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

Pathogens with Limited Distribution

Gulf of Maine and Scotian Shelf and West Coast Vancouver Island ecozones+

Plastic ingestion by marine birds

Authors: Pierre-Yves Daoust and Zoe Lucas

Ingestion of waste plastic by pelagic marine birds has been studied both to assess the impact on the birds themselves and as an index of pollution of the seas with plastic debris (Sievert and Sileo, 1993; Blight and Burger, 1997; Van Franeker, 2008). In the eastern Atlantic/North Sea, the number of avian species documented to have ingested plastic increased from two in the 1960s to more than 109 by the late 1980s. At the same time, global production of plastic increased from 30 million tonnes per year in the 1970s to 150 million tones per year in 2000 (Vlietstra and Parga, 2002).

Birds of the order Procellariiformes, which includes albatross, shearwaters, and northern fulmars, appear to ingest the largest amounts of plastic. Of 50 carcasses of northern fulmars collected between 2001 and 2005 during beached bird surveys on Sable Island (200 km east of Halifax, Nova Scotia), the stomachs of 49 contained plastic and/or styrofoam which varied in total weight from 0.015 to 13 g per bird (average, 1.7 g) (Walther et al., 2008) (Figure 5).

Figure 5. Indigestible material from the stomach of one northern fulmar from Sable Island, Nova Scotia.

Long Description for Figure 5

Photo: Ingestible material from the stomach of one northern fulmar from Sable Island, Nova Scotia. Materials include wire, plastic, glass, a lobster band, stone, cellophane, and wood.

Source: Walther et al. (2008)

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In 1987, plastic was found in the stomachs of 75 to 100% of eight different species of Procellariiformes caught in pelagic drift nets off the coasts of British Columbia (West Coast Vancouver Island Ecozone+), Washington, and Oregon (Blight and Burger, 1997). It is not clear to what extent plastic ingestion is harmful to these birds, although some evidence of nutritional problems has been reported (Sievert and Sileo, 1993). There is a clear trend for increasing pollution of the seas with plastic debris that can be and is ingested by marine birds (Sievert and Sileo, 1993; Blight and Burger, 1997) .

Prairies Ecozone+

Chronic wasting disease [Reportable]

Chronic wasting disease (CWD) is a fatal disease of members of the deer family (cervids) resulting from ingestion of a misfolded version of a normal body protein called the prion protein (Pruisner, 1982; Williams et al., 2001). Such diseases are classified as transmissible spongiform encephalopathies; other diseases in this same class include scrapie in sheep, bovine spongiform encephalopathy in cattle, and Creutzfeld-Jacob disease in people. These diseases result in progressive deterioration of the brain associated with accumulation in the brain of misfolded prion protein. All typically have long intervals (years) between exposure to the misfolded prion protein and the first clinical signs of disease. There are no conclusive medical tests to identify people or animals affected by these diseases prior to the onset of clinical signs, and a definitive diagnosis generally only occurs at autopsy. The abnormally-folded prion proteins which cause these diseases resist most available forms of deactivation such as formaldehyde, disinfectants, heat, and UV light. No effective vaccines or drugs currently are available to prevent or treat these diseases (Williams et al., 2001).

CWD was first recognized as a clinical disease in 1967 among mule deer housed at a research station in Colorado (Williams et al., 2001). It was first recognized to be a form of spongiform encephalopathy in 1978. At about this same time, it was found in captive mule deer in Wyoming and captive elk in Colorado, and then in wild elk, mule deer, and white-tailed deer in these same states. Since these first discoveries, the disease has spread widely in the United States and Canada (Figure 6), mainly in the Prairies Ecozone+ but also in the Boreal Plains Ecozone+, often in association with sale and transport of farmed cervids.

Figure 6. Distribution of chronic wasting disease in North America, 2011. Depopulated means that all cervids on the farm were killed by government authorities as per North American response to CWD.

Long Description for Figure 6

This map shows distribution of chronic wasting disease in North America for 2011. Incidences are concentrated around Wyoming, Utah, Colorado, Nebraska, and South Dakota in the United States and in the Prairies and Boreal Plains ecozones+.

