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D. E. Green

Publications and source records attributed to D. E. Green.

At least 19 recordsLinked to original sources
USGS2008

Widespread occurrence of the amphibian chytrid fungus Batrachochytrium dendrobatidis in the southeastern USA

From 1999 to 2006, we sampled >1200 amphibians for the fungal pathogen Batrachochytnum dendrobatidis (Bd) at 30 sites in the southeastern USA. Using histological techniques or PCR assays, we detected chytrid infection in 10 species of aquatic-breeding amphibians in 6 states. The prevalence of chytrid infection was 17.8% for samples of postmetamorphic amphibians examined using skin swab-PCR assays (n = 202 samples from 12 species at 4 sites). In this subset of samples, anurans had a much higher prevalence of infection than caudates (39.2% vs. 5.5%, respectively). Mean prevalence in ranid frogs was 40.7 %. The only infected salamanders were Notophthalmus viridescens at 3 sites. We found infected amphibians from late winter through late spring and in 1 autumn sample. Although we encountered moribund or dead amphibians at 9 sites, most mortality events were not attributed to Bd. Chytridiomycosis was established as the probable cause of illness or death in fewer than 10 individuals. Our observations suggest a pattern of widespread and subclinical infections. However, because most of the sites in our study were visited only once, we cannot dismiss the possibility that chytridiomycosis is adversely affecting some populations. Furthermore, although there is no evidence of chytrid-associated declines in our region, the presence of this pathogen is cause for concern given global climate change and other stressors. Although presence-absence surveys may still be needed for some taxa, such as bufonids, we recommend that future researchers focus on potential population-level effects at sites where Bd is now known to occur. ?? Inter-Research 2008.

Southeast↗
USGS2007

Occurrence of the amphibian pathogen Batrachochytrium dendrobatidis in Pacific Northwestern USA

Chytridiomycosis (infection by the fungus Batrachochytrium dendrobatidis ) has been associated with amphibian declines in at least four continents. We report results of disease screens from 210 pond-breeding amphibians from 37 field sites in Oregon and Washington. We detected B. dendrobatidis on 28% of sampled amphibians, and and we found - > 1 detection of B. dendrobatidi s from 43% of sites. Four of seven species tested positive for B. dendrobatidis , including the Northern Red-Legged Frog ( Rana aurora ), Columbia Spotted Frog ( Rana luteiventris ), and Oregon Spotted Frog ( Rana pretiosa ). We also detected B. dendrobatidis in nonnative American Bullfrogs ( Rana catesbeiana ) from six sites in western and central Oregon. Our study and other recently published findings suggest that B. dendrobatidis has few geographic and host taxa limitations among North American anurans. Further research on virulence, transmissibility, persistence, and interactions with other stressors is needed to assess the potential impact of B. dendrobatidis on Pacific Northwestern amphibians.

Oregon↗
USGS2007

Raptor mortality due to West Nile virus in the United States, 2002

West Nile virus (WNV) has affected many thousands of birds since it was first detected in North America in 1999, but the overall impact on wild bird populations is unknown. In mid-August 2002, wildlife rehabilitators and local wildlife officials from multiple states began reporting increasing numbers of sick and dying raptors, mostly red-tailed hawks ( Buteo jamaicensis ) and great horned owls ( Bubo virginianus) . Commonly reported clinical signs were nonspecific and included emaciation, lethargy, weakness, inability to perch, fly or stand, and nonresponse to danger. Raptor carcasses from 12 states were received, and diagnostic evaluation of 56 raptors implicated WNV infection in 40 (71%) of these cases. Histologically, nonsuppurative encephalitis and myocarditis were the salient lesions (79% and 61%, respectively). Other causes of death included lead poisoning, trauma, aspergillosis, and Salmonella spp. and Clostridium spp. infections. The reason(s) for the reported increase in raptor mortality due to WNV in 2002 compared with the previous WNV seasons is unclear, and a better understanding of the epizootiology and pathogenesis of the virus in raptor populations is needed.

