Tick-borne pathogens

Relative to the United States and many other countries, the burden of tick-borne pathogens that can infect pets and people is thought to be relatively low in Canada.


Relative to the United States and many other countries, the burden of tick-borne pathogens that can infect pets and people is thought to be relatively low in Canada.  There are, however, some pathogens that are important here, including Borrelia burgdorferi (the cause of Lyme disease in people and animals) and Anaplasma phagocytophilum (the cause of granulocytic anaplasmosis in dogs and people).  Although these infections are not common in Canada, they can be a significant clinical problem for individual animals.

Most prevalence data for vector borne diseases in dogs in North America are based on the Idexx 4Dx SNAP test administered in clinics or by diagnostic labs.  As such, they represent only a small, privileged portion of the companion animal population (largely in major urban centres), and are not likely representative of free-roaming, rural, or remote dogs and cats, who may well have higher exposure and less tick prevention.  In addition, this test detects antibodies for tick borne pathogens, which does not indicate active infection, and cross reactions are possible with novel, closely related pathogens.  Finally, there is no way to determine from amalgamated data if positive animals had a history of travel to endemic regions - which would be the major incentive for offering testing to a client in non-endemic regions.  Published national data for dogs seen in veterinary clinics in Canada in 2008 (n=86,251) for seroprevalences of tick-borne pathogens were: Borrelia burgdorferi ( 0.72%); Ehrlichia canis (0.05%); Anaplasma phagocytophilum (0.19%); and Dirofilaria immitis - transmitted by mosquitoes (0.22%).  Approximately 14% of dogs with seropositivity for one of these pathogens were clinically ill at the time of testing, and approximately 77% of dogs tested had never left their province of residence.  The highest seroprevalence rates for B. burgdorferi were eastern and central Canada, and for A. phagocytophilum in Manitoba and Saskatchewan. More recent studies (primarily dogs from ON, QC, and MB) show somewhat higher exposure to B. burgdorferi (2-2.5%), Ehrlichia spp. (0.2-0.5%), Anaplasma spp. (0.3-0.4%) and D. immitis (0.2-0.4%).  Dogs in Nova Scotia and Ontario had highest seropositivity for Borrelia, Nova Scotia and Manitoba had highest seropositivity for Anaplasma, and Saskatchewan had highest seropositivity for Ehrlichia.

Up to date annual data based on Idexx 4Dx testing in dogs in Canada are available on the CAPC website https://capcvet.org/maps/#/.  Bear in mind that these indicate only the location where a dog was tested, not where a dog was exposed, and no travel history information is provided.  At moment, % positive tests remain low in Canada (Anaplasma <1%, Borrelia ~3%, Dirofilaria <1% and Ehrlichia <1%).  


Anaplasma phagocytophilum zoonosis

Anaplasma phagocytophilum is a rickettsial pathogen that infects a wide variety of mammals, including dogs, cats, people, horses, livestock, and wildlife - especially small rodents, in many parts of the world.  Various species of mice and related rodents are the primary reservoirs.  The organism is transmitted by ixodid (hard) ticks.  In North America the vectors are Ixodes scapularis (eastern and central areas) and  I. pacificus (western coastal areas).  These ticks are also vectors for Borrelia burgdorferi (the cause of Lyme disease), and serological evidence of co-infections with both B. burgdorferi and A. phagocytophilum have been reported in dogs.

With important exceptions (see below), A. phagocytophilum generally occurs within areas where populations of the tick vectors are established (endemic).  In Canada currently, populations of I. scapularis are established in areas of Nova Scotia, New Brunswick, southern Ontario and Quebec, and south-eastern Manitoba.  Populations of I. pacificus are established in several areas of southern British Columbia, including the Fraser Delta, Vancouver Island and the Gulf Islands.  In these areas of Canada, however, clinical anaplasmosis is a very rare diagnosis in dogs and cats, and national Idexx testing data demonstrates that seroprevalence remains low.   In Canada, the only published reports of clinical anaplasmosis in a dog were from Vancouver Island, where I. pacificus is endemic and the the dog involved had never left the island, and in three dogs in Saskatoon, Saskatchewan, where two of the dogs had never left the region, and it is assumed that the infection was acquired from Ixodes scapularis tick vectors that had dropped from migratory birds.   It is estimated that several million ticks are carried by birds from the United States into Canada annually. 