Source: USGS National Wildlife Health Centre (2011)

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CWD was first reported in Canada in 1996 and again in 1998 in captive elk on game farms in Saskatchewan (Kahn et al., 2004). An eradication program for CWD in farmed cervids was carried out between 2000 and 2004, during which approximately 18,000 animals were destroyed on 42 farms in Saskatchewan and Alberta (Figure 6). However, in 2000, CWD was detected in a wild mule deer on the Saskatchewan side of the Saskatchewan-Alberta border. Since this first detection in wild populations, CWD has been detected in wild cervids progressively in four separate geographical areas of the Prairies Ecozone+ in mule deer, white-tailed deer, and elk (Figure 7). These affected areas have grown in size and the proportion of hunter-killed animals found affected with CWD within these areas has increased slowly but steadily since 2000 (Canadian Cooperative Wildlife Health Centre, 2008). Table 2 shows the data for Saskatchewan from 1997 to March 2009.

Figure 7. Detections of chronic wasting disease in wild deer in the Prairies.

Long Description for Figure 7

This map of southern Alberta and Saskatchewan show detections of chronic wasting disease in wild deer in the praries. Of 178 detections, 29 were in Alberta and 149 in Saskatchewan. Four separate geographical areas are outlined, the largest encircles Kindersley, Oyen, Empress and Swift Creek. Two areas are located in the south and northeastern regions of Lloydminster and the remaining location surrounds Nipawin.

Source: Canadian Cooperative Wildlife Health Centre (2008), Bollinger, pers. comm.

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Table 2. Summary of chronic wasting disease in wild cervids in Saskatchewan, 1997-March 2009.
YearMule Deer
Mule Deer
White-tailed Deer
White-tailed Deer
1999Footnote 1079057044000180
2000Footnote 111840726089001999
2001 SpringFootnote 1115405800001212
2001 Fall01,07702,23603400003,653
2002 Spring113402400001158
2002 Fall73,24422,41301630095,820
2003 Fall222,83001,922015300224,905
2004 Fall305,26521,4390900326,713
2005 FallFootnote 252,6351093804704353,624
2006 FallFootnote 2272,343221,4970164010494,014
2007 FallFootnote 2322,561131,72929004474,384
2008 FallFootnote 2433,66858281214027494,793

Notes: This table does not include those specimens that were deemed unsuitable for testing.


Footnote 1

Prior to the fall of 2000, only the brain section was used to diagnose CWD. Starting in 2001, tonsils and/or retropharyngeal lymph nodes were also examined.

Return to footnote Table 21

Footnote 2

Starting in the fall of 2005, animals under one year of age were no longer tested under the program because detectable infection is rare in a young animal and therefore not cost effective in terms of surveillance.

Return to footnote Table 2 2

Source: Canadian Cooperative Wildlife Health Centre, Western and Northern Regional Centre, unpublished data

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CWD is a serious ecological and economic concern to Canada. The approximately 1.8 million white-tailed deer, 350,000 mule deer, 100,000 elk and 900,000 moose in Canada are susceptible to CWD and there are no natural barriers to prevent its spread from its current locations to the rest of the country (Bollinger et al., 2004). It is not known whether or not Canada’s 4 million caribou also are susceptible to CWD. CWD is transmitted animal to animal through body secretions such as saliva, but also can be transmitted through exposure of susceptible animals to environments contaminated by the misfolded CWD prion protein, which persists for exceptionally long periods (Miller and Williams, 2003; Mathiason et al., 2006).

CWD is a new disease, caused by a whole new class of disease-causing agent, and thus predictions of its potential effects on cervid populations can only be approached through modelling. Such models are uncertain because large data sets and well-documented model parameters such as transmission rates for CWD are not available. However, as explored through models, a negative impact of CWD on wild cervid populations in the long term (100 years), moderate to extreme in extent, appears the most reasonable expectation (Gross and Miller, 2001). Wild cervids support a variety of commercial and subsistence human economies in Canada which form a large portion of the approximately $12 billion of Canada’s gross domestic product (1996) associated with wildlife (Federal-Provincial-Territorial Task Force on the Importance of Nature to Canadians, 2000). These species also are ecologically important herbivores across all terrestrial ecozones+. Thus, unless effective means of controlling the disease are developed and implemented, CWD is likely to reshape landscapes and economies in Canada in the 21st century.

