Systemic sarcocystosis in a wild turkey from Georgia.

Acute sarcocystosis was diagnosed in an adult female wild turkey (Meleagris gallopavo) that was collected from Early County (Georgia, USA) in February of 1998. Marked inflammatory lesions were seen in the heart, lung, and liver and were associated with protozoal schizonts and merozoites. The organisms were identified as Sarcocystis sp. (Acomplexa: Sarcocystidae) based on structure and antigenicity. Protozoa divided by endopolygeny, merozoites lacked rhoptries, and the organisms did not react to anti-S. falcatula antibodies but reacted to anti-S. cruzi antibodies.

The effect of dietary aflatoxin on wild turkey poults.

Aflatoxins, toxic metabolites of Aspergillus flavus or Aspergillus parasiticus, cause poor feed utilization, decreased weight gains, depressed immune function, liver dysfunction, coagulation abnormalities, and death in a wide variety of species including humans. Conservationists have become concerned that increasingly popular wildlife feeding or baiting practices could expose wildlife to toxic amounts of aflatoxin-contaminated grains. In particular, the effects of aflatoxins on the wild turkey (Meleagris gallopova silvestris) are of concern because the conspecific domestic turkey is highly susceptible to aflatoxins. To evaluate the effect of dietary aflatoxin on wild turkeys, four groups of 4-mo-old wild turkeys were fed diets containing either 0, 100, 200, or 400 micrograms aflatoxin/kg feed for 2 wk in September and October 1996. Aflatoxin-fed poults had decreased feed consumption and weight gains as compared with control poults. Decreased liver-to-body weight ratios, liver enzyme alterations, slightly altered blood coagulation patterns, and mild histologic changes indicated low-level liver damage. Compromise of cell-mediated immunity was indicated by decreased lymphoblast transformation. The effects were apparent in all treatment groups to variable levels, but significant differences most often were found at 400 micrograms aflatoxin/kg feed. This study shows that short-term aflatoxin ingestion by wild turkeys can induce undesirable physiologic changes; therefore, exposure of wild turkeys to feeds containing aflatoxin levels of 100 micrograms aflatoxin/kg feed or more should be avoided.

Normal hematologic and serum biochemical reference intervals for juvenile wild turkeys.

Blood samples taken from 48 4-mo-old wild turkeys (Meleagris gallopova silvestris) were used to establish reference intervals for hematology and serum chemistry values. The study was conducted during September and October 1996. Packed cell volume, total and differential white cell counts, total protein, albumin, glucose, calcium, uric acid, triglyceride concentrations, as well as aspartate transaminase (AST) and lactate dehydrogenase (LDH) activities were assayed. Reference intervals from wild turkeys are similar to those reported for domestic turkeys.

Granular cell tumour in an endangered Puerto Rican Amazon parrot (Amazon vittata ).

A 3 cm diameter mass from the metacarpus of a Puerto Rican Amazon parrot was diagnosed as a granular cell tumour based on light microscopy. The cytoplasmic granules were periodic-acid Schiff positive and diastase resistant. Ultrastructural characteristics of the cells included convoluted nuclei and the presence of numerous cytoplasmic tertiary lysosomes. This is only the second granular cell tumour reported in a bird. We speculate that most granular cell tumours are derived from cells that are engaged in some type of cellular degradative process, creating a similar morphologic appearance, but lacking a uniform histogenesis.

Gastrointestinal ulceration and pulmonary aspergillosis in a llama treated for parelaphostrongylosis.

A 9-year-old llama examined because of hind limb paresis was found to have parelaphostrongylosis. Despite treatment with ivermectin, fenbendazole, cimetidine, and ceftiofur, the llama developed gastrointestinal ulceration and pulmonary aspergillosis and was euthanatized. Parelaphostrongylus tenuis is a parasite of white-tailed deer, but ruminants can serve as aberrant or dead-end hosts after accidentally ingesting snails or slugs carrying third-stage larvae of the parasite. Gastrointestinal ulceration and pulmonary aspergillosis can develop secondarily in llamas with chronic disease. Treatment of gastrointestinal ulceration in llamas is difficult, because efficacy of commonly used antiulcer drugs in llamas has not been established.

In vitro replication of epizootic hemorrhagic disease and bluetongue viruses in white-tailed deer peripheral blood mononuclear cells and virus-cell association during in vivo infections.

