Distribution of the misfolded isoform of the prion protein in peripheral tissues and spinal cord of Rocky Mountain elk (Cervus elaphus nelsoni) with naturally occurring chronic wasting disease.

Chronic wasting disease (CWD) is an infectious transmissible spongiform encephalopathy of cervids associated with the presence of a misfolded prion protein (PrPCWD). Progression of PrPCWD distribution has been described using immunohistochemistry and histologic changes in a single section of brain stem at the level of the obex resulting in scores from 0 (early) to 10 (terminal) in elk with naturally occurring CWD. Here we describe the spread and distribution of PrPCWD in peripheral tissues and spinal cord in 16 wild and 17 farmed Rocky Mountain elk (Cervus elaphus nelsoni) with naturally occurring CWD and correlate these findings with obex scores. Spinal cord and approximately 110 peripheral tissues were collected, processed, stained with hematoxylin and eosin, and immunolabeled with the anti-prion protein monoclonal antibody F99/97.6.1. The medial retropharyngeal and tracheobronchial lymph nodes were the first tissues to accumulate PrPCWD, followed by other lymphoid tissues, myenteric plexus, spinal cord, and finally tissues outside of the lymphatic and neural systems. However, the only significant histological lesion observed was mild spongiform encephalopathy in the dorsal column of the lower spinal cord in elk with an obex score of ≥9. Initial exposure to CWD prions may be through the respiratory system and spread appears to occur primarily via the autonomic nervous system. Therefore, we suggest using obex scores as a proxy for stage of disease progression and verifying with key peripheral tissues.

Digeneans of northern fur seals Callorhinus ursinus (Pinnipedia: Otariidae) from five subpopulations on St. Paul Island, Alaska.

A parasitological survey of 651 northern fur seals Callorhinus ursinus L. from five subpopulations was conducted on St. Paul Island, Alaska, during July-August 2012-2014. Digenean trematodes were found in 210 of 651 fur seals with a total prevalence of 32.3%. Intensity of infection varied from 1 to 1540 parasites with mean intensity 18.4 ± 111.1 SD and median intensity of 2 specimens per host. Significant differences in prevalence and intensity of infection in northern fur seals between separate rookeries was not observed (Mann-Whitney test; p > 0.05). Four species of digeneans belonging to the families Heterophyidae (Apophallus zalophi Price, 1932, Phocitrema fusiforme Goto and Ozaki, 1930, and Galactosomum ubelakeri (Dailey, 1969)) and Troglotrematidae (Nanophyetus salmincola (Chapin, 1926)) were found. Nanophyetus salmincola is reported from C. ursinus for the first time. We obtained partial 28S rDNA sequences for all digenean species and conducted molecular phylogenetic analysis to demonstrate their phylogenetic relationships.

Shaggy Lame Fox Syndrome in Pribilof Island Arctic Foxes ( Alopex lagopus pribilofensis), Alaska.

A previously unrecognized condition is described in wild free-ranging Pribilof arctic foxes ( Alopex lagopus pribilofensis) from the Pribilof Islands, Alaska, USA. This condition is called shaggy lame fox syndrome (SLFS) denoting the primary clinical signs first observed. Criteria used to suspect SLFS on gross examination included emaciation, failure to shed winter pelage and moderate to severe polyarthritis. Criteria used to confirm SLFS histologically included polyarthritis (characterized by lymphoplasmacytic synovitis, tenosynovitis, bursitis, periosteal bony proliferation, and periarticular lymphoplasmacytic vasculitis) and systemic leukocytoclastic vasculitis. Other histological lesions often found included renal cortical infarcts, myocarditis with myocardial infarcts, lymphoplasmacytic meningitis, lymphoplasmacytic cuffing of meningeal and a few cerebral vessels, and cavitating infarcts of the brainstem and thalamus. The cause of SLFS is not known at this time; however, the gross and histological lesions suggest that the cause of SLFS may be a bacterial polyarthritis with a secondary immune-mediated vasculitis. These lesions are consistent with changes described with Erysipelothrix rhusiopathiae in domestic dogs; E. rhusiopathiae was identified from the synovial membrane of a swollen stifle joint and the kidney from one fox using real-time polymerase chain reaction and with culture from a fox that had gross and histological lesions of SLFS. Therefore, E. rhusiopathiae is a possible etiological agent for SLFS.

Anisakids (Nematoda: Anisakidae) from stomachs of northern fur seals (Callorhinus ursinus) on St. Paul Island, Alaska: parasitological and pathological analysis.