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Botulism type-C

Botulism is a form of food poisoning associated with ingestion of powerful toxins produced by various strains of the bacterium Clostridium botulinum, designated types A, B, C and so on, according to the type of toxin each produces. Although it has occurred in other ecozones+, type-C botulism, from ingestion of type-C botulinum toxin, has caused large and recurrent epidemics only in the Prairies Ecozone+. Waterfowl, especially ducks, regularly are affected by type-C botulism, with peak occurrence in July and August. Type-C botulism in ducks is a disease of complex ecology (Wobeser, 1997a; Rocke and Bollinger, 2007). C.botulinum is a decomposing bacterium which persists for long periods in soil and sediments as resistant spores and which proliferates in nutrient-rich environments such as animal carcasses. The bacterium carries no gene for botulinum toxin but can receive this gene when infected by a carrier bacteriophage virus. Epidemic mortality from type-Cbotulism occurs when toxin is produced and then ingested by susceptible animals. In the context of waterfowl on prairie wetlands, fly larvae (maggots) growing in carcasses of dead animals are the principal agents of toxin transfer from the dead to the living. Maggots are highly attractive food for birds of all kinds and are eaten voraciously. Maggots absorb but are unaffected by type-C toxin. Thus, the risk of epidemics of type-C botulism is highest when C. botulinum and toxin gene-carrying bacteriophage viruses are present in the environment, temperatures are within the range of flesh fly activity (above about 15C) and toxin production, a source of animal carcasses is present, and many susceptible ducks or other birds are present to find and ingest any toxin-bearing maggots that develop. Under these conditions, a cycle of positive feedback occurs in which the first toxin-bearing maggots are eaten by birds which then die and are substrate for putrefaction and further production of toxin-bearing maggots. Under these conditions, epidemics can grow logarithmically with each cycle of toxin production, transfer to living birds and consequent mortality adding to the biomass of putrefying carcasses producing toxin and maggots. Factors that reduce risk are high scavenging rates that remove carcasses, especially early in the season when only a few carcasses may be present, ambient temperatures below about 15° C, and a low density of susceptible live birds (Wobeser, 1997a; Rocke and Bollinger, 2007)

The alkaline wetlands of the Prairies Ecozone+ are habitats favourable to type-C botulism. It is likely that some mortality from botulism occurs every summer in this ecozone+, but often the outbreaks are small and go undetected. Some very large epidemics have been documented, however. In the mid-1990s, repeated years of high mortality occurred in southern Alberta, Saskatchewan, and Manitoba. For example, over 100,000 dead ducks were counted in late fall at Old Wives’ Lake in southern Saskatchewan in 1996, and a season-long study at this site in 1997 found total mortality from June to October to have been approximately one million birds (Rocke and Bollinger, 2007; Canadian Cooperative Wildlife Health Centre, 2008). These outbreaks were associated with drought conditions during which many of the small wetlands used by waterfowl for nesting were dry and large numbers of birds were concentrated on a small number of large wetlands where suitable habitat remained available. There was a marked reduction in mortality from botulism in subsequent years when precipitation relieved drought conditions (Canadian Cooperative Wildlife Health Centre, 2008).

C. botulinum and their bacteriophages are persistent residents of most wetlands in the Prairies Ecozone+. Thus, type-C botulism remains a potential source of mortality of wetland birds (virtually all species are susceptible to lethal intoxication). Occurrence of epidemics has been associated with factors such as low rainfall and high temperatures, both of which are predicted trends for the Prairies Ecozone+ in the coming decades (Ogden et al., 2006). The draining and other destruction of wetlands in the past 50 years already has greatly reduced the amount of habitat available to aquatic birds, and, by concentrating birds on remnant wetlands, this also may contribute to an increased risk of type-C botulism.

