Molecular characterization of Vibrio cholerae O1 El Tor strains in Malaysia revealed genetically diverse variant lineages.

Vibrio cholerae O1 El Tor variants have been the major causative agents of cholera worldwide since their emergence in the 2000s. Cholera remains endemic in some regions in Malaysia. Therefore, we aimed to investigate the genetic characteristics of the V. cholerae O1 El Tor strains associated with outbreaks and sporadic cases to elucidate the molecular evolution among the strains circulating in this region. A total of 45 V. cholerae O1 El Tor strains isolated between 1991 and 2011 were examined. All strains were subjected to phenotypic characterization, and molecular characterization including detection of virulence genes and CTX prophage (CTXΦ) by Polymerase Chain Reaction (PCR) and genotyping by Pulsed-Field Gel Electrophoresis (PFGE). All strains were phenotypically confirmed as El Tor biotype and were mostly Ogawa serotype (96%). Antimicrobial susceptibility testing showed that the outbreak strains isolated in 1991 (Sabah) and 2009 (Terengganu) were all multidrug-resistant while the sporadic strains were resistant to erythromycin and furazolidone only. All strains (n = 45) were resistant to erythromycin. The virulence genes ctxA, ctxB, ompW, rfb, rtxC, tcpA, tcpI, rstR, zot and hlyA were present in all strains. The outbreak strains isolated in 1991 harboured El Tor cholera toxin gene (ctxB3) while sporadic strains from 2004 to 2011 harboured classical ctxB1. Four distinctive CTXΦ arrays were identified among the El Tor variants, one of which co-occurred with El Tor strains during the 2009 outbreak in Terengganu. PFGE analysis revealed that a genetically diverse El Tor variants population persisted in Sabah. The co-existence of multiple El Tor variants together with the prototypic El Tor strains suggested a multiclonal emergence of V. cholerae O1 El Tor variants in this region.

Refractory hyperactive delirium in the dying: pharmacological management.

BACKGROUND: Delirium is a prevalent clinical presentation in advanced illness. The hyperactive phase can cause severe symptoms at the end of life. There is no published study of the pharmacological management of this symptom in Australian palliative medicine practice. OBJECTIVES: To describe the pharmacological management of hyperactive delirium at the end of life in an Australian inpatient palliative care setting. METHODS: Retrospective audit of deaths from October 2019 where a medication of interest (MOI) was used following admission to the palliative care unit (PCU) of Eastern Health. The clinical notes of those included were reviewed to further describe the clinical details surrounding the use of the MOI. RESULTS: Forty patients were included. Midazolam was the most common medication used (57.5%). The most common dual agent combination was midazolam plus levomepromazine. CONCLUSIONS: This audit is the first description of pharmacological management of severe hyperactive delirium at the end of life requiring sedation in an Australian PCU.