Beyond the landscape, other species in the community can influence CWD transmission. Empirical evidence supports the role of predators in the removal of sick and infectious prey across diverse disease systems (Packer et al., 2003). For example, grey wolf (Canis lupus) presence reduced seroprevalence of bovine-virus-diarrhea in elk (Barber-Meyer & White, 2005), and mountain lions (Puma concolor) selectively predate on CWD-infected mule deer (Krumm et al., 2010). Other native large predators, such as grey wolves and bears (Ursus spp.), may similarly influence the prevalence and geographic distribution of CWD in wild reservoirs, as demonstrated through modelling applications (Hobbs, 2006; Wild et al., 2011). Additionally, numbers and geographic range of predators, including wolves and black bears (Ursus americanus), can be successfully managed and controlled via wildlife management methods (Meagher & Phillips, 1980; Clark, Huber & Servheen, 2002; Soorae, 2013).
Research assessing the role of predators in CWD transmission requires a multidisciplinary approach integrating expertise in human dimension, epidemiology, and ecology. Alternatively, carnivores and scavengers could potentially facilitate CWD spread to distant areas by translocating infectious prions from prey. This has been suggested for scats of coyotes (Canis latrans), raccoons (Procyon lotor) (Hamir et al., 2007; Moore et al., 2019), and crows (Corvus spp.) (Fischer et al., 2013), but has not been tested empirically. Scats may also be of potential utility in CWD surveillance and early detection, as predators can selectively predate CWD-infected cervids (Nichols et al., 2015). Whether predators can significantly improve the control and surveillance of CWD is unknown but deserves deeper exploration. Predator or scavenger scats have not been used in CWD surveillance to date.
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Update on chronic wasting disease (CWD) III
EFSA Panel on Biological Hazards (BIOHAZ)
Kostas Koutsoumanis Ana Allende Avelino Alvarez‐Ordoňez Declan Bolton Sara Bover‐Cid Marianne Chemaly Robert Davies Alessandra De Cesare Lieve Herman Friederike Hilbert Roland Lindqvist Maarten Nauta Luisa Peixe Giuseppe Ru Panagiotis Skandamis Elisabetta Suffredini Olivier Andreoletti Sylvie L Benestad Emmanuel Comoy Romolo Nonno Teresa da Silva Felicio Angel Ortiz‐Pelaez Marion M Simmons … See fewer authors First published:11 November 2019 https://doi.org/10.2903/j.efsa.2019.5863
Correspondence: biohaz@efsa.europa.eu
Requestor: European Commission
Question number: EFSA‐Q‐2018‐00763
Panel members: Kostas Koutsoumanis, Ana Allende, Avelino Alvarez‐Ordoñez, Declan Bolton, Sara Bover‐Cid, Marianne Chemaly, Robert Davies, Alessandra De Cesare, Lieve Herman, Friederike Hilbert, Roland Lindqvist, Maarten Nauta, Luisa Peixe, Giuseppe Ru, Marion M. Simmons, Panagiotis Skandamis and Elisabetta Suffredini.
Acknowledgements: The EFSA Panel on Biological Hazards (BIOHAZ) wishes to acknowledge all European and North American researchers who provided data and information for this scientific output, and Maria Francesca Iulietto for her contributions to the draft.
Adopted: 26 September 2019
This article was originally published on the EFSA website www.efsa.europa.eu on 7 November 2019
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Using data from the NA CWD experience, 13 groups of risk factors have been identified based on their biological plausibility to spread CWD. Some of these are supported by epidemiological evidence from NA CWD studies with variable strength of evidence after applying the score‐based ranking, while others remain hypothetical:
Natural movement of live wild deer from infected areas,
Man‐mediated movement of live farmed/free‐ranging deer from infected areas,
Failure to separate live farmed and free‐ranging deer,
High deer density,
Species‐specific social organisation,
Sex‐related behaviours,
Natural or man‐mediated animal aggregation,
Consumption of forage grown on contaminated soil,
Fallen stock or inappropriate disposal of carcasses and slaughter by‐products,
***> Movement of other animals (working dogs, scavengers, predators),
Transfer of inanimate vehicles of contamination (fomites),
Environmental persistence of prions,
Host genetics.
