Parvovirus-induced encephalitis in a juvenile raccoon.

A juvenile raccoon was euthanized because of severe neurologic signs. At postmortem examination, no significant gross lesions were present. Histologic evaluation demonstrated nonsuppurative encephalitis in thalamus, brainstem, and hippocampus, cerebellar Purkinje cell loss, as well as poliomyelitis and demyelination of the spinal cord. Parvovirus antigen-specific immunohistochemistry revealed immunopositive neurons in the brainstem, cerebral cortex, and hippocampus. A few Purkinje cells were also immunopositive. DNA extracted from formalin-fixed, paraffin-embedded brain tissue (thalamus, hippocampus, cerebral cortex) yielded a positive signal using PCR targeting both feline and canine parvovirus. Sequencing analyses from a fragment of the NS1 gene and a portion of the VP2 gene confirmed the presence of DNA of a recent canine parvovirus variant (CPV-2a-like virus) in the cerebellum. Our case provides evidence that a recent canine parvovirus (CPV) strain (Carnivore protoparvovirus 1) can infect cerebral and diencephalic neurons and cause encephalitis in an otherwise healthy raccoon. Parvovirus-induced encephalitis is a differential diagnosis of rabies and canine distemper in raccoons with neurologic signs.

Detection and molecular characterization of a reovirus in black-capped chickadees (Poecile atricapillus) from Minnesota, USA.

In 2011, the Minnesota Rehabilitation Center submitted four dead Black-capped Chickadees (Poecile atricapillus) for necropsy to the Minnesota Veterinary Diagnostic Laboratory. All four chickadees were underweight and dehydrated and their intestinal contents were watery and yellowish. No significant lesions were observed upon histopathologic examination. Viral particles of the family Reoviridae were detected after negative-contrast electron microscopic examination of intestinal contents. Analysis by reverse transcriptase PCR and sequencing confirmed the presence of a reovirus. Based on phylogenetic analysis, the chickadee reovirus had 97.1% to 98.3% and 89.4% to 97.8% nucleotide identity with turkey enteric reoviruses from apparently healthy and enteritis-affected turkey poults, respectively. The chickadee reovirus had only 56.5% and 58.5% nucleotide and 54.5% and 56.8% amino acid identity with psittacine reovirus and Tvarminne avian virus, respectively. These results indicate that the chickadee reovirus is closely related to turkey reoviruses.

Sarcocystis calchasi has an expanded host range and induces neurological disease in cockatiels (Nymphicus hollandicus) and North American rock pigeons (Columbia livia f. dom.).

Pigeon protozoal encephalitis (PPE) is an emerging central nervous system disease of pigeons (Columba livia f. domestica) caused by the apicomplexan parasite Sarcocystis calchasi. The intermediate host specificity of S. calchasi had been considered high, as domestic chickens were resistant to experimental infection. Here, we have re-evaluated this concept and expanded the known host range of S. calchasi by experimental infection of cockatiels (Nymphicus hollandicus), a species distantly related to pigeons. In this work, a group of eight cockatiels were experimentally infected with S. calchasi, which resulted in a biphasic central nervous system disease that paralleled PPE in many aspects, albeit with a more diverse pathology. All cockatiels became lethargic and polyuric between days 7 and 13 pi and during that time schizonts of S. calchasi were found primarily in the liver and spleen accompanied by necrosis and inflammation. As with pigeons, neurological signs occurred during a chronic phase of the disease in three cockatiels between 57 and 63 dpi. However, all five cockatiels necropsied in that period, or at the end of the trial at 76 dpi, had a severe lymphohistiocytic and necrotizing encephalitis. No tissue cysts were found in the heart, and cockatiels infected with 10(5) sporocysts only had a negligible parasite load in skeletal muscles despite the presence of severe central nervous system lesions. Notably, intralesional schizonts were identified in the brain of one cockatiel. In contrast to previous results, intralesional schizonts were also identified in the brains of three of six naturally infected pigeons from Minnesota and Missouri examined as part of an epidemiological investigation. In both the cockatiel and the pigeons, tissue cysts were found concurrently with schizonts suggesting an uncommon phenomenon in the Sarcocystis life cycle. Based on the results of this study, transmission of S. calchasi to avian species other than the domestic pigeon is possible. These findings suggest a, so far, unmonitored prevalence of S. calchasi in avian populations and highlight a possible ongoing dissemination of this parasite in the Northern Hemisphere.