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	<title>wildlife disease &#8211; Science</title>
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	<title>wildlife disease &#8211; Science</title>
	<link>https://scienmag.com</link>
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		<title>Otters Face a Hidden Parasite Burden, and Most Species Have Never Been Surveyed</title>
		<link>https://scienmag.com/otters-face-a-hidden-parasite-burden-and-most-species-have-never-been-surveyed/</link>
		
		<dc:creator><![CDATA[Margaret Porter]]></dc:creator>
		<pubDate>Fri, 16 Oct 2026 22:06:36 +0000</pubDate>
				<category><![CDATA[Science News]]></category>
		<category><![CDATA[climate change effects on otter health]]></category>
		<category><![CDATA[conservation]]></category>
		<category><![CDATA[conservation challenges for otters]]></category>
		<category><![CDATA[Eurasian otter]]></category>
		<category><![CDATA[gaps in otter disease research]]></category>
		<category><![CDATA[human-wildlife contact and disease transmission]]></category>
		<category><![CDATA[impact of habitat loss on otters]]></category>
		<category><![CDATA[long-term study of otter parasitology]]></category>
		<category><![CDATA[Lutrinae]]></category>
		<category><![CDATA[Nematoda]]></category>
		<category><![CDATA[North American river otter]]></category>
		<category><![CDATA[otter disease surveillance]]></category>
		<category><![CDATA[Otter parasitic diseases]]></category>
		<category><![CDATA[otters]]></category>
		<category><![CDATA[parasites]]></category>
		<category><![CDATA[parasitic burden in semi-aquatic mammals]]></category>
		<category><![CDATA[Sarcocystis neurona]]></category>
		<category><![CDATA[sea otter]]></category>
		<category><![CDATA[systematic review]]></category>
		<category><![CDATA[systematic review of otter parasites]]></category>
		<category><![CDATA[threatened otter species]]></category>
		<category><![CDATA[Toxoplasma gondii]]></category>
		<category><![CDATA[underwater ecosystem health]]></category>
		<category><![CDATA[wildlife disease]]></category>
		<guid isPermaLink="false">https://scienmag.com/?p=290506</guid>

					<description><![CDATA[A systematic review of otter parasites cataloged 164 parasite species across ten otter species, but found no parasite studies at all for three threatened otters and limited data for seven more, with generalist pathogens such as Toxoplasma gondii and Sarcocystis neurona emerging as major conservation concerns.]]></description>
										<content:encoded><![CDATA[<p>Otters occupy a precarious ecological position. As semi-aquatic members of the mustelid subfamily Lutrinae, they forage in rivers, lakes, and coastal waters while denning and resting on land, which means their immune systems are challenged by pathogens drawn from two entirely different worlds. Twelve of the fourteen recognized otter species are currently listed by the IUCN as near-threatened, vulnerable, or endangered, and a new systematic review published in Frontiers in Mammal Science suggests that parasitic diseases, long an overlooked stressor, may be compounding the pressures of habitat loss, fragmentation, climate change, and increasing contact with humans.</p>
<p>The review, conducted by Stacy R. Cotey of Michigan Technological University and Mason V. Reichard of Oklahoma State University&#8217;s College of Veterinary Medicine, followed PRISMA guidelines and searched Google Scholar, Web of Science, and the ProQuest Dissertation and Theses databases using the terms otter plus parasite and otter plus disease. The initial sweep returned 4,515 sources. After duplicates were removed, titles and abstracts were screened by both researchers, and full papers were read in their entirety, the final dataset rested on 240 papers, the earliest of which dates to 1924. Publications have climbed steadily each decade, with 76 papers appearing between 2010 and 2019 and the 2020s on track to match or exceed that figure.</p>
<p>The headline numbers are striking. Across ten otter species, the authors cataloged 146 parasite genera representing 164 species, distributed across five major phyla: the apicomplexan protozoa, thorny-headed worms (Acanthocephala), roundworms (Nematoda), flatworms (Platyhelminthes), and arthropods such as ticks, mites, and insects, plus a residual category of tick-borne bacteria and other parasites spanning nine additional phyla. For each parasite-otter pairing with sufficient data, the team calculated prevalence and a 95 percent confidence interval using a modified Wald method for proportions.</p>
<p>Yet the coverage is profoundly lopsided. The Eurasian otter (Lutra lutra) dominated the literature with 89 papers and the highest parasite richness at 184 species, followed by the sea otter (Enhydra lutris) with 79 papers and 41 parasite species, and the North American river otter (Lontra canadensis) with 47 papers and 66 species. Three species, the smooth-coated otter (Lutrogale perspicillata), the hairy-nosed otter (Lutra sumatrana), and the Congo clawless otter (Aonyx congicus), have no published parasite studies at all in the databases searched. Seven additional otter species had fewer than 15 papers each. The newly recognized Neotropical species Lontra annectens, split from Lontra longicaudis on the basis of genome-wide data, has not yet been evaluated by the IUCN and has no parasite records of its own.</p>
<p>Among the protozoa, three parasites stand out as highly pathogenic: Toxoplasma gondii, Sarcocystis neurona, and Neospora caninum. Otters are accidental hosts of all three, and infections can be fatal. Toxoplasma gondii was the most heavily sampled apicomplexan, detected in five otter species, with prevalence of 12.6 percent in 5,307 sea otters, 14.3 percent in 1,008 Eurasian otters, 29.2 percent in 489 North American river otters, and 76.9 percent in a small sample of 13 southern river otters. Sarcocystis neurona, which together with T. gondii causes encephalitis and mortality in sea otters, showed an overall prevalence of 18.5 percent across 1,612 sea otters, and 5.1 percent of 1,350 sampled sea otters carried co-infections of both parasites. Neospora caninum reached 19.4 percent in 278 sea otters. The review also flags the considerable genetic diversity of T. gondii as a concern, because recombination among strains could generate more virulent variants with population-level consequences.</p>
<p>The helminths tell a story shaped by diet. Nematodes were the most species-rich group, with 58 genera and 58 species, a diversity the authors attribute largely to the otters&#8217; piscivorous feeding on fish, amphibians, and aquatic invertebrates. Several roundworms are otter specialists, including Dirofilaria lutrae (16.5 percent prevalence in North American river otters), Dracunculus lutrae (87.7 percent in the same host), Skrjabingylus lutrae, and Strongyloides lutrae. Highly pathogenic generalists such as Ancylostoma species, the mustelid specialist Skrjabingylus nasicola, Dirofilaria immitis, and Trichinella species also appear in the record. Flatworms, with 47 genera and 52 species, are likewise acquired through prey: Diphyllobothrium species use fish as intermediate hosts, Paragonimus kellicotti cycles through crayfish and causes lesions in the bile ducts and gall bladder, and both carry zoonotic potential. Notably, warmer temperatures, reduced rainfall, and fewer frost days have been linked to increased prevalence of the biliary trematodes Pseudamphistomum truncatum and Metorchis albidus in Eurasian otters, a direct climate signal.</p>