Anisakid nematodes parasitize the alimentary tracts of aquatic vertebrates, including northern fur seals (Callorhinus ursinus) (NFS). The main purpose of this study was to estimate the prevalence, intensity, and species composition of anisakids in NFSs on St. Paul Island, Alaska, and to analyze changes in NFS infection with these nematodes during the last decades. The study was carried out on St. Paul Island, Alaska, in July-August 2011-2013. Stomachs of 443 humanely harvested NFS males were collected from five separate haul-out areas. A total of 4,460 anisakid specimens were collected and identified by morphological criteria. Gross and histological examinations of stomachs were also performed. The overall prevalence of NFS infection was 91.2%; overall mean intensity 10.9, and overall median intensity 6. Five species, Anisakis simplex s. l., Contracaecum osculatum s. l., Pseudoterranova decipiens s. l., P. azarazi and Phocascaris cystophorae, were found. The prevalence of Anisakis was 46.5%, its intensity 7.5. The prevalence and intensity of Contracaecum, Pseudoterranova, and Phocascaris were 33.6% and 3.5, 81.9% and 6.5, and 5.2% and 1.7, respectively. Significant differences in the prevalence of NFS infection were observed between separate haul-outs. Comparison of the present data with the results of studies performed in the North Pacific in the 1960s, showed a significant decrease in the intensity of NFS infection with anisakids during the last decades. The prevalence of mucosal lesions in NFS stomachs caused by anisakids also decreased from 92 to 20.9%. Possible reasons for the changes in NFS infection with anisakids are discussed.

Ecological, morphological, and molecular studies of Acanthocheilonema odendhali (Nematoda: Filarioidea) in northern fur seals (Callorhinus ursinus) on St. Paul Island, Alaska.

Studies of northern fur seal (Callorhinus ursinus Linnaeus, 1758) infection by the filariid nematode Acanthocheilonema odendhali were carried out in 2011-2012 on St. Paul Island, Pribilof Archipelago, Alaska. Skins of 502 humanely harvested northern fur seals from haul-out areas of five rookeries, Polovina (n = 122), Morjovi (n = 54), Zapadni (n = 72), Lukanin (n = 109), and Gorbatch (n = 145), were examined. A. odendhali was found in 18% of northern fur seals. The prevalence of infection ranged from 12.5% up to 22.9% on different haul-out areas on the island. The mean intensity of infection was 1.3 (range 1-7). Detailed morphological examination of collected specimens was performed using light microscopy. Several characters were added to the morphological description of the species, among them lateral thickening of the body cuticle, especially prominent in males, variations in number and position of genital papillae in males, transverse striation of the cuticle, and terminal dilation on tail end in microfilariae. The adult specimens studied had a shorter esophagus than type specimens from the California sea lion described by Perry (1967). Comparison of partial sequences of the mitochondrial cox1 gene from specimens collected from five sampling sites on St. Paul Island and a specimen from the type host and territory in California showed no significant differences and strongly supported conspecificity of the material from Alaska with A. odendhali.

Neurolymphomatosis in a dog with B-cell lymphoma.

Lymphoma in the left femoral nerve of a 10-year-old English Cocker Spaniel caused complete paralysis of the affected limb. Neoplastic cells were immunopositive for CD79a and Pax5 and negative for CD3. Neoplastic cells were in multiple lymph nodes and one kidney but spared bone marrow. The clinical and histologic features in this case resemble those of the rare human condition of neurolymphomatosis.

Acanthocephalans in northern fur seals (Callorhinus ursinus) and a harbor seal (Phoca vitulina) on St. Paul Island, Alaska: species, prevalence, and biodiversity in four fur seal subpopulations.