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Newfoundland Boreal Ecozone+

Muscle worm of caribou (Elaphostrongylus rangiferi) [Immediately Notifiable]

The nematode parasite Elaphostrongylus rangiferi was brought to the island of Newfoundland in 1908 in infected reindeer, from which it spread to native caribou. It is now found in all major caribou populations on the island (Ball et al., 2001). The majority of infections appear to produce very little clinical disease, but infection with large numbers of worms can result in severe disease affecting the brain, a condition known as cerebrospinal elaphostrongylosis or CSE. The life cycle of this parasite is similar to that of the brain worm of white-tailed deer, Parelaphostrongylus tenuis (see page 22), although the adult worms come to rest in the connective tissue surrounding muscles, especially of the limbs, after undergoing a developmental stage on the surface of the brain (Lankester, 2001).

Two outbreaks of high mortality due to CSE in Newfoundland caribou have been recorded: in central Newfoundland in the mid 1980s and on the Avalon Peninsula beginning in 1996. In the latter outbreak, the affected caribou population was reduced from 7,000 to 2,500 animals over a three year period (Lankester and Fong, 1989). CSE in caribou in Newfoundland is associated with ingestion of large numbers of infective larvae and this, in turn, appears associated with moist conditions and moderate summer temperatures combined with mild winters which extend the period during which the intermediate hosts of the parasite, terrestrial snails and slugs, remain active in the fall and early winter and thus available to be eaten by grazing animals.

E. rangiferi in Newfoundland poses several different conservation and economic risks. Other cervids, as well as domestic goats, are susceptible to infection and to CSE. Moose are abundant and economically valuable in Newfoundland. Thus the parasite represents a potential threat to both caribou and moose populations on the island. Outbreaks of CSE, the severe disease associated with intense infections with E.rangiferi, appear related to climate in ways that may result in more frequent and intense outbreaks if winters become warmer. In North America, E.rangiferi exists only on the island of Newfoundland. Any translocation of infected animals from this island to the continent risks the introduction of a parasite that may readily infect and cause disease in most or all native cervids and some domestic livestock species. One such translocation of Newfoundland caribou already has taken place, fortunately from a herd that, at the time, probably was not infected with E.rangiferi (McCollough and Connery, 1991).

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Montane Cordillera Ecozone+

Adenovirus hemorrhagic disease of deer

Author: Gary Wobeser

Adenovirus hemorrhagic disease (AHD) is a severe virus disease of cervids (deer family) that has been recognized only in North America, and only since 1987. Knowledge of the geographic range and host species range of this virus has increased in the past two decades and AHDwas detected for the first time in Canadian wildlife in 2006.

AHD was first identified during an outbreak that killed thousands of deer in California in 1993 (Woods et al., 1996). Subsequently, examination of archived tissues revealed that adenovirus had caused an earlier outbreak in California in 1987 (Woods, 2001). AHD occurred in wild black-tailed deer in Oregon in 2001 and killed an estimated 400 or more black-tailed deer in one area of Oregon in 2002 (Oregon Department of Fish and Wildlife, 2002). AHD also has been diagnosed in captive deer: black-tailed deer in California, white-tailed deer in Iowa, and moose at the Toronto zoo (Boyce et al., 2000; Sorden et al., 2000; Shilton et al., 2002).

In 2006, AHDwas detected for the first time in wild deer in Canada, in Waterton Lakes National Park in southwestern Alberta (Montane Cordillera Ecozone+) (Canadian Cooperative Wildlife Health Centre, 2008). In July and August, nine mule deer fawns died in the park town site (mule deer and black-tailed deer are the same biological species). The virus of AHD was identified in tissues taken from two of these fawns, as were pathological changes typical of this disease (Woods et al., 1999; Wobeser, 2006).

A factor that complicates understanding the distribution and significance of AHD is its close resemblance to the more common hemorrhagic diseases of North American deer caused by orbiviruses (EHD and BT, see hemorrhage diseases of deer on page 7). Only detailed laboratory analysis can distinguish AHDfrom EHD or BT; their clinical characteristics are identical. The apparent increase in the geographic and host range of AHDsince 1987 may reflect no more than improved mechanisms of detection and identification. Several more decades of careful disease surveillance will be required to document any trends in its occurrence or its significance to host animal populations in Canada.

