Invasive Species Compendium

Detailed coverage of invasive species threatening livelihoods and the environment worldwide


lyme borreliosis



lyme borreliosis


  • Last modified
  • 14 July 2018
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • lyme borreliosis
  • Overview

  • Borrelia burgdorferi, a spirochaete bacterium, is the cause of Lyme borreliosis (LB), which is primarily of interest as a disease of humans. Modern studies date from an epidemic of juvenile arthritis in t...

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Preferred Scientific Name

  • lyme borreliosis

International Common Names

  • English: acrodermatitis chronica atrophicans; Bannwarth's syndrome; borreliosis, borrelia burgdorferi, lyme disease in cattle and sheep; borreliosis, lyme; erythema migrans; lyme disease

English acronym

  • LB


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Borrelia burgdorferi, a spirochaete bacterium, is the cause of Lyme borreliosis (LB), which is primarily of interest as a disease of humans. Modern studies date from an epidemic of juvenile arthritis in the town of Old Lyme, Connecticut. USA (Steere et al., 1977a).The causal agent, Borrelia burgdorferi, denoting all genospecies, was demonstrated in Ixodes ticks in the USA in 1982 (Burgdorfer et al., 1982) and in European ticks in the following year (Burgdorfer et al., 1983). Some of the symptoms had been described in Europe much earlier (Buchwald, 1883; Afzelius, 1910) and it is probable that the disease has been present in Europe for a very long time. Subsequent studies showed that LB occurs throughout temperate Asia as far as Japan (Kawabata et al., 1987, Korenberg et al., 1988). The most characteristic symptom of LB, an expanding rash (erythema migrans), eventually resolves spontaneously, but more serious neurological, cardiac, joint and chronic skin problems may occur weeks, months or even years after infection. Infection is usually asymptomatic but can cause significant, sometimes disabling, illness. The very few deaths associated with LB have usually occurred in immunocompromised patients.

Hosts/Species Affected

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Tick vectors

Only 9 species of ticks are proven vectors of B. burgdorferi worldwide, several other species have been incriminated as carriers (Gray, 1998). All of the vectors are Ixodes spp and 4 of them, the major vectors, I. persulcatus, I. pacificus, I. ricinus, I. scapularis, belong to the Ixodes ricinus species complex. I. ovatus transmits the non-pathogenic genospecies B. japonicum. Other species, such as I. dentatus, I. neotomae and I. spinipalpis in the New World and I. hexagonus in the Old World, seem to be involved in enclosed enzootic cycles and may have an important role in the maintenance of the spirochaetes in nature.

The 4 main vectors are 3-host ticks that quest for hosts from the vegetation.Each stage (larva, nymph, adult female) feeds on a host for a few days and then detaches and develops in the vegetation to the next stage, a process that takes several months. The males do not engorge and do not need to feed before mating, unlike many other ixodid ticks, but they may occasionally take small blood meals. The complete life-cycle takes 2-6 years depending on the tick species and the geographical area. Both questing and developing stages are sensitive to desiccation and require a relative humidity of at least 80% throughout the off-host periods, so that they are confined to areas where a good cover of vegetation is present. Distinct seasonality in host-seeking activity occurs, which is determined by diapause mechanisms mainly involving responses to photoperiod and temperature. The vector species all differ slightly in the way they utilize these environmental stimuli (Gray, 1991). The seasonality of early LB is determined by a combination of tick seasonal activity and the utilization of LB habitat by the public, so that in Europe most infections seem to be acquired in mid to late summer (Stanek et al., 1986).


The host requirements of the ticks are best met by a diverse mix of fauna, but a minimal requirement is that a significant number of large animals, such as deer, should be present in order to feed the adult female ticks. Female ticks, with few exceptions, only engorge successfully on animals as large as or larger than a hare (Lepus spp). The larvae and nymphs are more catholic in their host preferences and in addition to the larger hosts can feed on smaller mammals and on birds. The microclimatic and host requirements of these ticks mean that in most of their range they are found in mixed and deciduous woodlands, which harbour significant numbers of large animals, such as deer to maintain the tick population. However, ticks will also survive in coniferous forest as long as there is sufficient litter on the ground and the climate is moist. In some areas ticks may be found in large numbers in meadows and on open hillside and these areas are characterized by rough vegetation and high rainfall, and the major hosts involved are usually livestock such as cattle and sheep which feed all the tick stages.

