Diascopy and histopathological evaluation of nonblanching erythematous dermatoses in dogs.

BACKGROUND: Diascopy is a point-of-care diagnostic test used to differentiate skin erythema due to vascular dilation from haemorrhage. In the veterinary literature, only a handful of diseases have been described to be associated with a negative (nonblanching) diascopy result, and histological investigation of haemorrhage has been inconsistent. OBJECTIVES: Retrospective study to undertake a histopathological investigation of canine, nonblanching erythematous dermatoses for the presence or absence of haemorrhage and vascular changes. MATERIALS AND METHODS: Skin biopsies from dogs presented with moderate-to-severe nonblanching erythema were evaluated histologically. Additionally, clinical data about each patient were analysed. RESULTS: Twenty cases were identified with nonblanching erythema. Diagnoses included vasculopathy (n = 6), canine eosinophilic dermatitis (n = 3), cutaneous epitheliotropic T-cell lymphoma (n = 2), and one case each of sterile granuloma and pyogranuloma syndrome, German shepherd dog pyoderma, multiple mast cell tumours, haemangiosarcoma, exfoliative cutaneous lupus erythematosus, canine leishmaniosis with sebaceous adenitis, sebaceous adenitis with concurrent dermatophytosis, calcinosis cutis and canine atopic dermatitis with insect-bite reaction. One or more vascular changes were present in all 20 cases and included perivascular oedema, endothelial swelling and neutrophilic infiltration of vessel walls. Haemorrhage was identified in 17 of 20 cases (85%). Three cases without dermal haemorrhage were calcinosis cutis, sebaceous adenitis with dermatophytosis and canine atopic dermatitis with insect-bite reaction. CONCLUSIONS AND CLINICAL RELEVANCE: Negative diascopy was associated with haemorrhage and vascular pathological findings in the majority of cases, yet not all. Haemorrhage was identified histologically in all diseases previously reported as nonblanching as well as in a few additional diseases.

Vertebral Osteosarcoma in Two Cats-Diagnosis, Treatment, and Outcome.

In this case report, we describe the diagnosis, treatment, and outcome of two feline cases of vertebral osteosarcoma. Case 1: A 6-year-old female neutered domestic longhaired cat was presented with progressive paraparesis, ataxia, and spinal hyperesthesia. MRI of the thoracolumbar spinal cord and vertebral column revealed a strongly contrast-enhancing mass lesion originating from the dorsal lamina and spinous process of T13. The lesion caused extradural compression of the spinal cord. Surgical debulking was performed, and the histopathological evaluation of surgical biopsies was consistent with vertebral osteosarcoma. The cat was paraplegic with intact nociception post-surgery. Subsequently, the cat recovered ambulation while remaining mildly ataxic and paraparetic at long-term follow-up. Post-operative chemotherapy was started with doxorubicin. CT scans at 2, 4, 9, 13, and 20 months post-surgery showed no signs of local recurrence or metastasis. Case 2: A 15.5-year-old male neutered domestic shorthaired cat was presented with progressive paraparesis, tail paresis, and spinal hyperesthesia. Radiographs and CT scan of the lumbar vertebral column showed a large mass originating from the dorsal lamina and spinous process of L6, suggestive of neoplasia, with severe compression of the spinal cord. Surgical debulking was performed, and the histopathological evaluation was consistent with vertebral osteosarcoma. Post-operative chemotherapy was started with doxorubicin. Seven months post-surgery, the patient was neurologically normal with no signs of metastatic disease. This case report highlights the possibility of good outcomes after the surgical treatment of feline vertebral osteosarcoma supplemented with post-surgical chemotherapy.

Mechanism of reduction of virus release and cell-cell fusion in persistent canine distemper virus infection.

Canine distemper virus (CDV), a mobillivirus related to measles virus causes a chronic progressive demyelinating disease, associated with persistence of the virus in the central nervous system (CNS). CNS persistence of morbilliviruses has been associated with cell-to-cell spread, thereby limiting immune detection. The mechanism of cell-to-cell spread remains uncertain. In the present study we studied viral spread comparing a cytolytic (non-persistent) and a persistent CDV strain in cell cultures. Cytolytic CDV spread in a compact concentric manner with extensive cell fusion and destruction of the monolayer. Persistent CDV exhibited a heterogeneous cell-to-cell pattern of spread without cell fusion and 100-fold reduction of infectious viral titers in supernatants as compared to the cytolytic strain. Ultrastructurally, low infectious titers correlated with limited budding of persistent CDV as compared to the cytolytic strain, which shed large numbers of viral particles. The pattern of heterogeneous cell-to-cell viral spread can be explained by low production of infectious viral particles in only few areas of the cell membrane. In this way persistent CDV only spreads to a small proportion of the cells surrounding an infected one. Our studies suggest that both cell-to-cell spread and limited production of infectious virus are related to reduced expression of fusogenic complexes in the cell membrane. Such complexes consist of a synergistic configuration of the attachment (H) and fusion (F) proteins on the cell surface. F und H proteins exhibited a marked degree of colocalization in cytolytic CDV infection but not in persistent CDV as seen by confocal laser microscopy. In addition, analysis of CDV F protein expression using vaccinia constructs of both strains revealed an additional large fraction of uncleaved fusion protein in the persistent strain. This suggests that the paucity of active fusion complexes is due to restricted intracellular processing of the viral fusion protein.