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.

Carcasses of northern fur seal pups, Callorhinus ursinus , collected from the rookeries of Bering Island ( n = 133), were examined for hookworms Uncinaria spp. The parasite was found in 90% of the pups from the Severo-Zapadnoe rookery and in 45% of the pups from the Severnoe rookery. This difference in prevalence of nematode infection between the rookeries is associated with the type of substrate, as well as with the pattern of distribution of the seal reproductive groups on each of the rookeries.

Abstract To increase the currently limited knowledge addressing acanthocephalans parasitizing California sea lions (Zalophus californianus), 33 animals including pups, juvenile and adult males and females from the Marine Mammal Center (TMMC), Sausalito, California, USA were examined. Totally, 2,268 specimens of acanthocephalans representing five species from the genera Andracantha (A. phalacrocoracis and Andracantha sp.), Corynosoma (C. strumosum and C. obtuscens) and Profilicollis (P. altmani) were found. Profilicollis altmani and A. phalacrocoracis, predominantly parasitize fish-eating birds; they were registered in Z. californianus for the first time. Prevalence and intensity of California sea lion infection and transmission of acanthocephalans in these hosts of different age groups were analyzed and discussed. We provide brief morphological descriptions of the five species of acanthocephalan found in California sea lions.

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.

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.

Summary Necropsy and extensive parasitological examination of dead northern elephant seal (NES) pups was done on San Miguel Island, California, in February, 2015. The main interest in the current study was to determine if hookworms were present in NESs on San Miguel Island where two hookworm species of the genus Uncinaria are known to be present - Uncinaria lyonsi in California sea lions and Uncinaria lucasi in northern fur seals. Hookworms were not detected in any of the NESs examined: stomachs or intestines of 16 pups, blubber of 13 pups and blubber of one bull. The results obtained in the present study of NESs on San Miguel Island plus similar finding on Año Nuevo State Reserve and The Marine Mammal Center provide strong indication that NES are not appropriate hosts for Uncinaria spp. Hookworm free-living third stage larvae, developed from eggs of California sea lions and northern fur seals, were recovered from sand. It seems that at this time, further search for hookworms in NESs would be nonproductive.

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 %; overallmean 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.

Abstract Prevalence of Hookworms, Uncinaria lucasi (Ancylostomatidae), in Northern Fur Seals (Callorhinus ursinus) on St. Paul Island, Alaska. Lyons, E. T., Kuzmina, T. A., Carie, J. L., Tolliver, S. C., Spraker, T. R. — Review of main studies on biology and ecology of the hookworm Uncinaria lucasi Stiles, 1901 performed on St. Paul Island, Alaska, is presented. Current data on prevalence of adult hookworms parasitizing northern fur seals (NFS), Callorhinus ursinus Linnaeus, 1758, were obtained based on the examination of the intestines of dead NFS pups and subadult 3-4 year-old males in July and August of 2011-2013. In addition, blubber samples collected from subadult NFS males were examined for parasitic third stage hookworm larvae (L3). All current data were compared with previously published studies performed in 1950s-1960s. Current prevalence of U. lucasi in dead pups collected from Reef Rookery was 4.9 % in 2011, 0 % in 2012 and 10.5 % in 2013. This rookery has a rocky substrate. On sandy rookeries prevalence was up to 75 % on Morjovi Rookery and 50 % on Vostochni Rookery. Parasitic L3 were recovered in 2.5 % of subadult males examined in 2013. Decreasing prevalence of hookworm infection of dead pups and subadult males during the last several years follows the tremendous decline in the number of fur seals in the herd on St. Paul Island during last several decades.

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.