Clinical signs frequently associated with anaplasmosis in dogs include acute onset of lethargy, stiff limbs, inappetance, depression and fever.  Less common signs include vomiting and diarrhea.  Diagnosis is based on history, especially the presence of vector tick species on the animal, clinical signs, haematology (the organism has an affinity for leucocytes), serology,  microscopic detection of A. phagocytophilum in neutrophils in blood films, and/or detection of the organism in blood by PCR.  Affected dogs usually respond to treatment with doxycycline, although in some cases the clinical signs will resolve spontaneously.  Prevention depends on preventing infestation with the tick vector species and, if this is not practical, checking the animal daily for ticks - transmission of A. phagocytophilum from feeding tick to mammal usually takes 24 to 48 hours.

Anaplasma platys

Anaplasma platys is a related pathogen of dogs commonly found in tropical and sub-tropical areas. It has been reported in the US but not in Canada.  The vector for this organism in North America has not yet been identified with certainty, but is thought to be Rhipicephalus sanguineus, the brown dog tick. In dogs, A. platys causes a cyclic thrombocytopaenia which can cause bleeding, but in most dogs the infection tends to be self-limiting. Infections with this species are usually less severe than with A. phagocytophilum.  The serological test kit currently commercially available does not distinguish A. platys and A. phagocytophilumA. platys is often sympatric with Ehrlichia canis, and co-infections occur in some dogs. The zoonotic significance of A. platys is unknown.

Serological surveys of cats in the US have demonstrated exposure to A. phagocytophilum, and clinical disease has been reported in cats there, but much less frequently than in dogs.  Currently the situation in Canada is unknown.  Cats are not considered to be significant reservoirs for A. phagocytophilum.

Babesia canis (different subspecies exist)

Several sub-species of the protozoan Babesia occur in dogs in many parts of the world, particularly in the tropics and sub-tropics. IIn Canada, B. canis has been detected serologically in a small number of dogs in Ontario, most with a history of travel to the United States. In North America the vector for B. canis is Rhipicephalus sanguineus, but other ticks are important elsewhere in the world. There is also some evidence that the parasite can be transmitted by dog bites.

In the mammalian intermediate host, Babesia multiply asexually in erythrocytes and the merozoites produced invade additional erythrocytes. Eventually gametocytes are produced, which infect the tick vectors during blood feeding. In the tick definitive host, the gametocytes fuse to form a zygote which, by asexual reproduction, produces large number of kinetes which enter the body cavity of the tick and spread to a variety of organs, including the salivary glands. Here there is further asexual reproduction resulting in sporozoites in the lumen of the glands. This is the life cycle stage infective for the mammalian hosts, into which they are introduced during blood feeding. In some Babesia (e.g. B. canis canis) there is transovarial transmission in the ticks, and in all species there is transstadial transmission (transmission between life stages).

In the United States, some dogs infected with B. canis show a progressive haemolytic anaemia, which is usually mild. In most animals, the host immune response means that the infection is self-limiting. Some dogs remain persistently infected, however, with organisms sequestered in capillary networks. Stimuli such as stress can cause these parasites to infect erythrocytes in the peripheral circulation, resulting in clinical signs. These persistently infected animals can also act as reservoirs of the infection for the tick vectors and for other dogs. Currently, B. canis is not thought to be zoonotic. 


