Efficacy of Avian Botulism Surveillance and Mitigation Using Detection Canines Active
Avian botulism causes waterbird mortality in Hawai‘i's wetlands and elsewhere. We will evaluate using trained scent-detection canines (sniffer dogs) as a new tool to survey for the presence of avian botulism. Biologists will compare variables influencing detection probability and detection rates with traditional search methods. The pilot study will test the feasibility of this approach as a new tool for early detection and rapid response to wetland disease outbreaks.
National Wildlife Refuges and State Wildlife Sanctuaries in the subtropical Hawaiian Islands have experienced severe die-off events from avian botulism with increasing frequency. In the wetlands of Hanalei National Wildlife Refuge (Kaua‘i, Hawai‘i) and elsewhere, avian botulism is fatal and is caused by food poisoning from the bacteria Clostridium botulinum (strain C). The impact of avian botulism may increase globally as the bacteria Clostridium botulinum (strain C) favors warmer water temperatures. Hawaii’s non-migratory endemic waterbirds are especially vulnerable to avian botulism (type C) with epizootics causing mortality of thousands of endangered waterbirds in recent years. Migratory waterfowl and shorebirds are also affected. The endangered koloa maoli (Hawaiian duck; Anas wyvilliana) and critically-endangered Laysan duck (Laysan teal; A. laysanensis) have particularly high exposure because of their feeding behavior, limited wetland habitat, and small geographic ranges. Hawai‘i's endemic waterfowl are at high risk of extinction with small populations and thus are further jeopardized by high mortality due to avian botulism.
The paralytic food poisoning is caused by ingestion of prey containing neuro-toxin produced by the bacteria Clostridium botulinum. Undetected carcasses in avian habitats promote toxin production and mobilization of the toxin into avian food chains precipitating these mortality events. Avian botulism can spread from bird to bird quickly by way of the “carcass-maggot cycle”, if carcasses remain in areas used by waterbirds. Fly larvae (maggots) develop and bio-concentrate the toxin from waterbird carcasses. Invasive fish and wetland invertebrates also accumulate and concentrate the toxin, thereby expanding sources of the toxin within the wetland food chain. Waterfowl die from avian botulism after directly consuming toxin-laden maggots or from dabbling for invertebrates in infected wetlands. Each new undetected waterbird carcass develops more toxin-concentrating maggots, and the cycle accelerates with each additional carcass spreading across wetland food-webs, causing more and more mortality and morbidity.
For years wildlife managers have worked to remove carcasses from wetland habitats but some carcasses go undetected. Carcass detection before maggot development requires rapid response, high carcass discovery success, and is difficult in dense tropical vegetation. When the carcass-maggot cycle accelerates, management of botulism outbreaks exceeds refuge resources. Staff and volunteers at NWRs and other State wildlife sanctuaries are unable to keep up with intensive surveillance, carcass and maggot removal, emergency wetland management, and sick bird recovery and care.
Dogs have very sensitive and specific olfactory capacities and trained canines are used effectively for olfactory detection tasks including law enforcement and agricultural applications. In partnership with the USFWS, this pilot study will allow the USGS to evaluate if using skilled handler(s) and trained scent-detection dogs is feasible at Hanalei National Wildlife Refuge and if this approach is more effective than human only searches for early detection of waterbird carcasses for removal and early management of wetlands identified with avian botulism. Early detection of carcasses could help contain the spread of the waterbird toxin by allowing for rapid removal of dead birds and help pin point areas for water management.
Avian botulism causes waterbird mortality in Hawai‘i's wetlands and elsewhere. We will evaluate using trained scent-detection canines (sniffer dogs) as a new tool to survey for the presence of avian botulism. Biologists will compare variables influencing detection probability and detection rates with traditional search methods. The pilot study will test the feasibility of this approach as a new tool for early detection and rapid response to wetland disease outbreaks.
National Wildlife Refuges and State Wildlife Sanctuaries in the subtropical Hawaiian Islands have experienced severe die-off events from avian botulism with increasing frequency. In the wetlands of Hanalei National Wildlife Refuge (Kaua‘i, Hawai‘i) and elsewhere, avian botulism is fatal and is caused by food poisoning from the bacteria Clostridium botulinum (strain C). The impact of avian botulism may increase globally as the bacteria Clostridium botulinum (strain C) favors warmer water temperatures. Hawaii’s non-migratory endemic waterbirds are especially vulnerable to avian botulism (type C) with epizootics causing mortality of thousands of endangered waterbirds in recent years. Migratory waterfowl and shorebirds are also affected. The endangered koloa maoli (Hawaiian duck; Anas wyvilliana) and critically-endangered Laysan duck (Laysan teal; A. laysanensis) have particularly high exposure because of their feeding behavior, limited wetland habitat, and small geographic ranges. Hawai‘i's endemic waterfowl are at high risk of extinction with small populations and thus are further jeopardized by high mortality due to avian botulism.
The paralytic food poisoning is caused by ingestion of prey containing neuro-toxin produced by the bacteria Clostridium botulinum. Undetected carcasses in avian habitats promote toxin production and mobilization of the toxin into avian food chains precipitating these mortality events. Avian botulism can spread from bird to bird quickly by way of the “carcass-maggot cycle”, if carcasses remain in areas used by waterbirds. Fly larvae (maggots) develop and bio-concentrate the toxin from waterbird carcasses. Invasive fish and wetland invertebrates also accumulate and concentrate the toxin, thereby expanding sources of the toxin within the wetland food chain. Waterfowl die from avian botulism after directly consuming toxin-laden maggots or from dabbling for invertebrates in infected wetlands. Each new undetected waterbird carcass develops more toxin-concentrating maggots, and the cycle accelerates with each additional carcass spreading across wetland food-webs, causing more and more mortality and morbidity.
For years wildlife managers have worked to remove carcasses from wetland habitats but some carcasses go undetected. Carcass detection before maggot development requires rapid response, high carcass discovery success, and is difficult in dense tropical vegetation. When the carcass-maggot cycle accelerates, management of botulism outbreaks exceeds refuge resources. Staff and volunteers at NWRs and other State wildlife sanctuaries are unable to keep up with intensive surveillance, carcass and maggot removal, emergency wetland management, and sick bird recovery and care.
Dogs have very sensitive and specific olfactory capacities and trained canines are used effectively for olfactory detection tasks including law enforcement and agricultural applications. In partnership with the USFWS, this pilot study will allow the USGS to evaluate if using skilled handler(s) and trained scent-detection dogs is feasible at Hanalei National Wildlife Refuge and if this approach is more effective than human only searches for early detection of waterbird carcasses for removal and early management of wetlands identified with avian botulism. Early detection of carcasses could help contain the spread of the waterbird toxin by allowing for rapid removal of dead birds and help pin point areas for water management.