Monitoring studies of acanthocephalans in northern fur seals (Callorhinus ursinus Linnaeus, 1758) (NFSs) and a harbor seal (Phoca vitulina Linnaeus, 1758) were performed on St. Paul Island, Alaska, in July-August 2011. Gastrointestinal tracts of 105 humanely harvested NFS subadult males (SAMs) (3-4 years old) were collected during the annual Aleut subsistence harvest at four haul-out areas (HOAS): Lukanin (n = 26 NFSs), Polovina (n = 28), Gorbatch (n = 30), and Morzhovyi (n = 21). One gastrointestinal tract collected from a harbor seal (about 3-4 years old) found dead at Morzhovyi HOAS was also examined. The total prevalence of infection in NFSs with acanthocephalans was 29.52 % with variations from 7.69 % to 47.62 % between the four different HOAS. Eight acanthocephalan species of two genera-Corynosoma Lühe, 1904 (Corynosoma strumosum, Corynosoma alaskensis, Corynosoma cameroni, Corynosoma semerme, Corynosoma similis, Corynosoma validum, and Corynosoma villosum), and Bolbosoma Porta, 1908 (Bolbosoma nipponicum)-were found in the NFSs and a harbor seal. This is a new record of C. alaskensis for the NFSs. Short biological notes of the species found are presented. Differences in species composition as well as in prevalence of acanthocephalans parasitizing NFSs were observed in subpopulations from four different HOAS on St. Paul Island. The highest biodiversity of acanthocephalans and infection were found in subpopulations on Polovina and Morzhovyj HOAS, the lowest was on Lukanin HOAS. From 3.2 % (for C. validum) to 19.4 % (for C. villosum) of NFSs were infected by one acanthocephalan species; two species were found in 22.6 %; three in 9.7 %; and four in 3.2 %. Further studies of NFS parasites are necessary to follow the trends in parasitic infection rates and diversity in NFS population on the Pribilov Islands and for monitoring the influence of various ecological factors on NFS populations in Alaska.

Parasitological examination for presence of hookworms (Uncinaria spp.) in northern elephant seals (Mirounga angustirostris) at Año Nuevo State Reserve, California (2012).

Northern elephant seals (Mirounga angustirostris Gill, 1866), inhabiting rookeries on the mainland of Año Nuevo State Reserve in central California, were investigated in 2012 for presence of hookworms (Uncinaria spp.). Material collected and examined for hookworms included: blubber (n = 15), stomach and intestines (n = 21) from dead pups; feces from the rectum of weaned pups (n = 23); sand containing apparent feces in areas of weaned pups (n = 28) and sand without apparent feces in areas of weaned pups (n = 54); milk from females (n =23) at 5 days and about 23 to 26 days postpartum; and placenta from one female. Evidence of hookworm presence was not detected in any of the samples examined. Possible reasons why hookworms were not found in northern elephant seals on the mainland of Año Nuevo State Reserve are discussed.

Paranasal sinus masses of Rocky Mountain bighorn sheep (Ovis canadensis canadensis).

This article describes 10 cases of paranasal sinus masses in Rocky Mountain bighorn sheep (Ovis canadensis canadensis). Among 21 bighorns that were examined from 11 herds in Colorado, 10 individuals (48%) from 4 herds (36%) had masses arising from the paranasal sinuses. Affected animals included 9 of 17 females (53%) and 1 of 4 males (25%), ranging in age from approximately 2 years to greater than 10 years. Defining gross features of these masses included unilateral or bilateral diffuse thickening of the respiratory lining of the maxillary and/or frontal sinuses, with abundant seromucinous exudate in the affected sinus cavities. Defining histologic features of these masses included chronic inflammation and proliferation of mesenchymal and epithelial cells of the mucosa and submucosa. Epithelial changes included hyperplasia of mucosal epithelium, hyperplasia of submucosal glands and ducts, and neoplasia (adenocarcinoma). Mesenchymal changes included submucosal myxedema, submucosal fibroplasia/fibrosis, bone destruction, and neoplasia (myxomatous fibroma). Specific immunohistochemistry and polymerase chain reaction for Jaagsiekte sheep retrovirus and enzootic nasal tumor virus were performed with negative results.

Clinical and pathologic responses of American crows (Corvus brachyrhynchos) and fish crows (C ossifragus) to experimental West Nile virus infection.

West Nile virus (WNV)-associated disease has a range of clinical manifestations among avian taxa, the reasons for which are not known. Species susceptibility varies within the avian family Corvidae, with estimated mortality rates ranging from 50 to 100%. We examined and compared virologic, immunologic, pathologic, and clinical responses in 2 corvid species, the American crow (Corvus brachyrhynchos) and the fish crow (C ossifragus), following experimental WNV inoculation. Unlike fish crows, which remained clinically normal throughout the study, American crows succumbed to WNV infection subsequent to dehydration, electrolyte and pH imbalances, and delayed or depressed humoral immune responses concurrent with marked, widespread virus replication. Viral titers were approximately 3,000 times greater in blood and 30,000 to 50,000 times greater in other tissues (eg, pancreas and small intestine) in American crows versus fish crows. Histologic lesion patterns and antigen deposition supported the differing clinical outcomes, with greater severity and distribution of lesions and WNV antigen in American crows. Both crow species had multiorgan necrosis and inflammation, although lesions were more frequent, severe, and widespread in American crows, in which the most commonly affected tissues were small intestine, spleen, and liver. American crows also had inflammation of vessels and nerves in multiple tissues, including heart, kidney, and the gastrointestinal tract. WNV antigen was most commonly observed within monocytes, macrophages, and other cells of the reticuloendothelial system of affected tissues. Collectively, the data support that WNV-infected American crows experience uncontrolled systemic infection leading to multiorgan failure and rapid death.

