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

Pathogens Distributed Across Multiple Ecozones+ (Viruses)

Viruses

Rabies [Reportable]

Rabies is a fatal infection of the central nervous system caused by any of the several different strains of rabies virus, a rhabdovirus. It is transmitted from infected to uninfected animals primarily by bite wounds contaminated with infectious saliva. All mammals appear to be susceptible to all strains of rabies virus, but each strain persists in nature by transmission cycles within a single host species or a very small group of sympatric host species. The strains are named according to the principal maintenance host species, for example, skunk rabies, dog rabies, and raccoon rabies (Rupprecht et al., 2001).

Strains of rabies virus maintained in arctic foxes and in several different species of bats appear to have been present in Canada since prehistoric times. The domestic dog strain circulated in southern Canada from 1907 to 1934. Vaccination of domestic dogs began in the 1940s. The arctic fox strain persists in the Canadian Arctic and has spread southward periodically into southern Canada. A major southward incursion in the 1940s brought this strain of rabies into a large zone from British Columbia to New Brunswick (Tabel et al., 1974). The fox strain virus did not persist in southwestern Canada but became established in red foxes in Ontario and Quebec where it has persisted despite wildlife vaccination programs. There also were incursions of the arctic fox strain of rabies into insular Newfoundland in 1988 and 2002 (Whitney, 2004). In 1959, there was an incursion of a striped skunk rabies strain into southern Manitoba from adjacent North Dakota and Minnesota. This strain spread northwest, reaching Saskatchewan in 1963, and Alberta in 1970. Rabies persists in skunks in Manitoba and Saskatchewan. Further incursion into Alberta has been prevented thus far by an intensive program of skunk depopulation associated with rabies occurrences along the Saskatchewan-Alberta border. In 1977, an epidemic of the raccoon strain of rabies occurred in West Virginia because of importation of rabid raccoons into the state for hunting (Jenkins and Winkler, 1987). This epidemic swept through the rural and urban zones of the eastern United States and entered Ontario in 1999, New Brunswick in 2000, and Quebec in 2006. Epidemics of fox and raccoon strains of rabies are enormously costly to all affected areas due to the high rate of human exposure to potentially rabid raccoons, the high cost (approximately $2,000) of each post-exposure treatment, and the cost of the intensive surveillance, vaccination, and population control efforts used to try to stop its spread.

Several different species of bat in Canada carry different strains of rabies virus. Since 1970, all human infections with rabies acquired in Canada have been due to strains carried by bats (24 human cases of rabies have been recorded since 1924). The proportion of bats found dead and tested for rabies that have been found to carry the virus has been in 4-5% range in Canada in the past four decades (Johnstone, 2008).

Dog strain rabies is a conservation concern for several wild African canids, and is a world-wide human scourge, killing 25,000 to 50,00 people each year. Widespread vaccination of companion animals effectively has eliminated this concern in Canada. Control of fox strain rabies in Europe was followed by a pronounced increase in red fox populations with attendant new disease concerns including human echinococcosis (Rupprecht et al., 2001; Hegglin et al., 2003).

No clear trends in the occurrence of rabies in Canada are discernable from the historical record. Two exotic strains of rabies virus have invaded Canada in the past 50 years. Intensive and costly programs aimed at eradicating the fox (native) and raccoon (exotic) strains from southern Canada began 20 years ago and are still in operation, with renewed efforts directed against the newly-arrived raccoon strain.

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West Nile virus [Immediately Notifiable]

West Nile virus (WNV), a flavivirus, persists in nature through transmission cycles between a wide range of species of wild birds and a smaller species assemblage of bird-feeding mosquitoes. It was transported to North America from its Afro-Eurasian area of origin and first detected here in 1999. It spread rapidly across North America (McLean and Ubico, 2007). It was first detected in Canada in 2001, and affected all provinces from Nova Scotia to Alberta by 2003 (Figure 1) (Canadian Cooperative Wildlife Health Centre, 2008). The virus was detected in British Columbia for the first time in August 2009 in mosquitoes trapped in the Okanagan Valley. Although maintained in mosquito and bird populations, the virus also can infect and cause disease in a wide range of mammals, including people, and some species of reptiles. Most infected humans experience no illness. Some experience severe fever but readily recover. A small proportion experience severe neurological disease (encephalitis) which may be fatal or cause long-term debility. Despite the small proportion of exposed people who develop severe disease, WNV has caused the largest epidemic of infectious encephalitis in people ever recorded in North America (McLean and Ubico, 2007).

