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A scuticociliate causes mass mortality of Diadema antillarum in the Caribbean Sea
Echinoderm mass mortality events shape marine ecosystems by altering the dynamics among major benthic groups. The sea urchin Diadema antillarum , virtually extirpated in the Caribbean in the early 1980s by an unknown cause, recently experienced another mass mortality beginning in January 2022. We investigated the cause of this mass mortality event through combined molecular biological and veterinary pathologic approaches comparing grossly normal and abnormal animals collected from 23 sites, representing locations that were either affected or unaffected at the time of sampling. Here, we report that a scuticociliate most similar to Philaster apodigitiformis was consistently associated with abnormal urchins at affected sites but was absent from unaffected sites. Experimentally challenging naïve urchins with a Philaster culture isolated from an abnormal, field-collected specimen resulted in gross signs consistent with those of the mortality event. The same ciliate was recovered from treated specimens postmortem, thus fulfilling Koch’s postulates for this microorganism. We term this condition D. antillarum scuticociliatosis.
Pathology and case definition of Severe Perkinsea Infections of frogs
Severe Perkinsea infection (SPI) is an emerging disease of frogs responsible for mass mortalities of tadpoles across the United States. It is caused by protozoa belonging to the phylum Perkinsozoa that form a distinct group referred to as the Pathogenic Perkinsea Clade of frogs. In this work, we provide detailed description of gross and histologic lesions from 178 naturally infected tadpoles, including 10 species from 22 mortality events and 6 amphibian health monitoring studies from diverse geographic areas. On external examination, we observed abdominal distension (10, 5.6%), cutaneous erythema and petechia (3, 1.7%), subcutaneous edema (3, 1.7%), and areas of white skin discoloration (3, 1.7%). On macroscopic examination of internal organs, we found hepatomegaly (68, 38.2%), splenomegaly (51, 28.7%), nephromegaly (47, 26.4%), ascites (15, 8.4%), segmental irregular thickening and white discoloration of the intestine (8, 4.5%), pancreatomegaly (4, 2.2%), and pancreatic petechia (1, 0.6%). Histologically, over 60% of the liver (148/165, 89.7%), kidney (113/147, 76.9%), spleen (96/97, 99%), and pancreas (46/68, 67.6%) were invaded by myriad intracellular and extracellular Perkinsea hypnospore-like and trophozoite-like organisms. Numerous other tissues were affected to a lesser extent. Mild histiocytic inflammation with fewer lymphocytes or eosinophils was commonly observed in areas of infection that were not obscured by lympho-granulocytic hematopoietic tissue. In light of these observations, we suggest a logical pathogenesis sequence. Finally, we propose a “case definition” for SPI to promote standardized communication of results and prevent misdiagnosis with epidemiological and pathologically overlapping diseases such as ranavirosis.
Natural infections with pigeon paramyxovirus serotype 1: Pathologic changes in Eurasian collared-doves (Streptopelia decaocto) and rock pigeons (Columba livia) in the United States
Pigeon paramyxovirus serotype 1 (PPMV-1) is a globally distributed, virulent member of the avian paramyxovirus serotype 1 serogroup that causes mortality in columbiformes and poultry. Following introduction into the United States in the mid-1980s, PPMV-1 rapidly spread causing numerous mortality events in Eurasian collared-doves ( Streptopelia decaocto ) (ECDOs) and rock pigeons ( Columba livia ) (ROPIs). The investigators reviewed pathological findings of 70 naturally infected, free-ranging columbiforms from 25 different mortality events in the United States. Immunohistochemistry targeting PPMV-1 nucleoprotein was used to determine the tissue distribution of the virus in a subset of 17 birds from 10 of the studied outbreaks. ECDOs (61 birds) and ROPIs (9 birds) were the only species in which PPMV-1-associated disease was confirmed by viral isolation and presence of histologic lesions. Acute to subacute tubulointerstitial nephritis and necrotizing pancreatitis were the most frequent histologic lesions, with immunolabeling of viral antigen in renal tubular epithelial cells and pancreatic acinar epithelium. Lymphoid depletion of bursa of Fabricius and spleen was common, but the presence of viral antigen in these organs was inconsistent among infected birds. Hepatocellular necrosis was occasionally present with immunolabeling of hypertrophic Kupffer cells, and immunopositive eosinophilic intracytoplasmic inclusion bodies were present in hepatocytes of 1 ECDO. Immunopositive lymphocytic choroiditis was present in 1 ECDO, while lymphocytic meningoencephalitis was frequent in ROPIs in absence of immunolabeling. This study demonstrates widespread presence of PPMV-1 antigen in association with histologic lesions, confirming the lethal potential of this virus in these particular bird species.