Bartonella species POTENTIAL ZOONOSES

Bacteria of the genus Bartonella have been detected in a wide range of domestic and free-ranging mammal species, and in people around the world. There are many different species and subspecies.  Bartonella species can be transmitted among their mammalian hosts by a range of arthropods including biting flies, fleas, keds, lice, sand flies and ticks, as well as through arthropod feces, bites and scratches, and body fluids from infected animals. Not surprisingly, people who work closely with infected animals have an increased risk of acquiring the pathogen.

In North America, several species of Bartonella utilize reservoir hosts, primarily rodents, and for these species clinical disease tends to be more common in non-reservoir hosts that are infected "accidentally".  Currently in North America, B. vinsonii berkhoffii and B. henselae are the most important species causing disease in dogs, and B. henselae the most important in cats.  Both these species are zoonotic; B. henselae is  the cause of cat scratch fever and a range of other clinical problems in people.  Coyotes are an important reservoir for B. vinsonnii berkhoffii, and there is evidence that this species co-evolved with one or more species of free-ranging canid.  Similarly, in the United States and elsewhere, free-ranging felids are important reservoirs for B. henselae. The likely vector for B. vinsonii berkhoffii is Rhipicephalus sanguineus, and fleas (especially Ctenocephalides felis felis) are the vector for B. henselae

In Canada, two of 96 feral cats surveyed on Prince Edward Island were positive for Bartonella spp. by PCR. In Ontario, B. henselae was detected in three of  55 (5.5% prevalence) dogs surveyed serologically.  One animal had haemolytic anaemia, the second blastomycosis and the third chronic renal failure.   In the same study, none of 59 dogs surveyed showed serological evidence of exposure to B. vinsonii berkhoffii.  Also in Ontario, PCR and blood culture on healthy cats detected B. henselae in 46/646 (3.7%) and B. clarridgeiae in 4/646 (0.6%).   In western Canada, a serological survey of dogs and cats from four public parks across the southern prairies demonstrated overall seroprevalences of 0.178% for B. henselae in 242 cats and 0.186% for B. clarridgeiae in 242 dogs.  Seroprevalence of B. henselae in domestic cats in the US ranges from 5% to 40%, depending on location, with greater prevalences in the south-east and in Pacific coastal areas.  Although data are limited, the seroprevalence of B. vinsonii berkhoffii in domestic dogs in the US seems lower.  The incidence of disease associated with Bartonella in dogs and cats in Canada is unknown, but it appears to be low.  This situation could change, however, as awareness of the organism and its possible clinical effects increases.

Current opinion is that the preferred site for the development of Bartonella in its mammalian hosts is the vascular endothelium, although the organism is often found in erythrocytes and macrophages.  Some dogs and cats, and people, infected with Bartonella might not show any (obvious) ill effects.  Clinical signs, when present, can reflect disease in a wide range of organs and tissues.  While the clinical pictures associated with B. vinsonii berkhoffii and B. vinsoni are somewhat different, commonly affected are the heart (endocarditis, myocarditis, arrhythmias), the joints (polyarthritis) and, for B. vinsonii berkhoffii, the CNS (anterior uveitis, chorioretinitis, meningoencephalitis).  A similar range of clinical effects are seen in people infected with species of Bartonella.

Borrelia burgdorferi ZOONOSIS

Borrelia burgdorferi is a tick-borne spirochaete that causes Lyme disease in people and in dogs in many parts of the world, including North America.  Recent research has identified multiple species within the B. burgdorferi complex, only some of which occur in North America, and not all of which have been associated with clinical disease.   The risk of the disease closely follows the established populations of the tick vectors. Ixodes scapularis (the deer or black-legged tick) is the vector in the southern, south-eastern, north-eastern and north central states of the US and in foci in south-eastern Manitoba, southern Ontario and Quebec, New Brunswick, and Nova Scotia.  Climate warming is rapidly expanding the areas supportive of completion of the life cycle of the tick, where suitable habitat exists for both free living tick stages and wildlife hosts.  Ixodes pacificus (the western black-legged tick) is the vector in California, in the western regions of the other Pacific coastal states, as well as in areas of Arizona and Utah.  In Canada, established populations of I. pacificus are found in southern British Columbia, including Vancouver Island and the Gulf Islands.  Ixodes pacificus is thought to be a relatively ineffective vector for B. burgdorferi, in part because it often feeds on lizards which are not competent reservoirs for the infection.   All the life cycle stages of I. scapularis and I. pacificus (larvae, nymphs and adults) are very tiny (adults < 2 mm) and so are easily missed on people and on dogs. 
Ixodes scapularis has been found in Canada in many areas outside the established populations following transport by migratory birds.  This likely accounts for human and animal cases of Lyme disease in Canada reported outside areas with established vector populations.