Journal of Wildlife Diseases↗
USGS2006

Chlorfenapyr and mallard ducks: Overview, study design, macroscopic effects, and analytical chemistry

The first commercial pesticide derived from a class of compounds known as halogenated pyrroles was registered for use in the United States in 2001. Chlorfenapyr degrades slowly in soil, sediment, and water and is highly toxic to birds. Information on biochemical or histological endpoints in birds is lacking; therefore, a two‐year study was conducted to provide information needed to develop diagnostic criteria for chlorfenapyr toxicosis. In the first year, male mallard ducks were fed concentrations of 0, 2, 5, or 10 ppm technical chlorfenapyr or 5 ppm of a formulated product in their diet during a 10‐week chronic exposure study. Survival, body weight, feed consumption (removal), behavior, and molt progression were monitored. Feed and liver were analyzed for chlorfenapyr and two metabolites. Five of 10 ducks in the 10‐ppm group died, and neurotoxic effects were observed in the 5‐and 10‐ppm groups. Feed removal increased for ducks receiving chlorfenapyr and body weights of 5‐ and 10‐ppm ducks were reduced. Loss of body fat, muscle atrophy, and bile retention were suggestive of metabolic disruption or a decreased ability to digest and absorb nutrients. Liver and kidney weights and liver and kidney weight/body weight ratios exhibited a positive response to concentrations of chlorfenapyr in the diet. Emaciation and elevated organ weight/body weight ratios are candidates for a suite of indicators of chronic chlorfenapyr exposure. Liver is the preferred tissue for chemical confirmation of exposure.

Environmental Toxicology and Chemistry↗
USGS2005

Health evaluation of amphibians in and near Rocky Mountain National Park (Colorado, USA)

We conducted a health survey of amphibians in and adjacent to Rocky Mountain National Park (RMNP) to document current disease presence inside RMNP and identify disease outside RMNP with the potential to spread to the Park's amphibians. Amphibians from five sites within RMNP and seven sites within 60 km of Park boundaries were collected and examined. Necropsies (n - 238), virus isolation, bacterial and fungal cultures, and histological examinations were carried out on amphibian egg masses (outside RMNP/within RMNP: 26/22), larvae (30/42), imagos (recently metamorphosed individuals) (0/3) and adults (61/67) of five species. Marked infections by a pathogenic chytrid fungus (chyridiomycosis), Batrachochytrium dendrobatidis, were detected in three species (Bufo boreas, Pseudacris maculata and Rana sylvatica) from three of five sites within RMNP and in one of three species (P. maculata) from three sites outside RMNP. Of the fully metamorphosed individuals tested (B. boreas, P. maculata and R. sylvatica), chytridiomycosis was found in 60 % (n = 3), 46 % (n = 37) and 54 % (n = 7), respectively. Chytridiomycosis was the principal lethal pathogenic infectious disease detected in three amphibian species within or adjacent to RMNP. Higher fungi were isolated from the cloaca and skin of all five amphibian species. Watermolds (Oomycetes) were isolated from amphibian eggs or skin of all five species. No evidence of Ranavirus was found in cultures and histological examinations of 176 and 142 amphibians, respectively. Fifteen genera of bacteria were identified in larval and just metamorphosed amphibians, and a potentially pathogenic lungworm, Rhabdias sp, was identified in 61.1 % (n = 11) of B. woodhousii outside RMNP, but in only 2 (15.4 %) R. sylvatica within the Park.

