Systematic review of management strategies to control chronic wasting disease in wild deer populations in North America.

BACKGROUND: Chronic wasting disease (CWD) is a contagious, fatal prion disease affecting cervids in a growing number of regions across North America. Projected deer population declines and concern about potential spread of CWD to other species warrant strategies to manage this disease. Control efforts to date have been largely unsuccessful, resulting in continuing spread and increasing prevalence. This systematic review summarizes peer-reviewed published reports describing field-applicable CWD control strategies in wild deer populations in North America using systematic review methods. Ten databases were searched for peer-reviewed literature. Following deduplication, relevance screening, full-text appraisal, subject matter expert review and qualitative data extraction, nine references were included describing four distinct management strategies. RESULTS: Six of the nine studies used predictive modeling to evaluate control strategies. All six demonstrated one or more interventions to be effective but results were dependant on parameters and assumptions used in the model. Three found preferential removal of CWD infected deer to be effective in reducing CWD prevalence; one model evaluated a test and slaughter strategy, the other selective removal of infected deer by predators and the third evaluated increased harvest of the sex with highest prevalence (males). Three models evaluated non-selective harvest of deer. There were only three reports that examined primary data collected as part of observational studies. Two of these studies supported the effectiveness of intensive non-selective culling; the third study did not find a difference between areas that were subjected to culling and those that were not. Seven of the nine studies were conducted in the United States. CONCLUSIONS: This review highlights the paucity of evaluated, field-applicable control strategies for CWD in wild deer populations. Knowledge gaps in the complex epidemiology of CWD and the intricacies inherent to prion diseases currently pose significant challenges to effective control of this disease in wild deer in North America.

Myxobolus neurophilus Guilford 1963 (Myxosporea: Myxobolidae): a common parasite infecting yellow perch Perca flavescens (Mitchell, 1814) in Saskatchewan, Canada.

The goal of this study was to identify a myxosporidian parasite infecting the central nervous system of yellow perch Perca flavescens (Mitchell, 1814) observed while investigating a fish kill in Saskatchewan, Canada. Fish were collected from seven different lakes, from two distinct watersheds. Sixty-four per cent (54/86) of yellow perch contained myxozoan pseudocysts located throughout the spinal cord and brain. Myxospores measured 16.5 µm (range 16.2-16.8) long and 8.2 µm (range 7.9-8.4) wide and contained two pyriform, mildly dissymmetrical, polar capsules measuring 7.7 µm (range 7.3-8.1) long and 2.7 µm (range 2.4-3.0) wide. The polar capsules each contained a single polar filament, with 7-9 turns per polar filament coil. Sequencing of the 18S SSU rDNA gene demonstrated >99% similarity to Myxobolus neurophilus. In 60% of infected fish, there was a mild to moderate, non-suppurative myelitis or encephalitis, or both, associated with myxospores. Axonal degeneration was present in rare cases. These findings extend the geographical distribution of M. neurophilus and suggest it may be widespread in yellow perch populations in Saskatchewan.

Protostrongylid parasites and pneumonia in captive and wild thinhorn sheep (Ovis dalli).

