Lyme Borreliosis

Lyme borreliosis (LB) is a tick-transmitted inflammatory disease induced by spirochetes. In dogs the infection is common in the moderate climate regions of the Northern Hemisphere; prevalence of infection in dogs may range regionally as high as 85%, but generally is approximately 3 to 10%.

The infection is zoonotic and LB in humans is the most important reported vector-borne disease in Europe and the USA. The human disease was first identified in the North-Eastern part of the USA in the town Lyme during the 1970s, but retrospective analysis revealed its presence since the late 19th century in Europe and the US.

At least three closely interrelated elements must be present in nature to spread LB:

(1) the Lyme-borreliosis-causing bacteria of the Borrelia burgdorferi sensu lato (s.l.) complex,

(2) Ixodes ticks as transmitting vectors for the pathogens, and

(3) mammals (e.g. mice and deer) that provide a blood meal for the ticks through their various life stages.

Although a high proportion of dogs are positive for specific antibodies in endemic areas, not all infected animals develop clinical signs. Therefore, diagnosis should be based on both clinical signs and serologic testing. Therapy consists of antibiotic treatment for four weeks. Vaccines are available for the USA and other countries.


The genus Borrelia is included in the bacterial family Borreliaceae within the order Spirochaetales. The spirochete isolated from ticks and humans was identified as Borrelia by Willy Burgdorfer, et al. in 1982. In Europe, clinical signs of human borreliosis were described for the first time by Afzelius in 1910 and Lipschütz in 1913 in patients.

There are at least 52 Borrelia species, including 21 in the Lyme borreliosis (LB) group (Borrelia burgdorferi sensu lato (s.l.), gram-negative spirochetes which generally migrate within the host interstitially), 29 in the relapsing fever group (migrating haematogenously), and 2 undetermined members.

In dogs in North America, LB has only been associated with Borrelia burgdorferi sensu stricto (s.s.), of which several subtypes or strains exist, based on outer surface protein C (OspC, Osp=outer surface protein) genotyping. In Europe, coinfections of B. burgdorferi s.s. with other B. burgdorferi s.l. strains (i.e., Borrelia garinii) may predispose dogs to illness. Other B. burgdorferi s.l. species causing human LB (i.e., Borrelia mayonii in upper Midwestern states in the U.S.; Borrelia afzelii, Borrelia bavariensis, B. garinii, and Borrelia spielmanni in Europe) are not known to cause illness in dogs so far (Littman et al., 2018).

Two of the outer surface membrane proteins, OspA and OspB, are antigenic and are useful in differentiating these organisms from other spirochetal species.

Darkfield microscopical image of helical shaped Borrelia burgdorferi bacteria of approximately 10-25µm length.
Darkfield microscopical image of helical shaped Borrelia burgdorferi bacteria (about 10-25µm length)

B. burgdorferi can be cultivated from their arthropod vectors or vertebrate hosts in Barbour-Stoenner-Kelly (BSK II)-medium. Here especially Borrelia from ticks and skin biopsy samples have been successfully cultivated. B. burgdorferi grows slowly as compared to most other bacteria. Cultivation of Borrelia is very difficult, because of a long time needed for development (6-8 weeks) and a medium which also supports the growth of other bacteria and fungi, potentially reducing or even blocking Borrelia growth. Thus a sterile sampling technique is of major importance.


Geographic distribution

The pathogens of Lyme borreliosis (LB) are clearly distributed in the northern hemisphere. Borrelia burgdorferi sensu stricto (s.s.) is spread over the USA and Europe up to Asia, whereas Borrelia afzelii, Borrelia garinii, Borrelia spielmanii, and Borrelia bavariensis as further human pathogens seem to be endemic in the Eurasian area.

LB is found e.g. in Germany, Switzerland, Czech Republic, Slovakia, Austria, France, Portugal, United Kingdom, Ireland, Scandinavia and many regions in Eastern Europe including Russia. It has also been confirmed in Asia (China, Japan, Korea) while it is unlikely and still questionable whether the disease is present in Australia. In the United States, LB is mostly localized to states in the North-eastern, mid-Atlantic, and upper North-central regions, and to several counties in North-western California.

