Histopathological, ultrastructural and molecular phylogenetic analysis of a novel microsporidium in a loggerhead sea turtle Caretta caretta.

Microsporidial spores were identified in the musculature of a loggerhead sea turtle Caretta caretta found dead on the shore in New Brunswick, Canada. Gastroenteritis was diagnosed on gross postmortem examination, with no gross abnormalities detected in the skeletal muscle. Histologically, the microsporidial spores were associated with inflammation and muscular necrosis and measured 1.1-1.7 × 2.2-3.4 µm. Spores were typically identified within sporophorous vesicles and, less often, in sporophorocysts and were weakly Gram positive, had punctate PAS staining, and were occasionally strongly acid-fast. Ultrastructural characteristics included 7-10 polar filament coils and other standard features of microsporidial spores. PCR for the microsporidial small subunit rRNA gene sequence was performed on DNA extracted from the muscle and small intestine, and the resulting amplicon was sequenced and queried against published microsporidial genomes. DNA sequences shared 98.2-99.8% sequence identity to Clade III of the Marinosporidia. This is the first report of a microsporidial infection contributing to the mortality of a sea turtle.

Evaluation of tissue changes following intramuscular infiltration of lidocaine in rainbow trout Oncorhynchus mykiss.

Rainbow trout Oncorhynchus mykiss were infiltrated with either saline or lidocaine adjacent to the dorsal fin to assess histopathological changes. Infiltration was done as if it were being used as a local anaesthetic. Tissue lesions and associated tissue healing were examined over a period of 30 days. Most changes occurred at the cranial site of where the solution was first infiltrated. The infiltration of a dose of 10 mg kg-1 of lidocaine appears to have damaged the skeletal muscle and connective tissues more than a similar volume of saline, especially during the first 15 days. The primary changes included haemorrhage, inflammation and muscle degeneration and necrosis. By day 30 post-infiltration inflammatory lesions were either nearly or completely absent, signs of myofibre regeneration were noted in only one fish. This experiment shows local anaesthetics and saline can produce localized tissue damage, especially during the first 2 weeks post infiltration. Care should be taken to allow the fish to heal for at least 30 days and probably more, no matter the solution administered, especially if giving repeated injections or infiltrations at the same site.

Histological characterization of dilated cardiomyopathy in the juvenile toy Manchester terrier.

Dilated cardiomyopathy (DCM), the most common form of cardiomyopathy in the dog, most often occurs in certain breeds. The objective of this study was to describe a rapidly progressive form of DCM that has been recently recognized in juvenile Toy Manchester Terrier dogs (TMTs). The clinical history and gross findings were reviewed in a group of 14 TMTs, and histologic sections of heart were examined in 12 of those 14 TMTs with DCM. Histochemical and histomorphometric analyses were employed to compare the heart in TMTs affected by DCM with that of control dogs. TMTs ranged in age from 10 to 58.3 weeks, with males and females being equally affected. Affected TMT hearts contained foci of degeneration and loss of myofibers with fibrosis and mild lymphoplasmacytic infiltrates. Less prominent features included foci of acute myofiber degeneration and necrosis with or without intralesional mineralization and mild to moderate suppurative and lymphoplasmacytic infiltrates. Morphometric quantification demonstrated that the right ventricle was more severely affected (P ≤ .05) than the left ventricle with variable involvement of the interventricular septum. Immunohistochemistry for canine parvovirus was negative in all heart samples. However, the absence of parvoviral antigen does not rule out a possible viral or autoimmune cause. The presence of these myocardial lesions among closely related dogs suggests a genetic contribution to this disease process in the TMT.

Porcine circovirus 2 inclusion bodies in pulmonary and renal epithelial cells.

Porcine circovirus 2 (PCV2) is the cause of postweaning multisystemic wasting syndrome (PMWS). The most common lesions of PMWS are lymphohistiocytic to granulomatous lymphadenitis, interstitial pneumonia and interstitial nephritis, with intracytoplasmic amphophilic botryoid inclusion bodies in macrophages. In addition to these typical changes, intracytoplasmic botryoid inclusion bodies were observed in bronchial, bronchial glandular, and renal tubular epithelium of several pigs from 4 different farms in Western and Eastern Canada. PCV2 inclusion bodies were demonstrated to be located in the cytoplasm of epithelial cells by immunohistochemical staining for PCV2 and cytokeratin antigens and by ultrastructural demonstration of viral particles in the inclusion bodies within renal tubular epithelium.