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Hematology of healthy Florida manatees (Trichechus manatus)
Background: Hematologic analysis is an important tool in evaluating the general health status of free-ranging manatees and in the diagnosis and monitoring of rehabilitating animals. Objectives: The purpose of this study was to evaluate diagnostically important hematologic analytes in healthy manatees (Trichechus manatus) and to assess variations with respect to location (free ranging vs captive), age class (small calves, large calves, subadults, and adults), and gender. Methods: Blood was collected from 55 free-ranging and 63 captive healthy manatees. Most analytes were measured using a CELL-DYN 3500R; automated reticulocytes were measured with an ADVIA 120. Standard manual methods were used for differential leukocyte counts, reticulocyte and Heinz body counts, and plasma protein and fibrinogen concentrations. Results: Rouleaux, slight polychromasia, stomatocytosis, and low numbers of schistocytes and nucleated RBCs (NRBCs) were seen often in stained blood films. Manual reticulocyte counts were higher than automated reticulocyte counts. Heinz bodies were present in erythrocytes of most manatees. Compared with free-ranging manatees, captive animals had slightly lower MCV, MCH, and eosinophil counts and slightly higher heterophil and NRBC counts, and fibrinogen concentration. Total leukocyte, heterophil, and monocyte counts tended to be lower in adults than in younger animals. Small calves tended to have higher reticulocyte counts and NRBC counts than older animals. Conclusions: Hematologic findings were generally similar between captive and free-ranging manatees. Higher manual reticulocyte counts suggest the ADVIA detects only reticulocytes containing large amounts of RNA. Higher reticulocyte and NRBC counts in young calves probably reflect an increased rate of erythropoiesis compared with older animals. ?? 2009 American Society for Veterinary Clinical Pathology.
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.
Pathology of sea otters
In the months following the Exxon Valdez oil spill (EVOS), 994 sea otters ( Enhydra lutris ) from oil-spill-affected areas died (Doroff et al. 1993). Carcasses collected from these areas and otters that died in rehabilitation centers are included in this number. The actual number that died was probably much greater. Within days of the spill, the Exxon Company (USA) funded an effort to rehabilitate oil-contaminated sea otters (Davis 1990). Initially, clinical veterinarians working on the rehabilitation effort performed partial necropsies on some of the sea otters that died. Soon, veterinary pathologists from the University of Alaska and the U.S. Environmental Protection Agency provided assistance. Later, rehabilitation centers were constructed and other veterinarians with special training in pathology were hired by Exxon to provide diagnostic support. In late April 1989, veterinary pathologists from the U.S. Fish and Wildlife Service (USFWS) assumed responsibility for pathologic evaluation of oil-spill-affected sea otters. The USFWS requested assistance from veterinary pathologists of the Armed Forces Institute of Pathology (AFIP) in June 1989. Eventually, as part of the Natural Resources Damage Assessment program, AFIP veterinary pathologists were asked to carry out histopathological studies of the tissue specimens collected by all parties and to perform necropsies on carcasses that had been collected and frozen. A veterinary clinical pathologist was requested to assess hematology and clinical chemistry findings in otters that had been held in the rehabilitation centers. In spite of the best efforts of many dedicated people working under extremely difficult conditions, there are significant limitations in the pathological studies. The absence of a detailed necropsy protocol and of full documentation of necropsy findings during the first several weeks after the spill resulted in important data being lost. Often, samples of all major organs were not collected. In some cases, no necropsy report was available. Specimens for toxicologic analysis for petroleum hydrocarbons were not consistently collected. The absence of a detailed toxicology protocol suggests that the samples may not have been collected properly. The lack of a consistent numbering system for identification of specimens caused major problems; some samples were useless because they could not be identified. Many blood samples could not be transported to laboratories quickly enough to prevent significant deterioration of the samples because of inclement weather and the remote locations of the rehabilitation centers. Thus, in a number of cases, data could not be used because significant deterioration of the specimens was considered likely to have occurred. Since more than one laboratory was used to analyze blood samples, problems with comparability of results were encountered. The laboratory tests were performed to aid the clinical veterinarians in diagnosis and treatment of individual animals, not as part of a consistent protocol; thus, there is variation in the amount and type of laboratory data available for each otter. These problems illustrate the need for development of contingency plans that include detailed protocols before disasters occur.
