Current Advice on Parasite Control: Vector-Borne Diseases – Lyme Disease

Last reviewed and edited June 2015

Synopsis

CAPC Recommends

• Screening dogs for exposure to Borrelia burgdorferi due to rapid geographic expansion of endemic areas.
• In areas where Lyme disease is endemic or emerging, vaccinate dogs against Borrelia burgdorferi and reducing the risk of infection through year-round tick control and avoiding areas with ticks.
• Diagnosing Lyme disease based on a combination of clinical signs, including arthritis and renal disease, and positive serology.
• Veterinarians recognize that dogs can be sentinels for the risk of Lyme disease to people.

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 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 referred to as Ixodes dammini and given the incorrect common name of “deer tick.” However, southern and northern I. scapularis can interbreed and produce viable offspring, confirming they are the same species.) Other, less-common Ixodes spp. are reportedly infected, but it is uncertain how ofter these ticks feed 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 or nymphal ticks acquire B. burgdorferifrom wild rodents when feeding in nature and then transstadially transmit the infections to other hosts after these ticks molt to their subsequent developmental stage(s).
• Transovarial passage from infected adult females to newly hatched larvae does not occur, and thus the larvae 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 source of ticks that transmit B. burgdorferi due to the host preferences of immature I. scapularis and I. pacificus.

Stages

• 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, regional seroprevalence in dogs ranges from 1.4% in the West to as high as 13.3% in the Northeast.  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 B. burgdorferiinfections, creating a high risk of infection for pets living in a tick-infested environment.

Host Association 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 an important source of human infection due to the feeding behaviors of I. scapularis and I. pacificus.

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 ofB. 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 persistent infections with B. burgdorferi develop in individual dogs, these infections may persist for several years. In addition, reinfections or coinfections with other tick-transmitted organisms may occur following future infestations with infected ticks from the environment.

Site of Infection and Pathogenesis

• Ticks inoculate spirochetes directly into the feeding lesion. 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.
• It is important to remember that Lyme borreliosis differs among canine and human patients. For example, erythema migrans associated with spirochete migration from the tick feeding lesion is relatively common among people but rare among dogs.
• Subclinical infection with B. burgdorferi is common in dogs. Although the majority of naturally exposed dogs remain clinically normal, when canine Lyme disease does occur, 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. WhetherB. 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.
• It is important to remember that whole cell vaccines can invoke antibodies that are detectable by whole-cell-based indirect fluorescent antibody (IFA) or enzyme-linked immunosorbent assay (ELISA) tests. Therefore previous vaccination or prior exposure to related organisms may result in false-positive test results when using whole-cell-based IFA or 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. However, continued monitoring of such dogs for future signs of infection or disease may be warranted.
• 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. However, every conceivable precaution should be taken to minimize any chance that ticks could acquire B. burgdorferi from seropositive pets.

Control and Prevention

• Vaccines are available to limit Lyme borreliosis in dogs, and experimental studies testing efficacies of some of these vaccines were reported in peer-reviewed journals. The decision to vaccinate against Lyme borreliosis should be 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. Symptoms of human Lyme disease include erythema migrans (an ‘bull’s-eye-shaped’ rash expanding from the site of the tick bite), fever, myalgia, arthralgia, and headache. Persistent Lyme disease in people may be manifested by recurrent arthritis, neurologic disease, and myocarditis.
• People contract B. burgdorferi infection the same way that pets do: via the bite of an infected tick from a tick-infested environment. Pets are not an immediate source of infection to people, but the use of acaricides is nonetheless recommended to prevent tick feeding on both exposed and unexposed pets.
• Epidemiologists at the CDC reported a positive correlation between canine seroprevalence levels reported on the CAPC website to the incidence of human Lyme disease reported to the CDC. In this study, these investigators also reported that >5% canine seroprevalence at the county level was associated with emergence of human Lyme disease, while <1% canine seroprevalence was associated with little to no risk for emergence of human Lyme disease at the county level. Importantly, these results corroborated the feasibility of canine sentinels for risk of human exposure to B. burgdorferi. This study was not designed to test for a canine source of human infection. A subsequent report from the same group underscored the importance of maximal participation of veterinarians and veterinary clinics in these surveys to ensure sufficient amounts of data and to follow-up with travel histories of seropositive canine patients, in order to mitigate artifact associated with seroconverted dogs that have traveled to endemic areas.
• 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.

Selected References

• Littman MP, et al. 2006. ACVIM small animal consensus statement on Lyme disease in dogs: diagnosis, treatment, and prevention. J Vet Intern Med 2:422-34.
• Little SE, et al. 2010. Lyme borreliosis in dogs and humans in the USA. Trends Parasitol 26:213-8.
• Bowman D, et al. 2009. Prevalence and geographic distribution of Dirofilaria immitis, Borrelia burgdorferi, Ehrlichia canis, and Anaplasma phagocytophilum in dogs in the United States: results of a national clinic-based serologic survey. Vet Parasitol 160:138-48.
• Krupka I and Straubinger RK. 2010. Lyme borreliosis in dogs and cats: background, diagnosis, treatment and prevention of infections with Borrelia burgdorferi sensu stricto. Vet Clin North Am Small Anim Pract 40:1103-19.
• Mead P, et al. 2011. Canine serology as adjunct to human Lyme disease surveillance. Emerg Infect Dis17:1710-2.