Technical Thematic Report No. 7. - Wildlife pathogens and diseases in Canada
Pathogens Distributed Across Multiple Ecozones+ (Bacteria)
Avian cholera [Immediately Notifiable]
Avian cholera is the name given to infection of birds with disease-causing strains of the bacterium Pasteurella multocida. In poultry, the name fowl cholera often is used for this disease. Despite these names, this disease is not related in any way to human cholera (Samuel et al., 2008).
Avian cholera was recognized as an important cause of mortality in wild birds in North America only since the middle of the last century (Samuel et al., 2008). Large die-offs of wild birds, especially ducks and geese, were observed in California and Texas in winter in the 1940s. Beginning in the 1970s in Canada, avian cholera was recognized as occurring regularly in migrating geese in the Prairies Ecozone+, and in common eider nesting in the St. Lawrence Estuary (Wobeser, 1997b). More recently, epidemics also have occurred in double-crested cormorants in the Boreal Plains Ecozone+, in Arctic-nesting eiders in the Hudson Bay, James Bay & Foxe Basin Ecozone+, and in pelagic and coastal marine birds in winter in the Newfoundland and Labrador Shelves and the Gulf of Maine and Scotian Shelf ecozones+ (Canadian Cooperative Wildlife Health Centre, 2008; Buttler, 2009). In wild geese in Canada, (lesser snow, Canada, cackling, Ross, white-front), the disease has been recognized as a cause of annual but minor mortality during spring and fall migration through the Prairies Ecozone+, but occasionally causing larger epidemics among nesting geese in the Taiga Shield and Arctic ecozones+ (Canadian Cooperative Wildlife Health Centre, 2008; Samuel et al., 2008).
The strains of P. mulocida which cause avian cholera in wild birds are extremely powerful pathogens, rapidly transmissible within populations of birds and often producing very high levels of mortality. Although there often is collateral infection and mortality among other avian species using the same habitat as the main affected species during an epidemic, including avian predators and scavengers, each epidemic seems overwhelmingly to involve only one or a small number of species.
The emergence of avian cholera as an epidemic disease of wild birds in North America has been coincident with, and possibly related to, broad land use changes resulting in loss of wetland habitat, the consequent high densities of birds on refuges and other habitat remnants, and the associated unsanitary conditions and stress conducive to transmission of the bacterium among birds, particularly through contaminated water. However, too little is known about risk factors for these epidemics to attribute outbreaks to specific environmental factors (Samuel et al., 2008). Recognition of large outbreaks in double-crested cormorants also has been coincident with dramatic increases in the size of breeding colonies. Recent outbreaks in Arctic eiders and marine birds of the western Atlantic are unexplained. It is not yet possible to discern whether the record of occurrence of avian cholera in North American wild birds over the past 60 years represents the progressive expansion of an epidemic disease across an ever larger spectrum of species and populations, or a series of unconnected disease events, each with its own set of causal factors. Despite large epidemics affecting many thousands of birds, there is no evidence to date that avian cholera has had a significant impact on continental populations of the most-affected species.
Clinical disease in people due to infection with the bacterium Borellia burgdorferiwas first recognized in North America in a cluster of cases in the town of Old Lyme, Connecticut, and has been called Lyme disease ever since. This is not an important disease of wild animals, but wild animals are the source of infection for people. Lyme disease is a common and severe illness in the northeastern and northcentral United States and is of increasing importance in Canada. Infection is transmitted from the wildlife reservoir of the bacterium in small rodents, such as the white-footed mouse and eastern chipmunk, to people by two species of tick: Ixodes scapularis east of the Rocky Mountains and Ixodes pacificusin British Columbia. People are at risk of contracting Lyme disease in spring, summer, and fall in areas where the tick vector is a permanent resident and where local small rodents carry the bacterium (Brown and Burgess, 2001). Until very recently, these conditions prevailed only in a small area of the Mixedwood Plains along the north shore of Lake Erie and at the southern margin of the Pacific Maritime Ecozone+. In the past decade, however, zones of permanent human risk of Lyme disease in Canada have expanded to include a larger area of the Mixedwood Plains, a small area within the Atlantic Maritime, and small areas within the southern margin of the Boreal Shield and Boreal Plains (Public Health Agency of Canada, 2006).
