vitreous fluid), (3) Similarity to reported and confirmed clinical syndromes, (4) Laboratory testing of tissue or fluid by PCR and/ or histopathology (usually a lymphoplasmacytic, histiocytic or mixed monnuclear/neutrophilic inflammation), and (5) Most importantly ruling out other causes for the clinical signs! Diagnosis of neuroborreliosis should be based upon clinical signs such as ataxia, signs of peripheral neuropathy, cranial neuritis or radiculoneuritis, eg. muscle wasting, hyperesthesia, reluctance to hold the head up, cranial nerve dysfunction and uveitis, in addition to CSF pleocytosis ( 95% of humans with neuroborreliosis have a lymphocytic pleocytosis but in horses neutrophilic pleocytosis may be found); evidence of intrathecal production of antibodies to B. burgdorferi outer surface antigens and occasionally B. burgdorferi PCR positive CSF. The serum/CSF antibody ratio can be used to help determine intrathecal antibody production. This concept is similar to the commonly used EPM test where a serum to CSF antibody concentration (against surface proteins) ratio is both sensitive and specific for the disease. What is different for B. burgdorferi serum/CSF-ratio testing is that: the serum is diluted prior to testing in approximately the “normal ratio” of IgG in serum and CSF. I therefore, do not strongly consider a diagnosis of neuroborreliosis unless the CSF antibody against one or more OSP antigens is at least 2-fold more than serum values. It may be important diagnostically, if one of the Osp antigens has a markedly higher antibody ratio than do the others, as this would be further suggestive of intrathecal production of antibody against that particular antigen. It would be interesting to use the standard C6 snap test on CSF to see if that may be clinically useful. The most frequently used drugs for treatment of Lyme disease in horses are oxytetracycline (6.6 mg/kg q 12 or 8.4 mg/kg Q 24 intravenously) and doxycycline (10 mg/kg q 12 per os) or minocycline (4 mg/kg q12h per os). Minocycline has better oral bioavailability than doxycycline in the horse and it attains higher concentration in CSF and aqueous fluids because it is more lipophilic and less protein bound than doxycycline. Doxycycline and minocycline treatments for Lyme disease in horses may not have the same success as routinely reported in human Lyme treatment because of the relatively low bioavailability of both drugs in horses and the likelihood of more long-standing B. burgdorferi infections in horses than in humans prior to beginning treatment. Proper duration of treatment is unknown in horses but is commonly 1-2 months for doxycycline or minocycline. In experimentally infected ponies, oxytetracycline administered intravenously was superior to doxycycline (per os) in eliminating B. burgdorferi infection. The practical aspects of I.V. administration of Oxytetracycline and potential side effects (thrombophlebitis and renal failure) have prevented this from becoming a standard therapeutic treatment in equine practice. In our pony treatment study, ceftiofur at 2.2 mg/kg/ day I.M. for 28 days was moderately successful in eliminating the B. burgdorferi infection. In human Lyme disease, tetracyclines and beta lactams are the predominant antimicrobials used, and with excellent success. The use of metronidazole as treatment for possible cystic borreliosis currently lacks sufficient clinical information in either humans or domestic animals but could be a treatment option for chronic infections that do not respond to the more tradition treatments. Until more information is www.faep.net
available on actual incidence of clinical disease in the horse, treatment of asymptomatic but seropositive horses would seem highly questionable. Prevention of B. burgdorferi infection in horses has centered around avoiding tall grasses and other areas that ticks commonly reside, the use of preventative tick sprays and canine Lyme vaccines. Canine Lyme vaccines appear to be safe (based upon antidotal reports of hundreds of horses being vaccinated) and those that maintain high OspA antibody would be expected to provide protection against infection. Interestingly, natural infection is not believed to provide a high level of protection against re-infection possibly due to strain variation and the frequent lack of OspA antibody with natural infection. Dose and frequency of vaccination that have been empirically used are similar to what is suggested for dogs. Many horses appear to develop a good initial OspA antibody although the resulting antibody level is frequently of short duration. It is possible that subcutaneous or intradermal administration could better utilize dendritic cells and provide a better immune response and more prolonged protective antibody. Long term adverse but difficult to recognize effects from the vaccine are always possible as was implicated with the previously approved human vaccine. An OspA vaccine for humans was voluntarily withdrawn because of lack of sales; concerns over adverse effects were never proven. It is interesting, to me at least, that after litigations and a congressional hearing over possible adverse effects of the vaccine, one million dollars in legal fees was reportedly paid to the prosecuting lawyers, but no financial compensation was provided to the claimants who had been vaccinated.a Several canine-approved tick repellants are used in horses but dose, application sites and efficacy are unknown. An equine-approved permethrin and piperonyl butoxide product for tick prevention is available but I could not find published clinical studies on its efficacy in horses.
Footnote: a
Nigrovic LE, Thompson KM: The Lyme vaccine: a cautionary tale. Epidemiol Infect 135(1):1-6, 2007.
Additional Reading:
Brorson O, Brorson SH: An in vitro study of the susceptibility of mobile and cystic forms of Borrelia burgdorferi to metronidazole. Acta Pathol Microbiol Immunol Scand 107(6):566-576, 1999. Burgess EC: Borrelia burgdorferi infection in Wisconsin horses and cows. Ann NY Acad Sci 539:235-243, 1988. Chang YF, Novosol V, McDonough SP, Chang CF, Jacobson RH, Divers T, Quimby FW, Shin S, Lein DH.: Experimental infection of ponies with Borrelia burgdorferi by exposure to Ixodid ticks. Vet Pathol 37(1):6876, 2000. Chang Y, Novosol V, McDonough SP, Chang CF, Jacobson RH, Divers T, Quimby FW, Shin S, Lein DH: Vaccination against Lyme disease with recombinant Borrelia burgdorferi outer-surface protein A (rOspA) in horses. Vaccine 18(5-6)540-548, 1999. Chang YF, Ku YW, Chang CF, Chang CD, McDonough SP, Divers T, Pough M, Torres A: Antibiotic treatment of experimentally Borrelia burgdorferi-infected ponies. Vet Microbiol 107(3-4):285-294, 2005. DeVilbiss BA, Mohammed HO, Divers TJ: Perception of equine practitioners regarding the occurrence of selected equine neurologic diseases in the northeast over a 10-year period J Equine Vet Sci 29(4):237-246, 2009. Eugene D, Shapiro, MD: Lyme disease. N Engl J Med 370(18):1724-1731, 2014.
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