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Western Interior Basin and Montane Cordillera ecozones+

Wild sheep pneumonia syndrome

Author: Helen Schwantje

The historic decline of Rocky Mountain bighorn sheep in western North America is due, at least in part, to mortality from pneumonia. This disease syndrome has occurred in the Western Interior Basin and Montane Cordillera ecozones+ of British Columbia and Alberta, and in Rocky Mountain and California bighorn sheep ecotypes. The syndrome occurs as epidemics which are characterized by sudden or more gradual mortality at rates ranging from 10 to over 80% of affected populations. Low survival rates of lambs and periodic mortality of adults from pneumonia can persist for decades in sheep populations following these epidemics. Die-offs due to this syndrome have occurred in several herds constituting a metapopulation in southeastern British Columbia (Montane Cordillera Ecozone+) every 20 years from the early 1920s to, most recently, the 1980s. A second metapopulation in the Okanagan region (Western Interior Basin Ecozone+) was affected by an all-age die-off in 1999-2000. Die-offs in Alberta appear to occur sporadically in single herds on the eastern slopes of the Rocky Mountains (eastern Montane Cordillera Ecozone+). Die-offs have not been reported to occur in thinhorn sheep, but pneumonia in individuals has been reported sporadically (Schwantje, H., unpublished data).

Bacteria of the genera Pasteurella and Mannheimia have been the most commonly identified causes of pneumonia in bighorn sheep. However, other pathogens are often present as well, including viruses, other bacteria, and lungworm parasites, and combinations of these pathogens are thought to affect the occurrence and severity of disease outbreaks (Miller, 2001; Garde et al., 2005). Other factors that have been associated with the occurrence of bighorn all-age die-offs in Canada include reduction, fragmentation, and overall poor quality of habitat, inter- and intra-specific competition on winter ranges, human-related stressors such as intense disturbance of critical winter range habitat, inclement weather, and close contact with domestic sheep (Miller, 2001; Garde et al., 2005). Wild sheep are susceptible to a number of strains of Pasteurella and Mannheimia that may be carried by domestic sheep and goats, and disease outbreaks have occurred following close contact between these species (Rudolph et al., 2003; Garde et al., 2005; George et al., 2008).

Decline in bighorn sheep in Canada is a trend of the past several decades. Wild sheep pneumonia syndrome appears to be an outcome of multiple stressors imposed on wild sheep populations by human activities. One of the most important issues for wild sheep survival in Canada is contact with domestic sheep and goats, and the virulent pathogens these domestic species can carry and transmit to wild sheep. Habitat conservation, restoration and management, and exclusion of domestic sheep and goats from wild sheep habitat are considered the best approaches to reducing the impact of wild sheep pneumonia.

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Great Lakes and Mixedwood Plains ecozones+

Botulism type-E

Author : D. Campbell

Botulism is a form of food poisoning associated with ingestion of powerful toxins produced by various strains of the bacterium Clostridium botulinum, designated types A, B, C and so on, according to the type of toxin each produces. The strains of C. botulinum that produce type-E toxin are most common in aquatic and marine environments. The toxin can affect mammals, birds, amphibians, and fish. In 1963 to 1968, epidemic mortality due to type-E botulism occurred in fish-eating birds on Lake Michigan (U.S.). Thousands of loons, gulls, grebes, and mergansers were found dead on the lakeshore. This epidemic was coincident with a major change in the fish community of Lake Michigan in which native species declined and the invasive alewife (Alosa pseudoharangus) became the predominant fish in the lake (Fay, 1966; Fay, 1969). From the 1970s to the 1990s, type-E botulism occurred only sporadically in wild birds in North America. However, in 1998, an outbreak on Lake Huron became the first in a series of annual outbreaks on the Great Lakes that has expanded to include all of lakes Erie and Ontario and has affected at least 22 different species of wild birds (Figure 8) (Rocke and Bollinger, 2007; Leighton, 2007; Campbell, 2008; Canadian Cooperative Wildlife Health Centre, 2008).

