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Technical Thematic Report No. 7. - Wildlife pathogens and diseases in Canada

Pathogens Distributed Across Multiple Ecozones+ (Fungi and Parasites)



Chytrid fungus of amphibians [Reportable]

Author: Danna Schock

The amphibian pathogen Batrachochytrium dendrobatidis (Bd), a chytrid fungus which infects the skin of amphibians, has been linked to catastrophic amphibian declines around the world since the 1990s (Skerratt et al., 2007). The origin of Bd is unclear (Rachowicz et al., 2005; Morgan et al., 2007). In many regions of the world, patterns of disease and declines in affected species suggest Bd is a newly-introduced pathogen that has swept through susceptible host species, decimating amphibian diversity, and has then become established in suitable reservoir species (Retallick et al., 2004). Alternatively, Bd may be a historically widely distributed organism and recent declines associated with Bd may be linked to large-scale environmental changes that increase the impact of Bd on host populations (Ouellet et al., 2005; Pounds et al., 2006). Regardless of the ultimate source of Bd, this pathogen now is widespread and causing declines in many parts of the world.

Bdhas been isolated from several amphibians across Canada. In a large study of museum specimens, Bd was detected microscopically in amphibians collected in various parts of British Columbia, Ontario, Quebec, New Brunswick, and Nova Scotia (Ouellet et al., 2005). The majority of these specimens were from Quebec, especially along the St. Lawrence River (Mixedwood Plains, Atlantic Maritime, and Boreal Shield ecozones+). The authors argue that Bd is not linked with recent amphibian declines in eastern Canada because they detected high percentages of Bd-infected specimens collected as far back as 1960 from species that have not declined. However, there is strong evidence linking Bd to the declines of species in western North America (Briggs et al., 2005; Schlaepfer et al., 2007). The timing of the collapse of northern leopard frog (Rana pipiens) populations across western North America, including in Canada’s Prairies Ecozone+, in the 1970s and 80s, is consistent with Bd-related declines elsewhere in the west. However, the absence of necessary data makes it unlikely that the cause(s) of the declines will be conclusively determined. Bd has been isolated from multiple amphibian species in British Columbia (Pacific Maritime Ecozone+) and Alaska (Reeves and Green, 2006; Adams et al., 2007), Northwest Territories (Taiga Plains Ecozone+) (Schock, D., unpublished data), Alberta (Prairies and Boreal Plains ecozones+) (Kendell, K., 08, pers. comm.), and Saskatchewan (Prairies Ecozone+) (Canadian Cooperative Wildlife Health Centre, 2008).

Linking specific pathogens to declines in amphibian species is problematic. Most amphibians in Canada have boom-and-bust population cycles. Many species live ten or more years and may forego breeding activities altogether in years when rain and other environmental triggers are insufficient or occur too late in the year. Detection of steady downward declines, rather than fluctuations associated with expected boom-bust cycles, may require decades of monitoring (Alford and Richards, 1999). It is clear that Bd is causing significant declines in amphibian biodiversity in many parts of the world. In some instances, changing environmental conditions appear to enhance mortality due to Bd. It is not possible to predict whether or not similar negative impacts on amphibians in Canada will be triggered by impending changes in climate and land use.

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White nose syndrome in bats

Authors: I.K. Barker, Kim Taylor and F.A. Leighton

White nose syndrome (WNS) is a new disease that was first recognized in bats in New York State in the winter of 2006 and has since been found in bats in hibernation caves in the United States from New Hampshire to Tennessee and Missouri, and in Canada in southern Quebec, in the general regions of Ottawa-Gatineau and south of Sherbrooke, and in eastern Ontario, as far north as Kirkland Lake (Figure 3). These locations include the Mixedwood Plains, Boreal Shield and Atlantic Maritime ecozones+. The name of the disease refers to a ring of white fungus around the muzzles and elsewhere on the bodies of affected bats (Figure 4). The cause of this disease is not fully understood, but it is associated with the growth on the bats of a particular species of fungus, Geomyces destructans, which occurs during hibernation (Blehert et al., 2008; Gargas et al., 2009; Meteyer et al., 2009). The first occurrences of WNS in Canada were detected in the late winter of 2010 during active surveys of bat hibernacula in Ontario and Quebec; similar surveys in 2009 did not detect the disease.