<p>The acanthocephalans, though fewer in number with 6 genera and 10 species, include one of the review&#8217;s most consequential findings. Corynosoma enhydri, a specialist of the sea otter, showed an overall prevalence of 84.4 percent across 404 otters sampled in five studies. Recent work cited in the review found that this thorny-headed worm parasitizes sea otter pups at an early age, potentially suppressing their immune response and increasing susceptibility to other parasites or bacterial infections that led to mortalities. Heavy infestations of Profilicollis altmani and P. kenti have directly caused sea otter deaths. Arthropods, meanwhile, include the nasal mite Halarachne halichoteri, which causes respiratory disease and reached 25.6 percent prevalence in 156 sea otters, and the New World screwworm fly Cochliomyia hominivorax, whose tissue-eating larvae were found in a single giant otter. Ticks are relatively common on otters because several species survive prolonged submersion: Dermacentor reticulatus adults can survive up to 65 days underwater, Ixodes ricinus up to 44 days, and Amblyomma americanum up to 70 days, all three of which naturally infest otters and can vector pathogens such as Babesia, Anaplasma, and Rickettsia.</p>
<p>The review also documents parasites moving between humans, domestic animals, and wildlife in both directions. Giardia species were the most commonly reported of the tick-borne and miscellaneous group, detected in four otter species with prevalence ranging from 1 percent in sea otters to 20.8 percent in giant otters, and co-infections of Giardia and Cryptosporidium were found in Neotropical and giant otters. Agricultural runoff and untreated sewage are identified as routes by which these protozoa from domestic animals and humans enter aquatic systems. Growing support exists for the reverse hypothesis as well: Giardia duodenalis from human wastewater may infect aquatic mammals such as otters, which then serve as additional hosts for the parasite. Leishmania infantum, Encephalitozoon cuniculi, and the tick-borne bacterium Ehrlichia canis round out the list of highly pathogenic species recorded in otters.</p>
<p>The authors are candid about the biases threading through their dataset. Most studies were conducted in Europe and North America even though parasite diversity is higher in subtropical and tropical regions, a pattern reflecting publication bias toward English-language journals, limited access to study areas, and funding constraints. Prevalence estimates are further distorted by diagnostic method, since antibody tests detect previous infections while dissection and DNA methods detect active ones, and by the fact that most surveys sampled sick or dead animals, skewing prevalence upward relative to systematic surveillance and preferentially detecting parasites that cause visible symptoms. Opportunistic carcass sampling also biases the population toward dispersing young and toward sites near human development, where additional stressors impair otter immunity. Small sample sizes, sometimes fewer than ten animals, and repeated testing of the same otters for multiple parasites compound the uncertainty. The review notes that DNA amplification through PCR has broadened surveillance to environmental DNA and feces, but it has also revealed organisms such as the free-living soil nematodes Aphelenchus avenae, Diploscapter species, and Prionchulus species that otters likely ingested accidentally with prey rather than hosting as true parasites.</p>
<p>The broader ecological logic of the review is that generalist parasites, which infect a wide range of mammalian or vertebrate hosts, pose the greatest threat to vulnerable species because they can persist in tolerant hosts across broad ranges, continually exposing sensitive hosts to virulent stages. Fifteen of the cataloged parasites are specific to otters and eight to mustelids, but the majority, particularly the highly pathogenic ones, are generalists. Environmental degradation adds another layer: parasites with complex multi-host life cycles tend to decline in stressed environments, while single-host, monoxenous parasites such as Eimeria, Giardia, Cryptosporidium, and intestinal nematodes including Ascaris, Toxocara, and Trichuris, all of which have been found in otters, may thrive, especially when stress makes hosts more susceptible. The authors conclude that parasites must be treated as a factor when evaluating otter populations and designing conservation plans, and that systematic surveillance, detailed spatial data, and basic information on host sex, age, and behavior are the missing foundations for protecting twelve of the world&#8217;s fourteen otter species from a stressor that science has barely begun to measure.</p>
<p><strong>Subject of Research:</strong> A systematic review found 164 parasite species reported in ten otter species, with no parasite studies for three threatened otters and generalist pathogens posing the greatest conservation risk.</p>
<p><strong>Article Title:</strong> A systematic review of parasitic diseases of otters</p>
<p><strong>Article References:</strong> Cotey, S. R., &amp; Reichard, M. V. (2025). A systematic review of parasitic diseases of otters. <em>Frontiers in Mammal Science, 4</em>, Article 1673488. <a href="https://doi.org/10.3389/fmamm.2025.1673488" rel="noopener noreferrer">https://doi.org/10.3389/fmamm.2025.1673488</a></p>
<p><strong>Image Credits:</strong> AI Generated</p>
<p><strong>DOI:</strong> <a href="https://doi.org/10.3389/fmamm.2025.1673488" rel="noopener noreferrer">10.3389/fmamm.2025.1673488</a></p>
<p><strong>Keywords:</strong> otters, Lutrinae, parasites, Toxoplasma gondii, Sarcocystis neurona, sea otter, Eurasian otter, North American river otter, systematic review, wildlife disease, conservation, Nematoda</p>
]]></content:encoded>
					
		
		
		<post-id xmlns="com-wordpress:feed-additions:1">290506</post-id>	</item>
		<item>
		<title>Hidden Herpesvirus Found in Sea Turtles From Singapore&#8217;s Urban Waters</title>
		<link>https://scienmag.com/hidden-herpesvirus-found-in-sea-turtles-from-singapores-urban-waters/</link>
		
		<dc:creator><![CDATA[Margaret Porter]]></dc:creator>
		<pubDate>Fri, 16 Oct 2026 16:37:25 +0000</pubDate>
				<category><![CDATA[Science News]]></category>
		<category><![CDATA[coastal habitat degradation and disease prevalence]]></category>
		<category><![CDATA[disease surveillance in urban coastal waters]]></category>
		<category><![CDATA[environmental factors influencing marine turtle diseases]]></category>
		<category><![CDATA[fibropapillomatosis]]></category>
		<category><![CDATA[green and hawksbill turtle health risks]]></category>
		<category><![CDATA[green turtle]]></category>
		<category><![CDATA[hawksbill turtle]]></category>
		<category><![CDATA[herpesvirus]]></category>
		<category><![CDATA[Herpesvirus in sea turtles]]></category>
		<category><![CDATA[impact of eutrophication on marine turtle health]]></category>
		<category><![CDATA[implications of herpesvirus in conservation efforts]]></category>
