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D. E. Green

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

24 records · Page 2Linked to original sources
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↗
USGS1991

Subchronic hepatotoxicity of selenomethionine ingestion in mallard ducks

Twoyearold male mallards (Anas platyrhynchos) received a control diet (0.2 ppm Se) or diets containing 1, 2, 4, 8, 16, or 32 ppm Se as selenomethionine for 14 wk. Se accumulated readily in the liver in a dosedependent manner, reaching a mean concentration of 29 ppm (wet weight) in the 32 ppm group. Dietary Se of 2 ppm or greater increased plasma glutathione peroxidase activity. Mortality (10%) and histopathological effects, including bile duct hyperplasia and hemosiderin pigmentation of the liver and spleen, occurred in the 32 ppm group. These histopathological effects were accompanied by lower hemoglobin concentrations (16 and 32 ppm groups) and hematocrit (32 ppm group), and elevated plasma alkaline phosphatase activity (32 ppm group) indicative of cholestatic liver inJury. Other manifestations of hepatotoxicity included significant linear dose responses for hepatic oxidized glutathione (GSSG) concentrations and ratio of GSSG to reduced glutathione (GSH). Means for both of these responses differed from controls in groups receiving 832 ppm Se. Mean hepatic GSH and malondialdehyde (a measure of lipid peroxidation) concentrations were significantly elevated in the 16 and 32 ppm groups. Subchronic effects of selenomethionine, which occurs in vegetation, are of particular interest with respect to the health of wild aquatic birds in seleniferous locations.

Journal of Toxicology and Environmental Health↗