Figure 1. Distribution of birds testing positive for West Nile virus, 2001-2003.

Long Description for Figure 1

This map of Canada shows distribution of birds testing positive for West Nile virus from 2001 to 2003. Positive birds were concentrated around the Prairie and Mixedwood Plain ecozones+ with a few cases scattered as far east as the Atlantic Maritime Ecozone+.

Source: Health Canada (2003)

West Nile virus is not native to Canada and has the potential to produce ecological effects. Some native wild bird species experience high mortality when infected with WNV. Corvids (crows, jays, magpies, and their relatives) are highly susceptible; as are loggerhead shrike and greater sage grouse, two species of conservation concern. Late summer survival of greater sage grouse populations under study in 2003 in western Canada (Prairies Ecozone+) and the United States was reduced by 25% due to WNV infection (Naugle et al., 2004). Another study found declines in continental populations of American crow, blue jay, American robin, eastern bluebird, tufted titmouse, Carolina chickadee, black-capped chickadee, and house wren associated with WNV (LaDeau et al., 2007). Surveillance in Canada, from Nova Scotia to Alberta, has detected WNVas the cause of death in thousands of corvids and over 100 individuals representing 19 non-corvid bird species, including raptors (60%), passerines (15%), greater sage grouse (5%), and gulls (3%), and in two species of squirrel (red and eastern gray) (9%) (Canadian Cooperative Wildlife Health Centre, 2008).

West Nile virus is now firmly established in southern Canada from Alberta to the Maritime Provinces. The intensity of WNV activity has varied greatly among years and appears associated with a range of ecological factors affecting mosquito and bird population parameters. Climate is a key variable, but predictive modeling of likely future scenarios of climate change and WNV activity in Canada has not yet been done.

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Avian influenza

Avian influenza (AI) viruses are pathogens of intense current global concern because of the capacity of certain strains of these viruses to kill massive numbers of domestic poultry and the potential of some of these viruses to cause massive global human disease. Influenza viruses in birds all are members of the influenza A group of influenza viruses, and wild birds, particularly wild ducks, are the principal reservoir for influenza A viruses in the biosphere. In wild bird populations, influenza A viruses appear to persist as genetic strains with little capacity to cause disease. However, in other species, these viruses can undergo rapid genetic changes and develop into strains that can, and do, cause diseases, with affects ranging from mild to rapidly fatal. The H5N1 strain of current global concern, as well the H7N3 strains that caused epidemics in Canadian poultry in 2004 and 2007, appear to be recent genetic variants of non-disease causing strains present in wild birds (Capua and Alexander, 2006; Pasick et al., 2007; Berhane et al., 2009; Pasick et al., 2010).

Recent surveys of Canadian wild birds have found AI viruses to be abundant in wild ducks across the country and also to be present to a lesser extent in other species (Parmley et al., 2008; Canadian Cooperative Wildlife Health Centre, 2008). Table 1 shows the percentage of healthy live wild ducks sampled in Canada from 2005 to 2008 that were found to be infected with one or more AI viruses. None of the viruses detected was a highly pathogenic strain. In other species, the infection rate detected has been in the range of 0 to 13%, averaging less than 3%. None of the AI viruses found to date in Canadian wild birds has been a strain of direct concern to the health of people, poultry, or wildlife. However, many different strains of AI viruses have been found, indicating that a very large gene pool of AI virus persists in Canadian wild birds.

