Hibernation consists of extended durations of torpor interrupted by periodic arousals. The ‘dehydration hypothesis’ proposes that hibernating mammals arouse to replenish water lost through evaporation during torpor. Arousals are energetically expensive, and increased arousal frequency can alter survival throughout hibernation. Yet we lack a means to assess the effect of evaporative water loss (EWL), determined by animal physiology and hibernation microclimate, on torpor bout duration and subsequent survival. White-nose syndrome (WNS), a devastating disease impacting hibernating bats, causes increased frequency of arousals during hibernation and EWL has been hypothesized to contribute to this increased arousal frequency. WNS is caused by a fungus, which grows well in humid hibernaculum environments and damages wing tissue important for water conservation. Here, we integrated the effect of EWL on torpor expression in a hibernation energetics model, including the effects of fungal infection, to determine the link between EWL and survival. We collected field data for Myotis lucifugus, a species that experiences high mortality from WNS, to gather parameters for the model. In saturating conditions, we predicted healthy bats experience minimal mortality. Infected bats, however, suffer high fungal growth in highly saturated environments, leading to exhaustion of fat stores before spring. Our results suggest that host adaptation to humid environments leads to increased arousal frequency from infection, which drives mortality across hibernaculum conditions. Our modified hibernation model provides a tool to assess the interplay between host physiology, hibernaculum microclimate, and diseases such as WNS on winter survival.

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White-nose syndrome (WNS) has decimated hibernating bat populations across eastern and central North America for over a decade. Disease severity is driven by the interaction between bat characteristics, the cold-loving fungal agent, and the hibernation environment. While we further improve hibernation energetics models, we have yet to examine how spatial heterogeneity in host traits is linked to survival in this disease system. Here we develop predictive spatial models of body mass for the little brown myotis (Myotis lucifugus) and reassess previous definitions of the duration of hibernation of this species. Using data from published literature, public databases, local experts, and our own fieldwork, we fit a series of generalized linear models with hypothesized abiotic drivers to create distribution-wide predictions of pre-hibernation body fat and hibernation duration. Our results provide improved estimations of hibernation duration and identify a scaling relationship between body mass and body fat; this relationship allows for the first continuous estimates of pre-hibernation body mass and fat across the species’ distribution. We used these results to inform a hibernation energetic model to create spatially-varying fat use estimates for M. lucifugus. These results predict that WNS mortality of newly and soon-to-be infected M. lucifugus populations in western North America may be comparable to the substantial die-off observed in eastern and central populations.

24Hibernation consists of extended durations of torpor interrupted by periodic arousals. The 25 'dehydration hypothesis' proposes that hibernating mammals arouse to replenish water lost 26 through evaporation during torpor. Arousals are energetically expensive, and increased arousal 27 frequency can alter survival throughout hibernation. Yet we lack a means to assess the effect of 28 evaporative water loss (EWL), determined by animal physiology and hibernation microclimate, 29 on torpor bout duration and subsequent survival. White-nose syndrome (WNS), a devastating 30 disease impacting hibernating bats, causes increased frequency of arousals during hibernation 31 and EWL has been hypothesized to contribute to this increased arousal frequency. WNS is 32 caused by a fungus, which grows well in humid hibernaculum environments and damages wing 33 tissue important for water conservation. Here, we integrated the effect of EWL on torpor 34 expression in a hibernation energetics model, including the effects of fungal infection, to 35 determine the link between EWL and survival. We collected field data for Myotis lucifugus, a 36 species that experiences high mortality from WNS, to gather parameters for the model. In 37 saturating conditions we predicted healthy bats experience minimal mortality. Infected bats, 38 however, suffer high fungal growth in highly saturated environments, leading to exhaustion of 39 fat stores before spring. Our results suggest that host adaptation to humid environments leads to 40 increased arousal frequency from infection, which drives mortality across hibernaculum 41 conditions. Our modified hibernation model provides a tool to assess the interplay between host 42 physiology, hibernaculum microclimate, and diseases such as WNS on winter survival. 43 44 destructans, torpor, white-nose syndrome 3 45In periods of food scarcity, hibernators conserve energy by entering torpor, during which 46 body temperature (T b ) is maintained near hibernaculum temperature and metabolic rate is 47 lowered to reduce energy demands [1]. There are several hypotheses proposed to explain 48 periodic arousals, but two of the most prominent are linked to water balance: 1) the dehydration 49 hypothesis [2,3]; and 2) the need to excrete metabolic byproducts [4]. The dehydration 50 hypothesis suggests that hibernators arouse periodically after a threshold of total body water is 51 reached [5,6]. The metabolic byproducts hypothesis suggests that bats accumulate byproducts 52 from biochemical reactions during torpor, and these byproducts need to be excreted as waste as 53 they can be damaging to cellular function [4]. Both of these hypotheses are affected by 54 microclimate, which is supported by empirical evidence of the relationship between 55 hibernaculum temperature and relative humidity and torpor bout duration [3,5,7,8]. Hibernators 56 do not normally defecate or urinate during torpor [9], thus water lost during inactive periods of 57 hibernation is assumed to be from evaporation. Evaporative water loss (E...

Late detection of emerging viral transmission allows outbreaks to spread uncontrolled, the devastating consequences of which are exemplified by recent epidemics of Ebola virus disease. Especially challenging in places with sparse healthcare, limited diagnostic capacity, and public health infrastructure, syndromes with overlapping febrile presentations easily evade early detection. There is a clear need for evidence-based and context-dependent tools to make syndromic surveillance more efficient. Using published data on symptom presentation and incidence of 21 febrile syndromes, we develop a novel algorithm for aetiological identification of case clusters and demonstrate its ability to identify outbreaks of dengue, malaria, typhoid fever, and meningococcal disease based on clinical data from past outbreaks. We then apply the same algorithm to simulated outbreaks to systematically estimate the syndromic detectability of outbreaks of all 21 syndromes. We show that while most rare haemorrhagic fevers are clinically distinct from most endemic fevers in sub-Saharan Africa, VHF detectability is limited even under conditions of perfect syndromic surveillance. Furthermore, even large clusters (20+ cases) of filoviral diseases cannot be routinely distinguished by the clinical criteria present in their case definitions alone; we show that simple syndromic case definitions are insensitive to rare fevers across most of the region. We map the estimated detectability of Ebola virus disease across sub-Saharan Africa, based on geospatially mapped estimates of malaria, dengue, and other fevers with overlapping syndromes. We demonstrate "hidden hotspots" where Ebola virus is likely to spill over from wildlife and also transmit undetected for many cases. Such places may represent both the locations of past unobserved outbreaks and potential future origins for larger epidemics. Finally, we consider the implications of these results for improved locally relevant syndromic surveillance and the consequences of syndemics and under-resourced health infrastructure for infectious disease emergence.

Shiga toxin–producing Escherichia coli serogroup O26 is an important public health pathogen. Phylogenetic bacterial lineages in a country can be associated with the level and timing of international imports of live cattle, the main reservoir. We sequenced the genomes of 152 E. coli O26 isolates from New Zealand and compared them with 252 E. coli O26 genomes from 14 other countries. Gene variation among isolates from humans, animals, and food was strongly associated with country of origin and stx toxin profile but not isolation source. Time of origin estimates indicate serogroup O26 sequence type 21 was introduced at least 3 times into New Zealand from the 1920s to the 1980s, whereas nonvirulent O26 sequence type 29 strains were introduced during the early 2000s. New Zealand’s remarkably fewer introductions of Shiga toxin–producing Escherichia coli O26 compared with other countries (such as Japan) might be related to patterns of trade in live cattle.