Prion diseases are fatal neurodegenerative disorders by which the native cellular prion protein (PrPC) is misfolded into an accumulating, disease-associated isoform (PrPD). To improve the understanding of prion pathogenesis and develop effective treatments, it is essential to elucidate factors contributing to cellular permissiveness. We previously isolated five clones from an immortalized subline of ovine microglia, two of which had demonstrated differential permissiveness to a natural isolate of sheep scrapie and distinct transcriptomic profiles. To more robustly identify factors contributing to this activity, relative permissiveness, cell proliferation, selected gene transcript level, and matrix metalloproteinase 2 (MMP2) activity were compared amongst all five clones. Differences in cell proliferation were not detected between clones; however, significant correlations were identified between relative permissiveness and genes associated with cell growth (i.e., RARRES1 and PTN), protein degradation (i.e., CTSB and SQSTM1), and heparin binding (i.e., SEPP1). MMP2 activity varied amongst clones, but did not correlate with permissiveness. These associations support the contribution of cell division and protein degradation on the permissiveness of cultured ovine microglia to PrPD.
Three horses presented with variably painful, nonulcerated masses of the head or neck that were diagnosed as glomus tumours. Grossly, they were fleshy, pink to tan masses ranging from 0.4 to 9 cm in diameter, involving either the deep dermis and subcutis or the subcutis and underlying skeletal muscle. Microscopically, neoplastic epithelioid cells were arranged in sheets, cords and packets within lobules. The neoplastic cells frequently abutted and formed nodular bulges into large endothelium-lined vascular spaces, especially around the tumour periphery. Large nerve branches were associated with each tumour. As determined by immunohistochemistry, the neoplastic cells consistently expressed α-smooth muscle actin and vimentin, and some cells in two of the cases expressed desmin. A laminin- or collagen IV-positive basement membrane was demonstrated around individual tumour cells or small groups of cells in all three cases. Morphological features and immunohistochemistry supported the diagnosis of glomus tumour, most consistent with the solid type in humans. Applying a classification system used in humans, two of these tumours met criteria of malignancy (glomangiosarcomas). One horse was euthanized due to complications associated with recurrence and treatment-related necrosis and secondary infection.
Abstract. Dermatophilosis caused by Dermatophilus congolensis causes exudative dermatitis in a variety of species. The infection is generally limited to the cutaneous tissues, where infection is acquired from the environment and bacteria penetrate into keratinized epithelium through epithelial disruption. A 3-year-old pony filly was examined for enlarging mandibular lymph nodes during the preceding 10 months. Biopsy of the node revealed mixed and granulomatous inflammation and thick, filamentous Gram-positive bacteria. Dermatophilus congolensis, confirmed by biochemical testing and sequencing of the ribosomal RNA gene, was cultured from a sample aspirated from the infected site. Dermatophilus congolensis should be considered as a possible etiologic agent associated with lymphadenopathy and granulomatous inflammation in the horse.Key words: Dermatophilosis; Dermatophilus congolensis; horses; lymphadenopathy.Dermatophilus congolensis is a Gram-positive coccobacillary actinomycete that causes an exudative dermatitis in a variety of species, most notably in ruminants and horses, although rare infections occur in cats, dogs, and humans.1,2,12 Infection is generally restricted to the skin and subcutaneous tissue, although uncommon involvement of lymphoid tissue in ruminants and cats has been described. 3,4,12A 3-year-old female palomino pony was referred to the William R. Pritchard Veterinary Teaching Hospital at the University of California, Davis (Davis, CA) with the primary complaint of progressively enlarging bilateral mandibular lymphadenopathy during the previous 10 months. Intermandibular swelling was noticed the winter of the previous year (10 months before referral), and a biopsy of the affected area revealed inflamed lymphoid tissue. Prior to referral, the first premolar teeth had erupted and were removed; significant hooks on cheek teeth were treated with dental floatation. The pony was also reported by the owner to be lethargic and appeared pruritic, as evidenced by biting at or rubbing her sides. The filly had been regularly vaccinated and had most recently been dewormed with pyrantel pamoate 3 weeks prior to referral.The filly was slightly depressed on examination. Her temperature and heart rate were within normal limits. A slightly elevated respiratory rate of 25 breaths per minute was detected, although there were no abnormal lung sounds on thoracic auscultation. Large, firm, nonpainful multilobulated masses in the intermandibular space were palpable. The only other abnormalities on physical examination were small areas of superficial cutaneous excoriations over the flanks, thorax, and gluteal musculature. Dark, loose fecal material was observed after normal defecation.A complete blood count was unremarkable, and plasma fibrinogen was 300 mg/dl. A serum biochemistry panel was within normal limits, with the exceptions of slightly elevated alkaline phosphatase ( A lymph node aspirate and biopsy were performed on the affected tissue; a small amount of inspissated pus was observed during the biopsy procedu...
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