Table 1. Percentage of wild duck samples infected with Avian influenza virus.
Survey yearWild ducks
Number tested
Wild ducks
Number infected
Wild ducks
Percent infected
20054,2681,57237%
20064,0351,27532%
20075,5001,34024%
20081,445332%

Source: Canadian Cooperative Wildlife Health Centre (2009)

Globally, (AI) viruses seldom have been viewed as threats to ecological functions or conservation of endangered species. The currently-circulating H5N1 virus of concern to poultry and human health has also caused mortality in wild birds, including a large number of bar-headed geese in central Asia. This virus strain is a pathogen originating in domestic poultry populations that has been transmitted to wild bird populations, and is not a virus that originated in wild bird populations themselves. It is not known whether or not this or other disease-causing strains of AI viruses are able to persist in wild bird populations without periodic re-introduction from the poultry reservoir. However, such disease-causing strains originating in poultry are a potential risk to wild bird populations. The extraordinarily large global populations of domestic poultry that have been created in the past few decades are an enormous potential source of disease-causing AI viruses for wild birds (Steinfeld et al., 2006). This situation is unprecedented and the risk posed to wild birds is not known.

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Newcastle disease [Reportable]

Newcastle disease (ND) is the internationally accepted name for infection of birds with certain strains of avian paramyxovirus type 1 (APMV-1) that cause high mortality in experimentally-infected domestic chickens, and thus threaten poultry. The many strains of APMV-1 differ markedly in their capacities to cause disease. Newcastle disease is among the most serious epidemic diseases of poultry world-wide. It is highly contagious; any occurrence in any species threatens agricultural economies and the supply of affordable human dietary animal protein in affected regions (Alexander, 2000).

Strains of APMV-1 have been isolated from hundreds of different species of wild birds, particularly waterfowl, in Canada and all over the world. However, only two species of wild bird in Canada carry and maintain Newcastle disease viruses (NDV) strains of APMV-1 capable of causing severe disease in chickens: the double-crested cormorant (Phalacrocorax auritus) and the rock pigeon (Columba liva). NDV was first detected in wild birds in Canada in double-crested cormorants in the St. Lawrence Estuary in 1975. It was next detected in 1990 in double-crested cormorants in Saskatchewan, and subsequently has been detected regularly, if sporadically, from Alberta to the Atlantic coast. Antibodies to APMV-1 have been in found in double-crested cormorant eggs from British Columbia. On one double-crested cormorant colony in Saskatchewan monitored continuously from 1994 to 2008, ND occurred in 1995, 1997, 1999, 2001, 2003, and 2008 (Leighton, F. A., unpublished data; Leighton and Heckert, 2007). NDVin rock pigeons emerged in the Middle East in the 1970s, spread westward across Europe, and reached North America in 1984. It was first detected in Ontario in 1985 and had spread as far west as Saskatchewan by 1990 (Johnston and Key, 1992; Leighton and Heckert, 2007). This rock pigeon virus strain sometimes meets the criteria to be classified as NDV but often does not, and thus is usually referred to as pigeon paramyxovirus to avoid the national and international trade and legal implications of the term “Newcastle disease”.

Wild and feral rock pigeon populations appear to suffer high mortality when first infected with pigeon paramyxovirus, but recover quickly despite the persistence of the virus within the affected populations. The discovery in the early 1990s that true NDV is widespread in double-crested cormorant populations across North America was made during a rapid increase of the population of that species, restoring them to historical levels after two centuries of decline associated with human activities (Wires and Cuthbert, 2006). It is likely that mortality events are more readily detected on large colonies with thousands of nests than on the small colonies that were predominant prior to the 1970s. It is not, therefore, known whether NDV in double-crested cormorant is recent or ancient. ND has caused on the order of 40% immediate mortality of late fledgling and fledged hatch-year birds on one closely-studied colony, and additional, ultimately fatal, wing and leg paralysis in numerous surviving birds (Kuiken et al., 1998; Kuiken, 1999). Despite this regular high mortality, no population trends have yet been attributable to ND in double-crested cormorant. Adult double-crested cormorants appear unaffected by ND. NDVin large and wide-spread double-crested cormorant populations across North America is a constant risk to domestic poultry.