In Eurasia and northern Africa, the principal vectors are Ixodes ricinus and Ixodes persulcatus. The principal vectors in the U.S. are the Deer tick, Ixodes scapularis, in the North-east and Upper-midwest states and Ixodes pacificus along the West Coast of the United States.

Generally, the infection rate of ixodid ticks increases with the life cycle of the vector. The infection rates of adult ticks can reach up to 50% in the U.S. (I. scapularis) and up to 75% in central Europe (I. ricinus).

The trend of increasing incidence in some established endemic areas continues, as well as geographic spread of B. burgdorferi to new areas. One possible explanation for the rise of LB is that populations of deer, raccoon, opossum, birds, and other wildlife have rapidly expanded in the last few years, and proximity of domestic animals and humans to these hosts has increased as suburban development has encroached on woodlands and people spend more time outside due to their recreational activities. Migratory birds may partially account for the spread of this disease as well.


Seasonal distribution

The risk of LB infection depends on the seasonal activity of the transmitting ticks in the respective region. While I. ricinus is active from spring to fall with less intensity during hot and dry summer months, the peak months of the Deer tick are June and July.


Natural reservoirs for Borrelia burgdorferi s.l.

Ticks, small rodents, and other non-human vertebrate animals all serve as natural reservoirs for B. burgdorferi s.l.: the bacteria can live and grow within these hosts without causing a fatal disease. Larvae and nymph ticks typically become infected with B. burgdorferi s.l. when they feed on small animals that carry the bacteria in spring and summer. The pathogens remain in the tick during the developmental changes from larva to nymph or from nymph to adult in late summer or early fall. Infected nymphs transmit B. burgdorferi bacteria to other small rodents and other mammals through biting and sucking blood, all in the course of their normal feeding behaviour.

Deer are the preferred host for the adult ticks in the USA; in Europe it is the roe dear (Capreolus capreolus). Other mammals including humans and dogs can be incidental hosts and can develop Lyme disease.

There seems to be a host specifity for the different Borrelia species: B. burgdorferi s.s. and B. afzelii e.g. usually prefer rodents as reservoir, whereas B. garinii and B. valaisiana mainly occur in birds. Furthermore, the tick hosts seem to be differently competent as Borrelia reservoir. In case of a high prevalence of non-competent hosts in an area, the general risk of infection is massively reduced.


In Eurasia and northern Africa, the principal vectors for Borrelia burgdorferi are Ixodes ricinus and Ixodes persulcatus. The principal vectors in the U.S. are the Deer tick, Ixodes scapularis, and Ixodes pacificus.

Naïve ticks acquire the bacterium Borrelia burgdorferi while feeding on infected hosts, e.g. small rodents. In later stages, these ticks then transmit the Lyme borreliosis (LB) pathogen to other hosts, including dogs and man, during the feeding process. The bacteria are maintained in the tissues of the hosts.

The pathogens are localised in the mid gut of their vector ticks, where they are capable to adhere to the gut wall supposedly through expression of the outer surface protein A (OspA). Attachment of the tick to temperate host skin and the influx of blood into the tick’s gut are expected to cause a change in the surface structure of Borrelia. An increased expression of OspC is considered to facilitate that the bacteria penetrate the tick gut wall and migrate via the hemolymph to the salivary gland. From there the pathogens can be transmitted with the saliva during feeding of the tick. Besides OspC, host plasminogen and its activators also play a role during transmission. The change within the surface structure of the spirochete and the subsequent migration to the salivary gland of the tick usually takes about 24 to 48 hours. The so far shortest reported transmission time for Borrelia is that of Ixodes ricinus nymphs infected with Borrelia burgdorferi sensu lato (s.l.) inducing infection of gerbils after 16.7 hours (Kahl et al., 1998). The transmission efficiency increases with the duration of the blood meal, a fact which is observed in different Ixodes ticks and different Borrelia strains. Nevertheless the observed transmission time seems to be also depending on the vector and Borrelia species.