Figure 8. Distribution of confirmed type-E botulism mortality in wild birds in the Mixedwood Plains and Great Lakes ecozones+, 1998-2007.

Long Description for Figure 8

This map shows distribution of confirmed type-E boutulism mortality in wild birds in the Mixedwood Plains and Great Lakes ecozones+ from 1998 to 2007. In 1998, an outbreak on Lake Huron became the first in a series of annual outbreaks on the Great Lakes that has expanded to include all of lakes Erie and Ontario and has affected at least 22 different species of wild birds.

Source: Canadian Cooperative Wildlife Health Centre (2007)

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The first outbreak occurred on the southeastern shore of Lake Huron in autumn 1998, when type-Ebotulism killed hundreds of common loons. In 1999 and 2002, outbreaks in this same area killed gulls (Larus spp.) and grebes (Podicepsspp.) as well as loons. Lake Erie was first affected in 1999; dead gulls were found on the southern shore, at Presque Isle Pennsylvania, in the summer, and in autumn, type-Ebotulism killed about 6,000 red-breasted mergansers, loons, and grebes along the north shore of the west basin of Lake Erie. Over the next four years, the epidemic on Lake Erie acquired a regular pattern of small-scale mortality events (tens to hundreds affected in each) in summer of resident gulls, terns, double-crested cormorants, and shorebirds (Scolopacidae), and larger outbreaks (many hundreds to many thousands affected in each) in autumn of southbound migrant fish-eating birds (mainly red-breasted mergansers, common loons, grebes) and diving ducks (mainly long-tailed ducks). Fish-eating birds and diving ducks generally died off-shore and carcasses would be found on the leeward shore (Leighton, 2007; Canadian Cooperative Wildlife Health Centre, 2008).

The location of major outbreaks on Lake Erie shifted from the west basin (1999) to both the central basin and east basin (2000-2004), and then mostly the east basin (2002-2004). In 2000, about 6,000 fish-eating birds washed onto the New York shore at the east end of the lake; in 2001, 3,000 gulls, fish-eating birds and long-tailed ducks died along the New York shore; in 2002, over 3,000 ring-billed gulls died near Buffalo New York, and 12,600 long-tailed ducks and over 3,000 fish-eating birds came ashore on the New York coast; in 2003, 2,000 loons and hundreds of gulls and long-tailed ducks died on both sides of the east basin; in 2004, about 2,800 loons, 2,700 long-tailed ducks, and hundreds of birds of other species were found on the New York shore (Leighton, 2007; Canadian Cooperative Wildlife Health Centre, 2008).

Type-E botulism was first confirmed on Lake Ontario in 2002, when it occurred in gulls and affected about 675 long-tailed ducks along the New York shore. About 1,500 deaths attributed to botulism occurred in gulls, diving ducks, cormorants, and loons on the New York side of Lake Ontario in 2003, and botulism also occurred in great black-backed gulls at the east end of the lake on the Canadian side. In 2004, over 1,750 carcasses were counted on breeding colonies and beaches at the east and west ends of Lake Ontario in late summer and fall, mainly of double-crested cormorants, great black-backed gulls, long-tailed ducks, and white-winged scoters. On the New York shore, about 1,700 birds died, including long-tailed ducks, ring-billed gulls, cormorants, and common loons. Since 2004, botulism has occurred annually on Lake Ontario, following this same general pattern of incidents involving gulls, terns, and cormorants during the summer months, and diving ducks, loons, and grebes in the autumn (Leighton, 2007; Canadian Cooperative Wildlife Health Centre, 2008).

