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18 recordsLinked to original sources
USGS1956

Histopathology of kidney disease in fish

Kidney disease is one of the most puzzling fish diseases known to exist in the United States. In less than Io years it has invaded the Pacific Northwest, exacting a heavy toll of hatchery salmon. Its first appearance apparently was in Massachusetts where Belding and Merrill' described a disease similar to that now seen on the Pacific Coast. In I946 it was diagnosed in Washington2 and since that time has been observed in an ever increasing number of hatcheries. There are unpublished reports of the same or similar diseases in both California and Washington in the early I93o's.3 The latest outbreaks occurred in the Federal hatcheries at Berlin, New Hampshire, and Cortland, New York, in brook, brown, and rainbow trout.4 There is evidence to indicate that the disease may be much more widely spread in New York State.5 The disease is especially dangerous since little is known of the origin or source of the causative agent. Indeed, the classification of the diplobacillus associated with kidney disease is still uncertain. Thus, with our present knowledge, it is difficult or impossible to eradicate the malady from an infected hatchery. Histopathologic studies were undertaken to clarify the pathology of the disease and to compare the eastern form with the western form.

American Journal of Pathology↗
USGS1956

Ceroid in fish

Since the original description of ceroid in rats, many papers have appeared on the etiology and characteristics of this pigment. It was first seen as a yellow, granular pigment in hematoxylin and eosin sections of the cirrhotic livers of choline deficient rats. The pigment was more fully characterized by Endicott and Lillie, and additional stainging reactions were summarized recently by Lillie. The pigment is sudanophilic in paraffin sections, acid-fast, basophilic, isotropic, iron negative, and highly resistant to solution in water, alcohol, fat solvents, and dilute aqueous acids and alkalis. It is stained by Mallory's hemofuscin stain and Weigert's myelin stain. It reduces osmium tetraoxide and diamine silver carbonate but not ferric ferricyanide. The Gmelin reactions for bile pigments is negative. It has a greenish yellow fluorescence at 3650-3660 Å. It is Schiff positive with or without antecedent diastase digestion after performic or periodic acid oxidation.

The American Journal of Pathology↗
USGS1956

Jaundice and bilirubinemia as manifestations of canine distemper in raccoons and ferrets

1) Two strains of distemper virus have been isolated from wild raccoons and one strain from ferrets. 2) All strains isolated have induced bilirubinemia in raccoons and ferrets. Many raccoons with bilirubinemia also had jaundice. 3) Identification of these strains as members of the canine distemper virus complex has been by clinical and pathological findings consistent with this diagnosis as well as by cross-immunity tests.

American Journal of Veterinary Research↗
USGS1950

Phosphorus poisoning in waterfowl

Black ducks and mallards were found to be highly susceptible to phosphorus poisoning. 3 mg. of white phosphorus per kg. of body weight given in a single dose resulted in death of a black duck in 6 hours. Pathologic changes in both acute and chronic poisoning were studied. Data are presented showing that diagnosis can be made accurately by chemical analysis of stored tissues in cases of phosphorus poisoning.

Journal of the American Pharmaceutical Association↗
USGS2007

Two new species of Myxozoa, Myxobolus inaequus sp. n. and Henneguya theca sp. n. from the brain of a South American knife fish, Eigemannia virescens (V.)

Two new species of Myxozoa from the brain of the green knife fish Eigemannia virescens are described: Myxobolus inaequus sp. n. has an unusually large spore body and extremely unequal polar capsules, and Henneguya theca sp. n. has an attenuated spore encased in a sheath not previously described in other Myxozoa. Only spores of the two species were observed, and infections caused no obvious pathological changes in the brain.

Journal of Protozoology↗
USGS2011

Pathology of tissue loss (white syndrome) in Acropora sp. corals from the Central Pacific

We performed histological examination of 69 samples of Acropora sp. manifesting different types of tissue loss ( Acropora White Syndrome-AWS) from Hawaii, Johnston Atoll and American Samoa between 2002 and 2006. Gross lesions of tissue loss were observed and classified as diffuse acute, diffuse subacute, and focal to multifocal acute to subacute. Corals with acute tissue loss manifested microscopic evidence of necrosis sometimes associated with ciliates, helminths, fungi, algae, sponges, or cyanobacteria whereas those with subacute tissue loss manifested mainly wound repair. Gross lesions of AWS have multiple different changes at the microscopic level some of which involve various microorganisms and metazoa. Elucidating this disease will require, among other things, monitoring lesions over time to determine the pathogenesis of AWS and the potential role of tissue-associated microorganisms in the genesis of tissue loss. Attempts to experimentally induce AWS should include microscopic examination of tissues to ensure that potentially causative microorganisms associated with gross lesion are not overlooked.

