A Pelagic Outbreak of Avian Cholera in North American Gulls: Scavenging as a Primary Mechanism for Transmission?

Wille, Michelle; McBurney, Scott; Robertson, Gregory J.; Wilhelm, Sabina I.; Blehert, David S.; Soos, Catherine; Dunphy, Ron; Whitney, Hugh

doi:10.7589/2015-12-342

Cited by 20 publications

(23 citation statements)

References 28 publications

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“…This is consistent with results in geese, suggesting that adult birds can survived exposure to Pm (Samuel et al 2005a, b), although it had not been quantified. It, however, contrasts with the other waterfowl and seabird populations in which avian cholera induced high adult mortalities (Leotta et al 2006;Descamps et al 2012;Österblom et al 2004;Wille et al 2016). This heterogeneity is not surprising given what is generally known of the variability of Pm virulence depending on the strain and the host (Christensen and Bisgaard 2000).…”

Section: Immune Response After Natural Exposurementioning

confidence: 79%

“…Bacterial agents known for their pathogenicity in domesticated animals are commonly encountered in the wild, but variations in susceptibility among host populations and compartments of host populations are largely underestimated, especially when several strains circulate (Benskin et al 2009). For instance, avian cholera, caused by Pasteurella multocida (Pm), has been repeatedly implicated in mass mortality events of adult waterfowl and seabirds in the northern hemisphere (e.g., Descamps et al 2012;Österblom et al 2004;Wille et al 2016), while it seems to principally affect nestlings in the seabird community of Amsterdam Island (37°49ʹS, 77°33ʹE, southern Indian Ocean) where recurrent epizooties have been recorded since the mid-1980s (Weimerskirch 2004;Bourret et al 2018;Jaeger et al 2018). In addition, some evidence suggest that exposure of waterfowl to Pm results in a short-lived immune response (Samuel et al 2003(Samuel et al , 2005a, contradicting the suggested, but not fully explored, herd immunity effect leading to avian cholera epizootics fadeout in a population of common eiders (Somateria mollissima; Iverson et al 2016).…”

Section: Electronic Supplementary Materialsmentioning

confidence: 99%

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Exposure of breeding albatrosses to the agent of avian cholera: dynamics of antibody levels and ecological implications

et al. 2019

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Despite critical implications for disease dynamics and surveillance in wild long-lived species, the immune response after exposure to potentially highly pathogenic bacterial disease agents is still poorly known. Among infectious diseases threatening wild populations, avian cholera, caused by the bacterium Pasteurella multocida, is a major concern. It frequently causes massive mortality events in wild populations, notably affecting nestlings of Indian yellow-nosed albatrosses (Thalassarche carteri) in the Indian Ocean. If adults are able to mount a long-term immune response, this could have important consequences regarding the dynamics of the pathogen in the local host community and the potential interest of vaccinating breeding females to transfer immunity to their offspring. By tracking the dynamics of antibodies against P. multocida during 4 years and implementing a vaccination experiment in a population of yellow-nosed albatrosses, we show that a significant proportion of adults were naturally exposed despite high annual survival for both vaccinated and non-vaccinated individuals. Adult-specific antibody levels were thus maintained long enough to inform about recent exposure. However, only low levels of maternal antibodies could be detected in nestlings the year following a vaccination of their mothers. A modification of the vaccine formulation and the possibility to re-vaccinate females 2 years after the first vaccination revealed that vaccines have the potential to elicit a stronger and more persistent response. Such results highlight the value of long-term observational and experimental studies of host exposure to infectious agents in the wild, where ecological and evolutionary processes are likely critical for driving disease dynamics.

