Countdown to Lyme Season:

What Every Dog Owner Should Know About Lyme Disease

(revised and updated for 2000)

    Lyme disease, a tick-transmitted bacterial infection, can lead to recurrent arthritic symptoms in dogs and humans. Recent clinical studies indicate that Lyme disease in dogs may not be as benign as once believed: bacterial infection appears to persist in many dogs despite antibiotic therapy and even in individuals that are cured by treatment, there is evidence of progressive joint deterioration. Additionally, some breeds of dogs such as the Labrador retriever and Golden retriever may be at additional risk to a fatal kidney disease (Lyme nephritis) associated with Lyme infection. In light of these reports and the estimate that 80% of dogs living in endemic regions of the United States will become infected with Lyme disease, many clinicians are recommending Lyme prevention in the form of vaccination. The following article provides a detailed explanation of Lyme disease and explores the benefits and risks of the current commercial vaccines available for protecting dogs against Lyme disease.

Lyme Infection

The Lyme Organism. Borrelia burgdorferi is a bacterial spirochete that is responsible for causing Lyme disease. Unlike its distant relative, Leptospira spp. which cause canine leptospirosis, B. burgdorferi cannot live in water and soil but are dependent entirely on arthropod (insect) and vertebrate (mammals, reptiles) hosts to carry out their life cycle. Differences in strains of Borrelia spp. have been identified throughout the world and probably explain the different clinical syndromes associated with infection in the United States compared to other countries.

The Lyme Vector. For active Lyme infection to occur in dog or man, B. burgdorferi requires an intermediate host; that is, the disease cannot be directly transmitted from one host to another through contact with infected body secretions such as blood, saliva, urine, etc. The primary intermediate hosts for this spirochete are deer ticks belonging to the genus Ixodes. Though other biting insects may be intermediate hosts for B. burgdorferi, they were found to have an insignificant role in the spread of Lyme disease.
    Shortly after mating, the female tick will feed for 5-7 days on a host. In the spring, she will lay about 2000 eggs. Even if the female is infected with B. burgdorferi, the larvae that hatch from these eggs will not carry enough of the spirochetes to cause a threat of infection. It is only when the larvae begin to feed on a host, usually the white-footed mouse Peromyscus leucopus in the northeastern and midwestern US, that they will ingest enough bacteria to become a vector for Lyme disease. Interestingly, these infected mice do not develop disease and, therefore, act as a perfect reservoir for B. burgdorferi.. [As an indication of the importance of the role that white-footed mice have in the epidemiology of Lyme disease: in the mid-southern US where incidence of Lyme disease is low, Ixodes spp found in that region (I. scapularis) feed on lizards in which B. burgdorferi infection is not maintained.]
    The infected larvae molt into nymphs the following spring and will also feed on the white-footed mice or others animals or humans. At this point, an infected nymph may transmit B. burgdorferi to the host, however, studies indicate that nymphs are less effective at transmitting the bacteria than are adults. Uninfected nymphs are also capable of becoming infected at this point if they feed upon an already infected host. As a result, when nymphs molt again in the fall and become adults, it is estimated that at least 50% of the tick population in areas endemic for Lyme disease will carry B. burgdorferi. These adult ticks are the primary vectors for disease transmission.

Disease Transmission. Lyme disease is transmitted by tick bite. B. burgdorferi live in the midgut of ticks but will migrate to the salivary glands once the tick attaches to a host and begins to feed. Danger of infection with B. burgdorferi occurs when the tick becomes engorged, usually after 24 hours of feeding, thereby increasing the chances of bacteria-contaminated blood passing from tick to host. If an infected tick is removed prior to 24 hours of attachment, chances of the host acquiring Lyme disease are virtually non-existent.
    Several clinical studies exploring the transmission of Lyme disease indicate the necessity for the intermediate tick host. For example, inoculation of healthy dogs with contaminated blood or urine from infected dogs failed to produce clinical Lyme disease in the healthy dogs at a later time. These dogs did go on to develop a positive titer to Lyme disease, however, when blood from these dogs was examined, it was found that the bacteria were not viable. Furthermore, using experimental tick attachment models, clinicians found that pregnant bitches that became infected with B. burgdorferi did not transmit the bacteria to their fetuses. These studies support the need for the tick vector for Lyme disease transmission.

Disease Prevalence. It is estimated that although greater than 80% of dogs in high risk areas of the US will be exposed to infected ticks, only about 5% of these dogs will actually go on to manifest clinical Lyme disease. High risk areas of the US include all coastal states from Maine to North Carolina as well as New Hampshire and Pennsylvania. Other states considered to be mildly at risk for Lyme disease include Wisconsin, Minnesota, Michigan, Illinois, Missouri, Iowa, California and Oregon. The remaining states are considered to have a very minimal risk for Lyme disease.

Lyme Disease

Symptoms. Clinical studies exploring onset of Lyme disease following infection with B. burgdorferi suggest that symptoms appear usually 2-5 months after tick-induced infection. Primary symptoms include lameness and joint pain. These symptoms may be sudden and severe. Infected dogs also often exhibit depression, lethargy and loss of appetite. Fever may or may not be present, however, one or more affected joints are often swollen, hot and painful upon examination. In some cases, there may be lymph node enlargement. Rarely, infected dogs will develop complete heart block, renal failure, or neurological symptoms such as seizures, aggression or other behavioral changes. The rash typically appearing in the first stages of Lyme disease in humans is usually absent in dogs.

Diagnosis. Standard blood studies are not very helpful in the diagnosis of Lyme disease. Patient blood values are usually within normal ranges despite symptoms of infection. Analysis of joint fluid, however, often shows an increase in white blood cell count and changes in hematologic components indicative of infection and inflammation. Despite this, many canine disorders can present with similar symptoms. For this reason, clinicians propose 4 criteria for establishing a diagnosis of Lyme disease: 1) history of tick exposure; 2)typical clinical symptoms; 3) a positive serology and 4) a response to antibiotic treatment.
    In regard to serological tests, dogs exposed to B. burgdorferi begin to make antibodies within 4 to 6 weeks. The antibody titer will increase to high levels and then remain constant for about 18 months. Usually, by the time symptoms of Lyme disease manifest, antibody titers should be sufficient to rule out the possibility of false-negative tests. Though the enzyme linked immunosorbent assay (ELISA) and indirect fluorescence antibody (IFA) test are sometimes used for the diagnosis of Lyme disease, these methods are unable to distinguish antibodies made in response to infection from antibodies made in response to vaccination against Lyme disease. Therefore, false-positive results are a common limitation to serological testing with ELISA and IFA. However, another method called Western blotting is capable of distinguishing between these types of antibodies and, therefore, can determine if a dog is infected with B. burgdorferi even in the presence of a vaccine-induced antibody titer to B. burgdorferi.

Update: Advances in ELISA diagnosis
The standard enzyme linked immunosorbent assay (ELISA) for lyme disease utilizes whole cell antigen for detection of B. burgdoferi antibodies in dog sera. Naturally, the problem with utilizing whole cell antigen in ELISAs designed to diagnosis active disease is that dogs that have been immunized with either whole-cell vaccines or subunit vaccines (OspA) will also have antibodies that will react and cause false positive tests. This confounds the ability to differentiate dogs that have antibodies present from an active lyme infection from those dogs that have antibodies induced by vaccination. Currently, a new technology applied to ELISA design circumvents this problem by utilizing specific recombinant antigens (i.e. surface protein OspF, protein 35 and protein 39). This approach is based upon the observation that dogs that have been vaccinated with OspA subunit vaccines will not make antibodies to OspF (since their immune system has only seen the outer surface protein Osp A as part of the active vaccine component), however, dogs that have acquired natural infection with B. burgdoferi will make antibodies to many of the organism's antigens (i.e. OspA, OspB, OspF, p22, p37 and p41-G). Accordingly, if a dog that has been vaccinated with the subunit OspA vaccine is screened with the OspF ELISA and reacts positively, then it follows that the dog has had a natural exposure to the whole organism. Unfortunately, one limitation to the new ELISA is that it cannot be used to screen dogs that have received immunization with whole-cell (killed) lyme vaccines; that is, it can only differentiate active immunity [vaccine induced] from natural immunity [infection induced] in dogs that have been immunized with subunit vaccines).

Treatment. Antibiotic treatment is the current treatment of choice for Lyme disease. Doxycycline (tetracycline) for adult dogs or amoxicillin for young, growing dogs produce complete remission of clinical symptoms in dogs within 24-48 hours of initiation of treatment. Drug administration should be continued, however, for one month because of the slow reproduction cycle of the bacteria and its tendency to persist in dogs. Non-steroidal anti-inflammatory drugs are useful for alleviating arthritic symptoms associated with Lyme disease. However, many clinicians prefer not to use these drugs because they mask symptoms which may indicate possible progression of disease despite treatment with antibiotics. Clinical evidence suggests that corticosteroid (ex. prednisone) treatment is contraindicated for use in dogs with Lyme infection. In regard to this latter finding, studies have shown that the immunosuppression caused by these drugs may reactivate infection in dogs in which bacterial infection has not been totally eradicated.

Prognosis. In most cases, clinical symptoms of Lyme disease in the canine respond well to treatment with antibiotic therapy. Even without treatment, many dogs recover from symptoms spontaneously. Additionally, many dogs who are serologically positive for Lyme disease may never manifest clinical symptoms of disease. In cases where symptomatic dogs treated for Lyme disease develop recurrent symptoms at a later time in their lives, repeating the antibiotic treatment was found to be effective at controlling disease.
    Despite this, however, it is believed that antibiotic therapy may not completely cure dogs of Lyme disease. In fact, histological studies of tissues from asymptomatic and antibiotic-treated dogs suggests that even in the absence of clinical symptoms, mild arthritic changes continue to occur in affected joints that may limit mobility later in life. Furthermore, although clinical studies suggest that dogs are rarely at risk to the chronic arthritis and severe central nervous system syndromes that pose risks to humans who contract Lyme disease, some breeds of dogs such as the Labrador retriever and the Golden retriever are at risk to contracting a fatal kidney disease ( Lyme nephritis) caused by B. burgdorferi that is not treatable with antibiotics.

Prevention. Prevention of Lyme disease in the dog may occur at two levels: prevention of tick bites and inoculation against B.burgdorferi with a commercial vaccine. Prevention of tick bites includes the daily grooming of dogs to remove ticks and use of repellents or insecticides in the form of collars, dips, sprays or creams. A discussion of vaccination for the prevention of Lyme disease follows here.

The Need for Lyme Prevention. Early arguments directed against vaccinating for Lyme disease included the observation that although up to 80% of dogs in endemic regions become infected with B. burgdorferi, only 5% of these dogs actually go on to manifest clinical symptoms of disease. In light of this and the fact that clinical symptoms appear to respond well to antibiotic treatment, Lyme disease in the canine has not been viewed as a particularly life-threatening disease. Recent clinical information suggests, however, that Lyme disease may not be as benign as formerly believed. Examination of dogs experimentally infected with B. burgdorferi and then treated with the usual course of antibiotics has shown that despite reduction of joint lesions, bacterial infection was still present. This finding probably explains recurrent cases of Lyme disease observed in some dogs previously treated for infection. In another clinical study, histological examination of joints from dogs "cured" of Lyme disease showed progressive arthritis in joints previously infected with the bacteria. Furthermore, in some rare cases, B. burgdorferi infection transmitted by ticks leads to a fatal kidney disease, Lyme nephritis, for which Labrador retrievers and Golden retrievers appear to have a higher predisposition. Since vaccines that inoculate against B. burgdorferi only protect against infection if they are administered prior to infection, more clinicians are recommending preventative vaccination as the best defense against Lyme disease.

Commercial Lyme Vaccines. There are currently two Lyme vaccines available. The first vaccine has been around for nearly a decade and is a killed, whole-cell bacterin. Though administration of this vaccine is generally safe, observations supporting its efficacy to prevent infection are not very strong since laboratory animals (hamsters) immunized with this vaccine and later challenged with ticks infected with B. burgdorferi went on to develop arthritis several weeks or months later.
    A second vaccine which became available for dogs in 1996, consists of a recombinant outer surface protein A of B. burgdorferi (OspA). This vaccine induces a immune response to one specific protein on the surface of the bacterial organism. The same type of vaccine has recently been approved by the Food and Drug Administration for human immunization. Interestingly, the antibody induced by the OspA vaccine in the host actually works by stopping the bacteria while it is still in the tick. When a tick attaches to a vaccinated host and begins to feed, blood from the host contains the antibody to the bacteria. The antibody will bind to and block the bacteria in the mid-gut of the tick before it can migrate to the salivary glands of the tick and be passed to the host. As a result, the host does not become infected. Unfortunately, however, the antibodies cannot cure infection if the dog has already been exposed to B. burgdorferi.

Limitations to Safety and Efficacy. As with all vaccines, there are several limitations that may influence safety and efficacy of the OspA vaccine. In terms of safety, recent clinical studies exploring persistent arthritis in humans infected with, but treated for Lyme disease has identified a condition referred to as "molecular mimicry" involving B. burgdorferi. It has been observed that a small population of individuals have inherited a protein on their cells that is immunologically identical to OspA found on the surface of B. burgdorferi. When these people become infected with the Lyme disease organism, their bodies make antibodies to this protein in order to fight-off the infection. Once the infection is eradicated, however, these antibodies will continue to attack their own cells which have this same surface protein. Hence, symptoms of arthritis and inflammation will persist despite the fact that the bacterial infection is cured. Therefore, in a small population of individuals receiving the OspA vaccine, it is anticipated that the vaccine may induce symptoms of arthritic disease in the absence of infection. Though incidence of molecular mimicry has not been examined for occurrence in dogs specifically vaccinated with the OspA vaccine, some dogs develop Lyme symptoms even though they have antibodies only for the Lyme bacterin (vaccine-induced). This finding may be indicative of a vaccine-associated arthritic syndrome and suggests that similar to humans, a small population of dogs may be at higher risk for developing a reaction to vaccination with the OspA Lyme vaccine. This idea is further supported by a recent clinical study in which laboratory animals (hamsters) injected with recombinant OspA protein, the same protein used to manufacture the OspA Lyme vaccine, and then later challenged with B. burgdorferi developed severe destructive arthritis. Furthermore, when animals were immunized with another form of an OspA subunit vaccine, greater than half of them went on to develop this severe form of arthritis after infection with B. burgdorferi. When OspA was combined with aluminum hydroxide, a compound often added to vaccines to increase immunogenicity, all the vaccinated animals developed severe arthritis after being challenged with B. burgdorferi. These findings suggest the potential that OspA vaccines, though protecting against bacterial infection, may contribute to or even exacerbate an immune-mediated arthritic syndrome associated with Lyme disease in some individuals. In regard to this latter information, however, one must recognize that this is an experimental model and that these findings have not yet been explored in the dog.
    There are two considerations when addressing limitations of efficacy with the OspA vaccine. The first entails duration of protective immunity. In light of the recent controversy surrounding frequency of booster vaccinations, it is once again important to reiterate that the current consensus regarding long-term duration of immunity to viral antigens such as distemper, parvovirus, adenovirus, coronavirus, etc. should not be generalized to bacterin vaccines. Bacterin vaccines which provide immunity against Lyme disease, Leptospirosis and kennel cough are of short-term duration with immunity wearing-off within 12 months of vaccination. Indeed, clinical studies with the OspA vaccine for Lyme disease found complete and protective immunity up to 6 months following inoculation but the importance of a yearly booster vaccine, prior to the early spring and tick season, is necessary for continued protection against Lyme infection. The second limitation to efficacy with OspA is the potential for Lyme disease caused by infection with a different strain of B. burgdorferi for which antibodies directed at OspA will not recognize. Currently, this is not a concern in the US where 90% of the strains have the OspA, however, over the course of time it is not unheard of for less common, resistant strains to become more prevalent. This is currently an issue concerning Leptospirosis infection and vaccination (see Canine Leptospirosis: Current Issues on Infection and Vaccination).

    No. Although B. burgdorferi have been found in the urine and saliva of infected dogs, the bacteria do not survive well in these media and would not be viable to bring about clinical infection in another host.

Can my dog contract Lyme disease if he/she is bred to an infected dog?

    No. B. burgdorferi do not maintain viability in semen or vaginal secretions and therefore would not bring about clinical infection if transmitted during breeding.

Does owning a dog put me at higher risk for getting Lyme disease?

    Not likely. If your dog picks up infected ticks while out in the woods the risk that the dog may transport the infected tick to you is considered very unlikely. Once on the dog's hair, the ticks usually seek out the skin where they will embed. Since ticks are not intermittent feeders, once attached, the tick will only become detached once it completes its feeding or if it is removed.

What will happen if my dog already has Lyme disease, without any symptoms, and I vaccinate him?

    It is unknown what effects, if any, vaccinating an infected, asymptomatic dog will have. Clinical studies suggest that the vaccine will not assist in eliminating the present infection. Major health problems have not been reported for administering vaccine to dogs that already have the disease. To avoid potential complications, however, serological testing may be performed prior to vaccinating. If the dog is found to be sero-positive for Lyme, the dog can be treated with antibiotics first, then vaccinated to prevent re-infection at a later time.

What other diseases may appear as Lyme disease?

    Other diseases with symptoms that closely resemble Lyme disease include but are not limited to: rheumatoid arthritis, infectious or immune-mediated arthritis (e.g. systemic lupus erythmatosis), osteopathies, degenerative joint diseases, Rocky mountain spotted fever, ehrlichiosis, and bacterial endocarditis.

Should I keep my dog on antibiotics to prevent infection?

    Dogs in endemic areas are exposed to ticks too frequently to use prophylactic antibiotics on a regular basis. An alternative is to check your dog daily for ticks. Since ticks must be embedded for more than 24 hours to cause infection, removing ticks on a daily basis will decrease risk of infection in your dog.

I live in an endemic area, should I vaccinate for Lyme disease?

    When considering any vaccine, one must take into consideration and weigh the benefits and risks of administering the vaccine. It is estimated that at least 80% of dogs in endemic areas will become infected with Lyme disease. As such, this constitutes a high risk for dogs in these areas and reinforces the need for some form of prevention to protect dogs from infection. Alternatives to vaccines (such as daily grooming and removal of ticks with concomitant use of tick insecticides and repellents) are viable approaches for protection against Lyme infection, however, to be effective, they require firm commitment and diligence by the dog owner. If a dog owner is not meticulous in carrying out these alternatives, then the dog will remain in the high risk category for Lyme infection. In such an instance, vaccinating healthy dogs against Lyme disease becomes the next best form of protection. The ultimate decision to use the Lyme vaccine, however, should be discussed at length with your veterinarian. Some of the direct risks associated with Lyme vaccine are discussed above, for more information on general risks of vaccination please refer to Vaccines, Infectious Diseases, and the Canine Immune System.

For more information and links on Lyme disease visit the following sites:

Lyme Disease Foundation

Lots Of Links On Lyme Disease

CDC: Environmental Health; CDC; Lyme Disease

NIH/NLM: MEDLINEplus: Lyme Disease

Fighting Fleas and Ticks

Robin Camken's Health Infromation Links on Lyme Disease

References:

Appel MJ. Forty years of canine vaccination. Adv Vet Med, 41:309-24, 1999.

Appel MJG. Lyme Disease Vaccination. In: JD Bonagura, ed., Kirk's Current Veterinary Therapy XIII, W.B. Saunders, Philadelphia, 1999. pp 256-258.

Appel MJG and Jacobson RH. CVT Update: Canine Lyme Disease. In: JD Bonagura, ed., Kirk's Current Veterinary Therapy XII, W.B. Saunders, Philadelphia, 1995. pp 303-309.

Croke CL, Munson EL, Lovrich SD, et al. Occurrence of severe destructive lyme arthritis in hamsters vaccinated with outer surface protein A and challenged with Borrelia burgdorferi. Infect Immun, 68:658-63, 2000.

Dambach DM, Smith CA, Lewis RM, et al. 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, 1997.

Dickman, S. Possible cause found for Lyme arthritis (Immunology News Focus), Science, 281: 631-632, 1998.

Gomes-Solecki MJ, Wormser GP, Schriefer M, Neuman G, Hannafey L, Glass JD, Dattwyler RJ. Recombinant assay for serodiagnosis of Lyme disease regardless of OspA vaccination status. J Clin Microbiol 2002 Jan;40(1):193-7

Gross, D.M., Forsthuber, T., Tary-Lehmann, M., Etling, C., Ito, K., Nagy, Z.A., Field, J.A., Steere, A.C., and Huber, B.T. Identification of LFA-1 as a candidate autoantigen in treatment-resistant Lyme arthritis. Science, 281: 703-706, 1998.

Ma J, Hine PM, Clough ER, et al. Safety, efficacy, and immunogenicity of a recombinant Osp subunit canine Lyme disease vaccine. Vaccine, 14:1366-74, 1996.

Magnarelli LA, Levy SA, Ijdo JW, Wu C, Padula SJ, Fikrig E. Reactivity of dog sera to whole-cell or recombinant antigens of Borrelia burgdorferi by ELISA and immunoblot analysis.  J Med Microbiol 2001 Oct;50(10):889-95

Straubinger RK, Straubinger AF, Summers BA, Jacobson RH, Erb HN. Clinical manifestations, pathogenesis, and effect of antibiotic treatment on Lyme borreliosis in dogs. Wien Klin Wochenschr , 110:874-81, 1998.

Copyright © 1993, 2000. Pamela A. Davol. All rights reserved. Copyright & disclaimer.

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