Lyme disease (Proceedings)


Tick-transmitted disease caused by the spirochete Borrelia burgdorferi.


  • Tick-transmitted disease caused by the spirochete Borrelia burgdorferi.

  • “Borrelia burgdorferi sensu lato" is name given to the overall category. In North America there is just one genospecies variant - Borrelia burgdorferi sensu stricto. In Europe there are three categories Borrelia burgdorferi sensu stricto, B. garinii, and B. afzelii.

  • B. lonestari causes a “southern tick-associated rash syndrome” in the U.S.


  • Worldwide distribution

  • In the US, occurs mostly (> 90%) in the northeast, Minnesota and Wisconsin, less common in southeast, and midwest regions.

  • Recognized vectors:

  • Ixodes scapularis, in the northeastern and north central US

  • I. pacificus in the western US


  • Ticks

  • In the northeastern US from Maine to Maryland and in the north central states of Wisconsin and Minnesota

  • Highly efficient, horizontal cycle of B. burgdorferi transmission occurs among larval and nymphal I. scapularis ticks and certain rodents, particularly white-footed mice and chipmunks.

  • This cycle results in high rates of infection among rodents and nymphal ticks and many new cases of human Lyme disease during the late spring and early summer months.

  • Nymphs are the life stage most commonly involved in transmitting B. burgdorferi to dogs and humans.

  • White-tailed deer, which are not involved in the life cycle of the spirochete, are the preferred host of adult I. scapularis, Deer are not competent hosts for B. burgdorferi – their role is to maintain the ticks, not the Borrelia. Dogs, horses, cows, people, etc. are accidental victims of a hungry tick!

  • Vector ecology is different in other parts of the US where prevalence is lower.

  • Do not infect host until attached for 24 hours. This time is required for the bacteria to migrate from the tick midgut to the salivary glands

  • Dogs

  • Experimentally-infected dogs

  • Beagle pups

  • Clinical illness 2-5 months after exposure

  • Inappetence, lethargy, and lymphadenopathy

  • Episodic shifting leg lameness of 3-6 day duration

  • Arthritis develops first in the joint closest to the tick bite

  • After about 6 months, all arthritic episodes resolve

  • Adult beagles do not develop the disease

  • Natural disease not well characterized

  • Difficult to reproduce in an experimental setting.

  • Based on seroprevalence studies, only 5-10% of naturally infected dogs develop clinical signs.

  • Seroprevalence in endemic areas can be as high as 90%.

  • Considered a generalized, systemic infection

  • Connective tissues

  • Joint capsules

  • Muscle

  • Lymph nodes

  • Lyme disease can be seen throughout the active tick season, but it is most often diagnosed in late spring and fall, rather than in midsummer

  • Cats

  • Develop clinical signs if experimentally-infected

  • Clinical signs do not consistently develop in naturally-infected cats

  • More resistant than dogs?

  • Better at removing ticks

  • Rate of seropositivity is lower than in dogs

  • Connective tissues

Clinical Findings

  • Polyarthritis

  • Most common manifestation in dogs

  • May be septic or immunemediated

  • Transient, respond to antibiotic therapy

  • Few or many joints

  • Often subclinical

  • Chronic, non-erosive arthritis (persistent infection)

  • Systemic signs

  • Anorexia, weight loss, lethargy, lymphadenomegaly

  • Renal disease

  • Protein-losing nephropathy

  • Acute progressive renal failure (Lyme nephritis)

  • Syndrome described in Borrelia-seropositive dogs

  • Etiology not clearly established

  • Circumstantial evidence

  • Unique histopathologic lesions

  • Mostly in Labrador and Golden retrievers

  • Other manifestations

  • Lyme myocarditis

  • CNS inflammation (reported but poorly described)

Laboratory findings

  • Leukocytosis with left shift, monocytosis, mild anemia

  • Proteinuria

  • Azotemia

  • Joints

  • Neutrophilic inflammation


  • Clinical Signs + Serology

  • Prevalence of seropositivity is much higher than prevalence of disease

  • Whole cell body antibodies (ELISA or IFA)

  • Should not be used anymore

  • Poor specificity

  • Subclinical infection is common

  • Cross-reaction with vaccine

  • Non-specific reactivity

  • Snout test: so Sensitive that a Negative result rules OUT the disease

  • IgM cannot be used as an indicator of recent infection because IgM titers remain elevated for prolonged periods of time after infection

  • Western-blot

  • Can differentiate between vaccine and natural exposure

  • Some non-vaccinated dogs previously exposed to B. burgdorferi show Western-blot pattern compatible with both, vaccination and natural exposure.