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Whether the natural host range of CWD in North America extends beyond the family Cervidae is currently unclear and no natural infections have been reported so far in wildlife species with substantial overlapping geographical range and which could play a role in the spread of CWD, such as predators and scavengers.
3.2.1.2 Non‐cervid domestic species
The remarkably high rate of natural CWD transmission in the ongoing NA epidemics raises the question of the risk to livestock grazing on CWD‐contaminated shared rangeland and subsequently developing a novel CWD‐related prion disease. This issue has been investigated by transmitting CWD via experimental challenge to cattle, sheep and pigs and to tg mouse lines expressing the relevant species PrP.
For cattle challenged with CWD, PrPSc was detected in approximately 40% of intracerebrally inoculated animals (Hamir et al., 2005, 2006a, 2007). Tg mice expressing bovine PrP have also been challenged with CWD and while published studies have negative outcomes (Tamguney et al., 2009b), unpublished data provided for the purposes of this Opinion indicate that some transmission of individual isolates to bovinised mice is possible (Table 1).
In small ruminant recipients, a low rate of transmission was reported between 35 and 72 months post‐infection (mpi) in ARQ/ARQ and ARQ/VRQ sheep intracerebrally challenged with mule deer CWD (Hamir et al., 2006b), while two out of two ARQ/ARQ sheep intracerebrally inoculated with elk CWD developed clinical disease after 28 mpi (Madsen‐Bouterse et al., 2016). However, tg mice expressing ARQ sheep PrP were resistant (Tamguney et al., 2006) and tg mice expressing the VRQ PrP allele were poorly susceptible to clinical disease (Beringue et al., 2012; Madsen‐Bouterse et al., 2016). In contrast, tg mice expressing VRQ sheep PrP challenged with CWD have resulted in highly efficient, life‐long asymptomatic replication of these prions in the spleen tissue (Beringue et al., 2012).
A recent study investigated the potential for swine to serve as hosts of the CWD agent(s) by intracerebral or oral challenge of crossbred piglets (Moore et al., 2016b, 2017). Pigs sacrificed at 6 mpi, approximately the age at which pigs reach market weight, were clinically healthy and negative by diagnostic tests, although low‐level CWD agent replication could be detected in the CNS by bioassay in tg cervinised mice. Among pigs that were incubated for up to 73 mpi, some gave diagnostic evidence of CWD replication in the brain between 42 and 72 mpi. Importantly, this was observed also in one orally challenged pig at 64 mpi and the presence of low‐level CWD replication was confirmed by mouse bioassay. The authors of this study argued that pigs can support low‐level amplification of CWD prions, although the species barrier to CWD infection is relatively high and that the detection of infectivity in orally inoculated pigs with a mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity.
3.2.1.3 Other species
Studies have demonstrated that the CWD agent(s) can be transmitted by the IC route in several species of rodents, such as voles (Subfamily Arvicolinae), deer mice (Peromyscus maniculatus), mice and hamsters (Subfamily Cricetinae). The susceptibility was, however, variable, being high in voles and deer mice but lower in mice and hamsters (Raymond et al., 2007; Heisey et al., 2010; Kurt et al., 2011; Di et al., 2013; Lee et al., 2013). Mink (subfamily Mustelinae) (Harrington et al., 2008), ferrets (Mustela putorius) (Bartz et al., 1998; Sigurdson et al., 2008) and cats (Mathiason et al., 2013) were susceptible to IC challenge with NA CWD sources, while CWD transmitted poorly to raccoons (Procyon lotor) by the IC route (Moore et al., 2019).