Colorado↗
USGS2005

Diseases of frogs and toads

This chapter presents information on infectious diseases of free-living frogs and toads that have completed metamorphosis. The diseases discussed in this chapter pertain principally to sub-adult and adult frogs and toads that are at least 60-90 days removed from completion of metamorphosis. The main emphasis of this chapter is the diseases found in amphibians of Canada and the United States. Diseases of recent metamorphs, larvae and amphibian eggs are presented in the chapters Diseases of Amphibian Eggs and Embryos and Diseases of Tadpoles. The smallest disease agents (viruses and bacteria) are presented first, followed by fungi, protozoa, helminths and ectoparasites. Diseases presented in this chapter are Ranaviral (iridovirus) infection Lucke frog herpesvirus (kidney cancer) Frog erythrocytic virus West Nile virus Red-leg disease (bacterial septicemia) Salmonellosis Chytrid fungal infection Basidiobolus fungi Dermosporidiosis Ichthyophoniasis Dermocystidium & Dermomycoides Myxozoa Ribeiroia flukes and Amphibian malformations Clinostomum metacercaria Aspects of each disease are presented to assist the biologist with recognition of diseases in the field. Hence, the major emphases for identification of diseases are the epizootiological aspects (host species, life stage, casualty numbers, etc) and gross findings ('lesions'). Descriptions of the microscopical, ultrastructural and cultural characteristics of each infectious agent were considered beyond the scope of this text. Detailed cultural and microscopical features of these disease agents are available in other reviews (Taylor et al., 2001; Green, 2001). Some diseases, while common in captive and zoo amphibians, are exceptionally rare in free-living frogs and toads, and therefore are omitted from this review. Among the diseases not presented are infections by chlamydia and mycobacteria, which occur principally in captive colonies of African clawed frogs (Xenopus, Hymenochirus, et al.) and northern leopard frogs (Rana pipiens). Other interesting diseases could have been presented, such as a wart-like virus infection of Japanese newts and a group of protistan parasites, referred to as Dermocystidium and Dermomycoides, in European frogs and toads. The reader is referred to Green (2001) for a review of these diseases. Amphibians have a rich diversity of helminthic parasites (Poynton and Whitaker, 2001). In general, most cestodes, trematodes and nematodes of amphibians are innocuous and not linked to specific clinical signs ('symptoms') or mortalities. An important major exception to this generalization is the trematode, Ribeiroia, which has been linked to numerous and bizarre malformations of frogs, toads and salamanders (Johnson et al., 1999, Johnson et al., 2001, Schotthoefer et al., 2003). Two genera of trematodal parasites are discussed in this chapter: Ribeiroia because they cause malformations and Clinostomum because they are large and produce visible lumps in the skin. For a review of amphibian helminths, the reader is referred to the text by Flynn (1973).

Book chapter↗
USGS2005

Diseases of amphibian eggs and embryos

Amphibians generally are prolific egg producers. In tropical and semi-tropical regions, deposition of eggs may occur year-round or may coincide with rainy seasons, while in temperate regions, deposition of eggs usually occurs immediately after emergence from hibernation. Numbers of eggs produced by each species may vary from a few dozen to thousands. Accordingly, some eggs may be infertile and wastage of embryos is to be expected. Fertility, viability and decomposition of eggs and embryos must be considered before it is assumed that diseases are present. An important consideration in the evaluation of egg masses is the fact that some will contain infertile and non-viable eggs. These infertile and nonviable eggs will undergo decomposition and they may appear similar to eggs that are infected by a pathogen. Evaluation of egg masses and embryos for the presence of disease may require repeated observations in a given breeding season as well as continued monitoring of egg masses during their growth and development and over successive breeding seasons. Amphibian eggs rarely are subjected to a comprehensive health (diagnostic) examination; hence, there is scant literature on the diseases of this life stage. Indeed, the eggs of some North American amphibians have yet to be described. Much basic physiology and normal biomedical baseline data on amphibian eggs is lacking. For example, it is known that the aquatic eggs of some species of shrimp quickly are coated by a protective and commensal bacterium that effectively impedes invasion of the eggs by other environmental organisms and potential pathogens. In the absence of this bacterium, shrimp eggs are rapidly killed by other bacteria and fungi (Green, 2001). The possibility that amphibian eggs also have important symbiotic or commensal bacteria needs to be investigated. Furthermore, the quantity and types of chemicals in the normal gelatinous capsules of amphibian eggs have scarcely been examined. Abnormalities of the female oviduct, either due to infectious disease, nutritional status, hormonal imbalances, or sublethal intoxications, could affect the quality of secreted gelatinous capsules on eggs, thus rendering an egg mass susceptible to other stressors. Diseases of amphibian eggs and embryos presented in this chapter are Lucke frog herpesvirus Ranavirus (iridovirus) infection Bacteria Watermold infection (saprolegniasis) Algae Microsporidia

