Detection of arenavirus in a peripheral odontogenic fibromyxoma in a red tail boa (Boa constrictor constrictor) with inclusion body disease.

A captive bred red tail boa (Boa constrictor constrictor) was presented with a large intraoral mass originating from the buccal gingiva, attached to the right dentary teeth row. Based on the clinical features and histological examination, the diagnosis of a peripheral odontogenic fibromyxoma was made. Sections of liver biopsies and circulating lymphocytes contained relatively few eosinophilic intracytoplasmic inclusion bodies, indistinguishable from those observed in inclusion body disease-affected snakes. Inclusion bodies were not observed in cells comprising the neoplastic mass. Using reverse transcription polymerase chain reaction (RT-PCR), arenavirus was detected in the neoplastic tissue. Two years after surgical removal of the mass, recurrence of the neoplastic lesion was observed. Numerous large inclusion body disease inclusions were abundantly present in the neoplastic cells of the recurrent fibromyxoma. Sections of liver biopsies and circulating lymphocytes contained relatively few intracytoplasmic inclusions. The RT-PCR revealed the presence of arenavirus in blood, a liver biopsy, and neoplastic tissue. The present case describes the co-occurrence of an arenavirus infection and an odontogenic fibromyxoma in a red tail boa.

Sequence analysis of the Ras-MAPK pathway genes SOS1, EGFR & GRB2 in silver foxes (Vulpes vulpes): candidate genes for hereditary hyperplastic gingivitis.

Hereditary hyperplastic gingivitis (HHG) is an autosomal recessive disease that presents with progressive gingival proliferation in farmed silver foxes. Hereditary gingival fibromatosis (HGF) is an analogous condition in humans that is genetically heterogeneous with several known autosomal dominant loci. For one locus the causative mutation is in the Son of sevenless homologue 1 (SOS1) gene. For the remaining loci, the molecular mechanisms are unknown but Ras pathway involvement is suspected. Here we compare sequences for the SOS1 gene, and two adjacent genes in the Ras pathway, growth receptor bound protein 2 (GRB2) and epidermal growth factor receptor (EGFR), between HHG-affected and unaffected foxes. We conclude that the known HGF causative mutation does not cause HHG in foxes, nor do the coding regions or intron-exon boundaries of these three genes contain any candidate mutations for fox gum disease. Patterns of molecular evolution among foxes and other mammals reflect high conservation and strong functional constraints for SOS1 and GRB2 but reveal a lineage-specific pattern of variability in EGFR consistent with mutational rate differences, relaxed functional constraints, and possibly positive selection.

[Gingival fibromatosis (hereditary hyperplastic gingivitis) in a wild European red fox (Vulpes vulpes)]. / Gingivafibromatose (hereditäre hyperplastische Gingivitis) bei einem europäischen Wildrotfuchs (Vulpes vulpes).

This report describes a case of gingival fibromatosis in an otherwise healthy and well nourished wild European red fox (Vulpes vulpes), which was shot by a hunter and submitted to the state laboratory in the context of the rabies monitoring program of the federal state of Brandenburg, Germany. At necropsy, a severe papillomatous proliferation of the complete gingival tissue of the upper and lower jaw was present. This gingival proliferation had already resulted in malocclusion, loosening and loss of several incisival, premolar and molar teeth. Histologically, the primary lesion was a massive increase in the amount of collagen rich and relatively avascular connective tissue within the gingival lamina propria mucosae. A papillomavirus infection was excluded by electron microscopy, immunohistochemistry and molecular biological methods. The gingival lesions in the red fox are identical to those seen in hereditary hyperplastic gingivitis in farmed silver foxes and hereditary gingival fibromatosis in man. It is presumed that, in analogy to the genetic diseases in silver foxes and man, a still unidentified genetic defect is responsible for the development of the disease in the red fox, too.