Borrelia burgdorferi is maintained in ecosystems using small rodent and bird reservoir hosts.  Adult tick vectors feed on deer, where they mate, drop off and lay eggs in the environment in the spring.  Transovarial (adult to egg) transmission of B. burgdorferi is very inefficient, and so deer are considered to be dead-end hosts for the bacterium.  The tick eggs hatch in the summer and the released larvae feed on small mammals and birds, and it is from these hosts that the ticks first acquire B. burgdorferi.  The larval ticks then leave their hosts and moult to nymphs which become active the following spring and early summer, looking for small rodents and birds on which to blood feed.  Transstadial infection with B. burgdorferi (from larvae to nymphs and nymphs to adults) is relatively efficient, so the nymphs infected as larvae can spread the bacterium to other reservoir hosts.  Nymphs are also the primary source of human infections with B. burgdorferi, because timing of nymphal activity coincides with human outdoor pursuits, and nymphs are small and difficult to detect.  After a blood meal, the nymphs leave their hosts and moult to adults, which seek deer and other large animals.  Dogs most often acquire B. burgdorferi from adult ticks, and although dogs are not considered to be important reservoir hosts, they can bring infected ticks into close contact with people.  Adult Ixodes scapularis are most active in late fall and early spring.  The basic vector cycle takes two years, although there are climate-driven differences in the timing of its various phases. 
Most dogs (95%) exposed to B. burgdorferi remain clinically normal, and the acute phase of Lyme disease in dogs can have a range of clinical features, including fever, anorexia, lymphadenopathy and arthritis which often appear weeks or month after exposure to the tick vectors.  In chronic cases, glomerulonephritis can develop.  In contrast to human cases, skin lesions (erythema migrans) are not a feature of the disease in dogs.  Diagnosis of Lyme disease in dogs can be problematic because of the need to decide whether seropositivity reflects active infection or simply past exposure, and is usually based on a combination of factors (e.g. likelihood of exposure to infected vectors, clinical signs, and serology). Control relies on effective tick prevention and, in endemic regions, vaccination against Lyme disease, although this does not protect the dog against other tick-borne pathogens.  Testing is generally recommended only for clinically ill animals in endemic regions, at least 6-8 weeks after possible exposure (although it is often done in spring, in conjunction with annual heartworm screening).  Treatment is generally recommended only for animals with clinical evidence of Lyme disease (arthritis, proteinuria).  However, recommendations for testing and treatment of Lyme disease in dogs are controversial, and periodically updated by the ACVIM (see Littman MP, Gerber B, Goldstein RE, Labato MA, Lappin MR, Moore GE. ACVIM consensus update on Lyme borreliosis in dogs and cats. J Vet Intern Med. 2018 May;32(3):887-903. doi: 10.1111/jvim.15085. Epub 2018 Mar 22. PMID: 29566442; PMCID: PMC5980284.)


Ehrlichia canis, E. chaffeensis, and E. ewingi POTENTIAL ZOONOSES

The rickettsial genus Ehrlichia includes species of importance in veterinary medicine: E. canis; E. chaffeensis, and E. ewingi.  All three species utilize tick vectors: Rhipicephalus sanguineus and sometimes Dermacentor variabilis for E. canis; Amblyomma americanum (which likely occurs in Canada only in southern Ontario and southern Quebec) for E. chaffeensis; and A. americanum, D. variabilis and R. sanguineus for E. ewingiEhrlichia depends on reservoir hosts for persistence: dogs and wild canids for E. canis; white-tailed deer for E. chaffeensis; and probably dogs and deer for E. ewingi.

