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American Bison - Buffalo Field Campaign

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one) followed by its widespread dispersal and ecological<br />

establishment. Wild bison were abundant and widely distributed<br />

at the time of European colonisation. Once infected with anthrax<br />

they may have played an important early role in the ecological<br />

establishment and widespread dispersal of A.Br.WNA. The broad<br />

diversity of anthrax lineages represented in the industrialised<br />

south-eastern region of the continent (Van Ert et al. 2007) is<br />

suggestive of the accumulation of additional sub-group types<br />

over time. A likely mechanism is importation of contaminated<br />

animal products into mills and tanneries on the eastern seaboard<br />

and New England which process imported hair, wool, and hides.<br />

The World Health Organisation (WHO 2008) commented on<br />

the role of tanneries as a point source of anthrax outbreaks.<br />

Contaminated products come from animals that died of anthrax.<br />

Wastewater effluent from plants can contaminate downstream<br />

sediments and pastures with anthrax spores, providing a<br />

source of local outbreaks in livestock and further proliferation<br />

of novel introduced variants of the pathogen. Marketing of<br />

inadequately sterilised bone meals and fertilisers, rendered from<br />

contaminated materials, can result in long distance redistribution<br />

and introducing “industrial” strains to livestock remote from the<br />

original source (Hugh-Jones and Hussaini 1975).<br />

Under certain environmental conditions, concentrations of<br />

endospores have caused periodic outbreaks among wood bison<br />

in the Slave River Lowlands (SRL), Mackenzie <strong>Bison</strong> Sanctuary<br />

(MBS), and Wood <strong>Buffalo</strong> National Park (WBNP) (Dragon and<br />

Elkin 2001; Gates et al. 2001b; Pybus 2000). Between 1962 and<br />

1971, anthrax and the associated depopulation and vaccination<br />

programmes employed to control the disease, accounted for<br />

over 2,800 wood bison deaths (Dragon and Elkin 2001). Further<br />

outbreaks occurred in the MBS in 1993, in the SRL in 1978, 2000<br />

and 2006, and in WBNP in 1978, 1991, 2000, and 2001 (Gates<br />

et al. 1995; Nishi et al. 2002c). Four factors that are associated<br />

rather consistently with these epizootics are high ambient<br />

temperatures, intense mating activity, high densities of insects,<br />

and high densities of bison as they congregate and compete for<br />

diminishing water and food supplies (APHIS, USDA 2006). Based<br />

on these four factors, two hypotheses have been proposed to<br />

explain outbreaks of anthrax in bison in northern Canada: (1)<br />

“the modified host resistance hypothesis” (Gainer and Saunders<br />

1989) and (2) “the wallow concentrator hypothesis” (Dragon et<br />

al., 1999). These two hypotheses are not mutually exclusive.<br />

A recent outbreak was reported in a commercial herd in<br />

south-western Montana that killed over 300 bison pasturing<br />

on a large foothills landscape beneath the Gallatin Mountain<br />

Range (Ronnow 2008). Despite mass deaths of bison during<br />

anthrax outbreaks, the sporadic nature of outbreaks and<br />

predominance of male deaths suggest that the disease plays a<br />

minor role in long-term population dynamics unless operating<br />

in conjunction with other limiting factors (Joly and Messier<br />

2001b; Shaw and Meagher 2000). Anthrax is not treatable in<br />

free-ranging wildlife, but captive bison can be vaccinated or<br />

treated with antibiotics (Gates et al. 1995; Gates et al. 2001b).<br />

Carcass scavenging facilitates environmental contamination<br />

with anthrax spores (Dragon et al. 2005); therefore timely<br />

carcass treatment and disposal during an active outbreak in<br />

free-ranging bison is considered an important preventative<br />

strategy for reducing the potential for future outbreaks (Hugh-<br />

Jones and de Vos 2002; Nishi et al. 2002a). Anthrax is a public<br />

health concern and humans are susceptible, however, exposure<br />

from naturally occurring outbreaks requires close contact with<br />

animal carcasses or hides. In addition, humans have rarely been<br />

exposed to anthrax through the purchase of curios purchased by<br />

tourists (Whitford 1979).<br />

5.1.3 Bluetongue<br />

Bluetongue (BLU) is an insect-borne viral hemorrhagic disease<br />

affecting many ungulates in the lower latitudes of North America.<br />

The BLU virus is a member of the genus Oribivirus of the family<br />

Reoviridae. Worldwide there are 24 known BLU serotypes,<br />

but only six are active in domestic and wild ruminants from<br />

North America (Pearson et al. 1992). Bluetongue viruses are<br />

closely related to the viruses in the epizootic hemorrhagic<br />

disease and BLU is known to infect a wide variety of wild and<br />

domestic ruminants (Howerth et al. 2001). <strong>Bison</strong> are susceptible<br />

to BLU, and the virus has been isolated under field, captive,<br />

and experimental conditions (Dulac et al. 1988). The arthropod<br />

vectors of the bluetongue virus are various species of Culicoides<br />

midges (Gibbs and Greiner 1989; Howerth et al. 2001). Clinical<br />

symptoms include fever, stomatitis, oral ulcerations, lameness,<br />

and occasionally, reproductive failure (Howerth et al. 2001).<br />

There are subacute, acute, and even chronic expressions of the<br />

disease in many wild ungulates and domestic livestock. BLU<br />

typically occurs in the late summer and early fall depending<br />

upon the seasonal patterns of vector activity (Howerth et al.<br />

2001). Factors influencing the frequency and intensity of disease<br />

outbreaks are innate herd immunity, virulence factors associated<br />

with viruses, and vector competency and activity. BLU occurs in<br />

livestock over much of the U.S. and its distribution parallels that<br />

of domestic livestock. Its distribution is more limited in Canada<br />

where it once was a regulated disease until rules were relaxed<br />

in July 2006 (CFIA website). There is considerable difference in<br />

the epidemiology of the disease between northern and southern<br />

portions of North America depending on the consistency of<br />

vector activity. In the southern areas, vector activity is more<br />

common and animal populations exhibit a higher prevalence<br />

of seroreactivity and antibody protection. BLU has not been<br />

widely reported in bison herds in North America. Serologic<br />

surveys of several Department of Interior bison herds in the<br />

U.S. have not found seroreactors for bluetongue virus (T. Roffe<br />

personal communication; Taylor et al. 1997). The U.S. Fish and<br />

Wildlife Service (USFWS) has opportunistically examined bison<br />

<strong>American</strong> <strong>Bison</strong>: Status Survey and Conservation Guidelines 2010 29

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