The state of the art in raptor electrocution research: A global review
We systematically reviewed the raptor electrocution literature to evaluate study designs and methods used in raptor electrocution research, mitigation, and monitoring, emphasizing original research published in English. Specifically, we wondered if three decades of effort to reduce raptor electrocutions has had positive effects. The majority of literature examined came from North America, western Europe, and South Africa. In spite of intensive and often sustained effort by industry and governments across three continents for 30 years, reductions in the incidence of electrocution have been demonstrated in only a few studies. Reliable rate estimates of electrocution mortality generally are unavailable, with some exceptions. Nearly half of 110 studies we analyzed in detail were retrospective reviews of historical mortality records, banding data, or results of necropsies on dead birds received at pathology and veterinary facilities. Among prospective studies, less than half used unbiased approaches to sampling and many did not provide enough detail to assess the sampling design used. At this time, few researchers can demonstrate the reliability of standardized retrofitting procedures or the effectiveness of monitoring techniques. Future progress in reducing raptor mortalities on power lines will benefit from properly designed studies that generate rate estimates of mortality, address biasing factors, and include predictions concerning risk and techniques to reduce risk that can be tested in the field or laboratory.
Macroscopic, histologic, and ultrastructural lesions associated with avian keratin disorder in Black-capped Chickadees (Poecile atricapillus)
An epizootic of beak abnormalities (avian keratin disorder) was recently detected among wild birds in Alaska. Here we describe the gross, histologic, and ultrastructural features of the disease in 30 affected adult black-capped chickadees (Poecile atricapillus). Grossly, there was elongation of the rhamphotheca, with varying degrees of lateral deviation, crossing, and gapping between the upper and lower beak. Not uncommonly, the claws were overgrown, and there was alopecia, scaling, and crusting of the skin. The most prominent histopathologic features in the beak included epidermal hyperplasia, hyperkeratosis, and core-like intrusions of necrotic debris. In affected birds, particularly those with moderate to severe beak overgrowth, there was remodeling of premaxillary and mandibular bones and various dermal lesions. Lesions analogous to those found in beaks were present in affected claws, indicating that this disorder may target both of these similar tissues. Mild to moderate hyperkeratosis occurred in other keratinized tissues, including skin, feather follicles, and, occasionally, sinus epithelium, but typically only in the presence of microbes. We did not find consistent evidence of a bacterial, fungal, or viral etiology for the beak lesions. The changes observed in affected birds did not correspond with any known avian diseases, suggesting a potentially novel hyperkeratotic disorder in wild birds.
Dynamics of virus shedding and in situ confirmation of chelonid herpesvirus 5 in Hawaiian green turtles with Fibropapillomatosis
Cancers in humans and animals can be caused by viruses, but virus-induced tumors are considered to be poor sites for replication of intact virions (lytic replication). Fibropapillomatosis (FP) is a neoplastic disease associated with a herpesvirus, chelonid herpesvirus 5 (ChHV5), that affects green turtles globally. ChHV5 probably replicates in epidermal cells of tumors, because epidermal intranuclear inclusions (EIIs) contain herpesvirus-like particles. However, although EIIs are a sign of herpesvirus replication, they have not yet been firmly linked to ChHV5. Moreover, the dynamics of viral shedding in turtles are unknown, and there are no serological reagents to confirm actual presence of the specific ChHV5 virus in tissues. The investigators analyzed 381 FP tumors for the presence of EIIs and found that overall, about 35% of green turtles had lytic replication in skin tumors with 7% of tumors showing lytic replication. A few (11%) turtles accounted for more than 30% cases having lytic viral replication, and lytic replication was more likely in smaller tumors. To confirm that turtles were actively replicating ChHV5, a prerequisite for shedding, the investigators used antiserum raised against F-VP26, a predicted capsid protein of ChHV5 that localizes to the host cell nucleus during viral replication. This antiserum revealed F-VP26 in EIIs of tumors, thus confirming the presence of replicating ChHV5. In this light, it is proposed that unlike other virus-induced neoplastic diseases, FP is a disease that may depend on superspreaders, a few highly infectious individuals growing numerous small tumors permissive to viral production, for transmission of ChHV5.