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Section: Immune Response After Natural Exposurementioning

confidence: 79%

Section: Electronic Supplementary Materialsmentioning

confidence: 99%

Exposure of breeding albatrosses to the agent of avian cholera: dynamics of antibody levels and ecological implications

et al. 2019

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“…Understanding mechanisms by which pathogens transmit between hosts is key for defining disease risk and for planning effective control strategies. In addition to direct host‐to‐host or vector‐borne transmission, pathogens can spread through environmental sources, such as through contact with fomites (Allerson, Cardpna, & Torremorell, ), ingestion of contaminated drinking water (Breban, ; Kraay et al, ), contact with contaminated soil (Turner et al, ), contact with contaminated carcasses (Chenais, Ståhl, Guberti, & Depner, ), or carcass scavenging (Brown & Bevins, ; Wille et al, ). Environmental sources of infection can promote pathogen persistence by increasing their likelihood of contact with susceptible hosts because many pathogens can remain viable in the environment longer than they can keep a host infectious.…”

Section: Introductionmentioning

confidence: 99%

Ecological drivers of African swine fever virus persistence in wild boar populations: Insight for control

Pepin

Golnar

Abdo

et al. 2020

Ecology and Evolution

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Environmental sources of infection can play a primary role in shaping epidemiological dynamics; however, the relative impact of environmental transmission on host‐pathogen systems is rarely estimated. We developed and fit a spatially explicit model of African swine fever virus (ASFV) in wild boar to estimate what proportion of carcass‐based transmission is contributing to the low‐level persistence of ASFV in Eastern European wild boar. Our model was developed based on ecological insight and data from field studies of ASFV and wild boar in Eastern Poland. We predicted that carcass‐based transmission would play a substantial role in persistence, especially in low‐density host populations where contact rates are low. By fitting the model to outbreak data using approximate Bayesian computation, we inferred that between 53% and 66% of transmission events were carcass‐based that is, transmitted through contact of a live host with a contaminated carcass. Model fitting and sensitivity analyses showed that the frequency of carcass‐based transmission increased with decreasing host density, suggesting that management policies should emphasize the removal of carcasses and consider how reductions in host densities may drive carcass‐based transmission. Sensitivity analyses also demonstrated that carcass‐based transmission is necessary for the autonomous persistence of ASFV under realistic parameters. Autonomous persistence through direct transmission alone required high host densities; otherwise re‐introduction of virus periodically was required for persistence when direct transmission probabilities were moderately high. We quantify the relative role of different persistence mechanisms for a low‐prevalence disease using readily collected ecological data and viral surveillance data. Understanding how the frequency of different transmission mechanisms vary across host densities can help identify optimal management strategies across changing ecological conditions.

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“…Understanding mechanisms by which pathogens transmit between hosts is key for defining disease risk and for planning effective control strategies. In addition to direct host-to-host or vector-borne transmission, pathogens can spread through environmental sources, such as through contact with fomites (Allerson et al 2013), ingestion of contaminated drinking water (Breban et al 2013, Kraay et al 2018), contact with contaminated soil (Turner et al 2014), contact with contaminated carcasses (Chenais et al 2018), or carcass scavenging (Wille et al 2016, Brown and Bevins 2018). Environmental sources of infection can promote pathogen persistence by increasing their likelihood of contact with susceptible hosts because many pathogens can remain viable in the environment longer than they can keep a host infectious.…”

Section: Introductionmentioning

confidence: 99%

Ecological drivers of African swine fever virus persistence in wild boar populations: insight for control

Pepin

Golnar

Abdo

et al. 2019

Preprint

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16Environmental sources of infection can play a primary role in shaping epidemiological 17 dynamics, however the relative impact of environmental transmission on host-pathogen systems 18 is rarely estimated. We developed and fit a spatially-explicit model of African swine fever virus 19 (ASFV) in wild boar to estimate what proportion of carcass-based transmission is contributing to 20 the low-level persistence of ASFV in Eastern European wild boar. Our model was developed 21 based on ecological insight and data from field studies of ASFV and wild boar in Eastern Poland. 22 38 39

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A Pelagic Outbreak of Avian Cholera in North American Gulls: Scavenging as a Primary Mechanism for Transmission?

Cited by 20 publications

References 28 publications

Exposure of breeding albatrosses to the agent of avian cholera: dynamics of antibody levels and ecological implications

Exposure of breeding albatrosses to the agent of avian cholera: dynamics of antibody levels and ecological implications

Ecological drivers of African swine fever virus persistence in wild boar populations: Insight for control

Ecological drivers of African swine fever virus persistence in wild boar populations: insight for control

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