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Duck plague [Annually Notifiable]

Duck plague, also known as duck virus enteritis, is caused by anatid herpesvirus 1, a virus native to Eurasia that can infect and cause disease in ducks, geese, and swans. It was first recognized in North America in 1967 when it caused outbreaks of fatal disease in domestic ducks on Long Island, New York and a small outbreak in wild ducks (primarily American black duck and mallard) in adjacent wetlands. In January 1973, a major epidemic of duck plague occurred at Lake Andes Wildlife Refuge in South Dakota; 42,000 of the 100,000 mallards on the refuge died as did a number of Canada geese (Friend, 1999; Hansen and Gough, 2008). This event electrified North American wildlife managers, and the United States immediately established a national wildlife disease laboratory, now the National Wildlife Health Centre in Madison, Wisconsin. It was feared that similar outbreaks might destroy large numbers of wild waterfowl across the continent; regulations were put in place to permit strong and immediate actions to eradicate the virus.

Nevertheless, in the decades since 1973, duck plague has caused no major outbreaks in North America. It has caused small outbreaks, often in semi-domestic urban populations of ducks, in many parts of the United States and in five provinces in Canada: in a private waterfowl collection in Manitoba in 1973 (Prairies Ecozone+) (Bernier and Filion, 1975); in a small flock of captive muscovy ducks near Edmonton in 1974 (Prairies Ecozone+) (Hanson and Willis, 1976); in a zoo collection in Quebec in 1975 (Mixedwood Plains Ecozone+) (Bernier and Filion, 1975); in a single free-ranging mallard from a zoo pond in Saskatoon in 1984 (Prairies Ecozone+) (Wobeser and Docherty, 1987); perhaps in three mallards from southwestern Ontario in 1984 (Mixedwood Plains Ecozone+) (Wojcinski et al., 1991); and at three separate locations in British Columbia in captive barnacle geese and muscovy ducks in 1993 (Bowes, 1993). One outbreak, of moderate size but of no numerical importance to the affected populations, occurred in American black ducks and mallards in the Finger Lakes region of New York State in February 1994, just south of the Great Lakes and Mixedwood Plains ecozones+ (Hansen and Gough, 2008).

This virus now appears to be widespread in wild waterfowl populations across the continent, but does not appear to be the threat to those populations as once feared. Its behaviour and significance in North America now appears similar to the situation in Europe, where duck plague is associated with periodic, small mortality events, often in semi-domestic birds. Whether or not duck plague could again cause large-scale mortality in North America under changing environmental circumstances is not known, nor is it known if the virus now exerts sublethal effects on wild waterfowl populations (Hansen and Gough, 2008).

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Hemorrhagic diseases of deer [Reportable/Immediately Notifiable]

Hemorrhagic disease of deer is the general name given to diseases caused by infections of wild ungulates with various strains of two closely-related virus groups: bluetongue (BT) viruses and epizootic hemorrhagic disease (EHD) viruses, both of which belong to the orbivirus family. Records of diseases likely to have been hemorrhagic disease date back to the 19th century in North America. The viruses are transmitted from animal to animal by small biting flies of the genus Culicoides (midges, gnats, no-seeums). Although white-tailed deer and mule deer are the wild ungulates most affected, these viruses can cause disease in elk, pronghorn, bison, and wild sheep. At the northern edge of their range, where susceptible ungulate populations often have not been previously exposed to the viruses, periodic epidemics of fatal disease, often separated by several years or decades, are the usual expression of hemorrhagic disease. Further south, exposure to these viruses is more constant and a range of expressions, from pockets of epidemic mortality to various sub-lethal conditions, is seen annually (Howerth et al., 2001).