A recent serosurvey in the US showed evidence of exposure to E. canis in 0.6% of 982 336 dogs across most states in the southern two thirds of the country (except Utah and Nevada), in New England, and in Michigan, Wisconsin and Minnesota.  In Canada, a study published in 2006 revealed 1/271 dogs in Ontario were seropositive for E. canis, and of 41 tested by PCR, three were positive. Two of these three animals were seronegative.   There are published reports of three seropositive dogs with CNS signs in Ontario.  One of these dogs was seropositive to Ehrlichia risticii (now Neorickettsia risticii), the cause of Potomac horse fever.  None of the three dogs had a history of travel outside the province.  There is also a published report of a seropositive dog in Quebec with a variety of clinical signs attributed to a co-infection with Ehrlichia canis and Babesia canis.  This dog had recently been imported from Greece.  In more recent national studies in Canada (mostly dogs in Ontario, Quebec, and Manitoba), seropositivity for E. canis ranged from 0.05% to 0.5%. There are no large-scale, published data for the seroprevalence of E. chaffeensis or E. ewingi in dogs in North America.

Many dogs infected with Ehrlichia species show limited or no ill effects,  and E. canis is generally thought to be the most pathogenic of the three species in dogs.  Clinical effects include fever, depression, myalgia, and reduced leukocytes and platelets, the last sometimes causing bleeding, especially epistaxis (nose bleeds).  Ehrlichia chaffeensis and E. ewingi seem to cause only mild disease - clinically similar to that caused by E. canis - in otherwise healthy dogs.  Occasionally co-infections with Ehrlichia species and other pathogens have been reported, especially those that share R. sanguineus as a vector (e.g. Babesia species).  All three species of Ehrlichia infecting dogs can also infect people, and E. chaffeensis appears to be the most important as a cause of human disease.

A recent serosurvey of approximately 150 cats in the US found no evidence of exposure to Ehrlichia species.  There have been occasional reports, however, of clinical disease associated with Ehrlichia in cats in the US, but the specific identity of the organism involved has not been fully established and it is sometimes referred to as "E. canis -like".  Rhipicephalus sanguineus seems not to feed readily on cats unless the ticks are present in large numbers, but D. variabilis will feed on cats and so might be a more important vector.  Currently the occurrence of infection and disease associated with Ehrlichia in Canada is unknown.  Cats are not considered to be significant reservoirs for Ehrlichia.


Rickettsia ricketsii and other species of Rickettsia ZOONOSES

Rickettsia rickettsii infection is associated with Rocky Mountain Spotted Fever (RMSF) in people and in dogs.  The organisms are transmitted by ixodid ticks, in Canada, Dermacentor andersoni (in the west) and D. variabilis (in the east).  Recently, however, Rhipicephalus sanguineus served as the primary vector in  outbreaks of human RMSF in Arizona.  Rickettsia rickettsii is maintained in small rodent reservoir hosts and transmitted to dogs and people (accidental hosts) by the tick vectors. Transmission occurs between the life cycle stages of the tick - larva to nymph to adult (transstadial transmission), among adult ticks during mating, and from adult females to their eggs (transovarial transmission). 

