26 There has been no further evidence to suggest that Borrelia infections are in any way associated with recurrent uveitis in the horse. There is one published report of neurologic dysfunction in a horse attributed to Lyme disease, 22 and in another report, panuveitis was reported in a pony. One suspect horse the author examined had ataxia and severe lymphocytic infiltration of the meninges. Muscle wasting and pain over the thoracolumbar area have been present in a few horses with high serum titers. 21 – 25 Unlike human Lyme disease, joint effusion has been minimal in most Lyme-suspect horses, although it was pronounced in one horse. Clinical signs most often attributed to equine Lyme disease include low-grade fever, stiffness and lameness in more than one limb, muscle tenderness, hyperesthesia, lethargy, and behavioral changes. 9 – 11Ī wide variety of clinical signs have been attributed to Borrelia infection in horses, but cause and effect have been difficult to document. 8 Borrelia burgdoferi may also survive in the host by residing in collagen and connective tissue, having no requirement for iron and by possibly forming resistant cysts within the host. Many other components of the agent may be important for infection or virulence, but these are poorly understood. Other genes permit antigenic variation, ensuring survival in the host. 7 The changes in expression of surface proteins may be triggered by the blood meal. 6 Conversely, other surface proteins (e.g., OspE, OspF) that are in low concentration in the tick gut are upregulated to enhance complement resistance and other methods of immune evasion in the mammalian host. 5 This time may be needed for the organism to downregulate an outer membrane protein (OspA), which may be important to maintain survival in the mammalian host. Generally, 24 to 48 hours of attachment is required to transfer the organism successfully from the tick to the mammalian host. The organism lives in the tick gut and is transferred to animals during blood meals. 14 A lymphocytic plasmacytic reaction may occur within these tissues, and in experimentally infected ponies, this reaction was associated with the highest concentration of the Borrelia organism. After experimental infection of ponies, the organism appears to reside mostly in skin near the tick bite, as well as in connective tissue and muscle and around nerves and blood vessels near synovial membranes. Exact pathogenesis of Borrelia in the horse is not known. Once feeding begins, the organism begins its complicated up-and-down regulation of genes to enhance survival in the host. 5 It is not known if these stages transmit the spirochete to horses. Larvae and especially nymphs are responsible for a high percentage of infections in humans because they are small and often escape visual inspection. Female ticks are likely the competent vector and can be identified by the complete arch over the anus (see Fig. Infection in horses is caused by attachment and prolonged (>24 hours) feeding of infected adult Ixodes spp., ticks.
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