EHD and BT viruses are present on most continents, but none is currently established in Canadian ungulate populations. Both BT and EHD persist in wild and domestic ungulate populations across much of the United States, including states that border Canada, and both have made occasional late summer incursions into western Canada, probably due to wind-borne incursions of infected Culicoides sp.(Sellers and Maarouf, 1991). EHD occurred in southeastern Alberta (Prairies Ecozone+) in 1962 causing mortality in white-tailed deer, mule deer, and pronghorn, and in the Okanagan Valley of southern British Columbia (Western Interior Basin Ecozone+) in 1987 and 1999 causing mortality in wild white-tailed deer and bighorn sheep, and in several other species on a nearby game farm -- mule deer, American bison, elk, and mountain goat (Dulac et al., 1992; Pasick et al., 2001). Antibodies to EHD virus, but not to BT virus, were detected in domestic cattle in southcentral Saskatchewan (Prairies Ecozone+) in a survey conducted in 1986/87, but no disease was evident in the cattle or regional wildlife (Shapiro et al., 1991; Dulac et al., 1992). Incursions of BT viruses occurred in the Okanagan Valley in 1975, 1987, and 1998, but were detected only in domestic cattle and sheep (Dulac et al., 1992; Clavijo et al., 2000). Although mortality from these viruses in deer has not had a long-term impact on overall wildlife population sizes, they may pose a threat to small local or regional populations of species of conservation concern such as bighorn sheep and pronghorn.

EHD and BT are likely to affect Canadian wild ungulates more often in the future, associated with a warming climate. This is most likely to occur in ecozones+adjacent to areas in the United States where EHD and BT now occur, that is, southern regions of the Western Interior Basin, Montane Cordillera, Prairies, Boreal Shield, and Mixedwood Plains. The distribution of the Culicoides species which are competent vectors for these viruses and the rate of virus replication within these vectors both respond to temperature, among other environmental variables (Purse et al., 2008). There have been a few recent occurrences of EHD in the northeastern United States, close to Canada -- Michigan in 2006 and Pennsylvania and New York State in 2007 (including in Niagara County bordering the Mixedwood Plains Ecozone+) (New York State Department of Environmental Conservation, 2007; Pennsylvania Game Commission, 2008; Department of Natural Resources, 2009). However, these occurrences are not clearly related to trends in climate change. Recent incursions of BT viruses into Europe give warning of the rapid and massive shift in BT virus distribution that can occur in association with climate change and other factors (Purse et al., 2008). Canada is recognized as free of BT in domestic livestock for purposes of international trade; establishment of BT in Canada would negatively affect aspects of the Canadian livestock economy.

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Ranaviruses of amphibians [Reportable]

Author: Danna Schock

Ranaviruses (family Iridoviridae) infect fish, reptiles, and amphibians, and are of considerable concern in aquaculture (Chinchar, 2002; Williams et al., 2005). Lethal amphibian ranaviruses infect a wide range of species and die-offs have been documented world-wide (Collins et al., 2003). In Canada, ranaviruses have been isolated from amphibian populations in Ontario (Mixedwood Plains and southern edge of Boreal Shield) (Greer et al., 2005; Duffus et al., 2008), Manitoba, Saskatchewan and Alberta (Prairies and Boreal Plains) (Schock et al., 2008; Goater, C., 08, pers. comm.), and the Northwest Territories (Taiga Plains) (Schock, D., unpublished data). In a review of 64 amphibian mortality events in the United States, Green et al.. (2002) reported that ranaviruses affected only widespread and abundant amphibian species. However, amphibian ranaviruses isolated from abundant species such as barred tiger salamanders (Ambystoma mavortium) and wood frogs (Rana sylvatica) can cause lethal infections in multiple amphibian species (Schock et al., 2008). Thus, the potential exists for ranaviruses maintained in resilient populations of abundant species to serve as sources of infection to vulnerable rare species in the same habitat. Further, die-offs caused by ranaviruses can severely reduce numbers of amphibians at breeding sites and may affect amphibian populations in highly fragmented habitats where re-colonization is unlikely (Collins et al., 2003).