Ecological models of the effect of climate change on the public health risk of Lyme disease in Canada predict expansion of the range of the vector tick (I. scapularis) northward 200 km by 2020, to include the eastern Prairies, southern Boreal Plains, southern Boreal Shield, all of the Mixedwood Plains, and most of the Atlantic Maritime ecozones+, and up to 1,000 km by 2080, to include larger segments of the Prairies, Boreal Plains, southern Hudson Plains, Boreal Shield, Atlantic Maritime, and Newfoundland Boreal ecozones+ (Ogden et al., 2006). Thus, areas of permanent human risk of Lyme disease are predicted to include a majority of Canada’s human population within a few decades. Migratory passerine birds are a constant source of I.scapularis ticks to much of Canada. It is estimated that from 50 to 175 million I.scapularis are brought to Canada each year by spring migrant song birds (Ogden et al., 2008). Thus, any habitat made suitable to this tick through climate change may quickly be populated. These birds also transport the bacterium, either by transporting infected ticks or because the birds themselves are infected. Sporadic cases of Lyme disease in areas where the vector tick does not complete its life cycle are most likely due to the bites of infected ticks brought into the area by migratory birds. However, introduction and establishment of the bacterium in new populations of the tick may occur less frequently than does dissemination of the tick itself. This may extend the time required for Lyme disease itself to spread northward in association with the expanding range of the tick vector (Ogden et al., 2008). The recent expansion in Canada of the areas at risk of Lyme disease are consistent with these predictions and mechanisms.
Mycoplasma gallisepticum [Annually Notifiable]
The bacterium Mycoplasma gallisepticum (MG) is an important pathogen of domestic poultry. In 1994, infection with MG causing severe conjunctivitis (inflammation of the moist membranes of the outer eye and inner eyelid) was first detected in the eastern population of the house finch in Washington, DC.By June 1996, this infection had been recognized in house finches in all states east of the Mississippi River and in Ontario, Quebec, and the Maritime Provinces (Mixedwood Plains, Boreal Shield, and Atlantic Maritime ecozones+) (Fischer et al., 1997). Affected house finch populations underwent marked declines; infection has persisted in these populations and their numbers have not recovered (Dhondt et al., 1998; Nolan et al., 1998; Hochachka and Dhondt, 2000). Infection and disease also have been found in pine grosbeak and evening grosbeak in Quebec (southern Boreal Shield Ecozone+) and in American goldfinch in the United States (Fischer et al., 1997; Mikaelian et al., 2001). Possible effects on populations of these other species have not been studied. Live house finches with severely inflamed conjunctiva typical of MGinfection have been observed in the Prairies but the specimens required to confirm MG as the cause have not been available. Infection has been confirmed in adjacent Montana (Duckworth et al., 2003). This is evidence of spread of MG from the eastern to the western population of house finch.
MG in wild finches is a potential conservation concern for two reasons. The causative bacterium appears to be a strain of a poultry pathogen now adapted to and maintained within the wild house finch population. As such, it is an example of a pathogen transmitted from a domestic animal source to a wild species that has significantly reduced the population of the affected wild population. The effect of MG on house finch populations also appears to be significantly affected by climate. The prevalence of diseased birds was approximately three times higher in the southern than it was in central and northern areas of the eastern United States and prevalence appeared associated with minimum winter temperature (Altizer et al., 2004). Therefore, the impact of MG on house finch or other susceptible bird populations in Canada may increase with predicted climatic warming. On the other hand, the most affected population has been the eastern population of the house finch, which originated from a small number of birds taken from the normal range of this species in the western United States and released on the east coast in 1940 (Hill, 2008). Recent studies have shown that the eastern population may have reduced genetic variability due to its foundation on a small number of individuals and also that house finches with greater genetic heterozygosity are more resistant to the effects of MGinfection (Hawley et al., 2005; Hawley et al., 2006).
Bovine tuberculosis [Reportable]
Bovine tuberculosis (BTb) is caused by infection with the bacterium Mycobacterium bovis. It readily infects domestic cattle, and in people it causes a disease indistinguishable from human tuberculosis (infection with M.tuberculosis). Infection generally is permanent if untreated, and disease is prolonged and debilitating or fatal (Clifton-Hadley et al., 2001). Infected animals, meat products, and milk are significant health hazards for people, and for public health reasons, BTb was successfully eradicated from Canada’s domestic animal population through a long and costly program of testing all herds and slaughtering entire herds in which any infected animals were detected. Herd slaughter is necessary because the tests for BTbin live animals are unreliable and easily fail to detect infected individuals. These tests are quite accurate, however, when used to identify infected herds. BTb can infect and cause disease in a wide range of mammalian species. However, maintenance of infection in a population appears to require gregarious behaviour which affords the necessary rates of contact to achieve inter-generational infections. These maintenance populations also can provide a constant source of infection for susceptible scavenger species, such as wild or feral pigs, as occurs when these are sympatric with an infected maintenance population (Connelly et al., 1990; Clifton-Hadley et al., 2001).
