Diagnosis & Management of Dogs With Lyme Borreliosis

In North America, Lyme borreliosis is caused by the spirochete Borrelia burgdorferi sensu stricto. In the United States, >95% of cases in dogs and humans occur in the upper Midwest and Northeast regions.¹

In the upper Midwest, northeastern United States, and southeastern Canada, B burgdorferi is transmitted by Ixodes scapularis (black-legged tick). In the western United States, Lyme borreliosis is predominantly transmitted by Ixodes pacificus (western black-legged tick). The geographic range of I scapularis has expanded as a result of changing climate, conservation of white-tailed deer populations, and reforestation efforts.² The range of I pacificus has remained stable.³

Ask the Expert: How should dogs be tested and managed for Lyme borreliosis?

Diagnosis

Understanding the diagnostic approach to Lyme borreliosis in dogs requires knowledge of disease pathogenesis, clinical signs, and the timeline of antibody production. Following inoculation by a tick, the spirochete replicates and migrates through connective tissues.⁴ Transmission requires at least 24 hours of tick attachment.⁵

In humans, a characteristic bullseye rash (ie, erythema migrans) occurs acutely at the site of the tick bite, visualization of which can be helpful for diagnosis. In contrast, the first clinical sign of infection in dogs is usually lameness due to neutrophilic arthritis (with or without fever and thrombocytopenia), which complicates diagnosis because of its nonspecificity and typical onset several weeks after infection.⁶ In some dogs, persistent infection may be associated with protein-losing nephropathy (PLN) due to glomerulonephritis (ie, Lyme nephritis)⁵; however, >95% of infected dogs have no clinical signs of illness.⁶

Few detectable organisms are present in blood and tissue; diagnosis thus often relies on serum antibody detection in conjunction with clinical signs. Because signs are nonspecific, Lyme borreliosis should only be suspected in dogs with antibodies to B burgdorferi and either neutrophilic polyarthritis or evidence of PLN and when other specific etiologies have been ruled out.

In dogs with PLN, concurrent evidence of other clinicopathologic findings associated with seroreactivity may provide additional support for diagnosis of Lyme nephritis (see Suggested Case Definition for Lyme Borreliosis in Dogs in North America).⁷ Kidney biopsy with histopathology and, ideally, electron microscopy are needed for definitive diagnosis of glomerulonephritis.

In dogs, a seronegative result can rule out Lyme borreliosis because disease develops after an incubation period of at least 4 weeks, which is ample time for seroconversion.

For sick dogs, quantitative serology can be used to verify a positive qualitative antibody test result in regions where prevalence of infection is low (ie, to improve positive predictive value, as there is no clear correlation between titer magnitude and disease). Because dogs with Lyme disease have chronic infections, quantitative acute and convalescent serologic testing is not helpful for diagnosis.⁵

Treatment

Treatment of Lyme disease typically consists of doxycycline (5 mg/kg PO every 12 hours) for 4 weeks⁵; however, shorter durations (eg, 2 weeks) may be sufficient to resolve clinical signs. Resolution of signs should be the goal of treatment, as antibody titers can persist for months after disease resolution and subclinical reinfections can boost titers.⁵ There is no evidence that continuing treatment beyond resolution of clinical signs improves outcome; continued treatment of healthy dogs risks adverse effects of antimicrobials, adds expense and pet owner inconvenience, and contributes to selection of resistant nontarget bacteria (eg, enteric bacteria). Increased resistance to tetracyclines in clinical isolates of Escherichia coli was documented in the northeastern United States between 2004 and 2011.⁸ For these reasons, the author does not treat seropositive dogs that do not have signs consistent with Lyme borreliosis or simply have an incidental history of tick exposure. Prophylaxis with a single dose of doxycycline after a known Ixodes spp tick bite is widely used to prevent Lyme disease in humans but is considered controversial.^9,10 Evidence for doxycycline prophylaxis in dogs is lacking.

Amoxicillin (20 mg/kg PO every 8 hours) can be used in sick dogs that do not tolerate doxycycline (because of GI signs or hepatopathy).¹¹ Third-generation cephalosporins (eg, cefpodoxime, cefovecin) also have activity against B burgdorferi but are not recommended because they are designated as Critically Important, Highest Priority antimicrobials in human medicine.¹¹ An alternative diagnosis (eg, primary immune-mediated polyarthritis) should be pursued if lameness does not resolve within 72 hours of antimicrobial therapy.

For dogs with suspected Lyme nephritis, treatment should consist of doxycycline (5 mg/kg PO every 12 hours for 4 weeks) in conjunction with immunosuppressive therapy; doxycycline alone is typically ineffective.⁵ Mycophenolate mofetil has been recommended, possibly accompanied by a tapering dose of prednisone in dogs with rapidly progressive disease.^5,12

Depending on patient condition, other treatments for glomerulonephritis (eg, angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, antithrombotics, antihypertensives) may also be indicated.¹³

Prevention

Prevention strategies should aim to prevent Lyme nephritis, which does not typically respond simply to antimicrobial therapy and has a guarded prognosis, with death or euthanasia after 1 to 3 months due to irreversible kidney failure. Removal of ticks within 24 hours of attachment also prevents transmission, although ticks (especially nymphs) can be hard to find on dogs.

For dogs that live in or travel to endemic regions, prevention could consist of year-round tick chemoprophylaxis along with annual vaccines that stimulate an immune response to B burgdorferi outer surface protein A (OspA).¹⁴ OspA is the most critical antigen in all current vaccines because it is expressed throughout the transmission process.¹⁵ Products that kill ticks within 24 hours of attachment (eg, isoxazolines) can prevent transmission. Antibodies generated in response to vaccination are ingested by ticks when they feed; the antibodies neutralize the spirochete in the tick midgut and prevent host infection. Based on evidence that has shown reinfections in humans with recurrent erythema migrans, vaccination of dogs positive for B burgdorferi antibodies may prevent reinfection with new strains,¹⁶ although such studies are lacking in dogs.

Detection of antibodies to B burgdorferi during an annual wellness screening should prompt pet owner education regarding the need for prevention and potential for exposure of humans to B burgdorferi and other Ixodes spp–borne pathogens.

Conclusion

The spatial distribution of Lyme disease and its vector, I scapularis, is expanding in the upper Midwest, northeastern United States, and southeastern Canada. Diagnosis should be based on a combination of positive serologic test results, evidence of neutrophilic polyarthritis and/or PLN, attempts to rule out other secondary causes of these conditions, and (for dogs with polyarthritis) response to doxycycline therapy within 72 hours.

Prevention consists of parasiticides, with or without vaccines, that stimulate an immune response to OspA based on risk assessment.