Too little is known about ranaviruses and their effects on Canadian amphibian populations to identify trends or future trajectories of amphibian-ranavirus interactions. It is now clear that human activities, particularly the trade in fishing bait, has the potential to transport different strains of ranaviruses among widely-separated habitats (Collins, 2008), and there is strong experimental evidence that virus strains new to local populations can sometimes cause very high mortality (Schock, 2007).

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Morbilliviruses of terrestrial and marine carnivores

Morbilliviruses are a large virus group that includes human measles virus, several viruses important to livestock (rinderpest and peste des petites ruminants viruses), and an array of viruses in wild animals that are well-known but of uncertain virus taxonomy. Many morbilliviruses cause severe disease in susceptible wild species, often with high fatality rates. However, a virus that is fatal in one species may infect one or more other host species with little or no clinical disease. Thus, certain species serve as maintenance hosts for these viruses, and sources of infection for other, more susceptible species. For example, harp seals may be sources of infection with phocine distemper virus for harbor seals (Duignean et al., 1995a; Duignean et al., 1997; Barrett et al., 2003). Morbilliviruses have been named according to the animal host in which each was first discovered to cause disease, for example, canine distemper virus (domestic dogs), phocine distemper virus (seals), dolphin morbillivirus. Nevertheless, these names can be misleading; for example, canine distemper viruses cause severe disease in many non-canid species such as raccoons, skunks, ferrets, and several wild cats, and antibodies indicating exposure to dolphin morbillivirus and to phocine distemper virus have been found in land-locked grizzly bears in the Montane Cordillera Ecozone+ (Rossiter et al., 2001; Philippa et al., 2004).

Because they are known to infect such a wide range of widely distributed carnivores in Canada, morbilliviruses must be assumed to occur in Canadian wild carnivores in all ecozones+(Duignean et al., 1995a; Duignean et al., 1995b; Duignean et al., 1997; Rossiter et al., 2001; Philippa et al., 2004; Canadian Cooperative Wildlife Health Centre, 2008). The ecology, reservoirs, and transmission dynamics of these viruses in Canada are largely unknown, however. Morbilliviruses known to be present in Canadian wildlife include various strains of canine distemper virus (wide host range including canids, felids, procyonids, and mustelids, assumed to be in all terrestrial ecozones+) (Rossiter et al., 2001; Canadian Cooperative Wildlife Health Centre, 2008), phocine distemper virus (harbour, gray, harp, and hooded seals in the Gulf of Maine and Scotian Shelf and the Estuary and Gulf of St. Lawrence ecozones+, and ringed seals in the Canadian Arctic Archipelago, Beaufort Sea, and Hudson Bay, James Bay and Foxe Basin ecozones+) (Duignean et al., 1995b; Duignean et al., 1997), and porpoise morbillivirus (harbour porpoise) in the Gulf of Maine and Scotian Shelf Ecozone+ (Duignean et al., 1995a).

Morbilliviruses can threaten small populations of susceptible rare species when they are maintained in larger populations of sympatric species. Canine distemper virus was in the process of killing the last known wild population of black-footed ferrets when the last remnant animals were brought into captivity to prevent infection and permit captive breeding and release (Thorne and Williams, 1989). This virus continues to menace the success of restoration programs, including planned restoration to Canada’s Grasslands National Park (Prairies Ecozone+). Morbilliviruses have had significant impacts on conservation programs for African wild dogs and lions (Roelke-Parker et al., 1996; Van de Bildt et al., 2002), and have caused severe epidemics in harbour seals in the eastern Atlantic (phocine distemper) (Barrett et al., 2003) and seals of the Caspian Sea and Lake Baikal (canine distemper) (Kennedy et al., 2000). Potentially vulnerable populations of species at risk in Canada include the American badger population of the Western Interior Basin and Montane Cordillera ecozones+, the swift fox of the Prairies Ecozone+, and the beluga population in the St. Lawrence Estuary. Environmental or other changes that result in new range overlaps or intensified interactions among previously separated carnivore populations appear to be significant risk factors for epidemics due to morbilliviruses.

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