Gross and microscopic lesions in corals from Micronesia
The authors documented gross and microscopic morphology of lesions in corals on 7 islands spanning western, southern, and eastern Micronesia, sampling 76 colonies comprising 30 species of corals among 18 genera, with Acropora , Porites , and Montipora dominating. Tissue loss comprised the majority of gross lesions sampled (41%), followed by discoloration (30%) and growth anomaly (29%). Of 31 cases of tissue loss, most lesions were subacute (48%), followed by acute and chronic (26% each). Of 23 samples with discoloration, most were dark discoloration (40%), with bleaching and other discoloration each constituting 30%. Of 22 growth anomalies, umbonate growth anomalies composed half, with exophytic, nodular, and rugose growth anomalies composing the remainder. On histopathology, for 9 cases of dark discoloration, fungal infections predominated (77%); for 7 bleached corals, depletion of zooxanthellae from the gastrodermis made up a majority of microscopic diagnoses (57%); and for growth anomalies other than umbonate, hyperplasia of the basal body wall was the most common microscopic finding (63%). For the remainder of the gross lesions, no single microscopic finding constituted >50% of the total. Host response varied with the agent present on histology. Fragmentation of tissues was most often associated with algae (60%), whereas necrosis dominated (53%) for fungi. Two newly documented potentially symbiotic tissue-associated metazoans were seen in Porites and Montipora . Findings of multiple potential etiologies for a given gross lesion highlight the importance of incorporating histopathology in coral disease surveys. This study also expands the range of corals infected with cell-associated microbial aggregates.
West Nile virus infection in American singer canaries: An experimental model in a highly susceptible avian species
This study investigated the susceptibility of American singer canaries ( Serinus canaria ) to West Nile virus (WNV) infection. Adult canaries were inoculated with 10 5 , 10 2 , and 10 1 plaque forming units (PFU) of WNV. All birds became infected and mortality occurred by 5 days postinoculation. The load of viral RNA as determined by RT-qPCR was dose dependent, and was higher at all doses than the level of viral RNA detected in American crows ( Corvus brachyrhynchos ) challenged with 10 5 PFU of WNV. In a subset of birds, viremia was detected by virus isolation; canaries inoculated with 10 1 PFU of WNV developed viremia exceeding 10 10 PFU/mL serum, a log higher than American crows inoculated with 10 5 PFU of virus. In canaries euthanized at 3 days postinoculation, WNV was isolated at >10 7 PFU of virus/100 mg of lung, liver, heart, spleen, and kidney tissues. Pallor of the liver and splenomegaly were the most common macroscopic observations and histologic lesions were most severe in liver, spleen, and kidney, particularly in canaries challenged with 10 2 and 10 1 PFU. Immunoreactivity to WNV was pronounced in the liver and spleen. IgG antibodies to WNV were detected in serum by enzyme immunoassay in 11 of 21 (52%) challenged canaries and, in 4 of 5 (20%) of these sera, neutralization antibodies were detected at a titer ≥ 1:20. American singer canaries provide a useful model as this bird species is highly susceptible to WNV infection.
Ichthyophonus sp. Infection in Opaleye (Girella nigricans)
Over a 3-year-period, 17 wild-caught opaleye (Girella nigricans) housed in a public display aquarium were found dead without premonitory signs. Grossly, 4 animals had pinpoint brown or black foci on coelomic adipose tissue. Histologically, liver, spleen, heart, and posterior kidney had mesomycetozoan granulomas in all cases; other organs were less commonly infected. Four opaleye had goiter; additional substantial lesions were not identified. Granulomas surrounded melanized debris, leukocytes, and mesomycetozoa represented by folded membranes (collapsed schizont walls), intact schizonts (50- to >200 µm in diameter with a multilaminate membrane), plasmodia (budding from schizonts or free in tissue), or rarely germinal tubes (budding from schizonts). Ichthyophonus was grown from fresh tissues in tissue explant broth cultures of the heart, liver, and/or spleen. Polymerase chain reaction using 18S ribosomal DNA primers amplified a 1730-bp region, and the DNA sequence was most similar to Ichthyophonus hoferi, which is often associated with freshwater aquaculture fish.