Sporadic cases of RMSF occur in dogs in the US;  there are no data for the occurrence of clinical RMSF dogs in Canada. In the US, human disease is more common in the east than in the west, and between 1997 and 2002 nearly 4,000 cases were reported in people (RMSF in people is reportable in the US).  RMSF is not reportable in Canada, and so data on its occurrence in people here are very sparse.  A 1995 serological survey of 240 dogs from parks in the southern prairies of Canada revealed a prevalence of 0.025%.  A similar survey of dogs in Ontario from 2000 to 2003 revealed 3/68 dogs to be infected (4.4% prevalence).  Two of these animals had a history of travel to the US.  There is recent evidence that some, usually mild, cases of RMSF in people in the US might be due to R. parkeri and other species, and it is possible that some of these might also infect dogs, causing clinical disease.  In addition, infection of the tick vectors with  apparently non-pathogenic species of Rickettsia, for example R. peacockii, can block the transmission of R. rickettsii and perhaps other species.  In a recent PCR-based survey of approximately 1,300 adult ticks (mostly from Saskatchewan, but also from Alberta, Manitoba and northern Ontario),  Rickettsia rickettsii was not found in any of the ticks examined. 

The clinical signs associated with RMSF in dogs are highly variable, and include anorexia, fever, vomiting and lethargy.  If untreated, additional signs can appear including bleeding and neurological problems.  As in people, RMSF can be serious and even fatal in dogs, especially if appropriate antibiotic treatment is not started promptly.

Francisella tularensis ZOONOSES

Francisella tularensis, the causative agent of tularemia (or rabbit fever), is a gram-negative facultative intracellular coccobacillus related to Brucella spp. It can survive for weeks or months in a moist environment and is transmitted mechanically by arthropods (such as ticks, biting flies and mosquitoes), through exposure to infected water sources, or by direct contact with infected body fluids. There are three subspecies:  F. tularensis tularensis (type A tularemia), F. tularensis holarctica (type B tularemia) and F. novicida (type C tularemia - which rarely causes disease). Type A has been documented almost exclusively in North America and is more virulent; with mortality rates reaching as high as 30-60% in humans if left untreated. Rabbits and hares are thought to be reservoirs, and tick vectors such as  Dermacentor andersoni, Amblyomma americanum, and D. variabilis have been implicated in transmission (along with  Chrysops discalis, the deer fly). Transmission can occur between life cycle stages of ticks via transovarial and transstadial transmission. Type B is less virulent, associated with mosquito transmission and water-dwelling rodents (muskrats and beavers), and is widespread across the globe. Infections have been documented in over 200 animal species, with each developing differing degrees of disease severity. 

Rodents and lagomorphs are considered to be the most susceptible hosts and often develop fatal disease. Cats are more susceptible than dogs, though severity varies for both, ranging from mild localized infection (ulceroglandular form) to acute fatal disease (systemic). Kittens may develop a severe systemic disease (typhoidal tularemia) that is marked by lethargy, lymphadenopathy, hepatosplenomegaly and jaundice. Localized forms may manifest as a chronically draining abscess. Information for treatment of domesticated animals is limited. Gentamicin is typically used as the treatment of choice in humans. Tetracycline (doxycycline) and fluoroquinolones (administered for 2 weeks) have also been used for pets. Infection is confirmed through culture, serology, or PCR.

Little information is available for infection rates in dogs and cats across Canada and the US. In a very early study (1954), Francisella tularensis was detected in 0.4% of A. americanum ticks collected from Arkansas dogs. From 2006 to 2016, 1,814 U.S. human tularemia cases were reported, of which only 40% had any record indicating how the person became exposed. Of these, 3.3% were dog-related and 0.5% were due to tick exposure from dogs. In 1984, a tick-borne tularemia outbreak in twenty people from South Dakota was linked to dog exposures, with 17% of D. variabilis ticks from dogs found to harbor either Type A (12.5%) or Type B (87.5%) tularemia.Transmission from cats to humans via scratches and bites has been well documented. Blood samples collected from privately owned cats in Connecticut and New York State, USA in 1985-1990 revealed that 12% of animals had antibodies for F. tularensis (n=91). 