B. burgdorferi infection is usually acquired from a reservoir host by larval or nymphal ticks and transmitted horizontally by nymphs or adults. Transovarial transmission is thought to be uncommon and unfed larval ticks are rarely found to be infected. Larval ticks are therefore not considered to be an important source of disease, but the small proportion of infected ticks in the environment may still be important for the maintenance of B. burgdorferi in nature (Boer et al., 1993). The proportion of nymphs and adult ticks that are infected in a particular habitat may be highly variable, depending on tick species, spirochaete genospecies and reservoir hosts available. Nymphal infection rates may be as high as 50% but usually range between 10 and 20%, whereas adult ticks tend to show higher infection rates, usually ranging between 20 and 30%, sometimes more than 50%. A combination of relative abundance, willingness to bite humans (Robertson et al., 2000a) and the average infection rates incriminate the nymphs of I. pacificus, I. ricinus and I. scapularis as the main stage transmitting human disease. In I. persulcatus the adult female is the main vector because these nymphs rarely bite humans.

The abundance of reservoir hosts (usually small and medium-sized vertebrates) in a particular habitat is the most important factor in the establishment of significant infected tick populations. Different genospecies may be adapted to particular types of reservoir hosts, e.g. B. afzelii to rodents (Gern and Falco, 2000). Available evidence suggests that large animals such as deer, sheep and cattle are not important reservoir hosts (Gern and Falco, 2000), but they have a vital role in the maintenance of the tick population, since adult ticks only engorge successfully on larger animals (Gray, 1991). Some medium-sized animals such as hares and hedgehogs are not only reservoir hosts, but can also feed adult ticks (Tälleklint and Jaenson, 1993, Gray et al., 1994).


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Lyme borreliosis (LB) is restricted to temperate regions of the northern hemisphere and its distribution is approximately defined by the distribution of its tick vectors which are members of the Ixodesricinus species complex. In the New World the vectors are I. Pacificus, which occurs on the west coast extending from California to British Columbia and I. scapularis which is found on the east coast from Canada to Florida and southern Texas. I. scapularis is not found in many of the central states of the USA but occurs as far west as Wisconsin. Despite the presence of I. scapularis in the southern states of the USA, LB is not thought to occur there, though this view is not universally accepted. The principle vector in western and central Europe is I. ricinus, and in eastern Europe and temperate Asia the vector is I. persulcatus, which occurs as far east as Japan. In parts of the Baltic countries, such as Estonia, these two vector species are sympatric. B. burgdorferi is found throughout these areas and has also been recorded in North Africa where I. ricinus is present. However, LB is absent from southeast Europe, for example Greece, despite the presence of I. ricinus, an apparently analogous situation to that in the southern USA.

The different manifestations of LB do not show an even geographical distribution and this is at least partly due to the fact that several different genospecies of the causal agent (collectively referred to as B. burgdorferi are known to exist (Postic et al., 1994). Several of these genospecies seem to be especially associated with particular symptoms (Dam et al., 1993). Only one genospecies, B. burgdorferi sensu stricto, has been implicated as the cause of disease in North America, mainly causing arthritis. In Europe three genospecies, B. burgdorferi sensu stricto, B. afzelii and B. garinii are recognized as pathogens. Still others, such as B. valaisiana and B. lusitaniae are of unknown pathogenicity at present. B. afzelii is associated with a degenerative skin condition, acrodermatitis chronica atrophicans, and B. garinii with neurological symptoms. However, these associations are not clear-cut and there seems to be considerable overlap.