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10. Movement of other animals (working dogs, scavengers, predators)
I & II Working dogs are moved for hunting or sledging competitions
Defra (2016a,b) review F Y Faeces of dogs accompanying hunters returning from infected areas/countries can serve as a vehicle for prions contributing to the spread of the infectious agent in the environment (Defra, 2016a,b)
Scavengers Various species of (raptors, corvids) birds or mammals that feed on animal carcasses can act as spreaders of the infection. It has been shown that carcasses abandoned in the field in an area of Wisconsin were a source of food for at least 14 species of mammals and 14 species of birds. Carcasses could persist in the field from 18 to 101 days depending on the season and year. The involvement of the birds also suggests that the infectious agent could be transferred at great distances from the infected carcass (Jennelle et al., 2009) Jennelle et al. (2009) other F N
Predators. Prion‐infected deer were much more likely to be killed by mountain lions than uninfected deer (Miller et al., 2008). The presence of prions and their infectious ability in cervinised transgenic mice have been demonstrated in the faeces of coyotes (Canis latrans) 3 days after they had fed on with infected deer carcasses (Nichols et al., 2015). Faeces of predators (in North America e.g. coyotes or pumas) can serve as a vehicle for prions contributing to the spread of the infectious agent in the environment. Miller et al. (2008) cohort B N Nichols et al. (2015) other
11. Transfer of inanimate vehicles of contamination (fomites)
I & II Hunting clothing, boots or knives poorly cleaned and used in infected and areas, could help disseminate contaminated material (e.g. clods of soil attached to their boots) (Defra, 2016a,b) Defra (2016a,b) review F Y
During their activity, hunters have more opportunities than any other segment of the population for direct exposure to infected material (secretions, excreta, infected tissues) (Saunders et al., 2012). Saunders et al. (2012) review F
Wood, rocks, plastic, glass, cement, stainless steel and aluminium can all bind, retain and release prions and therefore act efficiently as fomites and transmit disease. Not every strain had the same affinities. Effective transmission only required contact with the contaminated surfaces – nothing more invasive. Good binding to wood and rock have implications for environmental contamination in natural/wildlife settings (Pritzkow et al., 2018) Pritzkow et al. (2018)
12. Environmental persistence of prions I & II Prions, due to their resistance to degradation, can persist for years by binding to soil particles without losing their infectious potential. For instance, it has been shown that BSE infectivity survives burial for 5 years with only limited spread (Williams and Young, 1992; Miller and Williams, 2003; Miller et al., 2004; Johnson et al., 2007; Saunders et al., 2012; Somerville et al., 2019) Williams and Young (1992) review F N
Miller and Williams (2003) cohort B
Miller et al. (2004) int A
Johnson et al. (2007) other F
Saunders et al. (2012) review F
Somerville et al. (2019) other F
Such a persistence allows an infected animal to cause secondary infections long after its death (Almberg et al., 2011). Almberg et al. (2011) simul E
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4.3 Answer to ToR3
To identify risk factors that can facilitate the spread of CWD in the European Union given the current situation of the disease.
Using data from the NA CWD experience, 13 groups of risk factors have been identified based on their biological plausibility to spread CWD. Some of these are supported by epidemiological evidence from NA CWD studies with variable strength of evidence, while others remain hypothetical:
1. Natural movement of live wild deer from infected areas.
2. Man‐mediated movement of live farmed/free‐ranging deer from infected areas.
3. Failure to separate live farmed and free‐ranging deer.
4. High deer density.
5. Species‐specific social organisation.
6. Sex‐related behaviours.
7. Natural or man‐mediated animal aggregation.
8. Consumption of forage grown on contaminated soil.
9. Fallen stock or inappropriate disposal of carcasses and slaughter by‐products.
10. Movement of other animals (working dogs, scavengers, predators).
11. Transfer of inanimate vehicles of contamination (fomites).
12. Environmental persistence of prions.
13. Host genetics.
All the identified risk factors may contribute to the spread of the disease when it is associated with the accumulation of infectivity in peripheral tissues, a host phenotype that is compatible with a contagious disease.
A subset of risk factors (1,2,6,8,9,10,11,12 and 13) are relevant to cases of disease that do not involve peripheral accumulation of infectivity and are therefore less contagious or non‐contagious and may contribute to the spread of the disease mainly via environmental contamination following death. Some risk factors are man‐mediated and are considered preventable. Their management could contribute to a decrease in the theoretical risk of spread of CWD.
The potential co‐localisation of cervid species and disease phenotypes mean that all the identified groups of risk factors should be taken into account when considering interventions.
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