In vitro and in vivo infections were conducted to determine if the epizootic hemorrhagic disease (EHD) and bluetongue (BT) viruses would replicate in peripheral blood mononuclear (PBM) cells of white-tailed deer (Odocoileus virginianus). All of the North American EHD and BT viruses (EHD virus serotypes 1 and 2, and BT virus serotypes 2, 10, 11, 13, and 17) replicated in vitro in cultures of white-tailed deer PBM cells. However, this replication appeared to be monocyte-dependent and was not enhanced by lymphocyte blastogenesis induced by the addition of concanavalin A. In white-tailed deer infected with either EHD virus serotype 2 or BT virus serotype 10, virus could be isolated consistently from PBM cells only from post-infection day 4 through 8, although they remained viremic through post-infection day 21. In deer, highest viral titers were associated with the erythrocyte fraction, and in no cases did viral titers detected in the platelet, PBM cell or polymorphonuclear cell fractions approach titers observed in whole blood. In the in vitro infections of white-tailed deer erythrocytes, the EHD and BT viruses were associated with pits in the erythrocyte membrane. This association may be important in the long-term viremia observed in deer.

Host defense responses associated with experimental hemorrhagic disease in white-tailed deer.

Our objectives were to examine the immunity conferred by epizootic hemorrhagic disease virus serotype 2 (EHDV-2) infection in white-tailed deer (Odocoileus virginianus) and determine if this immunity was protective during challenge with homologous (EHDV-2) or heterologous (bluetongue virus serotype 10; BTV-10) virus. Trials were conducted in the fall of 1992 and 1993. In the first experiment, naive white-tailed deer were infected intradermally and subcutaneously with EHDV-2 and monitored via physical examinations, complete blood counts, alpha and beta interferon (IFN) assays, viral isolation, and serology. Infected deer had a wide range of clinical signs in response to infection. Eleven of the 16 deer had body temperature elevations > or = 0.5 C between post-infection day (PID) 4 and 8. Infected deer had decreased lymphocyte counts between PID 6 and 10 that returned to normal levels by PID 17. Severely lymphopenic animals had the most severe clinical signs; five of 10 deer with lymphocyte counts less than 1000 cells/microliters succumbed to the infection. Viremia was detected in all 16 EHDV-2 infected animals by PID 4, and peak viremias occurred between PID 4 and PID 10. Three deer remained viremic until PID 56, the study endpoint. Interferon was first detected between PID 2 and 6. Peak alpha and beta IFN levels coincided with peak viremia in 11 deer. Precipitating and neutralizing antibodies were detected in infected deer by PID 10. In the second experiment, convalescent deer were challenged subcutaneously and intradermally with either EHDV-2 or BTV-10 and similarly monitored. Virus was detected in the blood of all four deer challenged with BTV-10, but viremia was not detected in three EHDV-2-challenged deer. Temperature fluctuations, blood cell parameter changes, and IFN and antibody responses seen in BTV-10-challenged deer were similar to those seen in the initial experiment. Deer challenged with EHDV-2 had mildly increased temperatures, but minimal IFN response and lymphocyte alterations.

Cell-mediated immune response and IL-2 production in white-tailed deer experimentally infected with hemorrhagic disease viruses.

Hemorrhagic disease, caused by various serotypes of two closely related orbivirus serogroups, the epizootic hemorrhagic disease viruses (EHDV) and the bluetongue viruses (BTV), is a major cause of morbidity and mortality in white-tailed deer (WTD) in the United States. Despite the importance of hemorrhagic disease in WTD, little is known about host defense mechanisms triggered by infection with either causative virus or how that immune response is modulated by challenge with closely related orbiviruses, as can occur under natural conditions. Initial experimental data from our laboratory showed WTD infected with EHDV serotype 2 (EHDV-2) had responded serologically but often became lymphopenic and had a reduced lymphocyte proliferative response in vitro to T-cell mitogens, suggesting possible suppression of cell-mediated immunity. The primary objective of this study was to more closely examine cell-mediated immunity of WTD when experimentally infected with EHDV-2 and subsequently challenged with BTV serotype 10 (BTV-10). The cell-mediated response was evaluated via in vitro lymphocyte proliferation and interleukin-2 (IL-2) production assays, and in vivo delayed type hypersensitivity tests. Deer infected with either EHDV-2 or BTV-10 responded similarly in all assays. Infected deer had decreased lymphocyte counts between post-infection days (PID) 6 and 10, with concurrent diminished lymphocytic response to concanavalin A in lymphocyte proliferation assays and phytohemagglutinin in delayed, type hypersensitivity tests. However, IL-2 production by peripheral blood lymphocytes of infected deer was comparable with that of non-infected control deer as measured using a IL-2-dependent bovine cell line (BT2). This suppression of T-cell proliferation, but not IL-2 production suggests selective inhibition of T-cells probably via altered signal transduction for either expression of the IL-2 receptor or for IL-2 receptor signal-induced T-cell proliferation.

