Page 99 - WSAVA2017
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H.L. Enemark1, S.M. Thamsborg2
1Norwegian Veterinary Institute, Department of Animal Health and Food Safety, Oslo, Norway
2University of Copenhagen, Department of Veterinary and Animal Sciences, Frederiksberg, Denmark
Heidi L Enemark, DVM, PhDa,b, Stig M Thamsborg, DVM, PhD, Dip. EVPCb,c
a. Norwegian Veterinary Institute, Department of Animal Health and Food Safety, Oslo, Norway Email: heidi. b. ESCCAP-DK c. University of Copenhagen, Department of Veterinary and Animal Sciences, Frederiksberg, Denmark
Alveolar echinococcosis (AE), a life-threatening zoonotic infection caused by the metacestode stage of the fox tapeworm Echinococcus multilocularis, is expanding in Europe. Globally, E. multilocularis is ranked third among food-borne parasites by FAO/WHO based primarily on public health concerns. However, applying the same multicriteria-based risk ranking analysis E. multilocularis is ranked first at the European level.1 The adult tapeworm, which is only few millimetres long, resides in the small intestine of wild carnivores (definitive hosts) such as e.g. red foxes, raccoon dogs and wolves. However, domestic dogs and cats may be involved in the lifecycle as definitive hosts if they prey on infected small mammals, predominantly rodents, serving as intermediate hosts. Dogs that have access to rodents and hunting dogs
run the highest risk of infection. Transmission to the intermediate host is faecal-oral via infective eggs excreted in the faeces of definitive hosts. The eggs are highly resistant to cold and capable of surviving for long periods in the environment. Based on a few experimental studies, the role of domestic cats in the transmission of E. multilocularis is thought to be small due to incomplete development and limited egg excretion. However, this has been questioned lately due to the detection of E. multilocularis eggs in a relatively high proportion of
cat stools2 including Danish cats. Humans and other mammals may become accidental hosts following ingestion of eggs e.g. from contaminated fruits and vegetables. Farming, gardening and contact with fox/dog fur are known risk factors for human infection. Although less commonly, dogs may also become accidental hosts and develop AE following ingestion of E. multilocularis eggs e.g. related to coprophagia or possibly following
autoinfection secondary to intestinal infection.3
E. multilocularis is widespread in the northern hemisphere with endemic areas in the near Near East, Russia, China, Northern Japan and North America. In Europe, the parasite was considered to be restricted to Central Europe i.e. Eastern France, southern Germany, parts of Switzerland and Austria until the 1990s. Yet, expansion in prevalence and geographic range into Northern, Eastern and Western Europe is ongoing and within the past three decades the parasite has been reported in 17 previously non-endemic countries in Europe. Increasing fox populations and colonisation
of residential areas are important underlying factors
but climate change, abundance of intermediate hosts, relocation of wildlife, globalization and traffic of pet dogs have also been proposed to play a role together with increased awareness and better diagnostic tools.4,5,6 So far, continuous surveillance of E. multilocularis in foxes
in Finland, Ireland, Malta, Norway (apart from Svalbard) and United Kingdom has documented absence of the infection in these countries6, but the risk of introduction with wildlife or due to pet travel is estimated to be high. To prevent introduction of E. multilocularis by dogs entering from endemic regions, requirements to show a veterinary deworming certificate at the border have been in place in most Scandinavian countries. Nevertheless, in Sweden the first case of E. multilocularis infection
was detected in a fox in 2011; and today the parasite
is considered endemic, although at a low prevalence,
in Denmark after detection of positive foxes in several locations.7
Currently, AE is considered a rare disease in endemic European countries with incidences of 0.03 to 0.3 per 100 000 inhabitants per year but numerous studies have documented a general increasing incidence, and in the actual population at risk, incidences from 4.7 to 8.1 cases per 100 000 inhabitants per year are observed.
In the Baltic countries, a 10-fold increase of the AE incidence has been reported reaching 0.5-0.77 per
100 000 inhabitants between 2009-12.4 The incidence of AE in dogs is unknown, but several studies have found shedding of eggs in less than 2% of the dogs in endemic regions. The fact that AE is a slowly developing disease means that change in definitive host ecology/ transmission patterns will not be reflected in increasing human incidence until 10-15 years later. Thus, the current increasing trend in human incidence may be the tip of the iceberg.
Clinical symptoms are absent in definitive hosts regardless of worm burden. In contrast, the symptoms may be severe in intermediate/accidental hosts. In humans, AE develops over a period of 5-15 years whereas the disease progresses more rapidly in dogs.
An Urban Experience

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