Figure 3. Spread of white nose disease in bats.

Long Description for Figure 3

This map of the Great Lakes region shows the spread of white nose disease in bats. First recognized in bats in New York State in the winter of 2006 and has since been found in bats in hibernation caves in the United States from New Hampshire to Tennessee and Missouri, and in Canada in southern Quebec, in the general regions of Ottawa-Gatineau and south of Sherbrooke, and in eastern Ontario, as far north as Kirkland Lake. These locations include the Mixedwood Plains, Boreal Shield and Atlantic Maritime ecozones+.

Source: Cal Butchkoski, Pennsylvania Game Commission, updated from Szymanski et al.(2009)

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Figure 4. Bats with white nose syndrome, Craigmont Mine, Ontario.

Long Description for Figure 4

Photo: Bats with white nose syndrome, Craigmont Mine, Ontario.

Photo credit: Lesley Hale, Ontario Ministry of Natural Resources, Peterborough

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Since its discovery in one hibernation cave in New York State in 2006, WNS has killed more than a million bats in the northeastern United States (Puechmaille et al., 2010). Deaths from WNS often exceed 75% of the bats in infected hibernacula, but in some hibernacula, 80 to 99% of the bats have been killed (Boyles and Willis, 2010; U.S. Fish and Wildlife Service, 2010; Puechmaille et al., 2010). Affected individuals suffer severe weight loss, and dead and dying emaciated bats have been found outside of major hibernacula during late winter, presumably searching for food when none is available and the bats should be hibernating. The bat species which have been affected as of 2010 include little brown bat (Myotis lucifugus), northern long-eared bat (Myotis septentrionalis), big brown bat (Eptesicus fuscus), Indiana bat (M.sodalis), and tri-colored bat (Perimyotis subflavus). Scientists are uncertain about the origin of the associated fungus, Geomyces destructans. The fungus, but not the disease, has been found in surveys of hibernating bats in Europe, and it has been suggested that European bats may be resistant to the disease due to a long evolutionary association with the fungus. This also suggests that the fungus may have been brought to North America quite recently (Wibbelt et al., 2010).

White nose syndrome is having an enormous impact on bat populations in North America and is likely to have a significant and long-term impact on the ecology of affected regions. The small insectivorous bats affected by the disease are long-lived and reproduce slowly. Therefore, the high mortality of adult bats associated with this disease has the potential to produce long-term population declines and extinctions. These bats consume large quantities of insects, including species damaging to agricultural crops and forests, and may play other important, if poorly understood, ecological roles (Boyles and Willis, 2010).

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Besnoitia is a genus of protozoan parasite which develops pin-head sized firm cysts in the skin and connective tissues of its herbivore intermediate host and typical coccidial forms in the intestines of its carnivore definitive hosts. No disease due to Besnoitia sp. has been recognized in definitive hosts, but intermediate hosts sometimes develop disease conditions associated with severe infections (Leighton and Gajadhar, 2001). In Canada, Besnoitia tarandi infects caribou and reindeer, and probably muskoxen, across their ranges in the Arctic, Taiga Cordillera, Taiga Plains, Taiga Shield, Hudson Plains, Boreal Plains, and Boreal Shield ecozones+. Infection is very common in barren ground caribou and has been described in woodland caribou. Infection rates in muskoxen are not known (Choquette et al., 1967; Wobeser, 1976; Gunn et al., 1991; Ayroud et al., 1995). Although occasional severe manifestations of infection on the skin have been seen, most infections appear to have little or no health consequences for these species.