  • C6 antibodies

  • “Snap-test” or Quantitative C6

  • Antibodies against C6 peptide

  • Not a part of OspA

  • Not affected by vaccination

  • Highly specific

  • Detectable 3 weeks post-exposure

  • May be able to use titer to gauge treatment succes


What to do with a seropositive dog?

  • Consider

  • Clinical signs

  • Proteinuria

  • Asymptomatic, non-proteinuric

  • No therapy

  • Symptomatic, non-proteinuric

  • Treat Lyme

  • Asymptomatic, proteinuric:

  • Recheck proteinuria periodically. If persistent or severe

  • Treat Lyme and proteinuria

  • Symptomatic, proteinuric

  • Treat Lyme and proteinuria


  • Doxycycline 10 mg/kg q12h for 28 days

  • Longer if nephropathy (?)

  • Drug of choice

  • Early treatment decreases titers and organism load

  • Clearance is not complete

  • Amoxicillin 20 mg/kg q8-12h for 28 days

  • Ceftriaxone is used in humans with menigitis


  • Strict tick-control

  • Vaccine

  • Bacterins + adjuvant vaccines: Reduce incidence of signs in seropositive dogs from 4.7% to 1%. Value is questionable

  • Single protein vaccines (OspA): protect from infection and disease

  • OspA antibodies block migration of the organism from the tick into the dog

  • Do not clear infection in the dog, because the change in temperature from the low temperature tick to the high temperature dog shifts expression of OspA to OspC.

  • OspC antibodies are not borrelicidal

  • Vaccinate at risk dogs before the tick season

  • Duration of immunity is at least 6 months

  • Western-blot and C6 antigen differentiate vaccine from exposure

Vaccine X Arthritis

  • Arthritis

  • Major clinical sign in human beings and dogs

  • Also detected in human beings following vaccination with Borrelia OspA and in dogs with the whole cell vaccine and presumably OspA vaccine

  • Arthritis is also found in animals following Borrelia vaccination with whole cell and OSPA followed by infection.

  • Should we vaccinate?

  • Arthritis is seen in about 3% of naturally-infected dogs

  • If prevalence of post-vaccination arthritis is assumed to be 0.04% (it is not known)

  • What would be the outcome in 3 different areas? (1,000 dogs, vaccine 70% effective)

  • High prevalence:  75% of dogs get infected

  • Without vaccine: 23 dogs with arthritis (Lyme-induced)

  • With vaccine: 11 dogs with arthritis (7 with Lyme, 4 vaccine-induced)

  • Moderate prevalence: 25% of dogs get infected

  • Without vaccine: 8 dogs with arthritis (Lyme-induced)

  • With vaccine: 6 dogs with arthritis (2 with Lyme, 4 vaccine-induced)

  • Low prevalence: 10% of dogs get infected

  • Without vaccine: 3 dogs with arthritis (Lyme-induced)

  • With vaccine: 5 dogs with arthritis (1 with Lyme, 4 vaccine-induced)


Barthold, S.W. et al. 1995. Serologic responses of dogs naturally exposed to or vaccinated against Borrelia burgdorferi infection. JAVMA. 207:1435-1440.

Brown, R.N.,R.S. Lane. 1992. Lyme disease in California: a novel enzootic transmission cycle of Borrelia burgdorferi . Science 256:1439-1442.

Burgess, E .C. et al. 1989. Testing for Borrelia burgdorferi. JAVMA. 195:844-845.

Burgess, E.C. 1992. Experimentally-induced infection of cats with Borrelia burgdorferi. A.J.V.R. 53:1507-1511.

Chang, Y.-F. et al. 2001. Experimental induction o f chronic borreliosis in adult dogs exposed to Borrelia burgdorferi infected ticks and treated with dexamethasone. AJVR. 62:1104-1112.

Chang, Y.-F., et. al. 1995. Recombinant ospA protects dogs against infection and disease caused by Borrelia burgdorferi . Infect. Imm. 63:3543-3549.

Chu, H.-J. et al. 1992. Immunogenicity and efficacy study of a commercial Borrelia burgdorferi bacterin. JAVMA. 201:403-411.

Dambach DM. et al. 1997. Morphologic, immunohistochemical, and ultrastructural characterization of a distinctive renal lesion in dogs putatively associated with Borrelia burgdorferi infection: 49 cases (1987-1992). Vet Pathol. 34:85-96.