Transovarial transmission does not occur or only occurs to a small percentage (in some species of the relapsing fever group), being of no importance for the transmission of LB pathogens in nature. Thus eggs and larvae are usually not infected with Borrelia. Feeding on an infected host will infect the larva. Another blood meal by the nymph can transmit the spirochetes to new mammalian or avian hosts; on the other hand it can cause an infection of still Borrelia-negative nymphs or a super-infection with additional spirochetes. In adult ticks, a large proportion can be infected in form of single, double or even triple infection with a variety of Borrelia species.


Borrelia burgdorferi enters the skin at the site of the tick bite. The infection may spread in lymph, producing regional adenopathy. From the site of entry the spirochetes spread to further distant tissues during the following weeks and months. With the dissemination of the spirochetes into the skin, joints, and connective tissues, local inflammatory reactions can cause pain, swelling, and lameness. Lameness was recognized first at the site of tick infestation, which reinforces the centrifugal spread of bacteria through the body.

The relative paucity of organisms in the involved tissue has suggested that manifestations of infection may be due to host immune response rather than to the destructive properties of the organism.

Although a high proportion of dogs may be seropositive in endemic areas, relatively few reports with clinical signs, like fever and lameness. Several mechanisms have been incriminated in causing joint damage in dogs. The production of the inflammatory mediator nitric oxide is up-regulated, as is interleukin 8, a cytokine that recruits neutrophils into infected synovial membranes.

Neurological abnormalities occur in some cases of borreliosis, cutaneous and cardiac diseases are rare and were not experimentally confirmed in dogs. Neuropathologic findings in experimentally infected dogs were described as an asymptomatic encephalitis, mild perineuritis, or meningitis only.

Additionally, in naturally infected dogs, glomerulonephritis with protein loss was described for certain breeds (e.g., labrador retrievers, golden retrievers). Fatal and progressive renal disease including peripheral edema, azotemia, uremia, proteinuria, and effusion into body cavities was often associated with emesis. Pathogenesis of Lyme nephritis so far is unknown.


Lyme borreliosis (LB) can mimic many other diseases, and it is very difficult to provide a reliable diagnosis. To substantiate the diagnosis of LB, according to Krupka and Straubinger (2010) four criteria should be checked carefully:

  1. Are the clinical signs seen in the patient associated with (typical for) LB?
  2. Are specific antibodies against Borrelia burgdorferi detectable (vaccination needs to be considered)?
  3. Does the patient improve substantially after an appropriate antibiotic therapy is applied?
  4. Does the patient live in an endemic area for LB and is there a real risk of exposure to Ixodes spp. ticks?


Clinical findings

Since dogs generally do not develop the characteristic skin lesions (e.g. erythema migrans) commonly found in humans, diagnosis is more difficult. Moreover, many dogs seroconvert in response to infection but never develop clinical signs. Nevertheless clinical signs may arise a suspicion of LB which should be confirmed or ruled out especially by laboratory tests.


Laboratory tests

The indirect detection of B. burgdorferi by detecting specific antibodies in blood or blood serum has become an important tool in diagnosing LB. In dogs, serology is regarded as the only recommended modality to evaluate for exposure to B. burgdorferi (Littman et al., 2018).

A number of serologic in-house and reference laboratory tests is available on the market with different capabilities of differentiating vaccinal versus natural exposure antibodies as well as acute versus chronic infection (see Littman et al., 2018 for a detailed summary).

The highly variable surface protein, VlsE, and the invariable region (IR6), respectively the even shorter peptide sequence of IR6 called C6 are often used as highly conserved and specific antigens of the B. burgdorferi sensu lato (s.l.) complex in enzyme-linked immunosorbent assays (ELISAs). Besides this ELISA-based serology, Western blot testing is performed. Some authors state that Western blotting may cause cross-reactions with other spirochetal infections (Littman et al., 2018), whereas others explain the two-tiered test system of an (ELISA) and subsequent immunoblotting (Western blotting) to be the method of choice (Krupka and Straubinger, 2010; Chomel, 2015): Namely a highly sensitive screening method based on an ELISA to filter out negative samples with high fidelity, a required confirmation of equivocal samples and Western blotting used in a second step to characterize positive samples further or to differentiate between infected or vaccinated animals. For details on B. burgdorferi proteins seen on serum incubated immunoblots of dogs see Krupka and Straubinger (2010).

