The Rise of Tick-Borne Disease in Northern Europe
World Small Animal Veterinary Association Congress Proceedings, 2017
Ian Wright, BVMS, Bsc, Msc, MRCVS
The Mews Studio, Malvern, UK

Risk of Tick-Borne Disease in Northern Europe

Introduction

Tick-borne disease represents an ongoing and growing risk to pets and their owners in Northern Europe. This comes from both increasing numbers of endemic ticks, and the increasing distribution of tick species and tick-borne diseases. This is driven by a combination of factors including habitat and climate change, increased wildlife reservoirs, pet travel, and human migration. Ixodes spp. ticks and Dermacentor reticulatus as vectors of Lyme disease and Babesia canis respectively, remain the most significant tick-borne disease threats in Northern Europe but pets travelling to, and being imported from, Rhipicephalus sanguineus endemic countries is leading to Ehrlichia canis being seen in Northern Europe. Tick­borne encephalitis is also spreading North and West through Europe, presenting a significant zoonotic risk.

Lyme Disease

Lyme disease is caused by spirochete bacteria of the Borrelia burgdorferi complex and transmitted by Ixodes spp. ticks. The sheep tick Ixodes ricinus is the most important vector throughout Europe and although I. hexagonus and I. canisuga are also implicated in Lyme disease transmission, they are not thought to be as significant vectors.

Where Lyme disease is endemic it is maintained by reservoir hosts that act as sub-clinical carriers of infection and reproductive hosts that do not carry infection but maintain populations of infected ticks. Small rodents and birds are the most significant reservoir hosts of Lyme disease but deer act as epidemiologically important reproductive hosts, carrying Lyme disease to new geographic areas.

Ticks mostly become infected as larvae and then remain infected as nymphs and adults. When these life-cycle stages of the tick feed, Borrelia spp. multiply in the gut and, over a period of several days, penetrate the gut epithelium and migrate to the salivary glands where they may then be potentially delivered to a new mammalian host. As a result, a tick has to feed for several hours and often 24–48 hours before transmission occurs. Nymphs are thought to be more significant in terms of overall transmission than adults as they are more abundant than adults and due to their size, less likely to be groomed off pets and missed when looking for attached ticks.

Although transovarian transmission of Borrelia spp. in ticks can occur, it is currently not thought to be epidemiologically significant.

Countries in Western Europe have a highly variable but increasing incidence of Lyme disease. The highest reported incidences have reported in southern Sweden with 464 cases per 100,000 people per year and the lowest in Italy of 0.001 per 100,000. The unweighted mean for the included data provided an incidence of 56.3 per 100,000 persons per year, equating to approximately 232,125 cases in one year throughout the region (Sykes 2014). Data of the incidence of disease in cats and dogs is lacking but prevalence in ticks was found to be 2.37% in the UK (Abdullah et al. 2016).

Most infections with B. burgdorferi are sub clinical with 5–10% of infected dogs going on to develop clinical signs. When Lyme disease does develop, this is often due to re-exposure to infection with an incubation period of 2–5 months. Dogs present primarily with acute or sub-acute arthritis in one or more joints with associated lameness, joint swelling and heat. Other acute signs may then follow including fever, anorexia, lethargy, and lymphadenopathy. The acute form is often transient with relapses occurring. The common primary human clinical presentation of a circular skin rash known as erythema migrans is not recognised in dogs. Chronic disease is often described in human infection but is less commonly seen in canines. When it does occur in dogs it tends to occur when acute cases have not been treated and consists of a non-erosive polyarthritis. Protein losing nephropathy can be a sign of renal disease in chronic Lyme disease patients. This should not be confused with the syndrome Lyme nephritis. This occurs in 1–2% of dogs diagnosed with Lyme disease in the USA with an average onset at 5–6 years. Labrador and Golden Retrievers are over represented and prior or concurrent lameness is described in 9–28% cases. Typically, these dogs present with an acute progressive protein-losing nephropathy with membranoproliferative glomerulonephritis, tubular necrosis, and interstitial nephritis, but possibly milder forms exist (Littman 2013). Fortunately, this syndrome is rare in Europe for reasons that are not understood.

Lyme disease should be considered as a differential in pets presenting with any of these clinical signs described throughout Northern Europe. PCR is a highly specific test and a sensitive method of diagnosis if synovial membrane or skin samples from the site of the original tick bite are used. PCR from blood or joint fluid however, carries low sensitivity and as a result serology is most commonly used as a diagnostic tool. Detection of antibodies in blood or synovial fluid samples is a highly sensitive and specific method of diagnosis. Results confirm exposure to Borrelia spp. exposure and correlate well with clinical infection. As early intervention improves prognosis, positive serology combined with relevant clinical signs is sufficient justification so start antibiotic therapy.

Doxycycline at 10 mg/kg per os once daily remains the mainstay of treatment as it is excreted via the faeces, is kidney sparing and may have some joint anti­inflammatory properties. Amoxicillin is as an effective alternative in growing animals. Treatment should be continued for a minimum of 4 weeks to maximise the chances of eliminating infection.