Hawai'i↗
USGS2024

Retrospective review of the pathology of American pikas

American pikas ( Ochotona princeps ) are small lagomorphs that live in mountainous talus areas of western North America. Studies on the histopathology of American pikas are limited. We summarize here the clinical histories, and gross and histologic findings of 12 American pikas, including 9 captive (wild-caught) and 3 wild animals. Death was often attributed to stress (transport, handling, anesthesia) with few-to-no premonitory clinical signs. Infection was the cause of death in 2 cases: 1 had bacterial pyogranulomatous dermatitis, cellulitis, and lymphadenitis with sepsis; the other case had oomycete-induced necrotizing colitis. Incidental parasitic infections included sarcocystosis, nematodosis (oxyurids), and ectoparasitism. Most animals with adequate nutritional status had periportal hepatic lipidosis; this finding was absent in all animals with adipose atrophy, and it is possible that periportal hepatic lipidosis is non-pathologic in American pikas. Three cases had myocardial necrosis that was considered the cause of death; the cause of necrosis was not determined, but it may have been caused by stress or vitamin E–selenium deficiency. Esophageal hyperkeratosis was noted in animals with a history of anorexia and negative energy balance; accumulation of esophageal keratin can result from lack of mucosal abrasion by ingesta. Several histologic findings that are likely normal in American pikas include splenic extramedullary hematopoiesis, thymic tissue in adults, and Clostridium sp. in the enteric lumen.

Journal of Veterinary Diagnostic Investigation↗
USGS2013

Pathologic and physiologic effects associated with long-term intracoelomic transmitters in captive Siberian sturgeon

Intracoelomic transmitters are commonly used to evaluate migratory patterns, distribution, and habitat use of many species of fish. Currently, transmitter implantation relies mostly on the assumption that transmitters do not cause any adverse physiological or pathological effects on the animal. To investigate these effects, we surgically implanted 60 Siberian Sturgeon Acipenser baeri with transmitters that weighed less than 2% of their body weight. Postoperative assessments were conducted at 1, 2, 8, 12, 26, and 55 weeks to evaluate surgical healing and transmitter retention. Blood samples were collected before and after the 55-week study for serum cortisol analysis. Overall transmitter loss was 32%. Minor to moderate adhesions were noted at necropsy but did not appear to affect organ function. One fish was noted to have an intraintestinal transmitter at necropsy, but the fish was in overall good health. Long-term transmitter presence does not appear to increase serum cortisol levels or affect overall growth more than nontransmitter fish. Although long-term telemetry studies can be undertaken with minimal concern for negative physiological or pathological effects from transmitters, researchers should be aware that transmitter loss rates may be higher than previously thought. Mechanisms for transmitter loss may include expulsion through the surgical incision, expulsion through the mucocutaneous junction between the large intestine and the vent, or intraintestinal capture and expulsion through the vent. Received February 10, 2013; accepted June 10, 2013

North American Journal of Fisheries Management↗
USGS1986

Acute oral toxicity of sodium cyanide in birds

Sensitivities of six avian species, black vulture ( Coragyps atratus ), American kestrel ( Falco sparverius ), Japanese quail ( Coturnix japonica ), domestic chicken ( Gallus domesticus ), eastern screech-owl ( Otus asio ), and European starling ( Sturnus vulgaris ), to acute poisoning by sodium cyanide (NaCN) were compared by single dose LD50's. Three species, domestic chickens, black vultures, and turkey vultures ( Cathartes aura ), were dosed with NaCN to determine cyanide residues in those that died and also in survivors, in addition to postmortem fate. Three flesh-eating species (black vulture, American kestrel, and eastern screech-owl; LD50's 4.0–8.6 mg/kg) were more sensitive to NaCN than three species (Japanese quail, domestic chicken, and European starling; LD50's 9.4–21 mg/kg) that fed predominantly on plant material. Elevated concentrations of cyanide were found in the blood of birds that died of cyanide poisoning; however, concentrations in birds that died overlapped those in survivors. Blood was superior to liver as the tissue of choice for detecting cyanide exposure. No gross pathological changes related to dosing were observed at necropsy.