In Canada, one study on rural dogs and cats in southern AB and SK found a seroprevalence of 0.089% for Francisella tularensisAcross Canada, wildlife have been actively surveyed for exposure to the bacteria. Antibodies have been documented in animals ranging from raccoons (11.3% from Ontario; n=177) to polar bears (68.4% of the Hudson Bay population; n=411). Climate change will likely increase the risk for both humans and pets in Canada, as warming temperatures improve vector survival and pathogen transmission. 



Evason, M., Stull, J.W., Pearl, D.L. et al. Prevalence of Borrelia burgdorferi, Anaplasmaspp., Ehrlichia spp. and Dirofilaria immitis in Canadian dogs, 2008 to 2015: a repeat cross-sectional study. Parasites and Vectors 12, 64 (2019). https://doi.org/10.1186/s13071-019-3299-9

Herrin, B.H., Peregrine, A.S., Goring, J. et al. Canine infection with Borrelia burgdorferi, Dirofilaria immitis, Anaplasma spp. and Ehrlichia spp. in Canada, 2013–2014. Parasites and Vectors 10, 244 (2017). https://doi.org/10.1186/s13071-017-2184-7

Villeneuve A et al. (2011) Seroprevalence of Borrelia burgdorferi, Anaplasma phagocytophilum, Ehrlichia canis and Dirofilaria immitis among dogs in Canada. Canadian Veterinary Journal 52: 527-530.

Blagburn BL et al. (2009) Biology, treatment and control of flea and tick infestations. Veterinary Clinics of North America Small Animal Practice 39: 1173-1200.

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: a national clinic-based survey.  Veterinary Parasitology 160: 138-148.

Gary AT et al. (2006) The low seroprevalence of tick-transmitted agents of disease in dogs from southern Ontario and Quebec. Canadian Veterinary Journal 47: 1194-2000.

Anaplasma phagocytophilum

Little SE (2010) Ehrlichiosis and anaplasmosis in dogs and cats. Veterinary Clinics of North America Small Animal Practice 40: 1121-1149.

Cockwill KR et al. (2009) Granulocytic anaplasmosis in three dogs from Saskatoon, Saskatchewan. Canadian Veterinary Journal 50: 835-840.

Lester SJ et al. (2005) Anaplasma phagocytophilum infection (granulocystic anaplasmosis) in a dog from Vancouver Island. Canadian Veterinary Journal 46: 825-827.

Babesia canis canis

King AR et al. (1991) Concurrent ehrlichiosis and babesiosis in a dog. Canadian Veterinary Journal 32: 305-307.

Bartonella species

Stovanovic V et al., (2011) Infectious disease prevalence in a feral cat population on Prince Edward Island, Canada. Canadian Veterinary Journal 52: 979-982.

Breitschwerdt EB at al. (2010) Bartonellosis: an emerging infectious disease of zoonotic importance to animals and human beings. Journal of Veterinary Emergency and Critical Care 20: 8-30.

Kamrani A et al. (2008) The prevalence of Bartonella, hemoplasma, and Rickettsia felis infections in domestic cats and in cat fleas in Ontario. Canadian Journal of Veterinary Research 72: 411-419.

Cockwill KR et al. (2007) Bartonella vinsonii subsp. berkhoffii endocarditis in a dog from Saskatchewan. Canadian Veterinary Journal 48: 839-844.

Leighton, F.A., Artsob, H.A., Chu, M.C. et al. A Serological Survey of Rural Dogs and Cats on the Southwestern Canadian Prairie for Zoonotic Pathogens. Can J Public Health 92, 67–71 (2001). https://doi.org/10.1007/BF03404848

Cimolai N et al. (2000) Bartonella henselae infection in British Columbia: evidence for an endemic disease among humans. Canadian Journal of Microbiology 46: 908-912.

Borrelia burgdorferi

Scott JD et al. (2010) Detection of Lyme disease spirochaete, Borrelia burgdorferi sensu lato, including three novel genotypes in ticks (Acari: Ixodidae) collected from songbirds (Passeriformes) across Canada. Journal of Vector Ecology 35: 124-138.