		<category><![CDATA[land reclamation effects on marine ecosystems]]></category>
		<category><![CDATA[marine]]></category>
		<category><![CDATA[marine conservation]]></category>
		<category><![CDATA[marine turtle fibropapillomatosis]]></category>
		<category><![CDATA[metagenomics]]></category>
		<category><![CDATA[molecular detection of herpesvirus in wild turtles]]></category>
		<category><![CDATA[Scutavirus chelonidalpha5]]></category>
		<category><![CDATA[sea turtles]]></category>
		<category><![CDATA[Singapore]]></category>
		<category><![CDATA[urban water pollution impact on marine wildlife]]></category>
		<category><![CDATA[Urbanization]]></category>
		<category><![CDATA[viral causes of tumor formation in marine animals]]></category>
		<category><![CDATA[whole genome sequencing]]></category>
		<category><![CDATA[wildlife disease]]></category>
		<guid isPermaLink="false">https://scienmag.com/?p=286902</guid>

					<description><![CDATA[Whole-genome sequencing has revealed a tumor-associated herpesvirus in every sampled sea turtle from Singapore, including apparently healthy individuals, in the first molecular detection of the virus in the city-state's waters.]]></description>
										<content:encoded><![CDATA[<p>In the crowded coastal waters of Singapore, where land reclamation and urban runoff have reshaped shorelines for decades, scientists have uncovered the first molecular evidence of a tumor-associated herpesvirus in the city-state&#8217;s sea turtles. A research team from Nanyang Technological University screened whole-genome sequencing data from green turtles and hawksbill turtles and detected Scutavirus chelonidalpha5, formerly known as chelonid alphaherpesvirus 5 or ChHV5, in every single animal tested. The virus is the leading candidate agent behind fibropapillomatosis, a disease that produces debilitating tumors in sea turtles around the world, yet had never been confirmed in wild turtles from Singapore.</p>
<p>Fibropapillomatosis is among the most consequential infectious diseases affecting marine turtles globally. It strikes green turtles most often, although cases have been documented in all sea turtle species, and its external tumors can grow around the eyes, neck, and flippers, impairing vision, movement, and feeding so severely that animals may starve or drown. The precise cause of the disease has never been fully resolved. Decades of research point to Scutavirus chelonidalpha5 as a key player, but the emergence and prevalence of fibropapillomatosis appear to be shaped by environmental conditions as well, particularly degraded water quality, eutrophication, and nutrient enrichment in coastal habitats.</p>
<p>Crucially, infection with the virus does not automatically mean illness. Numerous studies have found viral DNA in turtles that appear completely healthy, supporting the view that fibropapillomatosis is a multifactorial disease in which viral presence, host immunity, and environmental stressors interact to trigger tumor growth. This subtlety is what makes the Singapore findings so revealing: the virus was present not only in tumored animals but also in every apparently healthy individual sampled, suggesting that subclinical infections may be common in both species in the region.</p>
<p>The study began with two stranded green turtles found floating near East Coast Park and Lazarus Island in 2021 and 2022, both carrying multiple large external lesions on the neck and flippers. Internal examination revealed extensive pulmonary tumors that compromised lung integrity and buoyancy. Because veterinary diagnostic records were unavailable, the researchers classified the lesions based on gross morphology alone and describe them as suggestive of fibropapillomatosis rather than definitively diagnosed. The team then widened the net, analyzing whole-genome sequencing datasets from a total of four green turtles and four hawksbill turtles stranded or nesting in Singapore between 2020 and 2022, including individuals both with and without visible tumors.</p>
<p>The sequencing strategy was technically elegant. The team constructed Illumina TruSeq Nano paired-end libraries and sequenced them to roughly thirty-fold genome coverage on the HiSeq X platform. Because the viral genome is tiny, around 170 kilobases, compared with the roughly 2.1 gigabase turtle genome, viral sequences were expected to make up only a vanishingly small fraction of each dataset. To pull this signal out, the researchers used two complementary pipelines. The first, a reference-based approach using the BWA-MEM algorithm, aligned all quality-filtered reads against the reference viral genome, then filtered the results with SAMtools to retain only primary mapped read pairs. The second used Kraken2 metagenomic classification: host reads were subtracted, and the remaining reads were queried against the RefSeq viral database to count matches to the genus Scutavirus.</p>
<p>Both approaches told the same story. Viral sequences turned up in all eight genome datasets. After normalizing read counts to the smallest library size of roughly 223.8 million reads, reference-based viral counts ranged from about 30,869 to 98,326 reads, with the highest abundance found in a tumored green turtle from Lazarus Island. Kraken2 counts, between 178 and 488 normalized reads, mirrored the same pattern, and a Spearman&#8217;s rank correlation between the two methods was significant, indicating that the independent pipelines were capturing the same underlying viral signal. The concordance gives strong confidence that the detections are real rather than artifacts of any single analytical approach.</p>
<p>Perhaps the most striking result was what the statistics did not show. There was no significant difference in viral load between turtles with tumors and turtles without, and while green turtles carried somewhat higher counts than hawksbills, that difference also fell just short of significance with the small sample size. All four hawksbill turtles, none of which had visible tumors, still harbored detectable viral sequences. The authors caution that the sample sizes are small and unbalanced, and one green turtle muscle sample was excluded from statistical analysis because post-mortem contamination produced an unreliable taxonomic profile. Even so, the pattern is consistent with studies elsewhere showing that visual surveys based on tumors alone likely underestimate true infection rates.</p>
<p>That finding matters for conservation because turtles without symptoms may act as cryptic carriers, quietly maintaining the virus within populations. Viral infection can remain latent, and loads may drop below detection thresholds depending on tissue type, infection stage, and species, further limiting the reliability of external examinations. The researchers argue that host whole-genome sequencing, by enabling unbiased viral detection in both sick and healthy animals, offers a sensitive complement to existing viral, histological, and environmental DNA monitoring methods. Combined approaches of this kind could catch infections long before tumors appear.</p>