Journal of Wildlife Diseases↗
USGS2011

Microanatomy of passerine hard-cornified tissues: Beak and claw structure of the black-capped chickadee (Poecile atricapillus)

The microanatomy of healthy beaks and claws in passerine birds has not been well described in the literature, despite the importance of these structures in avian life. Histological processing of hard‐cornified tissues is notoriously challenging and only a few reports on effective techniques have been published. An emerging epizootic of beak deformities among wild birds in Alaska and the Pacific Northwest region of North America recently highlighted the need for additional baseline information about avian hard‐cornified structures. In this study, we examine the beak and claw of the Black‐capped Chickadee ( Poecile atricapillus ), a common North American passerine that is affected by what has been described as “avian keratin disorder.” We use light and scanning electron microscopy and high‐magnification radiography to document the healthy microanatomy of these tissues and identify features of functional importance. We also describe detailed methods for histological processing of avian hard‐cornified structures and discuss the utility of special stains. Results from this study will assist in future research on the functional anatomy and pathology of hard‐cornified structures and will provide a necessary reference for ongoing investigations of avian keratin disorder in Black‐capped Chickadees and other wild passerine species.

Journal of Morphology↗
USGS2017

In memoriam - William Toshio (Tosh) Yasutake, 1922-2016

William Toshio (Tosh) Yasutake, 1922-2016 passed away peacefully at home on December 12, 2016, at the age of 94. He is survived by Fumi, his wife of 66 years, as well as four children and six grandchildren. With his death, the fish health community has lost an outstanding scientist as well as a kind, unassuming, and wonderful human being. Tosh was born on June 10, 1922, in Seattle, Washington, to Jack and Hide Yasutake. He was in his first year of studies at the University of Washington when Pearl Harbor was attacked by Imperial Japan on December 7, 1941. Following the attack, Tosh and his family (father, mother, sister, and two brothers) were among the 110,000–120,000 people of Japanese ancestry who were forced from their homes on the Pacific coast and incarcerated in internment camps in the interior. In June 1942, Tosh enlisted in the U.S. Army, serving as an unarmed combat medic in the famed 442nd Regimental Combat Team, the most decorated unit for its size and length of service in the history of American warfare. Wounded in October 1944 during the Vosges Mountains campaign near Bruyères, France, Tosh was evacuated and missed the ensuing battle to rescue the “Lost Battalion,” at which his replacement was killed. Tosh returned to action in Italy in February 1945 and served until the end of the war in Europe, earning both a Purple Heart and a Bronze Star for bravery. In October 2010, the Congressional Gold Medal was awarded to the 442nd Regimental Combat Team, and in 2012 the surviving members were made chevaliers of the French Légion d’Honneur for actions contributing to the liberation of France in World War II. After the war, Tosh returned to the University of Washington on the GI Bill and received a B.S. degree in zoology in 1951. In 1953 he began his research career at the U.S. Fish and Wildlife Service’s Western Fish Nutrition Laboratory at Cook, Washington, where he conducted pioneering research on nutritional fish diseases with John Halver. Tosh was one of the first to recognize hepatomas in hatchery-reared Rainbow Trout and helped to trace the disease to an aflatoxin produced by the mold Aspergillus flavis , which grew during the storage of ingredients for fish diets. In 1960, he transferred to the Western Fisheries Research Center (WFRC) in Seattle (then called the Western Fish Disease Laboratory) to start a fish pathology diagnostic laboratory. There he described the histopathology of diseases of economically important fishes, identified etiologic agents, and worked with hatchery biologists to improve the health, quality, and survival of salmonids released from federal and state hatcheries. Tosh was instrumental in recognizing that the viruses of Oregon sockeye disease and Chinook Salmon virus disease were one entity and in giving the disease its present name: infectious hematopoietic necrosis. In recognition of his pioneering research, Tosh was awarded a doctorate in fish pathology by the University of Tokyo in 1980, the first American to have been so honored. In 1983, he published his classic textbook The Microscopic Anatomy of Salmonids: An Atlas , which quickly became a standard reference work in fish pathology and is still in wide use today. For his outstanding career achievements, in 1987 Tosh received the S. F. Snieszko Distinguished Service Award, the highest honor bestowed by the American Fisheries Society’s Fish Health Section (AFS–FHS). Tosh retired in 1988 but continued his research at the WFRC as a senior scientist emeritus, providing technical assistance to federal and state agencies and to the aquaculture industry worldwide. His culminating project was to digitize his lifetime collection of photomicrographs and prepare an atlas, “Histopathology of Selected Parasitic Salmonid Diseases: A Color Atlas,” that is now posted on the Web sites of the WFRC and the AFS–FHS. Although his presence will be sorely missed, his research contributions have become part of the foundation of today’s knowledge of fisheries biology and have assured him a place in history.

