Abstract. Thirty of 200 (15%) hatchling inland bearded dragons were found dead after a short period (48 hours) of weakness and lethargy. The most common clinical signs were head tilt and circling. Six bearded dragons with neurological signs were euthanized, and postmortem examination revealed no gross abnormalities. Microscopically, severe, randomly distributed hepatocellular necrosis with large basophilic intranuclear inclusion bodies in numerous hepatocytes was noted. Small-intestinal enterocytes contained intracytoplasmic coccidial protozoa (Isospora sp.) and occasional enterocytes had basophilic intranuclear inclusion bodies. Transmission electron microscopy revealed both 80-and 20-nm-diameter viral particles, which were consistent with adenoviruses and dependoviruses, respectively. Adenoviral outbreaks in groups of animals are uncommon. An adverse synergistic effect of the coccidiosis with the adenoviral infection may have played a critical role in the high morbidity and mortality in this case.Adenoviruses (Family Adenoviridae) are well-known pathogens in several mammalian and avian species. Adenoviruses are double-stranded DNA viruses, 70-90 nm in diameter, and have a characteristic nonenveloped, icosahedral structure. Generally, adenoviruses are host specific and are transmitted by the fecal-oral route or direct contact via oronasal secretions. Often, mammalian infections are subclinical, except for infectious canine hepatitis. Adenoviral disease generally occurs in immunocompromised or young animals. Outbreaks in groups of animals are uncommon. Recently, adenoviral infections also have been reported in several reptilian species, including crocodiles, snakes, and lizards. 3,4,[6][7][8][9][10][11][12]15,16 The Australian inland bearded dragon, Pogona vitticeps (Pogon: bearded in Greek), is one of the most popular reptiles in the pet trade. Two isolated cases of adenoviral infection in 4 neonatal inland bearded dragons have been reported, but the infections were limited mainly to the individuals affected. 10 No outbreak of adenoviral infection in a group of reptiles has been reported. This report describes an outbreak of adenoviral infection in a group of captive-bred inland bearded dragon hatchlings coinfected with dependovirus and Isospora sp. coccidia.Two hundred hatchling captive-bred inland bearded dragons, which had been purchased at different times by a reptile importer from different captive breeding populations, were placed in a holding facility. The ages of the dragons were uncertain; however, based on their weight (Ͻ5 g), the estimate age was less than 1 month. The bearded dragons were maintained at an environmental temperature of 29-32 C and were fed commercially obtained crickets and lettuce. Thirty of the 200 (15%) bearded dragons were found dead after a short period (48 hours) of weakness and lethargy. The most common clinical signs were head tilt and circling. Physical examination of tympanic bullae revealed no significant findings. Six of the bearded dragons with neurological signs were eut...

A bstract: West Nile virus (WNV) has been reported to affect various crocodilian species including the American alligator, Alligator mississippiensis, the Nile crocodile, Crocodylus niloticus, and the Morelet's crocodile, Crocodylus moreletii. In the Fall of 2003 an increased number of mortalities were observed at various alligator ranches in Louisiana. Affected animals were reported to have neurologic signs followed by death. At the time West Nile virus (WNV) had already been diagnosed in alligators from Georgia and Florida, but not Louisiana. This report outlines the findings of physical exam, necropsy, histopathology and diagnostic tests of affected animals. Viral isolation, real time RT-PCR and immunohistochemistry have proven to be useful tests for diagnosing WNV in alligators. One interesting aspect of these cases is that only one of the four affected facilities had alligators hatched in Louisiana. The other three had imported hatchlings from Florida and Texas.

Eastern equine encephalitis (EEE) was diagnosed in a flock of emus in southeastern Louisiana. The outbreak involved juvenile and adult breeders ranging in age from 20 to 36 months, with an attack rate of 76% and a case fatality rate of 87%. The diagnosis was confirmed by isolation and characterization of the viral agent, and by detection of EEE antibody in two recovered emus. High mortality was preceded by marked depression, hemorrhagic diarrhea, and emesis of blood-stained ingesta. On postmortem examination, hemorrhagic enteritis and multiple petechia of viscera were observed. Microscopic changes included severe necrosis of hepatocytes, intestinal mucosa, and necrotizing vasculitis of the spleen and lamina propria of the intestine. No nervous system lesions were observed. This outbreak occurred concurrently with EEE in horses and was attributed to unseasonably heavy rainfall with an abundance of arthropod vectors and proximity to free-living reservoir host species.

Eastern equine encephalitis (EEE) was diagnosed (postmortem) in a sheep with clinical signs attributable to a central nervous system disease. The sheep was febrile and initially had front limb incoordination, which progressed to paralysis of both front and hind limbs during a course of 2 days. The sheep maintained an alert attitude with the ability to eat up to the time of euthanasia. The only clinical pathologic abnormalities were neutrophilia and lymphopenia without appreciable leukocytosis, a moderate hyperglycemia, and an elevated creatine kinase. Treatment included hydrotherapy for lowering body temperature, intravenous fluids, thiamine hydrochloride, tetanus antitoxin, antibiotics, and corticosteroids. The only gross lesion at the time of necropsy was a wet glistening surface of the brain (leptomeninges). Microscopically, there was severe nonsuppurative meningoencephalitis, poliomyelitis, and polyradiculoneuritis with mild multifocal neutrophilic infiltration. The EEE virus was isolated from the brain, and subsequent fluorescent antibody testing for EEE was positive on cell culture.