Distribution Table

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The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes


ChinaPresentPresent based on regional distribution.
-FujianPresentPan et al., 1991
-HebeiPresentZhang, 1992
-HeilongjiangPresentAi et al., 1994
-JilinPresentZhang ZF(et al), et al
-LiaoningPresentZhang, 1992
-XinjiangPresentZhang, 1992
IsraelPresentBerger et al., 1993
JapanPresentPresent based on regional distribution.
-HokkaidoPresentNakao et al., 1994
-HonshuPresentCarlberg and Naito, 1991
-KyushuPresentCarlberg and Naito, 1991
-ShikokuPresentCarlberg and Naito, 1991
Korea, Republic ofPresentPark et al., 1993
KyrgyzstanPresentPostic et al., 1994
MongoliaPresentTakada et al., 1998
TaiwanPresentShih and Chao, 1998


TunisiaPresentZhioua et al., 1999

North America

CanadaPresentPresent based on regional distribution.
-British ColumbiaPresentKindree and, 1994
-OntarioPresentBarker and Lindsay, 2000
USAPresentPresent based on regional distribution.
-AlabamaPresentWright et al., 1997
-ArizonaPresentOlson et al., 1992
-CaliforniaLocalisedLane and Lavoie, 1988
-ConnecticutWidespreadSteere et al., 1977a; Steere et al., 1977b
-DelawareWidespreadWolfe et al., 1994
-FloridaPresentOliver et al., 1995
-GeorgiaPresentOliver et al., 1995
-IllinoisPresentNelson et al., 1991
-IndianaPresentPinger et al., 1991
-MainePresentGinsberg and Ewing, 1988
-MarylandWidespreadHofmeister et al., 1999
-MassachusettsWidespreadPiesman et al., 1986
-MichiganPresentPiesman et al., 1999
-MinnesotaPresentDrew and Loken, 1988
-New HampshirePresentAnderson et al., 1987; Anderson et al., 1987
-New MexicoWidespreadVarde et al., 1988
-New YorkWidespreadMagnarelli et al., 1986
-North CarolinaPresentMagnarelli et al., 1986
-OklahomaPresentKocan et al., 1992
-OregonPresentBurkot et al., 1999
-PennsylvaniaWidespreadLord and Lord, 1994
-Rhode IslandWidespreadAnderson et al., 1986
-South CarolinaPresentOliver and Clark, 2000
-TexasPresentTeltow et al., 1991
-VirginiaPresentSonenshine et al., 1995
-WisconsinWidespreadAnderson et al., 1987; Anderson et al., 1987


AustriaWidespreadRadda et al., 1986
BelarusWidespreadPostic and Korenberg, 1997
BelgiumWidespreadBigaignon et al., 1989
BulgariaWidespreadAngelov et al., 1990
CroatiaWidespreadRijpkema et al., 1996
Czech RepublicWidespreadHercogová et al., 1993
Czechoslovakia (former)WidespreadA
DenmarkWidespreadHansen, 1994
EstoniaWidespreadPostic and Korenberg, 1997
FinlandWidespreadJunttila et al., 1994
FranceWidespreadGilot et al., 1996
GermanyWidespreadWilske et al., 1987
HungaryWidespreadLakos and Nagy, 1991
IrelandLocalisedKirsten and Rijpkema, 1997
ItalyLocalisedBurioni et al., 1988
LithuaniaWidespreadMoteiunas and Shadzhene, 1990
MoldovaPresentPostic and Korenberg, 1997
NetherlandsWidespreadNohlmans et al., 1995
NorwayWidespreadBogsrud and Odegaard, 1987
PolandWidespreadWegner and Stanczak, 1994
PortugalLocalisedDe and Sewell, 2000
-MadeiraPresentMatuschka et al., 1994
RomaniaPresentCracea and Constantinescu, 1988
Russian FederationPresentPresent based on regional distribution.
-Central RussiaWidespreadVorob'eva and Volegova, 1995
-Northern RussiaWidespreadAleksee and Dubinina, 1998
-Western SiberiaWidespreadNaumov and Gutova, 1994
SlovakiaWidespreadDrgonová and Rehácek, 1995
SloveniaWidespreadStrle and Cheng, 1994
SpainLocalisedEstrada-Pena et al., 1995
SwedenWidespreadGustafson et al., 1995
SwitzerlandWidespreadAeschlimann and Chamot, 1987
UKLocalisedRobertson et al., 1999
UkraineWidespreadPostic and Korenberg, 1997
Yugoslavia (former)LocalisedStrle and Cheng, 1994
Yugoslavia (Serbia and Montenegro)PresentStajkovic and Obradovic, 1993