Clinical illness in a wild turkey with Laminosioptes cysticola infestation of the viscera and peripheral nerves.

Laminosioptes cysticola, the fowl cyst mite, was found in peripheral nerves and thoracic and abdominal viscera of an emaciated eastern wild turkey (Meleagris gallopavo) exhibiting severe torticollis, circling, loss of balance, and wing droop. Mites, sometimes accompanied by granulomatous inflammation, were abundant in brachial plexus and sciatic nerves. Mild lymphoplasmacytic perivascular cuffing was present in the cerebellum, but no direct evidence of mites or other infectious agents was found in the central nervous system. This is the first report of L. cysticola infestation in a wild turkey and of the invasion of nervous tissue by this mite.

Evaluation of low-level aflatoxin in the diet of white-tailed deer.

We evaluated the response of white-tailed deer (WTD) (Odocoileus virginianus) to dietary aflatoxin. Fourteen 4-to-5-mo-old WTD were used in this 8-wk study, conducted between November 1993 and January 1994. Seven animals received a ration containing 800 parts per billion (ppb) total aflatoxin (AF). Seven control animals received the same ration without AF. At 0, 1, 3, 6 and 8 wk, feed consumption, feed conversion, liver enzymes, bile acid levels, and immune function via lymphocyte proliferation assays and delayed type hypersensitivity reactions were determined. At the conclusion of the 8-wk feeding trial, deer were euthanized and necropsied. Clinical illness was not evident in any of the animals, but by the end of the study, AF-fed deer had reduced feed consumption and body weight as compared to control deer; the differences were not statistically significant. The AF-exposed group had a significant increase (P = 0.03) in serum bile acid concentration as compared to control deer. Two AF-exposed deer had gross and histologic hepatic lesions indicative of a mild degenerative hepatopathy. Residues of an aflatoxin metabolite, aflatoxin M1, were found in the livers of all treated animals. No differences in immune function were detected between the two groups. We conclude that consumption of 800 ppb AF in the diet of young WTD over an 8-wk period can produce subclinical hepatic injury.

Toxoplasmosis in wild turkeys: a case report and serologic survey.

Toxoplasmosis was diagnosed in a free-ranging wild turkey (Meleagris gallopavo) from West Virginia (USA) in June 1993. Gross findings included emaciation, splenomegaly, multifocal necrotizing hepatitis and splenitis, and crusting dermatitis on the head and neck. Histologically, multifocal necrosis with mononuclear inflammation was present in kidney, liver, spleen, heart, lungs, and pancreas. Toxoplasma gondii was confirmed in sections of liver by avidin-biotin immunohistochemical analysis. Subsequently, a retrospective serosurvey of wild turkeys for T. gondii antibodies was conducted using turkey sera collected between 1984 and 1989. An antibody prevalence of 10% was detected in 130 birds from 21 locations in the southeastern United States. While wild turkeys in the Southeast have T. gondii antibodies, this is only the second natural case of fatal toxoplasmosis reported; it appears that wild turkeys infrequently develop clinical disease when infected with T. gondii.

Apparent fatal snakebite in three hawks.

Based on histories and gross and histologic findings, snakebite was diagnosed in three dead raptors submitted for post-mortem examination from northern Florida and southern Georgia (USA). Two immature red-tailed hawks (Buteo jamaicensis) were found next to dead and partially eaten venomous snakes. An adult Cooper's hawk (Accipiter cooperii) was found adjacent to a den containing a cotton-mouth (Agkistrodon piscivorus) and an eastern diamondback rattlesnake (Crotalus adamanteus). Gross findings in all birds consisted of hemorrhage and gangrenous necrosis of one limb. Severe muscular degeneration was seen histologically.