Bison in Wood Buffalo National Park and adjacent areas (Boreal Plains, Taiga Plains, and Taiga Shield ecozones+) became infected with BTb in the 1920s when an infected herd of over 6,000 plains bison were translocated from the former Buffalo National Park in eastcentral Alberta (Nishi et al., 2006). Infection has persisted in this herd and surveys between 1997 and 1999 found that approximately 49% of these bison were infected (Joly and Messier, 2004a). (These bison also carry bovine brucellosis – see page 15) In the past two decades, other populations of wild bison, apparently free of infection with BTb, have become established in the Taiga Plains, Taiga Cordillera, Boreal Cordillera, and Boreal Plains ecozones+ to the north, west, and south of the range of the infected herds (Gates et al., 2001) (Figure 2). Effective measures to prevent the spread of BTb to these infection-free herds are not in place (Nishi et al., 2006). Thus, the potential spread of BTb from infected to non-infected wild bison, all of which are assessed as Threatened by the Committee on the Status of Endangered Wildlife in Canada, and also to livestock, is a major conservation and socio-economic issue.
Figure 2. Distribution of bovine tuberculosis-free and diseased free-ranging bison herds in northwestern Canada.
Long Description for Figure 2
This map shows distribution of bovine tuberculosis-free and diseased free-ranging bison herds in northwest Canada. Herds that are disease-free include Mackenzie, Nahanni, Norquist, Ethethin Lake, Pink Mountain, Hay Zama, and Syncrude/Fort McKay. With the exception of Syncrude/Fort MacKay (in northeastern Alberta) these herds are distributed west of the Great Slave Lake, across southern Northwest Territories and Yukon, and northern Alberta and British Columbia. The Hook Lake Recovery Project is another disease-free herd located south of Great Slave Lake.
Herds that have had disease presence confirmed or are assumed to be diseased include, Hook Lake, Little Buffalo River, Nyarling, Pine Lake, Garden River, Peace Delta, Wentzel, Wabasca, Birch Mountains, and Firebag. These herds are distributed south of Great Slave Lake across southern Northwest Territories and northeastern Alberta.
A bison control area is located between diseased and disease-free herds, in the southwestern region of Great Slave Lake.
Herds in blue are considered disease-free. Herds in red have had disease presence confirmed or are assumed to be diseased due to movement patterns into areas of confirmed disease status. WBNP = Wood Buffalo National Park, NH = Nahanni Herd, PM = Pink Mountain, HZ = Hay Zama, GR = Garden River Herd, HLRP = Hook Lake Recovery Project, LBR = Little Buffalo River, MB = Mackenzie Bison Herd, WZ = Wentzel, WA = Wabasca Herd, NL = Nyarling, PL = Pine Lake, PD = Peace Delta, BM = Birch Mountains, FB = Firebag, SY = Syncrude/Fort Mckay, Liard Reintroduction = Norquist herd Source: Elkin (2008)
The most extensive research on whether or not BTb (and brucellosis) have an impact on the demography of the infected bison herds found evidence that there is a negative impact (the disease alters the predation rate resulting in the predator having a larger impact than would be the case without the disease) and proposed a biological mechanism through which the impact will persist and keep the population well below the carrying capacity of the available habitat (Joly and Messier, 2004b). Others have disputed this interpretation (Bradley and Wilmshurst, 2004). The current rise in the population of infected bison in the area is compatible with either interpretation.
There is agreement among many scientists that BTb (and brucellosis) could be eliminated from wild bison through complete eradication of the infected herds and re-population with bison free of BTb and brucellosis, and also that such eradication is technically possible (Shuryet al., 2006). However, the governments of Canada, Alberta, and the Northwest Territories have not yet resolved this issue since it was first fully articulated in 1990 (Connelly et al., 1990; Nishi et al., 2006). It seems certain that without effective intervention of some form, BTb (and brucellosis) will spread to non-infected wild bison herds progressively over time, and that the vast majority of all wild bison in Canada will become infected (Gates et al., 2001). As recent controversies associated with the movement of diseased bison out of Yellowstone National Park in the United States illustrate, infection of wild bison with diseases of major public health and socioeconomic concern can limit the conservation options for this species (Brown, 2008).