<p>Singapore&#8217;s urban coastline makes the discovery especially poignant. Land reclamation, urban runoff, and pollution have drastically altered the island nation&#8217;s natural shores, and pollution is known to weaken immune function in marine organisms, potentially raising susceptibility to diseases like fibropapillomatosis. Globally, higher disease prevalence has been linked to eutrophic, polluted coastal habitats. The study&#8217;s authors are careful to note that environmental parameters were not measured in this work, so no direct link between pollution and viral presence can be drawn from the data. Still, the hypothesis that heavily impacted coastal ecosystems elevate disease risk fits the emerging picture that fibropapillomatosis reflects an interaction among viral exposure, host immune status, microbiome composition, and environmental stress rather than pathogen presence alone.</p>
<p>There are also broader geographic implications. Southeast Asia has long been a surveillance gap for this disease. The earliest known regional record dates to 1958, when fibropapillomatosis was reported in nesting green turtles at Malaysia&#8217;s Sarawak Turtle Islands, and subsequent studies have documented cases in Indonesia and Taiwan along with molecular evidence of the virus in green, hawksbill, and olive ridley turtles in Borneo. The Singapore data now fill in a missing piece of that map in one of the most heavily urbanized marine environments on Earth. The team calls for comprehensive health assessments across Singapore and the wider region, integrating water quality and pollutant monitoring with molecular and clinical surveillance, alongside more systematic sampling across species, life stages, and tissue types, and histopathological confirmation of lesions in future work. If the virus proves to be a sentinel of cumulative environmental stress, then tracking it genomics-first could benefit not just the turtles but the ecosystems they inhabit.</p>
<p><strong>Subject of Research:</strong> Detection of Scutavirus chelonidalpha5, the virus linked to fibropapillomatosis, in green and hawksbill turtles from Singapore using host whole-genome sequencing</p>
<p><strong>Article Title:</strong> Host whole-genome sequencing reveals Scutavirus chelonidalpha5 infection in sea turtles from Singapore</p>
<p><strong>Article References:</strong> Tanabe, L. K., Espinosa, A. G., Tiong, R. H. Y., &amp; Kim, H. L. (2026). Host whole-genome sequencing reveals Scutavirus chelonidalpha5 infection in sea turtles from Singapore. <em>Frontiers in Amphibian and Reptile Science, 4</em>, Article 1814588. <a href="https://doi.org/10.3389/famrs.2026.1814588" rel="noopener noreferrer">https://doi.org/10.3389/famrs.2026.1814588</a></p>
<p><strong>Image Credits:</strong> AI Generated</p>
<p><strong>DOI:</strong> <a href="https://doi.org/10.3389/famrs.2026.1814588" rel="noopener noreferrer">10.3389/famrs.2026.1814588</a></p>
<p><strong>Keywords:</strong> sea turtles, Scutavirus chelonidalpha5, fibropapillomatosis, herpesvirus, whole-genome sequencing, metagenomics, Singapore, green turtle, hawksbill turtle, marine conservation, urbanization, wildlife disease</p>
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		<post-id xmlns="com-wordpress:feed-additions:1">286902</post-id>	</item>
		<item>
		<title>Mating Season Turns Water Tanks and Scrapes into Prion Hotspots for Male Deer</title>
		<link>https://scienmag.com/mating-season-turns-water-tanks-and-scrapes-into-prion-hotspots-for-male-deer/</link>
		
		<dc:creator><![CDATA[Drew Townsend]]></dc:creator>
		<pubDate>Sat, 10 Oct 2026 18:33:48 +0000</pubDate>
				<category><![CDATA[Biology]]></category>
		<category><![CDATA[animal congregation sites]]></category>
		<category><![CDATA[camera traps]]></category>
		<category><![CDATA[cervid disease ecology]]></category>
		<category><![CDATA[chronic wasting disease]]></category>
		<category><![CDATA[chronic wasting disease transmission]]></category>
		<category><![CDATA[deer mating season]]></category>
		<category><![CDATA[elk]]></category>
		<category><![CDATA[environmental contamination of prions]]></category>
		<category><![CDATA[environmental transmission]]></category>
		<category><![CDATA[host competence]]></category>
		<category><![CDATA[indirect disease transmission]]></category>
		<category><![CDATA[mating season]]></category>
		<category><![CDATA[mule deer]]></category>
		<category><![CDATA[multi-host cervid community]]></category>
		<category><![CDATA[Nebraska]]></category>
		<category><![CDATA[prion hotspots in water tanks]]></category>
		<category><![CDATA[prion persistence in soil]]></category>
		<category><![CDATA[prions]]></category>
		<category><![CDATA[scrape sites]]></category>
		<category><![CDATA[seasonal disease risk]]></category>
		<category><![CDATA[white-tailed deer]]></category>
		<category><![CDATA[white-tailed deer behavior]]></category>
		<category><![CDATA[wildlife disease]]></category>
		<category><![CDATA[wildlife disease research]]></category>
		<guid isPermaLink="false">https://scienmag.com/?p=259550</guid>

					<description><![CDATA[Camera-trap data from Nebraska's Wildcat Hills show that male mule deer, white-tailed deer, and elk concentrate chronic wasting disease exposure risk at shared water tanks and scrape sites during the mating season.]]></description>
										<content:encoded><![CDATA[<p>Every autumn, as the rut grips North America&#8217;s deer country, male cervids abandon their usual caution. They travel farther, fight, court, scent-mark, and congregate at predictable places on the landscape. A new study in Ecology and Evolution suggests that this seasonal recklessness carries a hidden cost: it concentrates chronic wasting disease (CWD) exposure risk at a handful of shared sites, turning ordinary stock tanks and white-tailed deer scrapes into potential engines of prion transmission across an entire multi-host cervid community.</p>
<p>CWD is a fatal, transmissible prion disease that affects mule deer, white-tailed deer, elk, and moose. Infected animals shed infectious prions in saliva, urine, and feces, and those misfolded proteins can persist in soil and on surfaces for years. Transmission happens in two ways: directly, through animal-to-animal contact such as grooming or sparring, and indirectly, through contact with contaminated environments. Because sympatric cervid species rarely touch one another, scientists have long suspected that indirect, environmental exposure at so-called local infectious zones — places where prions accumulate and animals congregate — is the main bridge for transmission between species.</p>
<p>A research team led by Rebecca M. Windell of the U.S. Department of Agriculture&#8217;s National Wildlife Research Center, working with colleagues at Colorado State University and the Nebraska Game and Parks Commission, set out to quantify that risk during the mating season. Their study area was the Wildcat Hills of western Nebraska, roughly 9,100 square kilometers of buttes, canyons, ponderosa pine, and shortgrass prairie where CWD has been enzootic since it was first detected in 2000. Prevalence in mule deer in the surrounding management unit has hovered around 15 percent over the past decade, making the region an ideal natural laboratory for studying how a multi-host community shares — or fails to share — a prion disease.</p>