Book chapter↗
USGS2003

Chytridiomycosis in wild frogs from southern Costa Rica

In 1993, the amphibian fauna of Las Tablas, Costa Rica , began to decline, and by 1998 approximately 50% of the species formerly present could no longer be found. Three years later, at the Reserva Forestal Fortuna, in western Panama, a site approximately 75 km east southeast of Las Tablas, KRL encountered a mass die-off of amphibians and a subsequent decline in abundance and species richness. The epidemiological features of the anuran population declines and die-offs at both sites were similar, suggesting a similar cause. Herein we document the presence of the fungus, Batrachochytrium dendrobatidis, in dead and dying wild frogs collected at Las Tablas just prior to population declines of several anuran species.

Journal of Herpetology↗
USGS2003

Pseudacris triseriata (western chorus frog) and Rana sylvatica (wood frog) chytridiomycosis

The chytrid fungus Batrachochytrium dendrobatidis is a known pathogen of anuran amphibians, and has been correlated with amphibian die-offs worldwide (Daszak et. al. 1999. Emerging Infectious Diseases 5:735-748). In Colorado, B. dendrobatidis has infected Boreal toads (Bufo boreas) (Muths et. al., in review) and has been identified on museum specimens of northern leopard frogs (Rana pipiens) (Carey et. al. 1999. Develop. Comp. Immunol. 23:459-472). We report the first verified case of chytrid fungus in chorus frogs (Pseudacris triseriata) and wood frogs (Rana sylvatica) in the United States. We collected seven P. triseriata, and two adult and two juvenile R. sylvatica in the Kawuneeche Valley in Rocky Mountain National Park (RMNP) during June 2001. These animals were submitted to the National Wildlife Health Center (NWHC) as part of an amphibian health evaluation in RMNP. Chorus frogs were shipped in one container. Wood frog adults and juveniles were shipped in two separate containers. Histological examinations of all chorus frogs and 3 of 4 wood frogs were positive for chytrid fungus infection. The fourth (adult) wood frog was too decomposed for meaningful histology. Histological findings consisted of multifocally mild to diffusely severe infections of the epidermis of the ventrum and hindlimb digital skin. Chytrid thalli were confined to the thickened epidermis (hyperkeratosis), were spherical to oval, and occasional thalli contained characteristic discharge pores or zoospores (Green and Kagarise Sherman 1999. J. Herpetol 35:92-103; Fellers et al. 2001. Copeia 2001:945-953). We cannot confirm that all specimens carried the fungus at collection, because infection may have spread from one individual to all other individuals in each container during transport. Further sampling of amphibians in Kawuneeche Valley is warranted to determine the rate of infection and mortality in these populations.

Colorado↗
USGS2003

Hyla gratiosa (barking treefrog) intestinal hernia

Deformities and malformations in anurans occur in a variety of manifestations (Meteyer 2000. Field Guide to Malformations of Frogs and Toads with Radiographic Interpretations. Biol. Sci. Rep., USGS/BRD/BSR-2000-0005, 18 pp.). Most of those described in the literature are visible externally (e.g., ectromelia, brachydactyly, polydactyly, brachygnathia, kyphosis) (Ouellet et al. 1997. J. Wildlife Dis. 33:95-104). Internal malformations are less well known and seldom reported (Reeder et al. 1998. Environ. Health Persp. 106:261-266). Here we describe an unusual condition heretofore unreported for a hylid frog.

North Carolina↗
USGS2003

Investigation of frog abnormalities on national wildlife refuges in the Northeast U.S.

To address concerns about frog abnormalities, the U.S. Fish and Wildlife Service examined over 3,643 frogs and toads on National Wildlife Refuges (NWRs) in the Northeast U.S. The objectives were to: 1) determine if certain refuges had sites where abnormalities were frequently observed; 2) evaluate if the prevalence of abnormalities at a site was consistent within a season and among years; and 3) investigate possible causes. Sampling was conducted from 1999 through 2001. A complete sample from a site consisted of ???50 metamorphs of one species. The prevalence of abnormalities ranged from 0 to 15% and fluctuated within season and among years. The most common external abnormalities were truncated limbs, and missing limbs, feet, and digits. Frogs with duplication of limb segments were rare (6). Based on radiographical examinations of 89 abnormal frogs, 55 had abnormalities due to trauma, 22 due to malformations, and 12 could not be classified. Metacercariae of the trematode Ribeiroia were detected in substantial numbers in two species from Iroquois NWR, with one specimen having supernumerary hindlimbs. We recommend continued sampling and integrated, causal evaluations on NWRs where the prevalence of abnormalities exceeds 5% or where the types of abnormalities warrant further study.