BTb was discovered in elk, domestic cattle, and white-tailed deer in the area of Riding Mountain National Park in 1991 (Lees et al., 2003; Nishi et al., 2006). It appears that the bacterium had persisted undetected in this area in cattle and/or elk herds during the eradication program. In 2009, it was estimated that 3.5% of elk and 1% of white-tailed deer in the Riding Mountain National Park area are infected (Shury, T., unpublished data). There is evidence that BTb is maintained in populations of white-tailed deer only under conditions of unusually high population density, such as the large-scale deer feeding programs associated with BTb in deer in Michigan (Miller et al., 2003). This may be a factor in the maintenance of BTb in elk in the National Park area (Lees et al., 2003). Currently, a multi-stakeholder Task Group for Bovine Tuberculosis is taking a range of actions to reduce transmission of BTb among elk and from elk to cattle (Nishi et al., 2006).
Brucellosis is the name given to all diseases caused by infection with any of the several different species of the bacterial genus Brucella. The clinical manifestations of brucellosis are many, but the most common are infection and inflammation of the female and male reproductive tracts with resulting abortion and male infertility, and infection of joints and tendon sheaths resulting in progressive lameness. Infection persists, often for the lifetime of the animal. People are similarly susceptible to infection with Brucella sp., and brucellosis in animals with which people have contact is a public health risk (Chan et al., 1989; Forbes, 1991; Thorne, 2001).
In Canadian wildlife, infection with Brucella sp. is widespread and of potential ecological and public health significance in three areas: 1) in bison in and around Wood Buffalo National Park, where the bison populations infected with bovine tuberculosis are co-infected with bovine brucellosis caused by Brucella abortus(Boreal Plains, Taiga Plains and Taiga Shield ecozones+) (see bovine tuberculosis, above) (Tessaro, 1986); 2) in barren ground caribou populations, and one herd of reindeer near Tuktoyaktuk, Northwest Territories, which are infected with Brucella suis biotype 4 across the Arctic, Taiga Cordillera, Taiga Plains, Taiga Shield, and the northern edges of the Boreal Plains, Boreal Shield, and Hudson Plains ecozones+; (Forbes, 1991); and 3) in seals (harbour, harp, hooded, gray, and ringed seals, and walrus) and whales (beluga, narwal) in the Gulf of Maine and Scotian Shelf, Estuary and Gulf of St. Lawrence, Newfoundland and Labrador Shelves, Canadian Arctic Archipelago, Hudson Bay, James Bay and Foxe Basin, and West Coast Vancouver Island ecozones+ (Forbes et al., 2000; Nielsen et al., 2001).
Bovine brucellosis was eradicated from the Canadian cattle herd in 1985 and now is an issue for bison conservation, human health, and agricultural economies that parallels that posed by bovine tuberculosis (Connelly et al., 1990). Approximately 30% of bison in the Wood Buffalo National Park area are infected (Joly and Messier, 2004a). Brucellosis is widespread in arctic caribou, with 20 to 50% of animals in various herds infected (Leighton, F. A., unpublished data; Koller-Jones, M., 06, pers. comm.). However, its ecological impact, if any, on infected populations is not known. Infection of northern people with this bacterium occurs and is associated with consumption of caribou (Chan et al., 1989; Forbes, 1991). Whether or notB. suis biotype 4 is a naturally occurring pathogen in North America or a pathogen introduced from Europe in imported reindeer also is not known. There are no records of this infection in woodland caribou, including the George River herd of northern Quebec. Brucella infection in marine mammals was discovered only in 1994 (Forbes et al., 2000) and its importance to wild populations and to human health have not been assessed.
As noted for bovine tuberculosis, it seems certain that without effective intervention of some form bovine brucellosis will spread to non-infected wild bison herds progressively over time, and that the vast majority of wild bison in Canada then will be infected (Gates et al., 2001). This will place bison recovery efforts further at odds with livestock economies and public health interests. Too little is known about the ecology of Brucella in caribou or in marine mammals to identify current trends or predict future trajectories. A serological survey of a large herd of reindeer in the western edge of the Arctic Ecozone+ and of a barren ground caribou herd (Kaminuriak) in the Taiga Shield and adjacent Arctic ecozones+ of Manitoba and Nunavut in the 1960s found only 9% of reindeer and 4% of caribou infected (Broughton et al., 1970). The more recent infection rates of 20 to 50% may represent a trend of increasing prevalence. Any environmental changes that increase the overlap of barren ground caribou with woodland caribou carry the risk that Brucella suisbiotype 4 may become established in woodland caribou populations.