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Diagnosis of Lyme borreliosis (LB) is difficult and must be based on clinical signs taken together with history of exposure and supporting laboratory evidence. The only pathognomic manifestation of the disease is a 'typical' EM, which is frequently absent. Serological diagnosis is the most usual laboratory evidence provided, but due to cross reactions is difficult to perform and interpret correctly. Much mis-diagnosis took place in the early years after description of the disease and this is still a problem. The current recommended procedure is to use a two-step approach, consisting of a screening test such as ELISA followed by a confirmatory test of ELISA reactive-samples with a method of higher specificity such as immunoblotting. However, there is no standardization of either methodology or interpretation and inter-laboratory procedures and performance can vary widely (Robertson et al., 2000b). Polymerase chain reaction (PCR) depends on the reliable detection of frequently scarce organisms and is not recommended for routine use. Although culturing is the 'gold standard' for supporting evidence, this is frequently impossible because of the fastidiousness and scarcity of the pathogens.

List of Symptoms/Signs

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SignLife StagesType
Cardiovascular Signs / Tachycardia, rapid pulse, high heart rate Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer Sign
Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer Sign
Digestive Signs / Diarrhoea Sign
General Signs / Fever, pyrexia, hyperthermia Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer Sign
General Signs / Forefoot swelling, mass front foot, feet Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer Sign
General Signs / Forelimb lameness, stiffness, limping fore leg Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Sheep & Goats:Lamb Sign
General Signs / Forelimb swelling, mass in fore leg joint and / or non-joint area Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer Sign
General Signs / Generalized lameness or stiffness, limping Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Sheep & Goats:Lamb Sign
General Signs / Hindfoot swelling, mass rear foot, feet Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer Sign
General Signs / Hindlimb lameness, stiffness, limping hind leg Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer,Sheep & Goats:Lamb Sign
General Signs / Hindlimb swelling, mass in hind leg joint and / or non-joint area Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer Sign
General Signs / Inability to stand, downer, prostration Sign
General Signs / Pale mucous membranes or skin, anemia Sign
General Signs / Reluctant to move, refusal to move Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer Sign
General Signs / Swelling skin or subcutaneous, mass, lump, nodule Sign
General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift Sign
General Signs / Weight loss Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer Sign
Musculoskeletal Signs / Decreased mobility of forelimb joint, arthrogryposis front leg Cattle & Buffaloes:Cow,Sheep & Goats:Lamb Sign
Musculoskeletal Signs / Decreased mobility of hindlimb joint, arthrogryposis rear leg Cattle & Buffaloes:Cow,Sheep & Goats:Lamb Sign
Pain / Discomfort Signs / Forefoot pain, front foot Sign
Pain / Discomfort Signs / Hindfoot pain, rear foot Sign
Pain / Discomfort Signs / Pain mammary gland, udder Cattle & Buffaloes:Cow Sign
Pain / Discomfort Signs / Skin pain Sign
Reproductive Signs / Agalactia, decreased, absent milk production Sign
Reproductive Signs / Enlarged uterus Cattle & Buffaloes:Cow Sign
Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea Cattle & Buffaloes:Heifer,Cattle & Buffaloes:Cow,Cattle & Buffaloes:Steer Sign
Skin / Integumentary Signs / Skin erythema, inflammation, redness Cattle & Buffaloes:Cow Sign
Skin / Integumentary Signs / Warm skin, hot, heat Sign

Disease Course

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The vast majority of pathological data refer to human cases and only some of the manifestations have been described in animal species. The following account refers to the human disease (Stanek et al., 1996) and Lyme borreliosis (LB) of livestock species will be considered separately.

Lyme borreliosis in humans

The majority of infections with B. burgdorferi are subclinical and those that result in symptoms are often self-limiting. However, if early symptoms are left untreated the disease may progress to seriously debilitating manifestations involving the skin, joints, heart or nervous system. Very few manifestations of the disease are exclusive to B. burgdorferi infection and there are considerable diagnostic problems. Diagnosis must be made in the light of the clinical history and physical findings, exposure risk history and laboratory evidence.