Babesiosis

Infection with Babesia spp. occurs when the parasite is transmitted to dogs in the saliva of a feeding tick, occurring approximately 48 hours after the start of blood feeding (Matjila et al. 2004). Transmission has been reported through blood transfusions and in the case of B. gibsoni through dog bites. The parasite invades red blood cells and are described by their shape (piroplasms) and their size in relation to the red blood cell (large or small). There are five Babesias in Europe that can infect dogs. The large Babesia vogeli is of relatively low pathogenicity and is transmitted by Rhipicephalus sanguineus. Cases of babesiosis cause by the small Babesia annae and Babesia gibsoni are sporadic across Europe, with B. gibsoni potentially being transmitted by Ixodes spp. ticks. Babesia microti like organisms (B. vulpes) are thought to be transmitted by Ixodes hexagonus ticks and have been recorded sporadically across Europe, including Scandinavia (Sweden). Their clinical and epidemiological significance is unclear. The most pathogenic Babesia spp. endemic to Europe is the large Babesia canis and its distribution is closely linked with its main vector, D. reticulatus. Both B. canis and D. reticulatus are endemic in Northern Europe as far North as Poland, and while not thought to be endemic in Scandinavia, an untraveled case has been reported in Norway (Øines et al. 2010). Although B. canis was not thought to be endemic in the UK, the presence of D. reticulatus endemic foci in the South West of England and Wales (Smith et al. 2012) presented the possibility of B. canis being introduced to the UK and this subsequently occurred in Essex, confirming the potential for the spread of the parasite to new endemic foci (Phipps et al. 2016).

Infection can lead to immune mediated haemolytic anaemia with associated icterus, lymphadenopathy, pyrexia, secondary renal and hepatic disease, and in severe cases, death. Diagnosis can be achieved by demonstration of the parasite in peripheral blood smears stained with Giemsa or Diffquick®. The parasite presents as piriform (pear shaped) organisms, often paired, in the red blood cell, or by PCR on blood. Treatment consists of supportive treatment for anaemia and treatment for the parasite. Blood transfusion may be required if PCV drops below 15% and steroids may be indicated if PCV is slow to respond to treatment. Imidocarb given as 2 doses, 5–6 mg/kg IM, given 14 days apart is the most effective drug for elimination of the parasite. Atropine may be required to counteract anticholinesterase side effects and there is frequently pain at the injection site. Emesis is also sometimes seen in association with injection. If this drug cannot be immediately obtained, clindamycin given at 12.5 mg/kg orally twice daily also some efficacy. Either method of treatment is unlikely to eliminate the parasite, leaving infected dogs as subclinical carriers. As a result, infected dogs may have subsequent relapses and act as potential reservoirs of infection.

Rhipicephalus sanguineus, Anaplasma platys, and Ehrlichia canis

Rhipicephalus sanguineus is not currently endemic in Northern Europe as the climate is currently not favourable for establishment of an endemic population. This tick however, is moving Northwards and can now survive and develop in Belgium, France, the Netherlands, and Eastern Europe.

In addition to the potential for house infestation, R. sanguineus also carries a number of tick-borne pathogens with potential pathogenicity for Northern European dogs. These include E. canis and A. platys.

Ehrlichia canis is an obligate intracellular gram-negative bacteriam and the cause of canine monocytic ehrlichiosis. E. canis infects monocytes when introduced to dogs by feeding R. sanguineus ticks. Larvae and nymphs are infected while feeding on infected dogs and transmit the infection after moulting. Transmission has been demonstrated to take place within 3 hours of tick attachment, much faster than transmission of Lyme disease or babesiosis (Fourie et al. 2013).

Clinical signs start with an acute phase consisting of pyrexia, anorexia, and lymphadenopathy. Acute cases may also present with thrombocytopaenia. A subclinical period follows which may last many months or years. Subsequently, the organism is eliminated or severe chronic disease develops. The prognosis for chronic disease is grave with severe leukopaenia and thromboctopaenia and associated immune suppression and bleeding disorders developing. Ocular and neurological signs may also present in acute and chronic cases. German Shepherds are more susceptible to clinical signs and mortality rates are higher than in other breeds.

Diagnosis is based on IFAT serology, blood PCR, and identification of the organism in blood smears. The presence of the organism in peripheral circulation can be transient. Serology and PCR offers high sensitivity and specificity for diagnosis of infection. Although these tests demonstrate the presence of infection rather than the cause of clinical signs, treatment to eliminate the infection is important for prognosis and to avoid a carrier state with potential for chronic disease developing. Multiple tick-borne diseases are commonplace in dogs exposed to E. canis infection and co-infections causing clinical presentations should be considered.

Doxycycline is the treatment of choice for 3 weeks at 10 mg/kg daily per os. Supportive treatment for thrombocytopaenia may also be required.