Holding time or fixative formulation has no obvious effect on histology of Porites evermanni and Montipora capitata
Collection of coral for histologic examination requires holding of samples in seawater for a time before they are fixed for histologic processing. This could adversely affect the interpretation of morphologic changes during histologic examinations. We evaluated the microscopic morphology of Porites evermanni and Montipora capitata held (0–120 minutes) in seawater prior to fixation in Z-Fix formulated with raw or artificial seawater. We saw no evident effects of treatments on microscopic morphology. However, among 88 statistical comparisons, and after accounting for false discovery rate, holding time prior to fixation was associated with a significant increase in degree of mucosity of basal body walls.
Osteolipomatous metaplasia in the liver of cameloids
An aged male Bactrian camel ( Camelus ferus f. bactriana ), originally from the San Diego Zoo, died suddenly. Necropsy showed acute bloat and chronic liver disease. In samples of liver tissue fixed in 10% neutral buffered formalin, approximately 25% of the total volume of tissue was comprised of multiple white to cream-colored circumscribed nodules up to 1 cm in diameter, which were gritty when cut (fig. 1). Samples of liver were cut at 6 μ m for histologic examination. Microscopically, the nodules consisted of aggregations of large, vacuolated cells resembling fat cells with spicules of mature bone scattered throughout many nodules (fig. 2). Most nodules were circumscribed but not encapsulated. Single or small clusters of vacuolated cells, however, were scattered diffusely in the hepatic parenchyma surrounding the nodules. We found cholangitis and peribiliary fibrosis in some areas, but no generalized cirrhosis. Degeneration of hepatocytes was seen in some areas peripheral to the nodules. Compression of the hepatic architecture was evident in the liver parenchyma surrounding some nodules, but the primary change was infiltrative rather than expansive. Foci of lymphocytes and a few neutrophils were present in some nodules. Hematopoietic cells, described as a characteristic of myelolipomas, were not found in any of the nodules examined [2, 4].
Epizootic vacuolar myelinopathy of the central nervous system of bald eagles ( Haliaeetus leucocephalus ) and American coots ( Fulica americana )
Unprecedented mortality occurred in bald eagles ( Haliaeetus leucocephalus ) at DeGray Lake, Arkansas, during the winters of 1994-1995 and 1996-1997. The first eagles were found dead during November, soon after arrival from fall migration, and deaths continued into January during both episodes. In total, 29 eagles died at or near DeGray Lake in the winter of 1994-1995 and 26 died in the winter of 1996-1997; no eagle mortality was noted during the same months of the intervening winter or in the earlier history of the lake. During the mortality events, sick eagles were observed overflying perches or colliding with rock walls. Signs of incoordination and limb paresis were also observed in American coots ( Fulica americana ) during the episodes of eagle mortality, but mortality in coots was minimal. No consistent abnormalities were seen on gross necropsy of either species. No microscopic findings in organs other than the central nervous system (CNS) could explain the cause of death. By light microscopy, all 26 eagles examined and 62/77 (81%) coots had striking, diffuse, spongy degeneration of the white matter of the CNS. Vacuolation occurred in all myelinated CNS tissue, including the cerebellar folia and medulla oblongata, but was most prominent in the optic tectum. In the spinal cord, vacuoles were concentrated near the gray matter, and occasional swollen axons were seen. Vacuoles were uniformly present in optic nerves but were not evident in the retina or peripheral or autonomic nerves. Cellular inflammatory response to the lesion was distinctly lacking. Vacuoles were 8-50 microns in diameter and occurred individually, in clusters, or in rows. In sections stained by luxol fast blue/periodic acid-Schiff stain, the vacuoles were delimited and transected by myelin strands. Transmission electron microscopy revealed intramyelinic vacuoles formed in the myelin sheaths by splitting of one or more myelin lamellae at the intraperiodic line. This lesion is characteristic of toxicity from hexachlorophene, triethyltin, bromethalin, isonicotinic acid hydrazide, and certain exotic plant toxins; however, despite exhaustive testing, no etiology was determined for the DeGray Lake mortality events. This is the first report of vacuolar myelinopathy associated with spontaneous mortality in wild birds.