Emergence of diseases from wildlife reservoirs.

Interest in the epidemiology of emerging diseases of humans and livestock as they relate to wildlife has increased greatly over the past several decades. Many factors, most anthropogenic, have facilitated the emergence of diseases from wildlife. Some livestock diseases have "spilled over" to wildlife and then "spilled back" to livestock. When a population is exposed to an infectious agent, depending on an interaction of factors involving the host, agent, and environment, the population may be resistant to infection or may become a dead-end host, a spillover host, or a maintenance host. Each exposure is unique; the same species of host and agent may respond differently in different situations. Management actions that affect the environment and behavior of a potential host animal may allow the emergence of a new or as yet undetected disease. There are many barriers in preventing, detecting, monitoring and managing wildlife diseases. These may include political and legal hurdles, lack of knowledge about many diseases of wildlife, the absence of basic data on wildlife populations, difficulties with surveillance, and logistical constraints. Increasing interaction between wildlife and humans or domestic animals may lead to disease emergence and require innovative methods and strategies for disease surveillance and management in wildlife.

Detection of the abnormal isoform of the prion protein associated with chronic wasting disease in the optic pathways of the brain and retina of Rocky Mountain elk (Cervus elaphus nelsoni).

Eyes and nuclei of the visual pathways in the brain were examined in 30 Rocky Mountain elk (Cervus elaphus nelsoni) representing 3 genotypes of the prion protein gene PRNP (codon 132: MM, ML, or LL). Tissues were examined for the presence of the abnormal isoform of the prion protein associated with chronic wasting disease (PrP(CWD)). Nuclei and axonal tracts from a single section of brain stem at the level of the dorsal motor nucleus of the vagus nerve were scored for intensity and distribution of PrP(CWD) immunoreactivity and degree of spongiform degeneration. This obex scoring ranged from 0 (elk with no PrP(CWD) in the brain stem) to 10 (representing elk in terminal stage of disease). PrP(CWD) was detected in the retina of 16 of 18 (89%) elk with an obex score of > 7. PrP(CWD) was not detected in the retina of the 3 chronic wasting disease-negative elk and 9 elk with an obex score of < 6. PrP(CWD) was found in the nuclei of the visual pathways in the brain before it was found in the retina. Within the retina, PrP(CWD) was first found in the inner plexiform layer, followed by the outer plexiform layer. Intracytoplasmic accumulation of PrP(CWD) was found in a few neurons in the ganglion cell layer in the PRNP 132ML elk but was a prominent feature in the PRNP 132LL elk. Small aggregates of PrP(CWD) were present on the inner surface of the outer limiting membrane in PRNP 132LL elk but not in PRNP 132MM or 132ML elk. This study demonstrates PrP(CWD) accumulation in nuclei of the visual pathways of the brain, followed by PrP(CWD) in the retina.

Experimental chronic wasting disease (CWD) in the ferret.

Chronic wasting disease (CWD), a prion disease of North American deer, elk and moose, affects both free-ranging and captive cervids. The potential host range for CWD remains uncertain. The susceptibility of the ferret to CWD was examined experimentally by administering infectious brain material by the intracerebral (IC) or oral (PO) route. Between 15 and 20 months after IC inoculation, ferrets developed neurological signs consistent with prion disease, including polyphagia, somnolence, piloerection, lordosis and ataxia. Upon first sub-passage of ferret-adapted CWD, the incubation period decreased to 5 months. Spongiform change in the neuropil was most marked in the basal ganglia, thalamus, midbrain and pons. The deposition of PrP(CWD) was granular and was occasionally closely associated with, or localized within, neurons. There were no plaque-like or perivascular PrP aggregates as seen in CWD-infected cervids. In western blots, the PrP(CWD) glycoform profile resembled that of CWD in deer, typified by a dominant diglycosylated glycoform. CWD disease in ferrets followed IC but not PO inoculation, even after 31 months of observation. These findings indicate that CWD-infected ferrets share microscopical and biochemical features of CWD in cervids, but appear to be relatively resistant to oral infection by primary CWD inoculum of deer origin.

