Rate of contamination of hospital privacy curtains on a burns and plastic surgery ward: a cross-sectional study.

BACKGROUND: Surfaces in the patient environment may play a role in microbial transmission if they become colonized by bacteria. Patient privacy curtains are one such surface that may pose a high risk for transmission because they are high-contact surfaces, are infrequently cleaned, and healthcare workers are less likely to wash their hands after contacting inanimate objects such as curtains. AIM: To determine the amount and type of bacterial colonization of patient privacy curtains at a regional burns/plastic surgery unit. METHODS: Privacy curtain contamination on the burns/plastic surgery ward was determined for two separate occasions six months apart: 23 curtains on August 2015 and 26 curtains on January 2016. Dey-Engley neutralizing agar (DENA) replicate organism detection and counting (RODAC) contact plates were used daily to sample curtains near the edge hem where they are most frequently touched. Microbial contamination was reported as cfu/cm2 and the presence of meticillin-resistant Staphylococcus aureus (MRSA) was determined. Swabs were also taken of any open wounds and from tracheostomy sites on the ward. FINDINGS: Curtain contamination in August 2015 was 0.7-4.7 cfu/cm2 with 22% testing positive for MRSA, whereas contamination on January 2016 was 0.6-13.3 cfu/cm2 with 31% of curtains testing positive for MRSA. CONCLUSION: Curtains on the burns/plastic surgery ward become colonized with significant quantities of bacteria. Future studies will need to address the rate of colonization and the clinical impact of this colonization to better inform cleaning protocols.

The primacy of NF1 loss as the driver of tumorigenesis in neurofibromatosis type 1-associated plexiform neurofibromas.

Neurofibromatosis type 1 (NF1) is a common tumor-predisposition disorder due to germline mutations in the tumor suppressor gene NF1. A virtually pathognomonic finding of NF1 is the plexiform neurofibroma (PN), a benign, likely congenital tumor that arises from bi-allelic inactivation of NF1. PN can undergo transformation to a malignant peripheral nerve sheath tumor, an aggressive soft-tissue sarcoma. To better understand the non-NF1 genetic contributions to PN pathogenesis, we performed whole-exome sequencing, RNASeq profiling and genome-wide copy-number determination for 23 low-passage Schwann cell cultures established from surgical PN material with matching germline DNA. All resected tumors were derived from routine debulking surgeries. None of the tumors were considered at risk for malignant transformation at the time; for example, there was no pain or rapid growth. Deep (~500X) NF1 exon sequencing was also conducted on tumor DNA. Non-NF1 somatic mutation verification was performed using the Ampliseq/IonTorrent platform. We identified 100% of the germline NF1 mutations and found somatic NF1 inactivation in 74% of the PN. One individual with three PNs had different NF1 somatic mutations in each tumor. The median number of somatic mutations per sample, including NF1, was one (range 0-8). NF1 was the only gene that was recurrently somatically inactivated in multiple tumors. Gene Set Enrichment Analysis of transcriptome-wide tumor RNA sequencing identified five significant (FDR<0.01) and seven trending (0.01⩽FDR<0.02) gene sets related to DNA replication, telomere maintenance and elongation, cell cycle progression, signal transduction and cell proliferation. We found no recurrent non-NF1 locus copy-number variation in PN. This is the first multi-sample whole-exome and whole-transcriptome sequencing study of NF1-associated PN. Taken together with concurrent copy-number data, our comprehensive genetic analysis reveals the primacy of NF1 loss as the driver of PN tumorigenesis.

Postcoital generalised pruritus as a first symptom of polycythaemia vera.

Ploycythaemia vera (PV) is most common of chronic myeloproliferative disorder that involves the multipotent haemaotopoietic progenitor cells. PV has indolent course and recognised either by incidental discovery of high haemoglobin or haemtocrit. PV may present with aquagenic pruritus (AP) for years together without any other sign and symptoms. So advice of simple complete bood count as a routine in every case of pruritus can be helpful to diagnose it timely thereby dreaded complications of PV, related to hyperviscosity of blood like thrombosis both arterial and venous can be managed antecedently. A 50-year-old male doctor diagnosed as a case of PV presented to us with postcoital generalised pruritus (PCP) as a first, rarest symptoms and he remained undiagnosed for 10 years till he developed other features of PV like aquagenic pruritus, headache, red congestion in eyes and erythromelalgia symptoms complex erythema, burning pain and warmness of lower extremities. Then he was investigated and was found to have high haemoglobin or haemtocrit, JAK 2 genetic mutation changes were present, bone marrow biopsy and other biochemical investigations confirmed the diagnosis of PV. Initially he was managed with repeated phlebotomy to bring down high haemtocrit value in acceptable range (approximately 45%). Simultaneously he was put on hydroxyurea 500 mg twice daily doses. Since then his symptoms improved and monthly blood count was done to monitor the haemtocrit. So advice of simple blood count is highly informative in every case of generalised pruritus.