Early localized Lyme borreliosis

Erythema (chronicum) migrans (EM): Erythema migrans, the characteristic rash spreading from the site of a tick bite, typically starts about two to thirty days after the tick bite and is the direct result of the spirochaete migrating through the skin. Minor constitutional symptoms also may occur, for example mild 'flu-like' symptoms.

Borrelial lymphocytoma: Borrelial lymphocytoma is a very uncommon form of early localized LB, which is usually seen on the earlobe (especially in children), nipple or scrotum. Microscopic examination shows a very dense infiltrate of lymphocytes

Early disseminated Lyme borreliosis

The organism can spread through the bloodstream and lymphatic system to other tissues, which may include other parts of the skin, nervous system, musculoskeletal system and heart. The targeting of any of these systems can cause a wide variation of clinical features presenting from a few weeks to over a year after the initial infection.

Clinical features of this stage may include more severe constitutional symptoms, multiple erythema migrans, arthralgia, recurrent arthritis, carditis with conduction defects (usually partial heart block) and early neuroborreliosis. This latter manifestation may occur as facial palsy, other cranial nerve palsies, aseptic (viral-type) meningitis, polyradiculitis mild encephalitis and peripheral neuritis. Other rare manifestations reported, include cardiomyopathy, anterior and posterior uveitis, panophthalmitis, hepatitis, myositis and orchitis.

Late (chronic) Lyme borreliosis

This uncommon stage presents several years after the initial infection and may involve the joints (chronic Lyme arthritis), skin (acrodermatitis chronica atrophicans - a progressive fibrosing skin lesion, usually in elderly people) or, rarely, chronic neurological syndromes (e.g. memory loss, depression, sensory polyneuropathy, spastic paraparesis).

Lyme borreliosis in animals

Most data on LB in animals concerns dogs and horses. In dogs LB usually manifests as joint problems and in horses, particularly in North America, joints and eyes are reportedly affected.

Far fewer disease data are available for livestock species, however, there are many reports of the detection of anti-borrelia antibodies and there can be little doubt that most livestock can become infected. It is probable that most infections are subclinical and self-limiting, but it is also possible that infections are missed or mis-diagnosed because of the non-specificity of clinical symptoms and the considerable difficulties involved in laboratory diagnosis. Laboratory diagnosis of infection in animals has had practically none of the intense scrutiny received by LB diagnosis in humans. Finally, it should be borne in mind that the tick vectors of LB transmit other pathogens (e.g. Ehrlichia spp) that may confound both clinical and laboratory diagnosis (Gray, 1999).

Lyme borreliosis in cattle

There have been many reports of the detection of antibodies to B. burgdorferi sensu lato in the blood of cattle (e.g. Hovmark et al., 1986; Burgess, 1988; van den Bogaard, 1989; Morgan-Capner et al., 1989; Caracappa et al., 1992; Isogai et al., 1992; Wells et al., 1993; Blowey et al., 1994; Cabannes et al., 1997; Wan-KangLin et al., 1998). Seropositive rates have been shown to range as high as 65% (Burgess, 1988). However, relatively few cases of clinical LB in cattle have been documented. Several cases reported in the USA in the late 1980's and early 1990's were diagnosed by association of symptoms such as lameness, weight loss and abortion, with a number of factors. These include positive serology, isolation of B. burgdorferi from colostrum, serum, urine, milk or synovial fluids, apparent response to tetracyclines and with seroconversion in mice and a cat after exposure to urine and milk respectively (Burgess et al., 1987; Burgess, 1988; Post et al., 1988; Wells et al., 1993). Very few cases have been diagnozed subsequently, though isolated reports appeared from Australia (Rothwell et al., 1989), Japan (Isogai et al 1992) and the UK (Blowey et al., 1994).

Misgivings regarding the specificity of the tests used for B. burgdorferi serology have been reinforced by studies implicating Treponema spp as the causal agent of B. burgdorferi-seropositive cattle with digital dermatitis (Choi et al., 1997; Demirkan et al., 1999) and cross reactions to other spirochaetes have also been recorded (Rogers et al 1999). It seems likely that in some of the studies antibodies to other organisms were being detected, for example the Australian study (Rothwell et al., 1989) is compromised by the fact B. burgdorferi s.l. has yet to be isolated from any vector in that country (Russell, 1998).