We describe health significance of protostrongylid parasites (Parelaphostrongylus odocoilei and Protostrongylus stilesi) and other respiratory pathogens in more than 50 naturally infected Dall's sheep (Ovis dalli dalli) from the Mackenzie Mountains, Northwest Territories (1998-2002) as well as in three Stone's sheep (O. d. stonei) experimentally infected with P. odocoilei (2000-2002). Histological lesions in the brain and distribution of P. odocoilei in the muscles of experimentally and naturally infected sheep were consistent with a previously hypothesized "central nervous system to muscle" pattern of migration for P. odocoilei. Dimensions of granulomas associated with eggs of P. odocoilei and density of protostrongylid eggs and larvae in the cranial lung correlated with intensity of larvae in feces, and all varied with season of collection. Prevalence of P. stilesi based on the presence of larvae in feces underestimated true prevalence (based on examination of lungs) in wild Dall's sheep collected in summer and fall. Similarly, counts of both types of protostrongylid larvae in feces were unreliable indicators of parasitic infection in wild Dall's sheep with concomitant bacterial pneumonia associated with Arcanobacterium pyogenes, Pasteurella sp., and Mannheimia sp. Diffuse, interstitial pneumonia due to P. odocoilei led to fatal pulmonary hemorrhage and edema after exertion in one experimentally infected Stone's sheep and one naturally infected Dall's sheep. Bacterial and verminous pneumonia associated with pathogens endemic in wild Dall's sheep in the Mackenzie Mountains caused sporadic mortalities. There was no evidence of respiratory viruses or bacterial strains associated with domestic ruminants, from which this population of wild sheep has been historically isolated.

Pathology, isolation, and preliminary molecular characterization of a novel iridovirus from tiger salamanders in Saskatchewan.

All iridovirus was confirmed to be the cause of an epizootic in larval and adult tiger salamanders (Ambystoma tigrinum diaboli) from four separate ponds in southern Saskatchewan (Canada) during the summer of 1997. This organism also is suspected, based on electron microscopic findings, to be the cause of mortality of larval tiger salamanders in a pond over 200 km to the north during the same year. Salamanders developed a generalized viremia which resulted in various lesions including: necrotizing, vesicular and ulcerative dermatitis; gastrointestinal ulceration; and necrosis of hepatic, splenic, renal, lymphoid, and hematopoietic tissues. In cells associated with these lesions, large lightly basophilic cytoplasmic inclusions and vacuolated nuclei with marginated chromatin were consistently found. Virus was isolated from tissue homogenates of infected salamanders following inoculation of epithelioma papilloma cyprini (EPC) cells. The virus, provisionally designated Regina ranavirus (RRV), was initially identified as an iridovirus by electron microscopy. Subsequent molecular characterization, including partial sequence analysis of the major capsid protein (MCP) gene, confirmed this assignment and established that RRV was a ranavirus distinct from frog virus 3 (FV3) and other members of the genus Ranavirus. Intraperitoneal inoculation of 5 x 10(6.23) TCID50 of the field isolate caused mortality in inoculated salamanders at 13 days post infection. Field, clinical, and molecular studies jointly suggest that the etiological agent of recent salamander mortalities is a highly infectious novel ranavirus.

The 1992 epizootic of Newcastle disease in double-crested cormorants in North America.

In the summer of 1992, morbidity and mortality in juvenile double-crested cormorants (Phalacrocorax auritus; DCC) attributable to Newcastle disease virus (NDV) was observed for the first time in seven northern USA states and one Canadian province, and recurred in three western Canadian provinces. Based on clinical signs and laboratory diagnostic findings, DCC mortality from NDV occurred in 59 of the 63 nesting colonies and two of three non-colony sites investigated. An estimate of in excess of 20,000 DCC died, with mortality rates ranging from < 1 to 37% in Great Lakes colonies to 20 to 92% in Minnesota (USA) and North and South Dakota (USA) colonies. Sick juvenile white pelicans (Pelecanus erythrorhynchos) exhibiting signs similar to sick cormorants, and dead pelicans were observed in Minnesota and North Dakota. Mortality rates in pelican colonies were as high as in the adjacent cormorant colonies, but no cause for the mortality of an estimated 5,000 pelicans was determined. No evidence of NDV was found in other species nesting in proximity to affected cormorants. Although the source of the NDV infection is unknown in cormorants, the simultaneous onset of the epizootics in juvenile birds over a wide geographic area implies that the virus was acquired by adults prior to migration and was carried back to nest sites, exposing susceptible nestlings. The possible transmission of this virus from free-ranging wild birds to domestic poultry is a concern. Based on repeated epizootics in cormorants since 1990, NDV seems to be established in DCC.

