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عنوان فارسی مقاله:
تأثیر عمده تفکیک جزیی نیچ علوفه بر بروز بوتولیسم مرغی در پرستوها
عنوان انگلیسی مقاله:
Minor differentiation of foraging niche may have a major impact on the incidence of avian botulism in shorebirds
سال انتشار : 2016
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مقدمه انگلیسی مقاله:
1. Introduction
Avian botulism is a paralytic and often fatal disease of birds caused by ingestion of neurotoxinsthat are produced by Clostridium botulinum type C (Rocke and Bollinger 2007). Sporadic avianmortality has also been caused by typeEtoxin, although it has been reported almost exclusively for fisheating waterfowl (Brand, Schmitt, Duncan, & Cooley 1988; Hannett, Stone, Davis, & Wroblewski 2011). Under aerobic and other adverse conditions, C. botulinum forms dormant spores, which are harmless until they germinate into vegetative cells and begin multiplying. After germination, bacterial cells may start to produce neurotoxins which are encoded by specific bacteriophages that infect and replicate specifically within Clostridium bacteria (Eklund, Poysky, Reed, & Smith 1971). Optimal environmental conditions that promote germination of botulinum spores are relatively poorly recognized, but botulism outbreaks usually develop in shallow waters that are rich in decaying organic matter (Rocke and Samuel 1999). In order for a botulism outbreak to occur the toxin must become available for birds. In the early stages of epizootics the toxin is presumably transferred from the substrate to the birds through zooplankton and benthic epifauna. Invertebrates that feed on decaying matter remain unaffected by the toxin and may act as toxin reservoirs (Duncan and Jensen 1976; Rocke and Bollinger 2007). An alternative route to a massive botulism outbreak is through toxicoinfection, resulting from ingestion of C. botulinum spores, followed by multiplication of bacteria within the gastrointestinal tract, with subsequent toxigenesis and absorption of toxins (Critchley 1991; Trampel, Smith, & Rocke 2005). Thus, the incidence and numbers of C. botulinum spores and vegetative cells, as well as the concentration of botulinum neurotoxin in the environment could contribute significantly to the onset of a large outbreak. As soon as the first botulism-related casualties occur, an outbreak often becomes self-perpetuating, as foraging waterbirds tend to accidentally ingest toxic fly larvae that feed on the carcasses of infected birds. This, so called, carcass-maggot cycle rapidly acceleratesthe spread of the disease, causing massive avian botulism outbreaks (Espelund and Klaveness 2014). In fact, outbreaks with losses of up to 50,000 birds are relatively common and botulism epizootics with more than a million deaths have been reported (Rocke and Bollinger 2007). In consequence, avian botulism has been recognized as the most common cause of death in waterbirds worldwide. Most shorebirds (Charadrii) typically use shallow water and mudflat habitats to replenish fuel reserves during migration and, thus, are potentially highly exposed to avian botulism. However, this group of birds shows extraordinary divergence of micro-habitat use and foraging niche, mostly attributable to high inter-specific variation in bill morphology (Nebel, Jackson, & Elner 2005). One of the primary determinants of foraging behavior in shorebirds is bill length, as species/individuals with shorter bills are expected to peck epifaunal prey or probe near the sediment surface, while species/individuals with longer bills probe deeper into the sediments and feed mainly on infaunal invertebrates. We hypothesized that such differentiation of foraging niche may have an impact on the incidence of avian botulism, as botulinum toxins are available mostly at the sediment surface, especially during the carcass-maggot stage of botulism epizootics. To test this hypothesis we used capture-recapture methodsto estimate survivalrate oftwo shorebird species differing in bill morphology, wood sandpiper Tringa glareola and common snipe Gallinago gallinago, during a major avian type C botulism outbreak. Wood sandpiper has a relatively short bill (interquartile range: 27.0–28.8 mm, Fig. 1) and itfrequently catches free-living and mobile prey from the sediment surface (Krupa et al. 2009). Although common snipe is only slightly larger, its bill is overtwo timeslonger(interquartile range: 66.5–70.7 mm, Fig. 1) and adapted specifically for deep probing. As a result, we expected wood sandpipers to be more exposed to botulinum neurotoxins and, thus, to show elevated rate of botulism-related mortality.
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کلمات کلیدی:
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