses diagnosed with Lyme neuroborreliosis had chronic, necrosuppurative-to-nonsuppurative, perivascularto-diffuse meningoradiculoneuritis on necropsy examination. Hyperesthesia, lumbar pain and muscle wasting were the initial clinical findings followed by ataxia of all four limbs, facial nerve paralysis, and finally head tremors with depression in one horse. On necropsy, spirochetes were identified by Steiner silver impregnation in both cases, predominantly in the affected dura mater of brain and spinal cord. Borrelia burgdorferi was identified by polymerase chain reaction, with the highest spirochetal burdens in tissues with inflammation, including the spinal cord, muscle, and joint capsules. In another report, a horse with severe neck stiffness that progressed to ataxia had lymphohistiocytic meningitis and B. burgdorferi DNA in the cerebrospinal fluid (CSF). That horse originally responded to doxycycline treatment but relapsed after discontinuing the treatment. Another case was a Thoroughbred hunter that presented for lameness and ataxia and had lymphocytic pleocytosis and was PCR positive for B. burgdorferi on CSF analysis. The horse initially responded well to doxycycline but had some deterioration when treatment was discontinued. The author has examined three other suspect neuroborreliosis horses with ataxia and severe lymphocytic
or mixed cellular infiltration and thickening of the meninges. Based upon these few cases, it may be that ataxia and lumbar muscle wasting caused by lymphohistiocytic or neutrophilic meningitis and radiculoneuritis, with occasional fasciculations, cranial nerve dysfunction and neck stiffness, are common characteristics of neuroborreliosis in the horse. CSF would likely show a lymphocytic or mixed neutrophilic/lymphocytic or lymphocytic pleocytosis and, although uncommon in humans with neuroborreliosis, some horses have CSF that is PCR positive for B. burgdorferi. Bilateral uveitis has been reported in 2 horses associated with Borrelia burgdorferi infection of the eye. Borrelia burgdorferi was found on cytologic examination and confirmed by PCR in the vitreous in both horses. No organisms were observed in the aqueous although one aqueous sample was PCR positive. Borrelia burgdorferi was also observed with silver stain in the inflamed uveal tissue. In addition to the uveitis, a chronic, multifocal, lymphohistiocytic ganglioradiculitis and neuritis with presumptive neuronal degeneration in the spinal nerves was found in one of the horses with uveitis. Another report describes a horse with Lyme pseudolymphoma (multiple lymphohistiocytic cutaneous nodules). There was a complete resolution of signs following doxycycline treatment, as might be expected for a cutaneous form of borreliosis. The diagnosis of B. burgdorferi infection (but not clinical disease) can usually be determined by serology. Enzyme-linked immunosorbent assay (ELISA) and Western Blot testing are used as a two-step method for detection of antibodies in humans. The C6 SNAP test (IDEXX Laboratories, Westbrook, Maine), which is based on antibody to a peptide that reproduces the sequence of the invariable region 6 (an immunodominant, conserved region), has good correlation of results with whole cell or OspF ELISA results in horses; specificity of the C6 snap test may be better than sensitivity. Borrelia burgdorferi vaccination alone should not cause the C6 SNAP test to be positive. For canine Lyme testing, a quantitative C6 is available which is somewhat helpful in determining response to treatments in dogs but the quantitative test is specific for canine samples. A multiplex quantitative antibody bead test for OspA, OspC and OspF antibody detection is available for the serodiagnosis of equine B. burgdorferi infection. The interpretation concept is that high levels of OspA usually suggest vaccination, elevated OspC indicates recent infection (antibody against this antigen typically increases within a couple of weeks after infection and then becomes negative 3-5 months after the initial infection), and OspF elevations suggest either chronic infection or more long-lasting antibodies from a prior infection. Since the introduction of the multiplex assay, an increased number of unvaccinated horses have been found to be OspA antibody positive; importance of this is unknown, but a few horses with a rather solid diagnosis of Lyme disease have been seropositive for OspA and negative for OspC and OspF. Clinical diagnosis of Lyme disease is very difficult and should be based upon the following parameters: (1) Exposure to and infection with B. burgdorferi (i.e., geographic location and positive serologic testing which is present in most but not all cases), (2) Reasonable probability of the clinical signs being due to B. burgdorferi infection based upon knowledge of the most common anatomical locations for the organism to reside in the horse (synovial membranes, skin, meninges, nerves, and sometimes
Neuroborreliosis in a 10 TB Horse
22 The Practitioner
Issue 2 • 2015