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Amanda L. Guthrie

Publications and source records attributed to Amanda L. Guthrie.

2 recordsLinked to original sources

Detection of snake fungal disease due to Ophidiomyces ophiodiicola in Virginia, USA

Snake fungal disease (SFD) is an emerging disease of wildlife believed to be caused by Ophidiomyces ophiodiicola . Although geographic and host ranges have yet to be determined, this disease is characterized by crusty scales, superficial pustules, and subcutaneous nodules, with subsequent morbidity and mortality in some snake species. To confirm the presence of SFD and O. ophiodiicola in snakes of eastern Virginia, USA, we clinically examined 30 free-ranging snakes on public lands from April to October 2014. Skin biopsy samples were collected from nine snakes that had gross lesions suggestive of SFD; seven of these biopsies were suitable for histologic interpretation, and eight were suitable for culture and PCR detection of O. ophiodiicola . Seven snakes had histologic features consistent with SFD and were positive for O. ophiodiicola by PCR or fungal culture.

Virginia

Detection of Mycoplasma agassizii in the Texas Tortoise (Gopherus berlandieri)

Mycoplasma agassizii causes upper respiratory tract disease (URTD) in Texas tortoises (Gopherus berlandieri). To determine exposure to and shedding of M. agassizii, we collected blood samples and nasal swabs from 40 free-ranging Texas tortoises on public and private lands in Texas, USA, from May to October 2009. We used an enzyme-linked immunosorbent assay (ELISA) to detect M. agassizii–specific antibodies. Eleven (28%) tortoises were antibody positive, three (8%) were suspect, and the remaining 26 (65%) were negative. Nasal lavage samples were collected from 35 of the 40 tortoises for M. agassizii culture and PCR to detect shedding of M. agassizii. Current infection with M. agassizii was confirmed in one tortoise that had mild clinical signs of URTD and was positive by ELISA (antibody titer >512), PCR, and culture. The clinical isolate was confirmed as M. agassizii by restriction fragment length polymorphism and immunobinding.

Texas