Fritz CL, Kjemtrup AM. 2003. Lyme borreliosis. JAVMA. 223:1261-1270.

Gibson, M .D. et al. 1993. Borrelia burgdorferi in cats (lett). JAVMA. 202:1786.

Grauer GF et al. 1988. Renal lesions associated with Borrelia burgdorferi infection in a dog. JAVMA. 193:237-239.

Gustafson , J.M. et al. 1993. Intrauterine transmission of Borrelia burgdorferi in dogs. AJVR. 54:882-890.

Hinrichsen, V.L. et al. 2001. Assessing the association between the geographic distribution of deer ticks and seropositivity rates to various tick-transmitted disease organisms in dogs. JAVMA. 218:1092-1097.

Kazmierczak, J.J., F.E . Sorhage. 1993. Current understanding of Borrelia burgdorferi infection, with emphasis on its prevention in dogs. JAVMA. 203:1524-1528.

Levine, J.F. 1995. Ixodes-borne Borrelia sp p. infections. JAVMA. 207:768-775.

Levy, S.A. and L.A. Magnarelli. 1992. Relationship between development of antibodies to Borrelia burgdorferi in dogs and the subsequent development of limb/joint borreliosis. JAVMA. 200:344-347.

Levy, S.A. et al. 1993. Canine Lyme borreliosis. Comp. Cont. Ed. 15:8 33-846 .

Levy, S.A. et al. 1993. Performance of a Borrelia burgdorferi bacterin in borreliosis-endemic areas. JAVMA.202:1834-1838.

Lissman, B .A. et al. 1984. Spirochete-associated arthritis (Lyme disease) in a dog. JAVMA. 185:219-220.

Littman MP, et al. 2006. ACVIM small animal consensus statement on Lyme disease in dogs: diagnosis, treatment, and prevention. J Vet Intern Med. 20:422-34.

Lovrich, S.D. et al. 1994. Seroprotective groups of Lyme borreliosis spirochetes from North America and Europe. J.Infect. Dis. 170:115-121.

Magna relli, L.A. et al. 1990. Tick parasitism and antibodies to Borrelia burgdorferi in cats. JAVMA. 197:63-66.

Magnarelli, L.A. et al. 2005. Seroprevalence of antibodies against Borrelia burgdorferi and Anaplasma phagocytophilum in cats. AJVR. 66:1895-1899.

Mather, T.N. et al. 1994. Competence of dogs as reservoirs for Lyme disease spirochetes (Borrelia burgdorferi). JAVMA. 205:186-188.

Mathiesen, D.A. et al. 1997. Genetic heterogeneity of Borrelia burgdorferi in the United States. J. Infect. Dis. 175:98-107.

Moore, V.A. et al. 2003. Detection of Borrelia lonestari, putative agent of southern tick-associated rash illness, in white-tailed deer (Odocoileus virginianus) from the southeastern United States. J. Clin. Microbiol;. 41:424-427.

Philipp MT, et al. 2001. Antibody response to 1R6, a conserved immunodominant region of the V1sE lipoprotein, wanes rapidly after antibiotic treatment of Borrelia burgdorferi infection in experimental animals and in humans. J Infect Dis. 84:870-8.

Philipp MT, et al. 2003.C6 test as an indicator of therapy outcome for patients with localized or disseminated Lyme borreliosis. J Clin Microbiol. 41:4955-60.

Roush, J.K . et al. 1989. Rheumatoid arthritis subsequent to Borrelia burgorferi infection in two dogs. JAVMA.195:951-953.

Straubunger, R.K. et al. 1997. Persistence of Borrelia burgdorferi in experimentally infected dogs after antibiotic treatment. J. Clin. Microbiol. 35:111-116.

Varela, A.S. et al. 2004. First culture isolation of Borrelia lonestari, putative agent of southern tick-associated rash illness. J. Clin. Microbiol. 42:1163-1169.

Wasmoen, T.L. et. al. 1992. Examination of Koch's postulates for Borrelia burgdorferi as the causative agent of limb/joint dysfunction in dogs with borreliosis. JAVMA. 201:412-418.

Yang, L. et al. 1994. Heritable susceptibility to severe Borrelia burgdorferi-induced arthritis is dominant and is associated with persistence of large numbers of spirochetes in tissues. Infect. Imm. 62:492-500.


Related Videos
© 2023 MJH Life Sciences

All rights reserved.