Little SE et al. (2010) Lyme borreliosis in dogs and humans in the USA. Trends in Parasitology 26: 213-218.

Krupke I et al. (2010) Lyme borreliosis in dogs and cats: background, diagnosis, treatment and prevention of infections with Borrelia burgdorferi sensu stricto. Veterinary Clinics of North America Small Animal Practice 40: 1103-1119.

Mak S et al. (2010) Biological niche modeling of Lyme disease in Britsh Columbia, Canada. Journal of Medical Entomology 47: 99-105.

Ogden NH et al. (2009) The emergence of Lyme disease in Canada. Canadian Medical Association Journal 180: 1221-1224.

Littman MP et al. (2006) ACVIM small animal consensus statement on Lyme disease in dogs: diagnosis, treatment and prevention. Journal of Veterinary Internal Medicine 20: 422-434.

Ogden NH et al. (2006) Climate change and the potential for range expansion of the Lyme disease vector Ixodes scapularis in Canada. International Journal for Parasitology 36: 63-70.

Ehrlichia canis, E. chaffeensis, and E. ewingi

Little SE (2010) Ehrlichiosis and anaplasmosis in dogs and cats. Veterinary Clinics of North America Small Animal Practice 40: 1121-1149.

King AR et al. (1991) Concurrent ehrlichiosis and babesiosis in a dog. Canadian Veterinary Journal 32: 305-307.

Firneisz GD et al. (1990) Canine ehrlichiosis in Ontario. Canadian Veterinary Journal 31: 652-653.

Rickettsia ricketsii and other species of Rickettsia

Nicholson WL et al. (2010) The increasing recognition of rickettsial pathogens in dogs and people. Trends in Parasitology 26: 205-212.

Dergousoff SJ et al. (2009) Prevalence of Rickettsia spp. in Canadian Populations of Dermacentor andersoni and D. variabilis. Applied and Environmental Microbiology 75: 1786-1789.

Kamrani A et al. (2008) The prevalence of Bartonella, hemoplasma, and Rickettsia felis infections in domestic cats and in cat fleas in Ontario. Canadian Journal of Veterinary Research 72: 411-419.



Francisella tularensis

Gabriele-Rivet V et al. (2016) Eco-Epizootiologic study of Francisella tularensis, the agent of tularemia, in Quebec wildlife. J Wildl Dis 52 (2): 217–229.

Larson MA et al. (2014) Francisella tularensis Bacteria Associated with Feline Tularemia in the United States. Emerg Infect Dis. 20(12): 2068–2071. 

Leighton, F.A., Artsob, H.A., Chu, M.C. et al. A Serological Survey of Rural Dogs and Cats on the Southwestern Canadian Prairie for Zoonotic Pathogens. Can J Public Health 92, 67–71 (2001). https://doi.org/10.1007/BF03404848

Magnarelli L et al. (2006)  Detection of antibodies to Francisella tularensis in cats. Res Vet Sci. 82(1):22-6. 

Martin T et al. (1982) Tularemia in Canada with a focus on Saskatchewan. Can Med Assoc J 127(4):279-282.

Pennisi MG et al. (2013) Francisella tularensis Infection in Cats: ABCD guidelines on prevention and management. Journal of Feline Medicine and Surgery. 15(7). https://doi.org/10.1177/1098612X13489219

Pilfold N et al. (2021) Long-term increases in pathogen seroprevalence in polar bears (Ursus maritimus) influenced by climate change. Global Change Biology. https://doi.org/10.1111/gcb.15537

Smith et al. (2018) Powassan Virus and Other Arthropod-Borne Viruses in Wildlife and Ticks in Ontario, Canada. Am J Trop Med Hyg. 99(2): 458–465.

Zellner B and Huntley JF. (2019) Ticks and Tularemia: Do We Know What We Don't Know? Front. Cell. Infect. Microbiol. https://doi.org/10.3389/fcimb.2019.00146

Share this story