Antibodies often persist for months or years following successfully treated or untreated infection. Thus, seroreactivity has to be interpreted with caution, depending on the test systems and type of antigens used. In general, neither positive serologic test results nor a history of previous LB assures that an individual has protective immunity. Repeated infection with B. burgdorferi has been documented.


Further diagnostic measures, which are available are:

Cultivation: The diagnostic usefulness of this procedure is limited because of the need for a special bacteriologic medium (modified Barbour-Stoenner-Kelley (BSK II)-medium) and protracted observation of cultures. It may take 6-8 weeks until sufficient growth. Furthermore a high risk of contamination of the cultures exists, making sterile sampling essential. Only specialized laboratories should be consulted to obtain reliable test results.

Darkfield microscopy: It has especially been used for the diagnosis of Borrelia infection of ticks, but the technique is neither specific nor very sensitive. Different spirochetes cannot be differentiated.

Polymerase chain reaction (PCR): This technique is a very specific and sensitive tool. Besides different protocols and specific primers, the technique is limited by the type of tissue used and the number of bacteria available in the sample. It has been used to amplify genomic DNA of B. burgdorferi s.l. in skin, blood, cerebrospinal fluid, and synovial fluid. Meanwhile multiplex PCRs have been developed to detect several species and quantitative real time PCRs have been developed for a quantification of the pathogen. Nevertheless due to the mentioned limitations a negative result does not exclude an infection. For the detection of Borrelia in ticks this technique is used in laboratory diagnosis.

For cats, C6-based test systems labelled for dogs have been used in cats (Lappin and Huesken, 2015; Lappin et al., 2015). Seroconversion could be documented after experimental tick exposure using these test systems. Nevertheless, results were not always in accordance to positive skin PCRs and duration of positivity was partially very short. Thus further optimization experiments are recommended before using the kit for routine screening in cats (Littman et al., 2018).

Clinical Signs

Although a high proportion of dogs may be seropositive in endemic areas, not all intervals develop clinical signs. Rashes (erythema migrans) are rarely found in dogs and may not be readily apparent on dogs. Those that occur are localised and transient.

The incubation period for naturally infected dogs is not known. In a laboratory model, the humoral immune response developed within 4 to 6 weeks and clinical signs such as fever spikes and shifting leg lameness developed after 2 to 5 months. Lameness only lasted 3 to 4 days without treatment, but recurred at 2 to 4 week intervals in 60% of the dogs. Recurrences occurred commonly for 2 to 3 episodes, then resolved. However, histologic examination of tissue samples revealed lesions due to inflammatory responses (mild polyarthritis) more than one year after infection had occurred.

Acute clinical signs most commonly reported include fever, shifting leg lameness, lethargy, lymphadenopathy, and general malaise. Additionally, several distinct clinical symptoms may be recognized including polyarthritis and protein-losing nephritis. Other symptoms reported involve carditis, and neurologic abnormalities. While lameness is a common clinical sign in canine Lyme borreliosis (LB), the almost crippling, non-antibiotic responsive, chronic arthritis as in humans is rarely seen.

Summarizing, canine Lyme arthritis (in the field and experimentally) and Lyme nephritis (only in the field) have been reported in the U.S., whereas neurologic and cardiologic manifestations of  LB in dogs are not well-documented (Littman et al., 2018). Similar for Europe, seroprevalences in dogs are commonly found, but it is not proven that European LB causes clinical signs in dogs (Littman et al., 2018). Bernese Mountain dogs have been reported to be more often Borrelia burgdorferi sensu lato (s.l.) positive compared to other dog breeds.

Regarding cats, seroconversion in endemic areas is reported, as well as short-lived bacteraemia after experimental infection via spirochete inoculation. Furthermore, exposure to tick bites has been reported with lameness and multilocalized inflammations such as arthritis or meningitis in cats (Gibson et al., 1995) or has been reported without detectable clinical signs of disease in other studies (Burgess, 1992; Lappin and Huesken, 2015; Lappin et al., 2015). Studies proving clinical disease in naturally infected cats are missing so far, so that evidence excluding borreliosis as a cause of clinical illness in cats is as weak as the data indicating causation (Littman et al., 2018).