Besnoitia sp. (assumed to be B. tarandi) caused severe disease in mule deer in separate outbreaks in two zoos in the Prairies Ecozone+ in the 1980s (Glover et al., 1990; Leighton and Gajadhar, 2001). Based on experimental studies in cattle, it is assumed that Besnoitia was transmitted between infected caribou in the zoo collections and the zoos’ mule deer by biting flies (Bigalke, 1967). These disease occurrences in zoos indicated that transmission between infected caribou or reindeer and mule deer is possible and they occurred at a time when the farming of native deer species, including reindeer secured from the Canadian Arctic, was developing quickly in the Prairies. Regulations were put in place to prevent the importation and maintenance of infected caribou or reindeer within the geographic range of wild mule deer. As of 2008, Besnoitia has not been recognized in wild cervids in Canada other than caribou and reindeer (Lewis, 1989a; Canadian Cooperative Wildlife Health Centre, 2008).

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Brain worm of white-tailed deer (Parelaphostrongylus tenuis)

P. tenuis, the brain worm of white-tailed deer, is a parasitic nematode with a life cycle that involves two very different animal hosts: the white-tailed deer and several different species of terrestrial snails and slugs. The adult worms live in the connective tissue membranes on the outside of the brain (the meninges) of the deer. Here they mate and female worms deposit eggs into large veins. The eggs are carried to the lungs where larvae hatch (Lphase), move up the airways to the throat, are swallowed, and then expelled in the feces. These larvae burrow into snails and slugs attracted to the deer feces and develop within the snail to a new larval stage (L3) capable of infecting deer. Deer ingest these larvae inadvertently with vegetation. The ingested larvae penetrate the intestinal wall, follow large nerves up to the spinal cord, develop briefly in the cord, and then move anteriorly along the spinal cord to their final destination on the surface of the brain, developing into adults as they go (Lankester, 2001).

In white-tailed deer, this life cycle is completed and the adult worms live on the surface of the brain for the lifetime of the deer without causing significant damage or disease. However, in moose, caribou, mule deer, elk, and domestic sheep and goats, P. tenuis can produce fatal disease. The larvae do more damage by remaining longer and growing larger within the cord, and produce abnormal behaviour, paralysis, and death of the host in the process. P. tenuis does not complete its life cycle in any of these other hosts except elk and rarely moose. In elk, infection with small numbers of L3larvae can result in non-lethal infection and shedding of L1 larvae in elk feces, while infection with larger numbers of L3 can produce fatal infection before the worms mature and produce eggs. The few moose that pass larvae are likely short-lived. Thus, P.tenuis acts like a biological weapon of white-tailed deer, causing fatal disease in native and some non-native ungulates that compete for food resources with white-tails.

White-tailed deer have expanded their geographical range and numbers remarkably since historic times (Banfield, 1974). In eastern Canada, this expansion has been associated with decreases in moose populations and extirpation of caribou populations, for example in Nova Scotia and Maine. Efforts to re-establish caribou on their historic ranges newly inhabited by white-tailed deer have failed because of fatal infections with P.tenuis (Dauphine, 1975). However, although white-tailed deer have moved westward, arriving in Manitoba in the very early 1900s and are now present across the Prairies, in western British Columbia, and north to the southern Yukon and Northwest Territories, P.tenuis has not moved west beyond approximately the Manitoba-Saskatchewan border in the Prairies and southern margin of the Boreal Plains ecozones+. An array of biological or climatic factors currently appears to prevent the westward spread of P. tenuis. These include the drier conditions of the more western parts of these ecozones+ which are less favourable for terrestrial snails and slugs, the parasite’s intermediate hosts.

