Canine Lyme Disease: Treatment & Prevention

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Many dogs that present for annual preventive testing (eg, for heartworm, Lyme, other tick-borne diseases) are Lyme-positive without apparent signs. Infected dogs are at a 5%5 to 10% risk of developing signs of Lyme disease and are unlikely to survive if they develop renal disease. 

Vaccinating Lyme-positive dogs has been demonstrated to be safe.6 Treating asymptomatic positive dogs has been demonstrated to reduce antibody titers7; however, there is evidence that Lyme infections are persistent even after antibiotic therapy.8

When a patient is diagnosed with Lyme arthritis, antibiotic therapy is initiated with injectable penicillin, followed by 14 days of oral amoxicillin.  For dogs presumed to have Lyme nephritis, discuss with the client further testing (eg, blood chemistry, complete blood count, urinalysis), in-patient care, intensive therapy, and a guarded prognosis.


Vaccination of at-risk dogs before exposure to infected vector ticks is a part of disease prevention. Two types of vaccines with demonstrated safety and efficacy are available: a recombinant vaccine with a single protein from the causative organism, which immunogenicity studies have suggested may provide maximum protection with twice-yearly immunizations, and another vaccine that contains multiple proteins of B burgdorferi, which immunogenicity studies have suggested will maintain effective immunity with annual boosters.9

Preventing Transmission 

Successful transmission of the Lyme agent from a tick to a dog requires a minimum of 24 hours of tick attachment and feeding and is most efficient at 48 to 52 hours post-attachment. 

  • A rapidly acting acaricide will prevent tick feeding by either killing ticks or rendering them moribund before they attach. 
  • Spot-on products and some collars can achieve “clinical repellence,” essentially shielding dogs from ticks by rapid killing and attachment prevention. 
  • New oral products are highly effective at killing ticks but often allow some period of feeding, thus providing an opportunity for transmission of B burgdorferi or other tick-borne organisms. 


References Show
  1. Levy SA,  Barthold SW, Domback DM, et al. Canine Lyme borreliosis. Comp Cont Ed. 1993;15(6):833-846.
  2. Dambach DM, Smith CA, Lewis RM, Van Winkle TJ.  Morphologic, immunohistochemical, and ultrastructural characterization of a distinctive renal lesion in dogs putatively associated with Borrelia burgdorferi infection: 49 cases (1987–1992).Vet Pathol. 1997;34:85-96.
  3. Levy SA, Duray PH. Complete heart block in a dog seropositive for Borrelia burgdorferi. Similarity to human Lyme carditis. J Vet Intern Med. 1988;2(3):138-144.
  4. Azuma Y, Kawamura K, Isogai H, Isogai E. Neurologic abormalities in 2 dogs with suspected Lyme disease. Microbiil Immunol 1993;37(4):325-329.
  5. Levy SA, Magnarelli LA. Relationship between development of antibodies to Borrelia burgdorferi in dogs and the subsequent development of limb/joint borreliosis. JAVMA. 1992;200(3):344-347
  6. Levy SA, Lissman BA, Ficke CM. Performance of a Borrelia burgdorferi bacterin in borreliosis-endemic areas. JAVMA. 1993;202(11):1834-1838.
  7. Levy SA, O'Connor TP, Hanscom JL, e al. Quantitative measurement of C6 antibody following antibiotic treatment of Borrelia burgdorferi antibody-positive nonclinical dogs. Clin Vaccine Immunol. 2008;15:115-119.  
  8. Straubinger RK, Summers BA, Chang JF, et al.  Persistence of Borrelia burgdorferi in experimentally infected dogs after antibiotic treatment. J Clin Micro. 1997;35:111-116.
  9. Topfer KH, Straubinger RK. Characterization of the humoral immune response in dogs after vaccination against the Lyme borreliosis agent. A study with five commercial vaccines using two different vaccination schedules. Vaccine. 2007;25(2):314-316.

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