Clinical signs in humans

Human Lyme disease symptoms resemble many other diseases, like spirochete-caused syphilis. Three stages of infection can be distinguished: erythema migrans usually within the first month and often combined with flu-like symptoms, early dissemination of infection especially combined with lameness and the late disseminated disease after months to years associated with chronic changes in joints, skin and nervous system.

Treatment & Prevention

After a tick bite, Borrelia burgdorferi disseminates by active movement of the bacteria through the tissue. Therefore, even early infections require full dose antibiotic to penetrate all tissues in adequate concentrations to be bactericidal to the organism.


Antibiotic treatment

There is no universally effective antibiotic for treating Lyme borreliosis (LB). The choice of medication used and the dosage prescribed will vary for different individuals based on multiple factors. These include age, weight, gastrointestinal function, blood levels achieved, and patient tolerance.

The question of whether dogs (or cats) should be treated when specific antibodies are detected in the absence of clinical signs is controversial. It is often agreed that non-clinical, non-proteinuric, seropositive dogs should not be treated. For detailed considerations see also Littman et al. (2018).

Borrelia organisms are sensitive to tetracyclines (doxycycline), amoxicillin, azithromycin, and cephalosporines. The most commonly used drug is doxycycline, which is also effective in possible coinfections with Anaplasma and Ehrlichia. Amoxicillin is often preferred for sensitive and growing individuals. Additionally, cefovecin was also shown to be efficacious (Wagner et al., 2015). Encephalitis in humans caused by Borrelia is treated with cephalosporines, because these drugs penetrate the blood-brain barrier more efficiently (Krupka and Straubinger, 2010). Treatment regimens and more detailed considerations can be found in Krupka and Straubinger (2010) and Littman et al. (2018).

Special treatment considerations in cases of protein-loosing nephropathy can be found in Littman et al. (2018).


Duration of treatment

The spirochete has a very long generation time (12 to 24 hours in vitro and possibly much longer in living systems) and may have periods of dormancy, during which antibiotics will not kill the organism. Therefore, treatment has to be continued for a long time.

It has been observed for humans that symptoms will flare in cycles every four weeks. It is thought that this represents the organism's cell cycle, with the growth phase occurring once per month. As antibiotics will only kill bacteria during their growth phase, therapy is designed to brake at least one whole generation cycle. This is why the minimum treatment duration should be at least four weeks (also for dogs).

If antibiotics are effective, over time these flares will lessen in severity and duration. But a persistent infection with Borrelia even after antibiotic therapy is reported in dogs.



Measurements to prevent LB should be based on three columns:

  • daily tick checks; since it takes about 24 to 48 hours until borrelia reach the host skin after a tick bite had occurred, daily tick checks can dramatically reduce the risk of infection.
  • application of tick-killing or -repelling substances; many products are available for dogs and cats with tick-killing as well as tick repellent effect. These products reduce tick infestation significantly and therefore limit the risk of infection with Borrelia burgdorferi. Especially those products that quickly kill or prevent attachment and feeding by the tick are preferable.
  • vaccination; there are different approaches for generating antibodies against Borrelia burgdorferi transmission. Some vaccines induce anti-OspA antibodies, which when imbibed by a feeding tick will attack spirochetes which express OspA within the tick’s midgut by binding to the OspA-expressing borrelia in the tick, preventing their migration to the salivary glands and reducing their growth in the tick and thus halting transmission. But these anti-OspA titres are not boosted by natural exposure and wane in vaccinates, then allowing infection of the host. Hence frequent revaccination is essential. If borreliae have already infected the host, the bacteria are also not affected by OspA antibodies, because these borreliae have switched completely to OspC/VlsE surface expression. Other vaccines generate anti-OspC antibodies induced by bivalent bacterin vaccines or a chimeric recombinant vaccine and boosted by natural exposure, can eliminate transmitted organisms that express Osp. One of the vaccines available induces OspA and OspC antibodies against a number of B. burgdorferi strains. The decision whether to vaccinate or not should always be based on careful consideration of individual behaviour and circumstances, which include geographic location, outdoor activities, and risk of tick infestation, and prevention against B. burgdorferi infection should not be based on vaccination only (Krupka and Straubinger, 2010). There is much debate upon the efficacy and the usefulness of vaccination, which can be followed e.g. in Littman et al. (2018).