The aim of this study was to test the hypothesis that oxidative stress and glutamine synthetase (GS) redistribution occur in domoic acid (DA) toxicosis in California sea lions (CSLs, Zalophus californianus). Sections of archived hippocampi from seven control and 13 CSLs diagnosed with DA toxicosis were labelled immunohistochemically for GS and for two markers of oxidative stress, malondialdehyde (MDA) and 3-nitrotyrosine (NT). The distribution and intensity of labelling were compared with the pathological changes seen in haematoxylin and eosin-stained sections. Increased expression of MDA and NT occurred in neurons of the hippocampal formation of CSLs with lesions consistent with DA toxicosis. The degree of oxidative stress was not affected significantly by the chronicity or severity of hippocampal damage. In six out of seven CSLs with chronic effects of DA toxicosis, in addition to the normal glial distribution of GS, GS expression was very strong in some neurons of the subiculum. However, neuronal GS labelling was also seen in one control CSL, an effect that may have been due to previous exposure to DA. GS expression in neurons was associated with decreases in GS labelling in neighbouring glial cell processes. DA toxicosis therefore induces increased expression of markers of oxidative stress in neurons consistent with oxidative stress contributing to the initial DA insult and also the epilepsy that often develops in chronic DA toxicosis. GS redistribution occurred primarily in chronic DA toxicosis, perhaps leading to alterations of the glutamine-glutamate-GABA (gamma-aminobutyric acid) cycle and contributing to the excitotoxicity and seizures often seen in DA toxicosis.

Six bald eagles with severe, acute lead poisoning based on blood lead values were analyzed by Magnetic Resonance Imaging (MRI) of the brain and histopathology. The aims of the study were to use MRI to locate brain lesions and correlate the changes in MRI signal with the histological character of the lesions at necropsy. All of the bald eagles presented with neurologic and non-neurologic signs suggestive of severe lead poisoning and had blood lead levels in excess of 1.0 ppm. Areas of change in image intensity in the brainstem, midbrain and cerebellum were detected in the MRI scans. Histopathology confirmed the presence of all suspected lesions. The character of the lesions suggested vascular damage as the primary insult. MRI was useful for detecting lesions and defining their three-dimensional distribution and extent. Future studies are needed to evaluate the utility of MRI for detection of lesions in less severely lead poisoned eagles and determining prognosis for treatment.

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.

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.

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.

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.

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.

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 (PrPCWD). 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 PrPCWD immunoreactivity and degree of spongiform degeneration. This obex scoring ranged from 0 (elk with no PrPCWD in the brain stem) to 10 (representing elk in terminal stage of disease). PrPCWD was detected in the retina of 16 of 18 (89%) elk with an obex score of > 7. PrPCWD was not detected in the retina of the 3 chronic wasting disease–negative elk and 9 elk with an obex score of < 6. PrPCWD was found in the nuclei of the visual pathways in the brain before it was found in the retina. Within the retina, PrPCWD was first found in the inner plexiform layer, followed by the outer plexiform layer. Intracytoplasmic accumulation of PrPCWD 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 PrPCWD 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 PrPCWD accumulation in nuclei of the visual pathways of the brain, followed by PrPCWD in the retina.

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.

Intestines of dead northern fur seals (Callorhinus ursinus) on St. Paul Island (SPI), Alaska were inspected for specific internal parasites (hookworms and acanthocephalans) in July and August, 2007. Pups (n=64) were examined for adult hookworms (Uncinaria lucasi) and four (6.25%) were infected. The number of specimens per infected pup was 1, 2, 2, or 408. Low prevalence was similar to that determined in the last investigation (2001) in dead fur seal pups on SPI by two of the present authors (Lyons and Spraker). Subadult males (SAMS-3-4 years old, n=115) were examined for acanthocephalans and 25 (21.7.0%) were infected. Adult Corynosoma (C. obtuscens, C. strumosum, and C. validum) (n=56) and immature Bolbosoma spp. (n=4) were found. Apparently, this is a new host record for C. obtuscens and C. validum. Notes were made on finding tapeworms. in 114 of the 115 SAMs. Examination of some specimens revealed scolices characteristic of Diphyllobothrium spp.