<p>Between October 16 and December 7, 2023, the researchers deployed 38 camera traps at three kinds of sites: eight cattle-style water tanks, eleven white-tailed deer scrape sites marked by overhanging branches and pawed soil, and nineteen reference sites representing background deer activity such as game trails and agricultural edges. The cameras recorded ten-second videos whenever motion triggered them, capturing a total of 1,837 videos of antlered male mule deer, white-tailed deer, and elk. From this footage, the team built an ethogram of contact behaviors — drinking, foraging, investigating, scraping, thrashing, urinating, courting, and sparring — and measured exactly how many seconds each species spent performing them at each site type.</p>
<p>The results were striking. Male mule deer spent an average of 142 seconds engaged in environmental contact behaviors at water tanks and 105 seconds at scrape sites, compared with just 20 seconds at reference sites. White-tailed deer spent 104 seconds at scrapes versus 19 seconds at reference sites. Elk, remarkably, engaged in environmental contact behaviors only at water tanks, where they averaged 201 seconds — nearly three and a half minutes of drinking and investigating per encounter. Across the whole study, males logged 96.8 minutes of environmental exposure behaviors and 22.9 minutes of direct contact behaviors such as courting and sparring.</p>
<p>Spatial overlap told a complementary story. Mule deer were the only species that overlapped with both of the others, and the probability of overlap spiked at the local infectious zones: the odds of mule deer and white-tailed deer co-occurring were 7.6 times higher at scrape sites than at reference sites, and the odds of mule deer and elk overlapping were 8.7 times higher at water tanks. All three species appeared together at one water tank. Crucially, whenever two species overlapped, their environmental contact behaviors occurred exclusively at these shared sites — no interspecific exposure was recorded at reference locations at all.</p>
<p>To translate behavior into risk, the team calculated environmental exposure risk as the product of uptake behaviors, host competence, and shedding behaviors, drawing on a systematic literature review to estimate species-specific prevalence as a proxy for competence: roughly 15 percent for mule deer, 8 percent for white-tailed deer, and 3.3 percent for elk in comparable sympatric systems. Statistical models using Tweedie-distributed errors showed that mule deer intraspecific and total environmental exposure risk was more than 100 times higher at water tanks and scrapes than at reference sites, while white-tailed deer risk at scrapes was 6 to 15 times higher. Direct exposure risk, by contrast, showed no clear differences across site types, suggesting these hotspots matter mainly for environmental transmission.</p>
<p>The assumptions about host competence changed the picture in revealing ways. If all species were assumed equally competent, prions deposited by elk constituted the majority of mule deer&#8217;s environmental exposure risk at shared water tanks. But when the researchers used realistic prevalence-based competence values, most risk to both mule deer and elk traced back to mule deer themselves — positioning mule deer as the central node in the community&#8217;s transmission network. Because mule deer overlap heavily with both other species at local infectious zones and carry the highest prevalence, the authors argue they are both the main contributors to environmental transmission and the most vulnerable hosts, a conclusion consistent with the community epidemiology framework recently formalized by Atle Mysterud.</p>
<p>The findings carry immediate management implications. In areas where CWD spillover to elk is a concern, excluding cervids from shared water tanks or seasonally disinfecting metal tank surfaces — prions are known to bind to sediments and galvanized steel — could reduce emergence risk. Where mule deer populations are declining, managing densities and aggregation points may slow amplification, especially where white-tailed deer are abundant. The authors caution that host competence remains poorly understood and that their camera-trap window captured elk in post-rut recovery, but the approach itself is broadly applicable: any multi-host system with a horizontally transmitted pathogen and differential host competence could be dissected the same way, one behavior and one shared site at a time.</p>
<p><strong>Subject of Research:</strong> Chronic wasting disease exposure risk to male cervids at shared environmental sites during the mating season</p>
<p><strong>Article Title:</strong> Chronic Wasting Disease Exposure Risk to Male Cervids During the Mating Season in A Multi‐Host Community</p>
<p><strong>Article References:</strong> Windell, R. M., Malmberg, J. L., Bailey, L. L., Fesmire, S., Simpson, S., Roundtree, M. K., &amp; Titcomb, G. C. (2026). Chronic Wasting Disease Exposure Risk to Male Cervids During the Mating Season in A Multi‐Host Community. <em>Ecology and Evolution, 16</em>(10), Article e74463. <a href="https://doi.org/10.1002/ece3.74463" rel="noopener noreferrer">https://doi.org/10.1002/ece3.74463</a></p>
<p><strong>Image Credits:</strong> AI Generated</p>
<p><strong>DOI:</strong> <a href="https://doi.org/10.1002/ece3.74463" rel="noopener noreferrer">10.1002/ece3.74463</a></p>
<p><strong>Keywords:</strong> chronic wasting disease, prions, mule deer, white-tailed deer, elk, mating season, camera traps, host competence, environmental transmission, Nebraska, wildlife disease, scrape sites</p>
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		<post-id xmlns="com-wordpress:feed-additions:1">259550</post-id>	</item>
		<item>
		<title>Bats in Farmed Savannas Carry a Surprising Load of Potential Pathogens in Their Guts</title>
		<link>https://scienmag.com/bats-in-farmed-savannas-carry-a-surprising-load-of-potential-pathogens-in-their-guts/</link>
		
		<dc:creator><![CDATA[Morgan Morrow]]></dc:creator>
		<pubDate>Thu, 08 Oct 2026 10:30:47 +0000</pubDate>
				<category><![CDATA[Biology]]></category>
		<category><![CDATA[16S rRNA sequencing]]></category>
		<category><![CDATA[bacterial pathogens]]></category>
		<category><![CDATA[bat gut microbiome]]></category>
		<category><![CDATA[bats]]></category>
		<category><![CDATA[biodiversity hotspots in Eswatini]]></category>
		<category><![CDATA[conservation and public health implications]]></category>
		<category><![CDATA[disease ecology in agricultural landscapes]]></category>
		<category><![CDATA[effects of land use change on wildlife health]]></category>
		<category><![CDATA[Eswatini]]></category>
		<category><![CDATA[Gut microbiome]]></category>
		<category><![CDATA[human-wildlife interface in agriculture]]></category>
		<category><![CDATA[insectivorous bats in savannas]]></category>
		<category><![CDATA[land cover impact on bat microbiota]]></category>
		<category><![CDATA[land-cover change]]></category>
		<category><![CDATA[microbial analysis of fecal samples]]></category>
		<category><![CDATA[microbial diversity in bat populations]]></category>
		<category><![CDATA[Mops pumilus]]></category>
		<category><![CDATA[Mycoplasma]]></category>
		<category><![CDATA[One Health]]></category>
		<category><![CDATA[potential pathogens in bats]]></category>
		<category><![CDATA[Salmonella]]></category>
		<category><![CDATA[savanna]]></category>
		<category><![CDATA[wildlife disease]]></category>
		<category><![CDATA[zoonotic disease risk from bats]]></category>