Cattle are not regarded as reservoir hosts of B. burgdorferi s.l. (Gern et al., 1998), although infected ticks have been found on cattle pastures (Borko and Bole-Hribovsek, 1998). This association of B. burgdorferi s.l with cattle is probably due to the presence of other hosts in the same habitat. In study in Ireland infected ticks were only found in areas utilized by rodents and/or birds on the margins of cattle pastures, though uninfected ticks were abundant in the central areas of the pastures which were utilized mainly by the cattle (Gray et al., 1995).

Even when cattle are deliberately exposed to infection with all three pathogenic genospecies of B. burgdorferi s.l., it has not proved possible to provoke any clinical symptoms (Tuomi et al., 1998) and it seems likely that most strains of B. burgdorferi s.l. are non-pathogenic in cattle. However, a recent report strongly suggests that at least two genospecies may be pathogenic to cattle in certain circumstances (Lischer et al., 2000). In this study of two dairy cows, the clinical signs included erythema, loss of weight, swollen legs, swollen joints, stiff gait, acute laminitis and oligoarthritis. In order to decrease the possibility of erroneous results arising through contamination, real-time PCR was used as a diagnostic tool and B. burgdorferi sensu stricto. DNA was detected in synovial fluid and milk of one cow and B. afzelii DNA was detected in synovial fluid of the other.

LB in cattle is probably a rare disease, which as in humans, is difficult to diagnose due to the non-specific nature of symptoms and doubt surrounding the specificity of serology. The application of PCR technology as a diagnostic aid may result in more certain identification of cases in the future.

Lyme borreliosis in sheep

One of the main vectors of LB, Ixodes ricinus, is known in some parts of its range as the ‘sheep tick’ and it was initially assumed that sheep and also sheep-farmers may be at particular risk of LB. These assumptions have proved to be unfounded because the susceptibility of sheep to systemic infection appears to be low (Stuen and Fridriksdóttir, 1991). This limits the ability of B. burgdorferi s.l. to cause disease and also reduces the proportion of infected ticks in the immediate environment (Gray et al., 1995), thus limiting the risk to farmers. There is some evidence that adult ticks may become infected as a result of the transfer of the pathogens from infected to uninfected nymphal ticks co-feeding on sheep (Ogden et al., 1994), but this appears to have limited impact on the epidemiology of the disease.

There are several reports of the detection of anti-borrelia antibodies in the blood of sheep (Hovmark et al., 1986; Fridriksdóttir et al., 1992; Mitchell and Smith, 1994; Ciceroni et al., 1996; Wan-KangLin et al., 1998), but the same caveats regarding the specificity of the tests employed, apply here, as discussed above and some of these findings may be in question. There is at least one published report of possible LB in sheep (Fridriksdóttir et al., 1992) in which the disease manifested in seropositive Norwegian lambs as pronounced lameness in one leg. However, this is an isolated report and at present it must be concluded that B. burgdorferi s.l. infection of sheep rarely results in disease.

LB in other livestock

Antibodies to B. burgdorferi s.l. have been detected in the blood of goats (Doby and Chevrier, 1990; Ciceroni et al., 1996) but there are no reports of LB in these animals. Pigs have received no attention in this regard though wild boar have been found to be seropositive (Doby et al., 1991). Studies on the susceptibility of deer to B. burgdorferi s.l. suggest that infected animals do not exhibit clinical signs though seroconversion occurs (Lane et al., 1994; Luttrell et al., 1994). Deer are not considered to be reservoir hosts (Gern and Falco, 2000) but organisms may persist in skin long enough to infect some ticks by co-feeding (Kimura et al., 1995). B. burgdorferi DNA has been detected by PCR in a small number of ticks fed on experimentally infected white-tailed deer (Oliver et al., 1992). Some authors have suggested that deer may be utilized as serological sentinels for LB (Gill et al., 1994; Gray et al., 1996)