A. platys infection can lead to severe thrombocytopaenia approximately 2 weeks after infection. This spontaneously resolves after 3–4 days but with repeated episodes every 1–2 weeks. Infection may persist for months and the severity of clinical signs appears to be dependent on strain and coinfection with other tick­borne diseases such as E. canis. Chronic infection also puts dogs at increased risk of coagulopathy during surgery. Diagnosis and treatment is similar to E. canis with doxycycline at 10 mg/kg sid per os being effective.

Tick-Borne Encephalitis

Tick Borne Encephalitis (TBE) is a virus transmitted by feeding Ixodes ricinus ticks, although it has also been transmitted through unpasteurised milk and through exposure to infected tissues in abattoirs. It may infect a variety of mammalian hosts including dogs, foxes, and ruminants. It is a potentially severe zoonosis with infections most commonly resulting in a transient fever, but sometimes progressing to meningoencephalitis and CNS signs. Although human infection is uncommon with 1 case per 10,000 hours spent in woodland activity, it can be fatal and so concern about its spread through Europe has been high. In Europe, it is a parasite predominantly of Eastern Europe and the Mediterranean but it has been moving north and west in its distribution with cases beginning to emerge in Scandinavia, Austria, and Holland (Pettersson et al. 2014).

Prevention of Tick Borne Disease

Veterinary professionals play a vital role in giving accurate tick and tick-borne disease prevention advice, but also putting risks in perspective for the pet owning public. Lifestyle also puts some dogs at greater risk of infestation, such as those walked in rural areas, rough pasture, or land used by deer or ruminants. There may also be a history of previous tick attachment. Use of tick preventative products should, therefore, be based on risk assessment. No tick preventative product is 100% effective but use of isoxazolines or pyrethroid containing products are highly efficacious and will reduce disease transmission. It is important for pet owners to be vigilant and check for ticks on their pets every day, removing any ticks with a tick removal device or fine pointed tweezers. If tweezers are used the tick should be removed with a smooth upward pulling action. If a tick hook is used, then a simple “twist and pull” action is employed. It is important that owners are instructed how to remove ticks without stressing them and without leaving the head and mouth parts in situ. Squashing or crushing ticks in situ with blunt tweezers or fingers will stress the tick leading to regurgitation and emptying of the salivary glands, potentially leading to increased disease transmission. Traditional techniques to loosen the tick such as the application of petroleum jellies or burning will also increase this likelihood and are contra indicated.

Zoonotic tick-borne disease risk comes from infected tick bites. Avoiding high tick density areas is the most effective way of minimising this risk but these are also some of the most popular walking and outdoor recreational sport destinations in Europe. Precautions should be taken by people enjoying these areas such as wearing long sleeves and ensuring the lower body is covered. Pyrethroid washes for clothes or pre-prepared pyrethroid impregnated clothes give long lasting repellency. Deet and citronella can also be used with some efficacy but are much shorter acting. The body should be carefully inspected for ticks after being outdoors and any ticks found removed.

References

1.  Abdullah S, Helps C, Tasker S, Newbury H, Wall R. Ticks infesting domestic dogs in the UK: a large-scale surveillance programme. Parasit Vectors. 2016;9:391.

2.  Fourie JJ, Stanneck D, Luusa HG, Beugnet F, Wijnveld M. et al. Transmission of Ehrlichia canis by Rhipicephalus sanguineus ticks feeding on dogs and on artificial membranes. Vet Parasitol. 2013;197:595–603.

3.  Littman MP. Lyme nephritis. J Vet Emerg Crit Care (San Antonio). 2013;23:163–173.

4.  Matjila PT, Penzhom BL, Bekker CP, Nijhof AM, Jongejan F. Confirmation of occurrence of Babesia canis vogeli in domestic dogs in South Africa. Vet Parasitol. 2004;122:119–125.

5.  Øines Ø, Storli K, Brun-Hansen H. First case of babesiosis caused by Babesia canis canis in a dog from Norway. Vet Parasitol. 2010;171:350–353.

6.  Pettersson J, Golovljova I, Vene S, Jaenson TGT. Prevalence of tick­borne encephalitis virus in Ixodes ricinus ticks in Northern Europe with particular reference to Southern Sweden. Parasit Vectors. 2014;7:102.

7.  Phipps L, Del Mar Fernandez De Marco M, Hernández-Triana LM, Johnson N, Swainsbury C, et al. Babesia canis detected in dogs and associated ticks from Essex. Vet Rec. 2016;178:243–244.

8.  Smith FD, Ballantyne R, Morgan E, Wall R. Estimating Lyme disease risk using pet dogs as sentinels. Comp Immunol Microbiol Infect Dis. 2012;35:163–167.

9.  Sykes RA. An estimate of Lyme Borreliosis incidence in Western Europe. Res Medica. 2014;22:76–87.

 

Speaker Information
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Ian Wright, BVMS, Bsc, Msc, MRCVS
The Mews Studio
Malvern, Worcs, UK


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