Anthrax is the name given to all forms of disease caused by infection with the bacterium Bacillus anthracis. It is most typically a disease of wild and domestic ungulates, in which it usually is rapidly fatal. Mammalian predators and scavengers also die regularly during anthrax outbreaks in ungulates. Humans are susceptible to anthrax and disease in people ranges from a self-limiting infection of the skin to rapidly fatal disease following ingestion, inhalation, or contamination of wounds. Ungulates generally become infected from bacterial spores in soil. Environmental conditions that cause these spores to persist for decades or even centuries in soil and to concentrate on the soil surface, such as high-calcium soil chemistry for spore persistence, and flooding followed by dry periods for spore concentration, appear to be major risk factors in outbreaks of anthrax in wild and domestic ungulates. Animal to animal transmission of the bacterium plays only a minor role. Anthrax probably was introduced to North America by European exploration and settlement (Dragon and Rennie, 1995; Dragon et al., 1999; Hugh-Jones and de Vos, 2002).
In Canadian wildlife, anthrax has been recognized most often in bison in and around Wood Buffalo National Park. The first recognized outbreak was in 1962 and sporadic outbreaks have occurred ever since, often with inter-outbreak time spans of many years. Anthrax was recognized in bison in the Mackenzie Bison Sanctuary in 1993 (Taiga Plains Ecozone+) and in a bison herd associated with Prince Albert National Park (Saskatchewan, Boreal Plains Ecozone+) in 2008 (Dragon and Rennie, 1995; Dragon et al., 1999). Wild ungulates also have died in association with outbreaks of anthrax in domestic cattle in Canada. For example, small numbers of white-tailed deer and moose were found dead of anthrax in such an outbreak in central Saskatchewan in 2007 (Canadian Cooperative Wildlife Health Centre, 2008).
To date, outbreaks of anthrax in wildlife in Canada have affected relatively few individuals. The total number of bison and other species to have died of anthrax is unknown, but a minimum of 1,309 bison died of the disease in outbreaks between 1962 and 1993. Clearly, anthrax contributes to the overall effects of infectious diseases on these bison populations but has not, by itself, posed a significant risk to the survival of these populations (Joly and Messier, 2004b). Anthrax in bison does represent a potential health risk to people who hunt or handle infected bison or their tissues. The occurrence of outbreaks in wild bison and in livestock appear linked to climatic factors, particularly intense precipitation followed by drought. To date, no predictive models have been published with respect to outbreaks of anthrax in Canada and predicted climate change.
Plague is the name given to all forms of disease caused by infection with the bacterium Yersinia pestis. Synonyms for the disease in people include ‘bubonic plague’ and ‘the black death.’ The bacterium probably evolved quite recently (2 to 20,000 years ago) in central Asia as a pathogen of small rodent communities transmitted by fleas. Plague caused wide spread human disease in the Near East and Europe in the 6th to 8th centuries and again in the 14th to 19th centuries. In the late 1800s, an epidemic of plague spread from China around the world by newly available fast steam ship traffic, arriving in San Francisco in 1900. The bacterium became established in local wild rodent and flea communities and spread in wildlife east, north, and south over the ensuing three to four decades. It now is present in Canada in an area of uncertain size in the southern Prairies and Western Interior Basin ecozones+, and possibly the Montane Cordillera. Surveys conducted in the 1930s and 1990s detected Yersinia pestis in southern Saskatchewan and Alberta. Two bushy-tailed woodrats were found dead of plague in the Lillooet area of British Columbia in 1988 (Gibbons, 1939; Gibbons and Humphreys, 1941; Humphreys and Campbell, 1947; Barnes, 1982; Lewis, 1989b; Gage et al., 1995; Leighton et al., 2001).
Plague persists in communities of small rodents that are sufficiently resistant to severe disease that the bacterium can persist in their rodent-flea communities. However, populations of species such as colonial ground squirrels and prairie dogs suffer severe epidemics when plague is introduced into their colonies, with mortalities as high as 99% (Gage and Kosoy, 2005). These highly susceptible rodent populations are able to recover in one to three years. Nevertheless, the introduction of plague to North America is thought to have been a significant factor in driving the black-footed ferret to extinction in the wild by the late 1980s because of this animal’s dependence on prairie dogs for food and also its own susceptibility to plague (Biggins and Godbey, 2003). Plague in prairie dogs is now a significant factor affecting the long-term success of the black-footed ferret recovery program based on re-introduction of captive-bred animals in the United States and Canada (Grasslands National Park, Prairies Ecozone+). Only one case of plague in people derived from a wildlife source is on record in Canada (Gibbons and Humphreys, 1941), but there are 10 to 15 such cases each year in the United States (Division of Vector-Borne Infectious Disease, 2009). Plague in North American wildlife appears most prevalent in dry habitat at medium elevations in the American southwest (Gage et al., 1995). Currently, southwestern Canada is the northern limit of the geographic distribution of plague. It seems likely that a warming climate will change this distribution, with extensions northward toward major urban centers such as Calgary, Edmonton, Regina, and Saskatoon.
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