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Unformatted text preview: Eastern Equine Encephalitis Virus in Whooping Cranes Case History Seven whooping cranes (2 males, 5 females) died between 17 Sept. and 4 November 1984 Birds ranged in age from 1 to 16 years Only three birds exhibited clinical signs before death Blood Work Elevation in LDH, AST, and Uric Acid Results may be useful for monitoring cranes for Eastern Equine Encephalitis, but not diagnostic Post-mortem Findings All birds appeared in good nutritional condition Gross lesions were variable: mild to severe pathology in liver and spleen Fluid in anterior abdominal airsacs Histopathological Findings No evidence of nervous system involvement Acute necrosis of most organs, especially the liver and spleen Virology EEE virus isolated in tissue culture Characterized by electron microscopy Bird Number 72 72 72 72 74 74 74 74 Organ Titer in PFUs 7000 13000 6700 No virus No virus 300 No virus Kidney 6300 liver lung spleen Brain Colon Liver Lung Neutralizing Antibodies to EEE Virus
Species Feb-Nov. 1974 # pos./ # tested Whooping Crane Sandhill Crane Sandhill/whoop ing crane cross Totals 3/20 15 1/12 2/8 % 8 25 Nov. 1984 # pos./ # tested 14/32 13/38 1/1 % 44 34 100 28/71 39 Culiseta melanura Life Cycle Habitat Arboreal Late summer and fall Small puddles, such as occur when trees are uprooted are used for breeding Control Methods Limit access of susceptible mosquitoes to host Limit host's exposure to mosquitoes Vector control Vaccination Mosquito Monitoring Program History of EEE in Whooping Cranes Equine epizootics have probably occurred since 1831 on the East Coast Virus first isolated in Mid-Atlantic region in 1933 during equine epizootic Mortality in Ringed-necked Pheasants was seen in Connecticut in 1938 1984 EEE killed 7 Whooping Cranes at Patuxent Wildlife Research Center, Laurel, Maryland History of EEE in Whooping Cranes High virulence of EEE in exotic birds contrasts with inapparent infection or benign disease in native wild birds EEE Clinical Disease Two forms of disease: Neurotrophic infection with CNS involvement, fever depression diarrhea, ataxia, tremors, partial or complete paralysis of limbs, prostration and death Viscerotrophic infection, native birds and emus, lethargy, drooping wings, ataxia, death Transmission Arbovirus Enzootic foci in freshwater swamp habitats Summer in northern latitudes, longer periods in south Wild birds, primarily passerines, are natural hosts Primary enzootic vectors are avian feeding mosquitoes, Culiseta melanura Prevention in Cranes Vaccination trials at Patuxent in the 1980's identified two killed vaccines as developing titers to EEE in sandhill cranes Human killed EEE vaccine manufactured by Salk Company for US Army at Fort Derrick, Maryland Killed equine EEE vaccine from Fort Dodge and other companies EEE Vaccination Research Human killed EEE vaccine has become harder to obtain from only source, US Army Tested Fort Dodge EEE product again, comparing results with human EEE vaccine 5 year study showed either no differences in titers or higher titers with equine product Current EEE Vaccination Recommendations Vaccinate all exposed whooping cranes and susceptible sandhill cranes with 1.00 ml Fort Dodge EEE/WEE/tetnus vaccine annually Vaccinate chicks at day 21-24 and day 42-49 (two vaccines, 2-3 weeks apart) using 1.00 ml Fort Dodge EEE/WEE/tetnus/West Nile vaccine 1987 Crane Epizootic Case Report Juvenile endangered Mississippi sandhill crane found moribund 18 Sep. 1987 Thin, 2.6 kg, pale mucous membranes WBC count 23,000, Hct. 47%, TS 4.7ug/dl Coccidia and strongyles present in gastrointestinal tract Case Report Continued Second MSC and Florida sandhill crane found dead 2 days later Next day 2 FSC sick WBC 27,000, Hct 37%, TS 3.9 ug/dl Twenty other juvenile sandhill cranes examined, 18 found with similar but less pronounced signs 240 of 300 cranes found with signs Pathology 15 cranes died Often had 10-20% weight loss, died within 12 hours of signs of illness High WBC >40,000 in some cases Hematocrit initially normal (38-48%) decreased to 30-35% in 5-7 days Gross pathology and histopathology inconclusive: dehydration, atrophy of fat, renal failure, small spleen Treatment Captive endangered cranes highly valuable Treatment initiated Fluid therapy Antibiotics Treat parasites Supportive care with gavage mixture Differential Diagnosis Suspected toxic substance early Cranes had stopped eating pelleted food Cranes were excessively probing in pens for natural food Examined pens for poisonous plants not consistently found, no evidence of ingestion by cranes Removed pelleted diet Testing of Pelleted Diet Patuxent Analytical Control Facility tested diet for lead, mercury, arsenic, cadmium and selenium none found Also tested food for pesticides (organophosphates, chlorinated hydrocarbons, carbamates, polychlorinated biphenyls, and herbicides Water tested also Bioassays Suspect diet fed to cranes and bobwhite quail Cranes and bobwhite quail refused to eat diet Gavage fed to cranes produced signs consistent with epizootic Further testing of pelleted food indicated Mycotoxins Mycotoxins found in pelleted food from both gravity feeders from crane pens and from unopen feed bags T-2 mycotoxin found at 1-2 ppm Deoxynivalenol (DON or vomitoxin) found at 0.4 ppm Mycotoxins Tricothecenes: fusarium mycotoxin include: T-2 toxin is a naturally occurring mycotoxin, signs include yellow caseous plaque in mouth, beak edge, junction of mouth and tongue T-2 toxins cause gizzard erosion and necrosis of lining of proventriculus T-2 toxins can depress WBC counts and suppress immune system DON associated with depressed food intake and immunosuppression Diacetoxysirpenol/monoacetoxyscirpenol cause depressed egg production, depressed hatchibility,and depressed fertility ...
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