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Home arrow Environment arrow Bats in the Anthropocene: Conservation of Bats in a Changing World

II Emerging Disesases

White-Nose Syndrome in Bats

Winifred F. Frick, Sébastien J. Puechmaille and Craig K.R. Willis

Abstract White-nose syndrome (WNS) is an infectious disease of hibernating bats that has killed millions of bats since it first emerged in eastern North America in 2006. The disease is caused by a pathogenic fungus, Pseudogymnoascus (formerly Geomyces) destructans that was likely introduced to North America by human trade or travel, demonstrating the serious problem of global movement of pathogens by humans in the Anthropocene. Here, we present a synthesis of the current state of knowledge on WNS, including disease mechanisms, disease ecology, global distribution and conservation and management efforts. There has been rapid research response to WNS and much about the disease is now well understood. However, critical gaps in our knowledge remain, including ways to limit spread, or effective treatment options to reduce disease mortality. There are several hibernating bat species in North America that are threatened with extinction from WNS. Protecting those species has become a race against time to find and implement creative solutions to combat the devastating impacts of this disease.

Introduction

In late winter of 2007, biologists at the New York State Department of Environmental Conservation encountered a macabre scene during their annual winter surveys of hibernating bats in caves and mines in northern New York State: heaps of dead bats piled on cave floors (Fig. 9.1) (Veilleux 2008). Bats were also seen flying out in the middle of winter onto the snowy landscape and the number of citizen reports of dead bats found in backyards was much higher than normal. A white fuzzy growth was observed on muzzles and wings of the few remaining live bats, which led to the name white-nose syndrome (WNS) (Veilleux 2008; Reeder and Turner 2008; Turner and Reeder 2009). WNS is now recognized as one of the most devastating wildlife epidemics in recorded history and has caused the death of millions of bats in eastern North America. The research and management response to WNS has been rapid and we know much more about WNS than when those first dead bats were observed in New York, although there is still a great deal about this wildlife disease that is yet to be resolved.

The first evidence of WNS in North America is dated to a photograph taken by a caver at Howe's Cave in 2006 (Turner and Reeder 2009). Howe's Cave is a popular tourist attraction that receives hundreds of thousands of visitors each year, many of whom visit from other parts of the world. The white fuzzy growth visible on bats is caused by a pathogenic fungus, which was described as Geomyces destructans (Gargas et al. 2009; Blehert et al. 2009), but was recently re-named Pseudogymnoascus destructans after closer evaluation of its taxonomic allies (Minnis and Lindner 2013). The fungus infects the skin tissues, including the wings and tail membranes, and causes bats to arouse too frequently from torpor

Fig. 9.1 Bats that died from WNS during winter at Aeolus Cave in Vermont, USA. Photo by Al Hicks

Fig. 9.2 A hibernating little brown myotis (Myotis lucifugus) with typical WNS infection visible on skin tissues. Photo by Ryan von Linden

during hibernation (Lorch et al. 2011; Warnecke et al. 2012) (Fig. 9.2). Bats die before spring brings warmer weather and insects for food.

WNS has spread rapidly and by 2014 was found in 25 U.S. states and 5 Canadian Provinces (Fig. 9.3). A confirmed case of WNS is defined by the presence of cupping erosions on the skin caused by infection by P. destructans, which is determined by histopathological examination (Meteyer et al. 2009). There are currently seven hibernating species in North America that have been confirmed with infections characteristic of WNS, including Myotis lucifugus, Myotis septentrionalis, Myotis sodalis, Myotis leibii, Myotis grisescens, Eptesicus fuscus and Perimyotis subflavus. There are several additional species for which P. destructans has been detected on skin tissues using swab sampling and quantitative PCR methods (Muller et al. 2013), but that have not been confirmed with characteristic skin lesions that define the disease.

Two of the species confirmed with WNS (M. sodalis, M. grisescens) were already listed as federally endangered under the US Endangered Species Act before WNS emerged and several other species have been predicted to go globally or regionally extinct due to mortality from WNS (Frick et al. 2010; Langwig et al. 2012; Thogmartin et al. 2013). The US Fish and Wildlife Service listed

M. septentrionalis as federally threatened in 2015 due to the risk of extinction

Fig. 9.3 Map of current distribution and past spread of WNS across North America. Confirmed WNS cases are those where disease has been confirmed by histological examination of tissues. Suspect cases are those that are either a molecular detection of Pseudogymnoascus destructans by quantitative PCR (Muller et al. 2013) or by visual signs and/or aberrant behaviour consistent with WNS disease at a site. Updated versions of this map are made publically available at whitenosesyndrome.org

from WNS-associated mortality. In addition, a status review of M. lucifugus is being conducted to determine whether listing as federally endangered is warranted of this once common species (Frick et al. 2010). In Canada, three species, M. lucifugus, M. septentrionalis and P. subflavus were listed as endangered in 2015. The rapid spread and extensive mortality associated with WNS raise serious concerns about population viability for species that are being impacted by this disease.

In this chapter, we review what is currently known about WNS, focusing on mechanisms of disease, disease ecology, global distribution patterns and conservation and management. We first explain why WNS belongs in a volume addressing bats in the Anthropocene. We review what is known about disease mechanisms, including what we currently understand about the physiology of the disease and immune response in bats. We then review what is currently known about disease ecology of WNS, including the population impacts to species, and then highlight unanswered questions about transmission dynamics. We discuss global distributions patterns, focusing on what is known about WNS in Europe. We conclude by discussing current conservation and management strategies.

Wildlife disease is increasingly recognized as a major conservation threat (Daszak 2000). Global movements of humans increase the probability and rate at which we introduce pathogens into naïve ecosystems (Cunningham et al. 2003). This human-mediated spread of pathogens has been dubbed “pathogen pollution” to highlight the role of human trade and travel in the spread of wildlife pathogens (Cunningham et al. 2003). The fungus P. destructans was presumably introduced to North America from Europe by people, most likely from someone who had visited caves in Europe and subsequently visited Howe's Cave with contaminated boots or gear (Puechmaille et al. 2011c; Leopardi et al. 2015). No bats are known to migrate between the Americas and other continents, implicating human trade or travel in the trans-Atlantic arrival of the fungus (Wibbelt et al. 2010). Ironically, bats are often seen as reservoirs of diseases with consequences to human health

(e.g. rabies, SARS, etc.). In the case of WNS, humans were most likely the unwitting transcontinental carrier of a pathogen that has killed millions of bats and now threatens species with extinction.

The emergence of WNS has dramatically changed conservation planning and population monitoring of temperate bats in North America (Foley et al. 2011). On the positive side, this crisis prompted collaborative research efforts among bat conservationists in North America and in Europe. Although mortality from WNS is currently restricted to North America, the pathogen is a potential threat to hibernating bat populations in other parts of the globe and is a global concern for bats in the Anthropocene (Puechmaille et al. 2011c).

 
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