Coral disease and health workshop: Coral histopathology II, July 12-14, 2005
The health and continued existence of coral reef ecosystems are threatened by an increasing array of environmental and anthropogenic impacts. Coral disease is one of the prominent causes of increased mortality among reefs globally, particularly in the Caribbean. Although over 40 different coral diseases and syndromes have been reported worldwide, only a few etiological agents have been confirmed; most pathogens remain unknown and the dynamics of disease transmission, pathogenicity and mortality are not understood. Causal relationships have been documented for only a few of the coral diseases, while new syndromes continue to emerge. Extensive field observations by coral biologists have provided substantial documentation of a plethora of new pathologies, but our understanding, however, has been limited to descriptions of gross lesions with names reflecting these observations (e.g., black band, white band, dark spot). To determine etiology, we must equip coral diseases scientists with basic biomedical knowledge and specialized training in areas such as histology, cell biology and pathology. Only through combining descriptive science with mechanistic science and employing the synthesis epizootiology provides will we be able to gain insight into causation and become equipped to handle the pending crisis. One of the critical challenges faced by coral disease researchers is to establish a framework to systematically study coral pathologies drawing from the field of diagnostic medicine and pathology and using generally accepted nomenclature. This process began in April 2004, with a workshop titled Coral Disease and Health Workshop: Developing Diagnostic Criteria co-convened by the Coral Disease and Health Consortium (CDHC), a working group organized under the auspices of the U.S. Coral Reef Task Force, and the International Registry for Coral Pathology (IRCP). The workshop was hosted by the U.S. Geological Survey, National Wildlife Health Center (NWHC) in Madison, Wisconsin and was focused on gross morphology and disease signs observed in the field. A resounding recommendation from the histopathologists participating in the workshop was the urgent need to develop diagnostic criteria that are suitable to move from gross observations to morphological diagnoses based on evaluation of microscopic anatomy. As a continuation of building the foundation and framework for coral disease diagnostics, the CDHC convened the Coral Disease and Health Workshop: Coral Histopathology II in Charleston, South Carolina, July 11-14, 2005. The workshop was hosted by the Department of Pathology and Laboratory Medicine at the Medical University of South Carolina, Charleston, SC which provided expertise, facilities and equipment in support of the workshop. All of the histological slides and related photographs used in the discussions were prepared and supplied by the IRCP. This workshop brought together 15 experts in veterinary and medical pathology and coral biology from national and international research institutes and government laboratories. The mission was to devise a standardized approach to examining microscopic anatomy and pathology of corals and a standardized nomenclature to facilitate accurate descriptions of the microscopic morphology of corals and enhance communication among specialists investigating causes of coral death. 2 The participants of this workshop deliberated for 3 days to refine the nomenclature for gross and microscopic anatomy of corals and systematically described microscopic changes associated with selected coral diseases. The findings and recommendations from the deliberations will be submitted to the research community for peer review. The standardized nomenclature and descriptions produced at this workshop will ultimately be made available to the scientific community through a variety of media including the World Wide Web. An exciting highlight of this meeting was provided by Professor Robert Ogilvie (MUSC Department of Cell Biology and Anatomy) when he introduced participants to a new digital technology that is revolutionizing histology and histopathology in the medical field. The Virtual Slide technology creates digital images of histological tissue sections by computer scanning actual slides in high definition and storing the images for retrieval and viewing. Virtual slides now allow any investigator with access to a computer and the web to view, search, annotate and comment on the same tissue sections in real time. Medical and veterinary slide libraries across the country are being converted into virtual slides to enhance biomedical education, research and diagnosis. The coral health and disease researchers at this workshop deem virtual slides as a significant way to increase capabilities in coral histology and a means for pathology consultations on coral disease cases on a global scale.