P. tenuis is a conservation concern for native cervid species other than white-tailed deer. The rapid expansion of white-tailed deer across much of the continent is thought to be associated with human transformation of the landscape, including forestry, agriculture, removal of important predators, and some direct translocation of white-tails themselves (Banfield, 1974; Benson and Dodds, 1980; Hoefs, 2001). Translocation of white-tailed deer or elk infected with P. tenuis west of the Manitoba-Saskatchewan border has the potential to introduce the parasite into habitat in which it may be able to survive and complete its life cycle. For example, a related parasite with nearly identical life cycle, P.odocoilei, is widely distributed in western Canada, suggesting that these western environments, now inhabited with white-tailed deer, might support P.tenuis, if this parasite were transported across the ecological barrier that otherwise is preventing its spread. Large populations of mule deer, moose, elk, woodland caribou, and possibly wild sheep would then be at risk of significant reductions due to P.tenuis. Similarly, changes in climate or other ecological factors could change the distribution of P. tenuis, increasing or reducing its current range and impact depending on the nature of the change.

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Winter tick (Dermacentor albipictus)

Throughout most of their range in North America, moose suffer periodic events of high mortality in late winter associated with severe infestations with winter tick, Dermacentor albipictis. This tick is native to North America and infests a variety of other hosts including white-tailed deer, mule deer, elk, woodland caribou, bison, and also domestic horses and cattle. However, severe infestations frequently resulting in death are common only in moose. Winter ticks occur south of approximately 60° N latitude throughout the Atlantic Maritime, Boreal Shield, southern Hudson Plains, Boreal Plains, Prairies, Montane Cordillera, Western Interior Basin, southern Boreal Cordillera, and southern Taiga Plains ecozones+, and severe effects on moose have been recorded over most of this range in the past 100 years (Samuel, 2004).

The winter tick hatches from eggs laid on the ground in summer. Larvae climb vegetation and attach to passing ungulate hosts in the fall. They remain on the same individual host animal, maturing from larva to nymph to adult, and mated, blood-engorged adult females drop off the host in March-April. Females lay eggs on the ground and die. Moose are not clinically affected by the ticks until March, when adults develop and begin feeding. At this point, moose suffer significant blood loss, spend abnormally large amounts of time grooming which produces significant hair loss, and spend relatively little time feeding. The consequence is rapid deterioration in nutritional condition as moose expend large amounts of energy and take in very little; this is especially the case for young moose in their first year. On average, infested moose in western Canada have had on the order of 33,000 ticks; 6% had burdens of 80,000 and as many of 150,000 ticks have been found on some individuals, 5 to 8 ticks per square centimetre of skin. By comparison, numbers on elk, white-tailed deer, and bison have been on the order of 1,000, 500, and 100 ticks per animal (Samuel, 2004).

The winter tick was first identified by western science in 1869 and has been on record as a potentially deadly parasite of moose ever since. Large-scale mortality events often are described in association with severe cold, snow, and other challenging conditions for moose in March and April, including inadequate nutrition from poor habitat. Losses on the order of 1,000 out of a total population of 5,000 moose were reported in Riding Mountain National Park in 1999, for example (Samuel, 2004). Often, these events occur over a very large area, for example simultaneously across the entire Boreal Plains, Prairies, and western half of the Boreal Shield ecozones+ in 1999. It is clear that weather events affect the abundance of the ticks, particularly conditions in April when gravid adult female ticks drop to the ground and either do or do not survive to lay eggs, thus affecting the numbers of larvae available to infest moose the following fall. Environmental conditions also affect the resilience of the moose, particularly conditions in late winter and early spring the following year when infested moose must endure the ticks. The historical record does not provide data sufficient to determine any temporal trend in the effect on moose populations by the winter tick. Neither is it possible to make predictions based on climate change scenarios and existing knowledge of host and tick ecology. Winter ticks have been imported into southwestern Yukon (Boreal Cordillera Ecozone+) by way of importation and release of infested elk and there is reason to believe that translocation of the tick further west into Alaska, where currently it does not exist, would result in establishment of the tick in many of Alaska’s moose populations (Zarnke et al., 1990; Samuel, 2004; Merchant, P., 09, pers. comm.). Hunters along the MacKenzie River in the Northwest Territories recently have reported moose in spring with severe hair loss typical of winter tick infestation, a phenomenon new to the traditional knowledge of local First Nations (Elkin, B.T., 09, pers. comm.).

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