Using an alumni survey to target improvements in an emergency medicine training programme.

INTRODUCTION: The Accreditation Council for Graduate Medical Education (ACGME) is the governing body responsible for accrediting graduate medical training programme in the USA. The Emergency Medicine Milestones (EM-Milestones) were developed by the ACGME and American Board of Emergency Medicine as a guide and monitoring tool for the knowledge, skills, abilities and experiences to be acquired during training. Alumni surveys have been reported as a valuable resource for training programme to identify areas for improvement; however, there are few studies regarding programme improvement in emergency medicine. We aimed to use the EM-Milestones, adapted as an alumni self-assessment survey, to identify areas for training programme improvement. METHODS: This study was conducted at an urban, academic affiliated, community hospital in New York city with an emergency medicine training programme consisting of 30 residents over 3 years. Alumni of our emergency medicine training programme were sent an EM-Milestones-based self-assessment survey. Participants evaluated their ability in each EM-Milestones subcompetency on a Likert scale. Data were analysed using descriptive statistics. RESULTS: Response rate was 74% (69/93). Alumni reported achieving the target performance in 5/6 general competencies, with Systems-Based Practice falling below the target performance. The survey further identified 6/23 subcompetencies (Pharmacotherapy, Ultrasound, Wound Management, Patient Safety, Systems-Based Management and Technology) falling below the target performance level. DISCUSSION: Alumni self-evaluation of competence using the EM-Milestones provides valuable information concerning confidence to practice independently; these data, coupled with regular milestone evaluation of existing trainees, can identify problem areas and provide a blueprint for targeted programme improvement.

Cell type specific accumulation of the major latency-associated transcript (LAT) of herpes simplex virus type 2 in LAT transgenic mice.

We performed in situ hybridization to determine the cell type specific accumulation of the intron of the latency-associated transcript (LAT) in tissues in HSV-2 LAT transgenic mice in which LAT expression is driven by its native promoter. We identified LAT in multiple cell types in most tissues analyzed from HSV-2 LAT transgenic mice. While weak to moderate signals were seen in brain and spinal cord neurons, epithelial cells, and muscle cells, the strongest signals were detected in neurons from dorsal root and trigeminal ganglia. About 70-86% of neurons in these ganglia were LAT-positive with varying signal intensities, while cells surrounding the neurons were LAT-negative. The frequency of A5 or KH10-positive neurons was similar in LAT-positive and total neurons. These data indicate that HSV-2 LAT promoter activity is not restricted to neurons and that LAT accumulation in ganglionic neurons is likely regulated by cell-specific factors.

Diverse herpes simplex virus type 1 thymidine kinase mutants in individual human neurons and Ganglia.

Mutations in the thymidine kinase gene (tk) of herpes simplex virus type 1 (HSV-1) explain most cases of virus resistance to acyclovir (ACV) treatment. Mucocutaneous lesions of patients with ACV resistance contain mixed populations of tk mutant and wild-type virus. However, it is unknown whether human ganglia also contain mixed populations since the replication of HSV tk mutants in animal neurons is impaired. Here we report the detection of mutated HSV tk sequences in human ganglia. Trigeminal and dorsal root ganglia were obtained at autopsy from an immunocompromised woman with chronic mucocutaneous infection with ACV-resistant HSV-1. The HSV-1 tk open reading frames from ganglia were amplified by PCR, cloned, and sequenced. tk mutations were detected in a seven-G homopolymer region in 11 of 12 ganglia tested, with clonal frequencies ranging from 4.2 to 76% HSV-1 tk mutants per ganglion. In 8 of 11 ganglia, the mutations were heterogeneous, varying from a deletion of one G to an insertion of one to three G residues, with the two-G insertion being the most common. Each ganglion had its own pattern of mutant populations. When individual neurons from one ganglion were analyzed by laser capture microdissection and PCR, 6 of 14 HSV-1-positive neurons were coinfected with HSV tk mutants and wild-type virus, 4 of 14 were infected with wild-type virus alone, and 4 of 14 were infected with tk mutant virus alone. These data suggest that diverse tk mutants arise independently under drug selection and establish latency in human sensory ganglia alone or together with wild-type virus.