		<guid isPermaLink="false">https://scienmag.com/?p=247126</guid>

					<description><![CDATA[A new study of 109 little free-tailed bats in Eswatini reveals highly individual gut microbiomes rich in potential bacterial pathogens such as Mycoplasma and Salmonella, yet surprisingly unresponsive to agricultural land cover change.]]></description>
										<content:encoded><![CDATA[<p>Deep in the savannas of northeastern Eswatini, one of Africa&#8217;s most adaptable bats is quietly carrying a microbial cargo that has caught the attention of disease ecologists. The little free-tailed bat, Mops pumilus, is a small, fast-flying insectivore that roosts in buildings, forages over sugarcane plantations, and thrives in landscapes transformed by human agriculture. A new study published in the journal Web Ecology has now provided the first detailed characterization of this species&#8217; gut microbiome, and the results are striking: the bats harbor a remarkably diverse community of gut bacteria, including several genera that contain species pathogenic to humans and other animals, yet the composition of that microbial community appears largely indifferent to the dramatic land cover changes reshaping the region.</p>
<p>The research, led by Julie Teresa Shapiro of the University of Florida and the French Agency for Food, Environmental and Occupational Health and Safety, together with colleagues from the University of Copenhagen, Aarhus University, the University of Pretoria, and the University of Eswatini, analyzed fecal samples from 109 individual little free-tailed bats captured between November 2015 and July 2016 at 28 sites across the Lowveld region of eastern Eswatini. This area, part of the Maputaland-Pondoland-Albany biodiversity hotspot, is dominated by commercial sugarcane plantations, subsistence maize fields, grazing lands, rural villages, and protected parks, making it an ideal natural laboratory for asking how anthropogenic disturbance shapes the invisible ecosystems inside wildlife.</p>
<p>The team used a molecular technique called amplicon sequencing, targeting the V3–V4 region of the 16S ribosomal RNA gene, a genetic marker widely used to identify bacteria. After extracting DNA from fecal samples preserved with silica gel, the researchers amplified the bacterial marker, sequenced the products on an Illumina MiSeq platform, and processed the reads through the DADA2 pipeline, which identifies distinct amplicon sequence variants, or ASVs, the finest practical resolution of bacterial identity. Rigorous contamination controls, including extraction blanks, PCR blanks, and the requirement that a bacterial variant appear in at least two of three PCR replicates before being counted, ensured the results reflected genuine biology rather than laboratory artifacts.</p>
<p>The scale of bacterial diversity they uncovered was impressive. Across the 109 bats, the team identified 2,249 unique bacterial ASVs, and a statistical technique called rarefaction, which plots species accumulation against sampling effort, showed the curves reaching a clear asymptote. The Chao1 estimator, a method for extrapolating total richness from observed data, suggested the true diversity was between 2,250 and 2,253 species, meaning the researchers had captured essentially the complete bacterial inventory of this species&#8217; gut in the region. Individual bats carried anywhere from 3 to 185 ASVs, with a mean of 47, and phylogenetic diversity, measured with Faith&#8217;s index, ranged from 0.6 to 24.1.</p>
<p>Perhaps the most striking pattern was the extraordinary individuality of each bat&#8217;s microbiome. Fully 72 percent of the identified bacterial variants, some 1,622 of them, were found in only a single bat, and fewer than 1 percent appeared in more than a quarter of the animals sampled. The most common single variant, an unknown species of Mycoplasma, was still detected in only 66 percent of bats. The dominant phyla across the population were Proteobacteria and Firmicutes, present in every individual, followed by Actinobacteria in 84 percent and Bacteroidota in just over half. The researchers suggest this high individual variability likely reflects the bat&#8217;s generalist insectivorous diet: previous molecular diet studies have shown that Mops pumilus feeds on a wide and individually variable array of insect prey, and since diet is a major driver of gut microbial composition, no two bats end up with quite the same internal community.</p>
<p>Then came the pathogen findings. Screening the ASV table against a list of bacterial genera known to be potentially zoonotic and frequently found in bats, the team detected five: Mycoplasma, Rickettsia, Salmonella, Bartonella, and Campylobacter. Four of these occurred at remarkably high prevalence. Mycoplasma topped the list at 88 percent of individuals, present at all but two of the 17 roosts surveyed in the landscape analysis. Rickettsia was found in 36 percent of bats, Salmonella in 34 percent, and Bartonella in 23 percent, while Campylobacter appeared in just 4 percent. Co-occurrence was common: 27 bats carried two of these genera simultaneously, 23 carried three, seven carried four, and one individual harbored all five.</p>
<p>Crucially, none of the bats showed signs of illness. The researchers found no correlation between bacterial richness or phylogenetic diversity and body condition, calculated as mass divided by forearm length, a standard health proxy in bats. This absence of disease, combined with the sheer prevalence of the bacteria, suggests the animals are likely asymptomatic carriers, or that the detected DNA originated in their insect prey rather than establishing infection in the bats themselves. Rickettsia in particular is a common insect endosymbiont, and its presence in feces could simply reflect a recent meal of infected insects or ticks groomed off the fur. Salmonella, by contrast, is usually reported in bats at prevalences below 12 percent, making the 34 percent figure here notably high, and raising questions about environmental reservoirs such as contaminated water, which has been implicated in other studies.</p>
<p>The central hypothesis of the study, however, was largely not borne out. Drawing on prior work showing that habitat degradation can reduce gut microbial diversity in primates, rodents, and other bats, the researchers expected that anthropogenic land covers and fragmentation would diminish bacterial richness and shift community composition. They classified the landscape from Landsat 8 satellite imagery into savanna, sugarcane, rural settlement, and water, then calculated composition metrics and configuration metrics such as savanna edge density and a fragmentation index at both a fine scale around roosts and a landscape scale matching the bats&#8217; nightly foraging ranges, which can exceed four kilometers. Using generalized linear mixed models and distance-based redundancy analysis, they found no association between any land cover variable and bacterial richness, phylogenetic diversity, or the prevalence of potentially pathogenic genera. Land cover explained only a small fraction, about 6.7 percent, of the variation in community composition, with fine-scale rural and savanna cover and landscape-scale sugarcane cover and savanna splitting emerging as statistically significant but weak predictors.</p>