Biomedical and veterinary science can increase our understanding of coral disease
A balanced approach to coral disease investigation is critical for understanding the global decline of corals. Such an approach should involve the proper use of biomedical concepts, tools, and terminology to address confusion and promote clarity in the coral disease literature. Investigating disease in corals should follow a logical series of steps including identification of disease, systematic morphologic descriptions of lesions at the gross and cellular levels, measurement of health indices, and experiments to understand disease pathogenesis and the complex interactions between host, pathogen, and the environment. This model for disease investigation is widely accepted in the medical, veterinary and invertebrate pathology disciplines. We present standard biomedical rationale behind the detection, description, and naming of diseases and offer examples of the application of Koch's postulates to elucidate the etiology of some infectious diseases. Basic epidemiologic concepts are introduced to help investigators think systematically about the cause(s) of complex diseases. A major goal of disease investigation in corals and other organisms is to gather data that will enable the establishment of standardized case definitions to distinguish among diseases. Concepts and facts amassed from empirical studies over the centuries by medical and veterinary pathologists have standardized disease investigation and are invaluable to coral researchers because of the robust comparisons they enable; examples of these are given throughout this paper. Arguments over whether coral diseases are caused by primary versus opportunistic pathogens reflect the lack of data available to prove or refute such hypotheses and emphasize the need for coral disease investigations that focus on: characterizing the normal microbiota and physiology of the healthy host; defining ecological interactions within the microbial community associated with the host; and investigating host immunity, host-agent interactions, pathology, pathogenesis, and factors that promote the pathogenicity of the causative agent(s) of disease.
Hematology of the West Indian manatee (Trichechus manatus)
Hemograms on blood obtained from 10 clinically normal West Indian Manatees ( Trichechus manatus ) were studied. The red cells were large and in lower number than in most terrestrial species. The manatee does not have a neutrophil as is present in most species, but it has a heterophil whose granules stain pink with the Wright-Giemsa stain. The eosinophil has uniform red-staining granules that make its differentiation from heterophils difficult. Both large and small lymphocytes, monocytes and basophils are present. The total number of white blood cells was comparable to that of common domestic species as were the platelet numbers. No reticulocytes were found.
Clinical and clinical laboratory correlates in sea otters dying unexpectedly in rehabilitation centers following the Exxon Valdez oil spill
Following the Exxon Valdez oil spill, 347 oiled sea otters ( Enhydra lutris) were treated in rehabilitation centers. Of these, 116 died, 94 within 10 days of presentation. Clinical records of 21 otters dying during the first 10 days of rehabilitation were reviewed to define the laboratory abnormalities and clinical syndromes associated with these unexpected deaths. The most common terminal syndrome was shock characterized by hypothermia, lethargy, and often hemorrhagic diarrhea. In heavily and moderately oiled otters, shock developed within 48 hours of initial presentation, whereas in lightly oiled otters shock generally occurred during the second week of captivity. Accompanying laboratory abnormalities included leukopenia with increased numbers of immature neutrophils (degenerative left shift), lymphopenia, anemia, azotemia (primarily prerenal), hyperkalemia, hypoproteinemia/hypoalbuminemia, elevations of serum transaminases, and hypoglycemia. Shock associated with hemorrhagic diarrhea probably occurred either as a direct primary effect of oiling or as an indirect effect secondary to confinement and handling in the rehabilitation centers. Lightly oiled otters were less likely to die from shock than were heavily oiled otters (22% vs. 72%, respectively). Heavily oiled otters developed shock more rapidly and had greater numbers of laboratory abnormalities, suggesting that exposure to oil was an important contributing factor.
An introduction to lesions and histology of scleractinian corals
Stony corals (Scleractinia) are in the Phylum Cnidaria (cnidae referring to various types of stinging cells). They may be solitary or colonial, but all secrete an external, supporting aragonite skeleton. Large, colonial members of this phylum are responsible for the accretion of coral reefs in tropical and subtropical waters that form the foundations of the most biodiverse marine ecosystems. Coral reefs worldwide, but particularly in the Caribbean, are experiencing unprecedented levels of disease, resulting in reef degradation. Most coral diseases remain poorly described and lack clear case definitions, while the etiologies and pathogenesis are even more elusive. This introductory guide is focused on reef-building corals and describes basic gross and microscopic lesions in these corals in order to serve as an invitation to other veterinary pathologists to play a critical role in defining and advancing the field of coral pathology.