Gross and histopathologic effects of medroxyprogesterone acetate and progesterone on the mammary glands of adult beagle bitches.

Adult beagle bitches received 0.2 to 75 mg/kg doses of medroxyprogesterone acetate (MPA) once every 3 months for 1 to 1.5 years. Doses greater than 2.0 mg/kg prevented the recurrence of ovarian cycles; lower doses did not. MPA (10 and 75 mg/kg) induced a dose-related development of multiple, large (greater than 5 mm diameter) mammary nodules that occurred earlier in older dogs than in younger dogs. MPA-induced mammary hyperplasia and nonnodular dysplasias were also noted. Most of the large (5 to 110 mm in diameter) MPA-induced nodules were, in nearly equal numbers, nodules of lobular hyperplasia, simple adenomas, or complex adenomas. Such benign mammopathies all appear to have histopathologic counterparts in human breast disease. However, simple adenomas are uncommon in both humans and dogs. Some of the MPA-induced nodules were benign mixed tumors with cartilaginous metaplasia. No malignant tumors were found. Induction of mammary tumors by 75 mg MPA/kg was not affected by prior ovariectomy but was reached by prior hypophysectomy, suggesting involvement of pituitary secretion in MPA-induced mammary gland disease.

Ascaridoid nematodes and associated lesions in stomachs of subadult male northern fur seals (Callorhinus ursinus) on St. Paul Island, Alaska: (1987-1999).

Stomachs from subadult male northern fur seals (SAMs) (Callorhinus ursinus) (n = 5,950) from St. Paul Island, Alaska, were examined from 1987 to 1999 for lesions and parasites. On gross examination of these stomachs, parasite nodules were evident in 92% of the stomachs and active and healing ulcers were found in 14% and 10%, respectively. Prevalence of nematodes from 1987 to 1997 was 88% for 5,700 SAMs for which numbers of parasites were estimated but not identified to the genus level. All nematodes recovered from 250 SAMs examined in 1998 (n = 124; 99% infected) and in 1999 (n = 126; 91% infected) were identified and counted. Prevalences in 1998 and 1999 were 5% and 0% for Anisakis spp., 52% and 18% for Contracaecum spp., and 96% and 89% for Pseudoterranova spp., respectively.

Epizootic malignant catarrhal fever in three bison herds: differences from cattle and association with ovine herpesvirus-2.

Three bison herds in Colorado experienced high mortality from malignant catarrhal fever (MCF). In comparison with cattle, the bison had a more rapidly progressive disease, fewer clinical signs, and milder inflammatory histologic lesions. There was consistent association with ovine herpesvirus-2 (OHV-2). Contact with sheep was not consistent. Of 17 animals in herd A, 15 died of acute MCF; 1 was slaughtered while healthy; and 1 developed clinical signs of MCF, was treated with corticosteroids and antibiotics, and died of fungal abomasitis and rhinitis after 5 months. In herds B and C, approximately 300 of 900 and 18 of 20 died of MCF following brief clinical disease. The nearest sheep were 1 mile away from herd A, but direct contact with sheep could be documented in herds B and C. Complete gross and histologic examinations were conducted on 34 animals, including all animals in herd A, and MCF was diagnosed in 31. In addition, field necropsies were performed on all dead animals in herd B and most in herd C and MCF was diagnosed on the basis of the gross lesions in most animals. Clinical signs of each animal in herd A were recorded. Illness was brief, usually 8-48 hours. Clinical signs were subtle; separation from the herd was often observed. In all 3 herds, hemorrhagic cystitis and multifocal ulceration of the alimentary tract were consistently found at necropsy. Mild lymphocytic vasculitis was present in multiple organs. Ovine herpesvirus-2 was found by polymerase chain reaction (PCR) in 71 of 105 formalin-fixed tissue specimens from 29 of 31 animals with MCF. In herd A, blood samples from 13 animals were collected at 5 time points and tested by PCR for the presence of OHV-2 viral sequences in peripheral blood leukocytes. Nine bison with a positive PCR test and 4 with negative results prior to clinical illness died of MCF.

Validation of monoclonal antibody F99/97.6.1 for immunohistochemical staining of brain and tonsil in mule deer (Odocoileus hemionus) with chronic wasting disease.

