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Lyme Borreliosis
Meryl P. Littman, VMD, DACVIM (SAIM)

University of Pennsylvania, School of Veterinary Medicine, Philadelphia, PA, USA

Etiology/Pathophysiology Lyme nephritis in dogs is not due to spirochetal renal
invasion but rather Lyme‐specific antigen–antibody
Lyme borreliosis is caused by gram‐negative spirochetes of complex deposition and immune‐mediated glomerulo­
the Borrelia burgdorferi sensu lato complex, including 21 nephritis, with secondary changes of tubular necrosis/
species and at least 30 strains of B. burgdorferi sensu stricto regeneration and interstitial nephritis. There is no exper­
in North America and Europe, and B. afzelii, garinii, and imental model of Lyme nephritis, but genetic predisposi­
others in Europe. At least 52 Borrelia spp. exist; some 29 tion appears to play a role.
cause relapsing fever or rash in people, mimicking Lyme dis­
ease (e.g., B. andersonii, B. hermsii, B. lonestari, B. miyamo-
toi, B. parkeri, B. recurrentis, B. turicatae). Fever, lameness, Epidemiology
anterior uveitis, splenomegaly, thrombocytopenia, and
spirochetemia were associated with B. turicatae in dogs Ixodes ticks are the main vector of B. burgdorferi. The
in Florida and Texas; B. hermsii was isolated in a febrile main reservoirs are mice, small mammals, and birds. In
spirochetemic pancytopenic dog in Washington. the US, 95% of human cases are seen in the Northeast,
Lyme spirochetes are mainly transmitted via Ixodes tick MidAtlantic, and Midwest states. Bird migration and cli­
bites after two days of host attachment, as outer surface mate changes are extending the habitat of infected ticks
protein A (ospA, the organisms’s attachment to tick to adjacent areas.
midgut) is downregulated and other antigens (e.g., ospC)
become expressed. The organisms live extracellularly, Signalment
associated with fibroblasts and collagen. Disease signs are
due to immune‐mediated reactions, not bacterial toxins or Most affected dogs are middle‐aged, large‐breed dogs
cellular damage by the organisms. Although many exposed with outdoor lifestyles exposing them to field ticks
people develop acute signs of illness (rash, flu‐like signs) questing in leaf litter, hedges, bushes, and tall grasses.
and later possible arthritis, neurologic, and/or cardiac man­ Lyme nephritis can occur in any breed, but Labrador and
ifestations, most exposed dogs and cats seroconvert with­ golden retrievers appear predisposed.
out illness. The experimental model in 6–12‐week‐old
beagle puppies showed no illness until 2–5 months after
infected tick exposure. Carrier status and antigenic varia­ History and Clinical Signs
tion account for recurrent self‐limiting episodes of ano­
rexia, fever, and lameness. Only <5% of seropositive dogs in Lyme Arthritis
the field show Lyme arthritis. In some endemic areas,
70–90% of healthy dogs are seropositive. Canine Lyme The experimental tick exposure model shows that dogs
nephritis is rare (<2% of those exposed), even among sero­ seroconvert and become nonclinical carriers of spiro­
positive retrievers (predisposed breeds). Other manifesta­ chetes for many years, based on positive spirochetal cul­
tions in dogs are not well documented. Lyme arthritis is rare tures and polymerase chain reaction (PCR) tests of skin
in seropositive cats; signs may be due to co‐infection with and subcutis biopsies from tick bite sites. Very young
Anaplasma phagocytophilum. (6–12 weeks old) puppies showed signs of illness 2–5

Clinical Small Animal Internal Medicine Volume II, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical