Lyme Disease (Borrelia burgdorferi)

Species

Canine
Borrelia burgdorferi

Feline*
Borrelia burgdorferi

*Despite the common finding of antibodies reactive to B. burgdorferi in cats in endemic areas, natural disease caused by infection in cats—if it occurs at all—is poorly understood. Accordingly, little is known about the prevalence of infection, disease manifestations, and treatment recommendations for feline infections with this agent.

Overview of Life Cycle

Dogs and cats become infected with B. burgdorferi when feeding ticks inoculate the organisms. In North America, only Ixodes scapularis and Ixodes pacificus, the eastern and western black-legged tick, respectively, have been shown to transmit the infection to dogs. (Formerly, northern strains of I. scapularis were erroneously referred to as Ixodes dammini and given the incorrect common name of “deer tick.” However, southern and northern I. scapularis interbreed and produce viable offspring, confirming they are indeed the same species.) Other, less-common Ixodes spp. are reported to be infected in nature but are not often found feeding on pets or people.
The Ixodes spp. that transmit B. burgdorferi are three-host ticks that feed on animals as larvae, nymphs, and adults.

The immature larval and nymphal ticks acquire B. burgdorferi from wild rodents when feeding in nature and then maintain the infection transstadially and can transmit after molting to the nymphal or adult stage.
Transovarial transmission from infected adult females to newly hatched larvae does not occur, and thus the larvae (“seed ticks”) do not serve as a source of infection.
In the wild, adult I. scapularis and I. pacificus feed largely on deer, and deer populations facilitate large tick populations in a given area. However, deer are not known to serve as a reservoir host for B. burgdorferi.

Stages (see image on right)

Spirochetes of B. burgdorferi enter connective tissue upon inoculation and thus are not found by microscopy in circulating blood and are only rarely visualized directly in tissue sections from infected dogs.
The Ixodes spp. ticks that can transmit B. burgdorferi can be identified by the presence of an anal groove arching anterior to the anus (arrow) on the ventral surface of nymphal or adult ticks.

Disease

Most dogs exposed to B. burgdorferi appear to develop subclinical infections.
Dogs with acute Lyme borreliosis may present with fever, shifting leg lameness, swollen joints, enlarged lymph nodes, lethargy, depression, and anorexia. In general, clinical improvement is observed following initiation of antibiotic therapy.
Chronic disease is also associated with shifting leg lameness caused by transient, persistent polyarthritis accompanied by progressive joint changes; polyarthritis may persist even in the face of aggressive antibiotic therapy. Protein-losing glomerulopathy leading to acute progressive renal failure has also been described.
Mild focal meningitis and encephalitis without concomitant neurologic signs have been described in experimentally, but not naturally, infected dogs.

Prevalence

Infection with B. burgdorferi is common in the northeastern, upper midwestern, and West Coast states. In endemic areas, seroprevalence rates in dogs vary widely, ranging from 6.5% to as high as 85.2%. Similarly, up to 47% of cats in regions where B. burgdorferi is endemic show evidence of exposure to or infection with this agent. However, in nonendemic areas such as the southern United States, infection is rarely documented in pets without a travel history to an endemic area.
Borrelia burgdorferi infection is more common in areas where tick infestation pressure is high and routine acaricide use is not practiced. In some surveys, over half of questing nymphal and adult ticks have been shown to harbor infection with B. burgdorferi, creating a high risk of infection for pets living in a tick-infested environment.

Host Associations and Transmission Between Hosts

Pets become infected with B. burgdorferi upon inoculation of organisms by tick feeding. Ticks are not able to transmit infection immediately upon first attachment to a host but instead require a period of approximately 24 to 48 hours of initial feeding before organisms are able to pass across the salivary glands and into the vertebrate host.
Although experimentally infected dogs have been shown capable of infecting ticks and thus theoretically could serve as a reservoir host of B. burgdorferi, dogs are not considered important in maintaining a source of infection to people in nature.

Prepatent Period and Environmental Factors

Whole-cell-based serologic assays (see Diagnosis) for IgG reactive to B. burgdorferi first become positive 4 to 6 weeks following infection; IgG titers reach their peak approximately 3 months postinfection and may persist in the absence of reexposure for several years. In naturally infected dogs, whole-cell-based IgM titers persist for several months and thus cannot be used to confirm a recent infection.
Antibody titers to C6—a diagnostic peptide based on an invariable region of the VlsE surface protein of B. burgdorferi that has become widely used for serologic testing—increase quickly upon initial infection. However, most dogs that are seropositive to C6 do not have any evidence of clinical disease and do not go on to develop chronic disease.
When chronic infection with B. burgdorferi does develop in individual dogs, infection may persist for several years. In addition, reinfections or coinfections with other tick-transmitted organisms may occur following acquisition of infected ticks from the environment.

Site of Infection and Pathogenesis

Ticks inoculate spirochetes directly into the bite wound. However, transmission does not occur for 24 to 48 hours after initial attachment by an infected tick. Once inoculated, the spirochetes migrate in connective tissues, disseminate, and eventually establish long-term infections in peripheral sites including the heart, joints, and occasionally neural tissue. Resident bacteria incite inflammation with tissue damage. The spirochetes evade the host immune response and persist in tissues.
Subclinical infection with B. burgdorferi is common in dogs. When Lyme disease occurs, the most common signs are fever, polyarthritis, lymphadenopathy, and anorexia. Other, atypical signs may occur in association with protein-losing nephropathy and include edema, weight loss, anorexia, vomiting, and diarrhea. Whether B. burgdorferi is capable of causing arrhythmias and neurologic signs in dogs is not clear.
Clinical disease has not been described in naturally infected cats.

Diagnosis

A clinical diagnosis of Lyme borreliosis usually depends on the presence of compatible clinical signs and positive serology for B. burgdorferi. Although dogs with protein-losing nephropathy may develop azotemia, hypoalbuminemia, and proteinuria, hematology and serum chemistry do not reveal specific evidence of infection in most dogs with Lyme disease. Thromobocytopenia or leukopenia in a dog from an area where B. burgdorferi is endemic is more likely attributable to infection or coinfection with a rickettsial pathogen rather than an indication of Lyme borreliosis.
Serology is the mainstay of confirming a clinical impression of Lyme disease. Because of the prolonged incubation period, diseased dogs are almost always seropositive. However, because asymptomatic dogs in endemic areas are also often or even usually seropositive, accurate interpretation of a positive serologic test result is complicated.

Sensitive and specific patient-side assays are available that identify the presence of antibodies caused by natural infection and not prior vaccination.
Previous vaccination or prior exposure to related organisms may result in false-positive test results using such serologic assays as the whole-cell-based indirect fluorescent antibody (IFA) assay or enzyme-linked immunosorbent assay (ELISA), necessitating a follow-up Western blot assay for any dogs testing positive on the initial whole-cell-based screening technique. For this reason, many veterinarians consider the specific C6-based assay the initial screening method of choice for evaluating a dog for exposure to and potentially infection with B. burgdorferi.

Other, less clinically applicable approaches to diagnosis of Lyme borreliosis in dogs include microscopy, culture isolation, and polymerase chain reaction (PCR).

Spirochetes cannot be detected in blood smears by microscopy. Indeed, B. burgdorferi is only transiently present in circulating blood, and whole blood is not considered a useful diagnostic specimen for evaluation of infection. Spirochetes reportedly may be found in synovial fluid using dark-field microscopy, but low numbers of organisms are present in clinical specimens, precluding direct visualization.
Cell culture isolation requires specialized media and is challenging because of the relatively low density of organisms present in chronic infections.
Molecular diagnosis of B. burgdorferi infection in pets via PCR of affected tissues is available. However, the sensitivity of these assays may be limited by the low density of spirochetes in clinical specimens, and results (both positive and negative) should be interpreted with caution because the techniques used in different diagnostic laboratories vary. To maximize the utility of molecular diagnostics, samples should be collected before the initiation of antimicrobial therapy and submitted to experienced diagnostic laboratories with stringent quality control measures in place.

Treatment

The standard treatment for disease caused by B. burgdorferi infection in dogs is doxycycline at 10 mg/kg orally every 24 hours for 30 days. Longer courses of treatment may be necessary in some dogs, particularly those with nephropathy.
Prophylactic use of antibiotics following a tick bite is not recommended in dogs given the high frequency of exposure in the face of a relatively low incidence of clinical disease.
Antibiotic treatment of a clinically normal, seropositive dog is controversial. Most seropositive dogs do not have any evidence of clinical disease. However, because the course of infection can be prolonged, treating in the subclinical phase is viewed by some veterinarians as potentially beneficial in preventing the development of chronic disease. Currently, CAPC recommends that seropositive dogs be tested for the presence of other, coinfecting tick-borne disease agents and for evidence of abnormalities on hematology or urinalysis and that a tick-control program be instituted. Antibiotic treatment of seropositive dogs in the absence of clinical or pathological abnormalities is not recommended.

Control and Prevention

Vaccines are available to prevent Lyme borreliosis in dogs. The decision to vaccinate against Lyme borreliosis should be made based on a risk assessment of the individual dog that includes information about where the dog lives and how often it frequents a tick-infested area. Routine vaccination of dogs against Lyme disease is not warranted in areas of the United States where B. burgdorferi infection is not endemic.
Vaccination against Lyme borreliosis does not replace the need for stringent tick-control programs in pets. Vaccines may not protect against all strains of B. burgdorferi, and ticks harbor multiple pathogens for which vaccines are not yet available. For this reason, CAPC recommends that all pets be maintained year-round on highly effective acaricides with residual activity against ticks.
Attached ticks found on pets should be promptly removed to prevent transmission of B. burgdorferi or any other pathogens they may harbor. To avoid both zoonotic infection and accidental inoculation of pathogens into the pet during the removal process, ticks should be retracted using forceps or a commercial tick-removal device, and care should be taken to avoid contact with tick contents, ideally by wearing gloves. Careful attention to handwashing following tick removal is also recommended.
Tick infestations and resultant infection with B. burgdorferi can be prevented by avoiding tick-infested areas whenever possible and by modifying the habitat around the home through such basic measures as keeping shrubbery and grass closely clipped to discourage both tick populations and the wildlife species that often harbor them from flourishing. Immature ticks on rodents may be controlled through the use of acaricide-treated cotton that the rodents then use to line their nest, or by bait stations constructed to allow self-application of acaricides to rodents. Broadcasting acaricides across large outdoor areas is difficult, expensive, and largely ineffective in controlling many tick species.

Public Health Considerations

Lyme borreliosis caused by B. burgdorferi is the most common vector-borne disease of people in the United States. Clinical signs include erythema migrans (an expanding rash at the site of the tick bite), fever, myalgia, arthralgia, and headache. Chronic Lyme borreliosis may be manifested by signs of recurrent arthritis, neurologic disease, and myocarditis.
People contract B. burgdorferi infection the same way that pets do: via the bite of an infected tick acquired from a tick-infested environment. Pets are not an immediate source of infection to people.
Prevention of human infection with B. burgdorferi relies on preventing tick bites in people through many of the same measures that prevent tick bites on animals. In addition to stringent adherence to the routine use of acaricides on pets to limit infestations, people should take basic precautions when in tick-infested areas. Such precautions include wearing light-colored, protective clothing; performing frequent tick checks and promptly removing any ticks found; and using repellent products specifically labeled as effective at preventing tick attachment.

The Companion Animal Parasite Council