<p>The authors interpret this muted response as a reflection of the species&#8217; ecological flexibility. Unlike bats that avoid disturbed habitats, Mops pumilus actively uses and even prefers agricultural landscapes, roosting in buildings and feeding over irrigated monocultures where water and insect prey remain available year-round. Because its activity and foraging are not negatively affected by human land use, its gut microbiome may be similarly buffered. The researchers also point to factors their sampling design could not fully disentangle, including social transmission of microbes within roosts, local environmental microbial communities, and roost characteristics, any of which might outweigh landscape composition in shaping these internal ecosystems. Seasonal effects, too, remain untested, although the species neither migrates nor hibernates, which may dampen the seasonal microbiome shifts documented in other bat species.</p>
<p>The findings carry real weight for the One Health framework, the principle that human, animal, and environmental health are interconnected. Bats are already recognized as reservoirs of numerous viruses, and bacterial genera such as Bartonella and Mycoplasma have documented links to human disease, including Bartonella mayotimonensis carried by Myotis bats in northern Europe and Mycoplasma haemohominis carried by flying foxes in New Caledonia. While there is currently no evidence that the bacteria detected in Eswatini cause illness in the bats or can infect people, Mycoplasma species are considered emerging pathogens that have caused mortality in other wildlife, and the authors argue that continued surveillance of this abundant, human-associated bat species is warranted. As savannas across southern Africa continue to convert to agriculture, understanding which species tolerate, and which are quietly transformed by, the changing landscape will be essential for conserving both the bats and the health of the systems they inhabit.</p>
<p><strong>Subject of Research:</strong> Gut microbiome diversity and potentially pathogenic bacteria in the little free-tailed bat (Mops pumilus) in relation to land cover change in Eswatini</p>
<p><strong>Article Title:</strong> Gut microbiomes of the little free-tailed bat (Mops pumilus) show high prevalence of potential bacterial pathogens but limited responses to land cover</p>
<p><strong>Article References:</strong> Shapiro, J. T., Barnes, C., Nielsen, I. B., Rasmussen, L., Monadjem, A., McCleery, R. A., &amp; Hansen, A. J. (2026). Gut microbiomes of the little free-tailed bat ( Mops pumilus ) show high prevalence of potential bacterial pathogens but limited responses to land cover. <em>Web Ecology, 26</em>(2), 223-242. <a href="https://doi.org/10.5194/we-26-223-2026" rel="noopener noreferrer">https://doi.org/10.5194/we-26-223-2026</a></p>
<p><strong>Image Credits:</strong> AI Generated</p>
<p><strong>DOI:</strong> <a href="https://doi.org/10.5194/we-26-223-2026" rel="noopener noreferrer">10.5194/we-26-223-2026</a></p>
<p><strong>Keywords:</strong> gut microbiome, bats, Mops pumilus, 16S rRNA sequencing, bacterial pathogens, Mycoplasma, Salmonella, land cover change, Eswatini, One Health, wildlife disease, savanna</p>
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		<post-id xmlns="com-wordpress:feed-additions:1">247126</post-id>	</item>
		<item>
		<title>Past Chytrid Infection Leaves Harlequin Toads More Vulnerable, Not Resistant, to Re-infection</title>
		<link>https://scienmag.com/past-chytrid-infection-leaves-harlequin-toads-more-vulnerable-not-resistant-to-re-infection/</link>
		
		<dc:creator><![CDATA[Kristina Jarvis]]></dc:creator>
		<pubDate>Sun, 04 Oct 2026 20:05:39 +0000</pubDate>
				<category><![CDATA[Biology]]></category>
		<category><![CDATA[amphibian conservation]]></category>
		<category><![CDATA[amphibian disease management strategies]]></category>
		<category><![CDATA[amphibian immune gene expression profiling]]></category>
		<category><![CDATA[amphibian skin microbiome and disease resistance]]></category>
		<category><![CDATA[antifungal treatments in amphibian conservation]]></category>
		<category><![CDATA[Atelopus glyphus]]></category>
		<category><![CDATA[Batrachochytrium dendrobatidis]]></category>
		<category><![CDATA[Batrachochytrium dendrobatidis immune response]]></category>
		<category><![CDATA[BMC Genomics]]></category>
		<category><![CDATA[Chytrid fungus re-infection in amphibians]]></category>
		<category><![CDATA[chytridiomycosis]]></category>
		<category><![CDATA[effects of prior Bd infection on amphibian vulnerability]]></category>
		<category><![CDATA[harlequin toads]]></category>
		<category><![CDATA[immune gene expression]]></category>
		<category><![CDATA[immune memory and pathogen]]></category>
		<category><![CDATA[immunosuppression]]></category>
		<category><![CDATA[impact of chytridiomycosis on amphibian extinction]]></category>
		<category><![CDATA[itraconazole]]></category>
		<category><![CDATA[Pirre harlequin toad conservation]]></category>
		<category><![CDATA[re-infection]]></category>
		<category><![CDATA[re-infection susceptibility in critically endangered toads]]></category>
		<category><![CDATA[skin microbiome]]></category>
		<category><![CDATA[wildlife disease]]></category>
		<guid isPermaLink="false">https://scienmag.com/?p=235590</guid>

					<description><![CDATA[A new study shows that prior infection with the chytrid fungus Bd leaves critically endangered harlequin toads immunosuppressed and more likely to die upon re-infection.]]></description>
										<content:encoded><![CDATA[<p>A devastating fungal pathogen has driven hundreds of amphibian species toward extinction over the past few decades, and conservationists have long hoped that surviving an infection might confer some measure of protection against future encounters. A new study of the critically endangered Pirre harlequin toad, Atelopus glyphus, delivers a sobering counterexample. Researchers found that toads previously infected with the chytrid fungus Batrachochytrium dendrobatidis, commonly known as Bd, and then cleared of the infection with antifungal treatment fared significantly worse when re-exposed to the pathogen than animals facing it for the first time. The work, published in BMC Genomics, combined infection experiments, immune gene expression profiling, and skin microbiome sequencing to reveal why prior infection failed to protect this highly susceptible species.</p>
<p>The experimental design was unusually thorough for a wildlife disease study. The team, led by Brian Gratwicke of the Smithsonian&#8217;s National Zoo and Conservation Biology Institute and Owen Osborne of Bangor University, divided toads into five treatment groups. One group of twenty animals was infected with Bd, then cleared using itraconazole, a standard antifungal used in amphibian rescue programs, and then infected again. A second group of twenty received a mock infection, underwent the same itraconazole treatment, and was then exposed to Bd for the first time. Two smaller groups of ten animals each served as controls that experienced infection or mock infection without re-exposure, and a final group of ten remained untreated throughout. This structure allowed the researchers to disentangle the effects of prior infection, antifungal treatment, and re-infection on survival, pathogen load, immune gene expression, and the communities of bacteria and fungi living on the skin.</p>