Effects of the intestinal flagellate, Cochlosoma anatis, on intestinal mucosal morphology and disaccharidase activity in Muscovy ducklings.

Newly hatched female Muscovy ducklings were randomly separated into 2 groups of 12 and 1 group of 13. Ducklings in the first 2 groups were each orally inoculated with 0.5 ml of sterile normal saline containing 0 and 3 x 10(6) trophozoites of Cochlosoma anatis, respectively. Birds in the third group were each orally inoculated with 3 x 10(6) trophozoites for 5 consecutive days. Birds were weighed daily for the first 5 days and then on days 7, 14 and 21 post-inoculation (p.i.). On days 6, 7, 8, 13, 14, 15, 20, 21 and 22 p.i., 1 bird from each group was killed and samples of intestine at 7 levels were taken for trophozoite counts, mucosal disaccharidase analyses and morphometric analysis. Body weights did not differ among treatment groups at any time during the experiment. Trophozoite numbers did not change over the period 6-22 days p.i. Trophozoite numbers were lowest in the anterior small intestine and increased distally, but very few were observed in the caecum. Crypt depth was greater in all regions of the small intestine in inoculated groups compared to uninoculated controls, and was significantly increased in the duodenum, proximal jejunum and mid-jejunum (P < 0.05). Villus height was greater in inoculated groups compared to controls at all levels of the intestine and was significantly increased in the duodenum, proximal jejunum and ileum (P < 0.05). Mucosal palatinase and maltase activity in the small intestine were reduced in inoculated groups compared to uninoculated controls; palatinase activities were significantly reduced in the proximal and mid-jejunum and maltase activities were significantly reduced in the mid-jejunum (P < 0.05). Sucrase activities were significantly increased at all levels of the small intestine in inoculated ducklings compared to uninoculated controls (P < 0.05). Although no clinical signs were evident, Cochlosoma infection significantly altered intestinal morphometrics and mucosal enzyme concentrations in ducklings, in several cases in a counter-intuitive direction.

Runting of ducklings associated with Cochlosoma anatis infection.

Ducklings, especially common goldeneye (Bucephala clangula), experiencing poor weight gain and delayed development were reported from a waterfowl park during June and July of 1990. Runting was first noticed between days 5 and 10 post-hatch in the "brooder" building, and although ducklings appeared active and were feeding, they developed at a slower rate than other members of their clutch. Many ultimately died of emaciation and gram-negative bacterial septicemia. Necropsies of affected ducklings revealed large numbers of the intestinal flagellate Cochlosoma anatis, in both the small and the large intestine; however, autolysis impaired histological interpretation in many cases. Inoculation of 1-day-old Muscovy ducklings with feces containing large numbers of C. anatis resulted in poor weight gain and delayed tail-feather development compared with uninoculated control ducklings. Weight gain improved after treatment with metronidazole. Cochlosoma anatis is associated with the runting syndrome observed in ducklings at the waterfowl park.

Lupus-type "anticoagulant" in a dog with hemolysis and thrombosis.

A circulating anticoagulant was detected in a 2-year-old Chesapeake Bay Retriever with hemolytic anemia, nephrotic syndrome, thrombocytopenia, polyarthropathy, and pulmonary thromboembolism. A persistent prolongation of the activated partial thromboplastin time (aPTT) was detected, and it did not correct with repeated administration of fresh frozen plasma. The aPTT was still prolonged, with a 1:1 mixture of patient's plasma and normal dog plasma in vitro, suggesting the presence of a circulating inhibitor. Results of assays to characterize the inhibitor were compatible with those described for the lupus anticoagulant in human patients with systemic lupus erythematosus. Paradoxically, patients having the lupus anticoagulant are at increased risk for thrombosis. Pulmonary thromboembolism has been described as a frequent complication of immune-mediated hemolytic anemia in the dog, and the presence of a circulating anticoagulant should be considered as a potential mechanism.