Conference Paper↗
USGS2002

Epizootiology of sixty-four amphibian morbidity and mortality events in the USA, 1996-2001

A total of 44 amphibian mortality events and 20 morbidity events were reviewed retrospectively. The most common cause of amphibian mortality events was infection by ranaviruses (Family: Iridoviridae). Ranavirus epizootics have abrupt onset and affect late-stage larvae and recent metamorphs. Mortality events due to ranavirus infections affected only widespread and abundant amphibian species, and there was a clear association with high population densities. Chytrid fungal infections accounted for seven mortality events in postmetamorphic anurans only. Chytrid epizootics are insidious and easily overlooked in the field. While both ranavirus and chytrid fungal epizootics were associated with >90% mortality rates at affected sites, only the chytrid fungal infections were linked to multiple amphibian population declines. Three primitive fungal organisms in the newly erected clade, Mesomycetozoa, caused morbidities and mortalities in anurans and salamanders.

Conference Paper↗
USGS2001

Oral chytridiomycosis in the mountain yellow-legged frog (Rana muscosa)

The chytrid fungus Batrachochytrium dendrobatidis was originally reported in wild frog populations in Panama and Australia, and from captive frogs in the U.S. National Zoological Park (Washington, DC). This recently described fungus affects the keratinized epidermis of amphibians and has been implicated as a causative factor in the declines of frog populations. We report here the presence of B. dendrobatidis in larval and recently metamorphosed mountain yellow-legged frogs ( Rana muscosa ) in or near the Sierra Nevada Mountains of California, an area where declines have been documented in all five species of native anurans. Forty-one percent (158 of 387) of larval R. muscosa examined in the field with a hand lens and 18% (14 of 79) of preserved larvae had abnormalities of the oral disc. Twenty-eight larvae were collected from 10 sites where tadpoles had been observed with missing or abnormally keratinized mouthparts, and 24 of these were examined for infection. Sixty-seven percent (16 of 24) of these tadpoles were infected with B. dendrobatidis. Batrachochytrium dendrobatidis was cultured from both tadpoles and recent metamorphs from one of these sites. Tadpoles with mouthpart abnormalities or confirmed chytrid fungus infections were collected at 23 sites spanning a distance of > 440 km and an elevational range from 1658-3550 m. Life-history traits of R. muscosa may make this species particularly susceptible to infection by Batrachochytrium . We recommend that biologists examine tadpoles for oral disc abnormalities as a preliminary indication of chytridiomycosis. Further, we believe that biologists should take precautions to prevent spreading this and other amphibian diseases from one site to another.

California↗
USGS1999

Cutaneous mastocytomas in the neotenic caudate amphibians Ambystoma mexicanum (axolotl) and Ambystoma tigrinum (tiger salamander)

Spontaneous mastocytomas studied in 18 axolotls ( Ambystoma mexicanum ) and six tiger salamanders ( Ambystoma tigrinum ) were gray-white, uni- to multilobular cutaneous protrusions from 2 mm to 2 cm in diameter. Tumors were moderately cellular unencapsulated masses that usually infiltrated the dermis and hypodermis with the destruction of intervening tissues. Some tumors were invading superficial bundles of the underlying skeletal muscle. Tumors consisted of mitotically active cells derived from a single lineage but showing a range of differentiation. Immature cells had nearly smooth to lightly cleft or folded basophilic nuclei bordered by a band of cytoplasm with few cytoplasmic processes and containing a few small uniform eccentric granules. Mature cells had basophilic nuclei with deep clefts or folds and abundant eosinophilic cytoplasm with multiple long intertwining cytoplasmic extensions packed with metachromatic granules. The axolotls were old individuals from an inbred laboratory colony. The tiger salamanders were wild animals from a single polluted pond. They could have been old and inbred. Both groups were neotenic. These are the first mastocytomas discovered in cold-blooded animals.