<p>The survival results were unambiguous and troubling. Toads that had been previously infected and cleared developed detectable Bd infections faster and died sooner after re-infection than naïve animals that had never encountered the fungus. In other words, the infection-clearance-infection protocol, which mirrors the approach used in some captive breeding and reintroduction programs, did not improve survival. It actively worsened outcomes. This finding stands in sharp contrast to earlier studies in other amphibian species, in which surviving a Bd infection and being cleared of it sometimes produced acquired resistance or reduced susceptibility upon re-exposure. For Atelopus glyphus, one of the most Bd-susceptible species known, no such protective effect emerged.</p>
<p>To understand the mechanism behind this heightened vulnerability, the researchers turned to transcriptomics, sequencing RNA from the toads&#8217; skin to measure the activity of immune-related genes. Their analysis revealed that even after Bd had been cleared from previously infected animals, the fungus left a lasting imprint on the immune system. Animals in the Bd-mock group, which had been infected and cleared but never re-exposed, showed downregulation of immune genes that normally respond to Bd compared with animals that were re-infected. This sustained immunosuppression, the authors suggest, likely reduced the effectiveness of the immune response when the pathogen returned, explaining the accelerated infection dynamics and earlier mortality in the previously infected group.</p>
<p>When the researchers examined what happened upon re-infection in more detail, they found that as fungal loads climbed, Bd itself became the dominant force shaping both immune gene expression and bacterial community composition, regardless of whether an animal had prior infection history. Previously infected animals did not mount any novel immune response upon re-exposure. Instead, their gene expression patterns resembled those of naïve infected animals, only more pronounced. This suggests that the initial infection produced no long-lasting immunological memory that could be mobilized against the pathogen a second time, and that the immune system was simply responding more intensely to a heavier fungal burden.</p>
<p>The skin microbiome added another layer to the story. Prior infection and itraconazole treatment shifted the toads&#8217; bacterial and fungal skin communities into a new state, one enriched in bacteria that are putatively capable of inhibiting Bd. On its face, this might seem like a beneficial change, a kind of microbial vaccination induced by the pathogen itself. Yet the enriched anti-Bd bacteria clearly did not translate into protection, since previously infected animals died faster. The researchers noted that observed differences in bacterial communities were closely tied to host immune gene expression, indicating that the skin microbiome and the immune system are tightly coupled, and that microbial shifts alone cannot compensate for a compromised immune response.</p>
<p>Intriguingly, the fungal component of the skin microbiome told a different story. While the initial infection and treatment period reshaped fungal communities, those communities did not shift again in response to re-infection. The authors concluded that the fungal community changes were most likely a side effect of itraconazole treatment rather than a host- or pathogen-driven response, a reminder that antifungal therapy itself can perturb the delicate microbial ecosystems on amphibian skin. This has practical implications for rescue programs that routinely use itraconazole to clear infections before releasing animals back into the wild.</p>
<p>The broader significance of the study lies in its demonstration that disease outcomes following pathogen clearance are species-specific and cannot be generalized across amphibian diversity. Bd has caused the steepest disease-driven biodiversity loss ever recorded, and harlequin toads of the genus Atelopus have been among its most catastrophic victims, with many Central and South American species vanishing or collapsing to remnant populations. Captive assurance colonies, such as those maintained by the Panama Amphibian Rescue and Conservation Project, a collaboration involving the Smithsonian Tropical Research Institute, Zoo New England, the Cheyenne Mountain Zoo and other partners, represent a lifeline for these species. The new results suggest that simply clearing Bd from captive animals before release may not only fail to protect them but could actively sensitize them to the pathogen awaiting them in their native streams.</p>
<p>For conservation practitioners, the message is that reintroduction strategies must account for the immunological legacy of prior infection. The integrative approach used here, pairing survival data with gene expression and microbiome sequencing, offers a template for evaluating whether any intervention intended to reduce susceptibility actually works before animals are committed to the wild. The researchers emphasize that strategies to improve survival of wildlife impacted by emerging infectious disease remain urgently needed for species of conservation concern, but that such strategies must be tested rigorously in the species they are meant to help. In the case of Atelopus glyphus, the hope that infection history could serve as a shield has been replaced by a more nuanced and challenging reality: for some of the world&#8217;s most endangered amphibians, the scars left by chytrid fungus run deeper than the infection itself.</p>
<p><strong>Subject of Research:</strong> Effects of prior Batrachochytrium dendrobatidis infection on immunity, skin microbiome and re-infection mortality in harlequin toads</p>
<p><strong>Article Title:</strong> Prior infection of harlequin toads by Batrachochytrium dendrobatidis alters their immune-microbial state and increases mortality upon re-infection</p>
<p><strong>Article References:</strong> Gratwicke, B., Osborne, O. G., Hartmann, A., Ávila, N., Baitchman, E., Togna, G. D., Figueroa, Y., Guerrel, J., Illueca, E., Linhoff, L., Madison, J. D., Ellison, A., Grayfer, L., Ibáñez, R., &amp; Muletz-Wolz, C. R. (2026). Prior infection of harlequin toads by Batrachochytrium dendrobatidis alters their immune-microbial state and increases mortality upon re-infection. <em>BMC Genomics</em>. <a href="https://doi.org/10.1186/s12864-026-13310-9" rel="noopener noreferrer">https://doi.org/10.1186/s12864-026-13310-9</a></p>
<p><strong>Image Credits:</strong> AI Generated</p>
<p><strong>DOI:</strong> <a href="https://doi.org/10.1186/s12864-026-13310-9" rel="noopener noreferrer">10.1186/s12864-026-13310-9</a></p>
<p><strong>Keywords:</strong> Batrachochytrium dendrobatidis, harlequin toads, Atelopus glyphus, chytridiomycosis, amphibian conservation, immune gene expression, skin microbiome, itraconazole, re-infection, immunosuppression, wildlife disease, BMC Genomics</p>
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		<post-id xmlns="com-wordpress:feed-additions:1">235590</post-id>	</item>
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