Chickens have been infected experimentally in order to determine their possible reservoir status and it was found that these animals quickly became immune to B. burgdorferi s.s. and did not show any clinical symptoms (Piesman et al., 1996). In one publication mallard ducks were implicated as reservoir hosts following infection by both oral and intravenous routes and subsequent detection of antibodies and isolation of organisms from the blood, kidneys and cloacal material (Burgess, 1989). No pathology was reported. These unusual findings were not confirmed and are now discounted, perhaps explained by lack of specificity in the serological tests and by culture contamination. More recent studies have shown that pheasants are reservoir hosts of B. garinii and B. valaisiana in the UK (Kurtenbach et al., 1998), but no symptoms of disease in infected birds have been reported.


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In the USA approximately 5/100,000 reported cases occur each year in the human population, mostly in the New England area. In Europe annual case incidence increases from west to east and from south to north, ranging from 120/100,000 in Slovenia to 0.6/100,000 in Ireland and 89/100,000 in southern Sweden to zero in southern Greece (O'Connell et al., 1998). Seroprevalences are generally far higher than case rates. The main risk factors appear to be the presence of highly heterogeneous mixed or deciduous woodland containing a vector tick species, a diverse vertebrate fauna, including large animals such as deer, and the use of such areas by the public for recreational purposes (Gray et al., 1998).

Zoonoses and Food Safety

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Despite early suggestions that Borrelia burgdorferi sensu lato may occur in milk and that infections can become established in laboratory mice by the oral route (Post et al., 1988), these findings have not been supported by subsequent research. At present it must be concluded that B. burgdorferi sensu lato is not a food borne pathogen.

Disease Treatment

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Borrelia burgdorferi sensu lato is susceptible to several classes of antibiotics, including tetracyclines, penicillins and cephalosporins. Despite continuing controversy over a small proportion of cases, treatment recommendations for human Lyme borreliosis (LB) are now well established (Weber and Pfister, 1994; Nadelman and Wormser, 1998). Two week oral regimens of tetracyclines, such as doxycycline, and penicillins, such as amoxicillin, are effective against early LB, whilst 2-3 weeks intravenous treatments with penicillin or cephalosporins, such as ceftiaxone, are indicated for late stage LB. At present there is no data on the successful treatment of confirmed LB cases in cattle or sheep with antimicrobial agents, though tetracyclines have been used in suspected cases and the satisfactory responses were interpreted as evidence for correct diagnosis (Post et al., 1988; Rothwell et al., 1989). An anti-inflammatory (phenylbutazone ) has been used with a satisfactory outcome in one case (Lischer et al., 2000).

Vaccination against canine LB using a whole cell preparation (Fisher, 1991) is available and recombinant vaccines for dogs (Ma et al., 1996) and horses (Chang et al., 2000) are under development. In view of the apparent rarity of LB in livestock the development of a vaccine for its prevention in these animals seems unlikely at present.

LB may also be prevented by directing control measures at ticks and since ticks transmit other diseases to livestock within some LB endemic areas, such as babesiosis, ehrlichiosis and anaplasmosis, treatment of livestock against ticks may be desirable. With the advent of highly efficacious pour-on formulations of synthetic pyrethroids, such as flumethrin, this has become comparatively easy, but at present does not seem justified to prevent LB alone.


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Aeschlimann A, Chamot E et al. , 1987. Borrelia burgdorferi in Switzerland. Zentralbl Bakteriol Mikrobiol Hyg [A], 263(3):450-458.

Afzelius A, 1910. Verhandlungen der dermatologischen Gesellschaft in Stockholm; Sitzung vom 16 Dezember 1909 Arch. Dermatol. Syph., 101:405-406.

Ai ChengXu; Zhang WeiFen; Zhao JienHua, 1994. Sero-epidemiology of Lyme disease in an endemic area in China. Microbiology and Immunology, 38(7):505-509; 23 ref.

Aleksee AN, Dubinina HV et al. , 1998. Tick-bourne borrelioses pathogen identification in Ixodes ticks (Acarina, Ixodidae) collected in St. Petersburg and Kaliningrad Baltic regions of Russia. Journal of medical entomology, 35(2):136-142.

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