Texas↗
USGS1997

Diagnostic criteria for selenium toxicosis in aquatic birds: Histologic lesions

Chronic selenium toxicosis was induced in 1-yr-old male mallard ducks ( Anas platyrhynchos ) by feeding selenium, as seleno-DL-methionine, in amounts of 0, 10, 20, 40, and 80 parts per million (ppm) to five groups of 21 ducks each for 16 wk during March to July 1988. All mallards in the 80 ppm group, three in the 40 ppm group, and one in the 20 ppm group died. Histologic lesions in mallards that died of selenosis were hepatocellular vacuolar degeneration progressing to centrolobular and panlobular necrosis, nephrosis, apoptosis of pancreatic exocrine cells, hypermaturity and avascularity of contour feathers of the head with atrophy of feather follicles, lymphocytic necrosis and atrophy of lymphoid organs (spleen, gut-associated lymphoid tissue, and lumbar lymph nodes), and severe atrophy and degeneration of fat. Histologic lesions in surviving mallards in the 40 ppm group, which had tissue residues of selenium comparable to mallards that died, were fewer and much milder than mallards that died; lesions consisted of atrophy of lymphoid tissue, hyalinogranular swelling of hepatoeytes, atrophy of seminiferous tubules, and senescence of feathers. No significant histologic lesions were detected in euthanized mallards in the 0, 10 and 20 ppm groups. Based on tissue residues and histologic findings, primarily in the liver, there was a threshold of selenium accumulation above which pathophysiologic changes were rapid and fatal. Pathognomonic histologic lesions of fatal and nonfatal selenosis were not detected. Criteria for diagnosis of fatal selenosis in aquatic birds include consistent histologic lesions in the liver, kidneys, and organs of the immune system. Although histologic changes were present in cases of chronic non-fatal selenosis, these were inconsistent. Consistent features of fatal and non-fatal chronic selenosis were marked weight loss and elevated concentrations of selenium in organs.

Journal of Wildlife Diseases↗
USGS1996

Diagnostic criteria for selenium toxicosis in aquatic birds: dietary exposure, tissue concentrations, and macroscopic effects

A feeding study with mallard ducks ( Anas platyrhynchos ) was conducted during March to July 1988 in Laurel, Maryland (USA), to identify diagnostic criteria for selenium toxicosis in birds. One-year-old male mallards in groups of 21 were fed diets containing 0, 10, 20, 40, or 80 parts per million (ppm) selenium, as seleno-DL-methionine, for 16 weeks. All ducks receiving 80 ppm died. Ducks receiving 40 or 80 ppm selenium consumed less feed than ducks in the other treatment groups. Body weights of ducks receiving 40 or 80 ppm selenium declined during the study. The post-breeding molt was delayed in ducks receiving 40 ppm; most ducks receiving 80 ppm selenium died prior to the onset of molt. At necropsy, numerous abnormalities were observed in ducks that died but only a small number of abnormalities were observed in ducks surviving to the end of the study in the 40 ppm group. Weights of the heart, spleen, and pancreas were mostly lower and weights of the kidney were higher for ducks dying during the study than for euthanized ducks. Liver weights were unaffected. Selenium accumulated in soft tissues approximately in proportion to dietary concentrations. Selenium concentrations in tissues of all ducks that died were different from those of surviving ducks in the 0, 10, and 20 ppm groups, but were not different from those of surviving ducks in the 40 ppm group. Proposed diagnostic criteria for fatal chronic selenosis were derived from body weight, macroscopic abnormalities, organ weights, and concentrations of selenium in the liver. Proposed diagnostic criteria for non-fatal chronic selenosis were derived from body weight, plumage condition, macroscopic abnormalities, concentrations of selenium in the liver, reproductive failure, and alterations of blood and tissue chemistries. Lead or dioxin poisoning have diagnostic criteria most similar to selenium toxicosis.

Journal of Wildlife Diseases↗