Journal of Aquatic Animal Health↗
USGS2008

Pathology, physiologic parameters, tissue contaminants, and tissue thiamine in morbid and healthy central Florida adult American alligators (Alligator mississippiensis)

An investigation of adult alligator (Alligator mississippiensis) mortalities in Lake Griffin, central Florida, was conducted from 1998-2004. Alligator mortality was highest in the months of April and May and annual death count peaked in 2000. Bacterial pathogens, heavy metals, and pesticides were not linked with the mortalities. Blood chemistry did not point to any clinical diagnosis, although differences between impaired and normal animals were noted. Captured alligators with signs of neurologic impairment displayed unresponsive and uncoordinated behavior. Three of 21 impaired Lake Griffin alligators were found to have neural lesions characteristic of thiamine deficiency in the telencephalon, particularly the dorsal ventricular ridge. In some cases, lesions were found in the thalamus, and parts of the midbrain. Liver and muscle tissue concentrations of thiamine (vitamin B"1) were lowest in impaired Lake Griffin alligators when compared to unimpaired alligators or to alligators from Lake Woodruff. The consumption of thiaminase-positive gizzard shad (Dorosoma cepedianum) is thought to have been the cause of the low tissue thiamine and resulting mortalities. ?? Wildlife Disease Association 2008.

Journal of Wildlife Diseases↗
USGS2021

Pathology of Lagovirus europaeus GI.2/RHDV2/b (rabbit hemorrhagic disease virus 2) in native North American lagomorphs

Rabbit hemorrhagic disease, a notifiable foreign animal disease in the US, was reported for the first time in wild native North American lagomorphs in April 2020 in the southwestern US. Affected species included the desert cottontail ( Sylvilagus audubonii ), mountain cottontail ( Sylvilagus nuttallii ), black-tailed jackrabbit ( Lepus californicus ), and antelope jackrabbit ( Lepus alleni ). Desert cottontails ( n =7) and black-tailed jackrabbits ( n =7) collected in April and May 2020 were necropsied at the US Geological Survey National Wildlife Health Center and tested positive for Lagovirus europaeus GI.2, also known as rabbit hemorrhagic disease virus 2 (GI.2/RHDV2/b), by real-time PCR at the US Department of Agriculture's Foreign Animal Disease Diagnostic Laboratory. Gross and microscopic lesions were similar to those reported in European rabbits ( Oryctolagus cuniculus ) and other hare ( Lepus ) species with GI.2/RHDV2/b infection; they included epistaxis (12/13; 92%); massive hepatocellular dissociation (14/14; 100%) and necrosis or apoptosis (11/11; 100%); pulmonary congestion (12/12; 100%), edema (12/13; 92%), and hemorrhage (11/12; 92%); and acute renal tubular injury (3/8; 38%). As in previous reports, massive hepatocellular dissociation and necrosis or apoptosis were the most diagnostically distinct finding. As North American Sylvilagus and Lepus species appear to be susceptible to fatal GI.2/RHDV2/b infection, additional work is needed to understand the host range, pathogenicity, and potential population effects of GI.2/RHDV2/b in North America.