The source of the toxin in these epidemics and the ecology of type-E botulism in the Great Lakes has yet to be fully determined. Identification of the stomach contents of birds dying during botulism events indicates that a substantial proportion of affected fish-eating birds had fed recently on round gobies (Neogobius melanostomas). This fish is an invasive species, having arrived within the last 15 years from the Black Sea area, likely in the ballast water of ocean-going ships. This goby is a predator of the zebra and quagga mussels (Dreissena polymorpha and Dreissena rostriformis bugensis), which also are newly-introduced non-native species originating from the Black Sea area (zebra mussel) and Dnieper River in the Ukraine (quagga mussel). These mussels themselves have been found in the stomachs of many of the diving ducks found dead during botulism episodes. Thus, there appears to be a link between these invasive mussels and gobies, and type-E botulism in the Great Lakes Ecozone+. It is possible that the mussels are dying in large numbers due to an unknown cause. Their tissue, in an anoxic environment within their closed shells, could provide the substrate for growth of C. botulinumand toxin production. Consumption of these dead mussels by either ducks or fish would move toxin, respectively, directly to mussel-eating ducks or, via gobies, upwards in the food chain to fish-eating birds (Rocke and Bollinger, 2007; Leighton, 2007).

Therefore, based on current evidence, this epidemic of type-E botulism in birds on the Great Lakes appears linked to the changed ecology of the lakes associated with at least three introduced species. While the scale of mortality in birds is locally impressive and alarming, it may not be high enough at present to have a significant impact on continental or global populations of the species suffering the highest mortality (for example, common loon, population of 500,000 to 700,000; red-breasted merganser, 249,000 in Canada and Alaska; double-crested cormorant, over 226,000 breeding pairs (Canadian Wildlife Service, 1996; Rose and Scott, 1997; Wires and Cuthbert, 2006). The epidemic has shown a rapid eastward expansion but also a slower expansion northward along the Bruce Peninsula and into Georgian Bay (Figure 8). A better understanding of the ecology of type-Ebotulism on the Great Lakes is required before any possibly useful predictions of its future extent or behaviour can be made.

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Viral hemorrhagic septicemia virus type-IV ‘b’

Author: J. Lumsden

Viral hemorrhagic septicemia (VHS) viruses infect freshwater and marine fish. Infection may result in severe and fatal disease or have little effect on the fish, depending on the virus strain and the species of fish involved. However, VHS viruses are important pathogens in aquaculture and are therefore listed by the World Organization for Animal Health as pathogens against which trade restrictions can be declared by importing nations. VHS viruses have been classified into four different genotypes (I, II, III, and IV), of which only genotype-IV currently occurs on the Atlantic and Pacific coasts of North America (Gagne et al., 2007). A new strain of VHSV type-IV,referred to as type-IV ‘b’, was discovered in the Great Lakes Ecozone+ in Lake Ontario in 2005 associated with a large mortality event in freshwater drum (Aplodinotus grunniens) (Lumsden et al., 2007) and was subsequently identified in Lakes Erie, St. Clair, Huron, and Michigan, and in inland fresh water bodies in New York, Michigan, Wisconsin, and in the Thames River in Ontario. From archived samples of muskellunge from Lake St. Clair, this virus is now known to have been present in the ecozone+ at least since 2003 (Elsayed et al., 2006). The western Atlantic strains of type-IV are most closely related to the newly recognized Great Lakes strain (Gagne et al., 2007) but the origin of this type-IV ‘b’ strain is not known. All of the strains of type-IV ‘b’isolated from the Great Lakes have been virtually identical (Garver, K., 08, pers. comm.), which suggests either a recent evolution or recent arrival of this virus strain.

The most important pathogenic feature of this type-IV ‘b’ strain is its very broad host range; dozens of different fish species now are known to be susceptible to infection. To date, freshwater drum, yellow perch, muskellunge, gizzard shad, and the introduced round goby seem to have experienced the most significant mortalities. Assessment of the true impact of the virus will require the sustained efforts of fisheries agencies on both sides of the border, as population surveys are performed and year-class recruitment numbers are documented, particularly for high profile or commercially important species like muskellunge and yellow perch. Economically, the virus already has had a substantial effect (Garver, K., 08, pers. comm.) on the day-to-day operations of baitfish harvesters, aquaculture and fish enhancement activities, on anglers, and on fish health personnel around the Great Lakes, all due to the restrictions imposed in Canada and the United States on trade in Great Lakes fish when this virus was discovered.

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