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.
The pathogenesis of a North American H5N2 clade 2.3.4.4 group A highly pathogenic avian influenza virus in surf scoters (Melanitta perspicillata)
Background Aquatic waterfowl, particularly those in the order Anseriformes and Charadriiformes , are the ecological reservoir of avian influenza viruses (AIVs). Dabbling ducks play a recognized role in the maintenance and transmission of AIVs. Furthermore, the pathogenesis of highly pathogenic AIV (HPAIV) in dabbling ducks is well characterized. In contrast, the role of diving ducks in HPAIV maintenance and transmission remains unclear. In this study, the pathogenesis of a North American A/Goose/1/Guangdong/96-lineage clade 2.3.4.4 group A H5N2 HPAIV, A/Northern pintail/Washington/40964/2014, in diving sea ducks (surf scoters, Melanitta perspicillata ) was characterized. Results Intrachoanal inoculation of surf scoters with A/Northern pintail/Washington/40964/2014 (H5N2) HPAIV induced mild transient clinical disease whilst concomitantly shedding high virus titers for up to 10 days post-inoculation (dpi), particularly from the oropharyngeal route. Virus shedding, albeit at low levels, continued to be detected up to 14 dpi. Two aged ducks that succumbed to HPAIV infection had pathological evidence for co-infection with duck enteritis virus, which was confirmed by molecular approaches. Abundant HPAIV antigen was observed in visceral and central nervous system organs and was associated with histopathological lesions. Conclusions Collectively, surf scoters, are susceptible to HPAIV infection and excrete high titers of HPAIV from the respiratory and cloacal tracts whilst being asymptomatic. The susceptibility of diving sea ducks to H5 HPAIV highlights the need for additional research and surveillance to further understand the contribution of diving ducks to HPAIV ecology.
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.
Experimental infection studies demonstrating Atlantic salmon as a host and reservoir of viral hemorrhagic septicemia virus type IVa with insights into pathology and host immunity
In British Columbia, Canada (BC), aquaculture of finfish in ocean netpens has the potential for pathogen transmission between wild and farmed species due to the sharing of an aquatic environment. Viral hemorrhagic septicemia virus (VHSV) is enzootic in BC and causes serious disease in wild Pacific herring, Clupea pallasii, which often enter and remain in Atlantic salmon, Salmo salar, netpens. Isolation of VHSV from farmed Atlantic salmon has been previously documented, but the effects on the health of farmed salmon and the wild fish sharing the environment are unknown. To determine their susceptibility, Atlantic salmon were exposed to a pool of 9 isolates of VHSV obtained from farmed Atlantic salmon in BC by IP-injection or by waterborne exposure and cohabitation with diseased Pacific herring. Disease intensity was quantified by recording mortality, clinical signs, histopathological changes, cellular sites of viral replication, expression of interferon-related genes, and viral tissue titers. Disease ensued in Atlantic salmon after both VHSV exposure methods. Fish demonstrated gross disease signs including darkening of the dorsal skin, bilateral exophthalmia, light cutaneous hemorrhage, and lethargy. The virus replicated within endothelial cells causing endothelial cell necrosis and extensive hemorrhage in anterior kidney. Infected fish demonstrated a type I interferon response as seen by up-regulation of genes for IFNα, Mx, and ISG15. In a separate trial infected salmon transmitted the virus to sympatric Pacific herring. The results demonstrate that farmed Atlantic salmon can develop clinical VHS and virus can persist in the tissues for at least 10 weeks. Avoiding VHS epizootics in Atlantic salmon farms would limit the potential of VHS in farmed Atlantic salmon, the possibility for further host adaptation in this species, and virus spillback to sympatric wild fishes.