A new monoclonal antibody (MAb), F99/97.6.1, that has been used to demonstrate scrapie-associated prion protein PrP(Sc) in brain and lymphoid tissues of domestic sheep with scrapie was used in an immunohistochemistry assay for diagnosis of chronic wasting disease (CWD) in mule deer (Odocoileus hemionus). The MAb F99/97.6.1 immunohistochemistry assay was evaluated in brain and tonsil tissue from 100 mule deer that had spongiform encephalopathy compatible with CWD and from 1,050 mule deer outside the CWD-endemic area. This MAb demonstrated abnormal protease-resistant prion protein (PrP(res)) in brains of all of the 100 mule deer and in 99 of the 100 tonsil samples. No immunostaining was seen in samples collected from deer outside the endemic area. MAb F99/97.6.1 demonstrated excellent properties for detection of PrP(res) in fresh, frozen, or mildly to moderately autolytic samples of brain and tonsil. This immunohistochemistry assay is a sensitive, specific, readily standardized diagnostic test for CWD in deer.

Comparative biology of Uncinaria spp. in the California sea lion (Zalophus californianus) and the northern fur seal (Callorhinus ursinus) in California.

Studies on several aspects of the life cycle of hookworms (Uncinaria spp.) in the California sea lion (Zalophus californianus) and northern fur seal (Callorhinus ursinus) were conducted on material collected on San Miguel Island (SMI), California and at The Marine Mammal Center, Sausalito, California in 1997, 1998, and 1999. Examination of Z. californianus intestines for adult hookworms and feces for eggs revealed that longevity of these parasites in pups is about 6-8 mo, and infections are probably not present in older sea lions. Parasitic third-stage larvae (L3) were recovered from the ventral abdominal tissue of Z. californianus, suggesting transmammary transmission. Callorhinus ursinus pups had no hookworm eggs in their feces or adult worms (except for 1 probable contaminant) in their intestines in the fall and early winter, revealing that adult Uncinaria spp. are spontaneously lost at <3 mo of age of the pups. Sand samples from rookeries, used by both Z. californianus and C. ursinus, on SMI were negative for free-living, L3 in summer months but positive in fall and winter months, indicating seasonality occurred.

Abomasal erosions in feedlot cattle.

The abomasa of 1,949 slaughtered feedlot cattle, 45 necropsied feedlot cattle that died 2 to 45 days after arrival, and 45 necropsied pastured cattle were opened and examined. Of these organs, 484, 1, and none, respectively, contained erosions. The slaughtered cattle were fattened at 3 locations: 1,305 with 430 eroded abomasa were fed a ration of corn in northeastern Colorado; 144 cattle with 4 affected abomasa fed a ration of milo in south-central Arizona; and 500 cattle with 50 affected abomasa fed a ration of milo and corn in northwestern Texas. The red-brown lesions developed late during the second semester of fattening and were located mostly on fundic folds. Those on fold edges were linear and were 2 to 15 cm long, whereas those on fold sides were punctate and were 2 to 15 mm in diameter. Normal fold edges contained fewer goblet cells and less surface mucus than did fold sides. Eroded folds had disruption of surface epithelium, damage to endothelial cells, and dilated, thrombosed, congested, and ruptured capillaries. Mean pH values of 16 normal and 17 eroded abomasa were 4.7 and 3.9, respectively. Necrosis of all tissue toward the mucosal surface of erosions was extensive. The cause of gastric erosion in cattle is not known.

Capture myopathy in wild turkeys (Meleagris gallopavo) following trapping, handling and transportation in Colorado.

Sixty wild turkeys were necropsied following trapping, transporting and handling during the winters of 1980-1981, 1981-1982, and 1982-1983 in order to determine the incidence of subclinical capture myopathy. Gross lesions characterized by small to large patchy, pale white streaked areas within skeletal muscle were found in 13 of 27 birds trapped with a drop net in the winter of 1982-1983. Microscopic lesions within myocardium characterized by irregular areas of coagulative necrosis, collapse of intercellular stroma and myocardial nuclear proliferation were found in two of 14 birds in 1980-1981, five of 19 birds in 1981-1982 and 11 of 27 birds in 1982-1983. Microscopic lesions within skeletal muscle characterized by rhabdomyolysis were found in 16 of 19 birds in 1981-1982 and 25 of 27 birds in 1982-1983. These findings suggest that wild turkeys are susceptible to capture myopathy and particular caution should be exercised in capturing and handling these birds.