A vaccine for the prevention of human Lyme disease based on recombinant outer-surface protein specific to B. burgdorferi has been launched in 1998, but was withdrawn from the market in 2002.



Littman MP, Gerber B, Goldstein RE, et al.: ACVIM consensus update on Lyme borreliosis in dogs and cats. J Vet Intern Med. 2018, 32, 887-903



Kahl O, Janetzki-Mittmann C, Gray JS, et al.: Risk of infection with Borrelia burgdorferi sensu lato for a host in relation to the duration of nymphal Ixodes ricinus feeding and the method of tick removal. Zentralbl Bakteriol. 1998, 287, 41-52



Chomel B: Lyme disease. Rev Sci Tech. 2015, 34, 569-76

Krupka I, Straubinger R: 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. 2010, 40, 1103-19

Lappin MR, Chandrashekar R, Stillman B, et al.: Evidence of Anaplasma phagocytophilum and Borrelia burgdorferi infection in cats after exposure to wild-caught adult Ixodes scapularis ticks. J Vet Diagn Invest. 2015, 27, 522-5

Lappin MR, Huesken R: Anaplasma phagocytophilum and Borrelia burgdorferi infections in cats exposed repeatedly to Ixodes scapularis. J Vet Intern Med. 2015, 29, 1201 (ID03)

Littman MP, Gerber B, Goldstein RE, et al.: ACVIM consensus update on Lyme borreliosis in dogs and cats. J Vet Intern Med. 2018, 32, 887-903


Clinical Signs

Appel MJG: Lyme disease in dogs. Comp Cont Educ Pract Vet. 2002, 24 (Suppl.), 19-23

Burgess EC: Experimentally induced infection of cats with Borrelia burgdorferi. Am J Vet Res. 1992, 53, 1507-11

Gibson MD, Omran MT, Young CR: Experimental feline Lyme borreliosis as a model for testing Borrelia burgdorferi vaccines. Adv Exp Med Biol. 1995, 38, 373-82

Lappin MR, Chandrashekar R, Stillman B, et al.: Evidence of Anaplasma phagocytophilum and Borrelia burgdorferi infection in cats after exposure to wild-caught adult Ixodes scapularis ticks. J Vet Diagn Invest. 2015, 27, 522-5

Lappin MR, Huesken R: Anaplasma phagocytophilum and Borrelia burgdorferi infections in cats exposed repeatedly to Ixodes scapularis. J Vet Intern Med. 2015, 29, 1201 (ID03)

Littman MP, Gerber B, Goldstein RE, et al.: ACVIM consensus update on Lyme borreliosis in dogs and cats. J Vet Intern Med. 2018, 32, 887-903


Treatment & Prevention

Krupka I, Straubinger R: 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. 2010, 40, 1103-19

Littman MP, Gerber B, Goldstein RE, et al.: ACVIM consensus update on Lyme borreliosis in dogs and cats. J Vet Intern Med. 2018, 32, 887-903

Wagner B, Johnson J, Garcia-Tapia D, et al.: Comparison of effectiveness of cefovecin, doxycycline, and amoxicillin for the treatment of experimentally induced early Lyme borreliosis in dogs. BMC Vet Res. 2015, 11, 163

Further Reading

Appel MJG: Lyme disease in dogs. Comp Cont Educ Pract Vet. 2002, 24 (Suppl.), 19-23

Chomel B: Lyme disease. Rev Sci Tech. 2015, 34, 569-76

Krupka I, Straubinger R: 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. 2010, 40, 1103-19

Littman MP, Gerber B, Goldstein RE, et al.: ACVIM consensus update on Lyme borreliosis in dogs and cats. J Vet Intern Med. 2018, 32, 887-903

Straubinger RK, Dharma Rao T, Davidson E, et al.: Protection against tick-transmitted Lyme disease in dogs vaccinated with a multiantigenic vaccine. Vaccine 2002, 20, 181-93


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