Arizona, New Mexico, Texas↗
USGS2010

Prevalence and pathology of West Nile virus in naturally infected house sparrows, western Nebraska, 2008

Nestling birds are rarely sampled in the field for most arboviruses, yet they may be important in arbovirus amplification cycles. We sampled both nestling and adult house sparrows ( Passer domesticus ) in western Nebraska for West Nile virus (WNV) or WNV-specific antibodies throughout the summer of 2008 and describe pathology in naturally infected nestlings. Across the summer, 4% of nestling house sparrows were WNV-positive; for the month of August alone, 12.3% were positive. Two WNV-positive nestlings exhibited encephalitis, splenomegaly, hepatic necrosis, nephrosis, and myocarditis. One nestling sparrow had large mural thrombi in the atria and ventricle and immunohistochemical staining of WNV antigen in multiple organs including the wall of the aorta and pulmonary artery; cardiac insufficiency thus may have been a cause of death. Adult house sparrows showed an overall seroprevalence of 13.8% that did not change significantly across the summer months. The WNV-positive nestlings and the majority of seropositive adults were detected within separate spatial clusters. Nestling birds, especially those reared late in the summer when WNV activity is typically greatest, may be important in virus amplification.

Nebraska↗
USGSDate not supplied

Perspectives on the diagnosis, epizootiology, and control of the 1973 duck plague epizootic in wild waterfowl at Lake Andes, South Dakota

An epizootic of duck plague occurred in early 1973 in a population of 163,500 wild waterfowl, primarily mallards (Anas platyrhynchos), wintering on Lake Andes and the nearby Missouri River in southeastern South Dakota (USA). The diagnosis was based on pathologic lesions and confirmed by virus isolation. Control measures included quarantine, attempts to reduce virus contamination of the area, dispersal of waterfowl, and monitoring of wild waterfowl populations for mortality. The epizootic resulted in documented mortality of 18% and estimated mortality of 26% of the waterfowl at risk. Prompt implementation of control measures might have limited mortality to approximately 8%. Losses during the epizootic were equivalent to 0.12% of the annual mortality in the North American 1996 fall population of 80,000,000 wild ducks. The most likely sources of the infection were free-flying wild mallard or American black duck (Anas rubripes) carriers from the upper midwestern or northeastern United States. Duck plague serum neutralization antibodies were demonstrated in 31% of 395 apparently healthy mallards sampled prior to dispersal of the flock at Lake Andes, suggesting that tens of thousands of potential duck plague carriers entered the wild waterfowl populations of all four major flyways. Consequently, the absence of major epizootics of duck plague in wild waterfowl in the subsequent two decades is evidence that substantial numbers of duck plague carriers can occur in wild waterfowl populations without resulting in epizootic mortalities. The failure to isolate duck plague virus from apparently healthy mallards sampled during the epizootic raises questions concerning the validity of conclusions regarding the status of duck plague in wild waterfowl based upon negative results of random surveys conducted in the absence of epizootics. © Wildlife Disease Association 1997.

South Dakota↗
USGS2019

Pathogen prevalence in American black bears (Ursus americanus) of the Jemez Mountains, New Mexico, USA

Informed management of American black bears ( Ursus americanus ) requires knowledge of the distribution and pathology of diseases affecting the species. Little information is available on pathogen prevalence from black bear populations in the Southwest, US, and it is unknown how these infections may influence black bear populations or disease transmission. We captured New Mexico black bears ( Ursus americanus amblyceps ) during 2016–17 as part of a long-term monitoring project and opportunistically collected 36 blood samples from 12 female and 17 male black bears. We wanted to determine prior exposure to canine distemper virus, canine parvovirus, Yersinia pestis , Francisella tularensis , West Nile virus, Toxoplasma gondii , and the tick-borne pathogens, Anaplasma spp., Ehrlichia spp., Borrelia burgdorferi , Rickettsia spp., and Babesia spp. Approximately half (55%, 16/29) of the individuals sampled had antibodies to Y. pestis , and 37% (10/27) had antibodies to T. gondii . Prevalence of antibodies to West Nile virus, F. tularensis , and canine parvovirus were lower (i.e., 11, 10, and 3%, respectively). We detected no antibodies to canine distemper, B. burgdorferi , Rickettsia spp., or Babesia spp. We documented changes in antibody titer levels for both sexes of several recaptured black bears. Our data will inform managers of pathogen prevalence and distribution in black bears in north-central New Mexico and provide a vital baseline dataset for future pathogen monitoring. Additionally, these data support actions to minimize exposure through handling wild individuals or through hunter harvest activities.

New Mexico↗