ABSTRACT
Three years after a prospective study on wound infections in a rural hospital in Ghana revealed no emergence of carbapenem-resistant bacteria we initiated a new study to assess the prevalence of multidrug-resistant pathogens. Three hundred and one samples of patients with wound infections were analysed for the presence of resistant bacteria in the period August 2017 till March 2018. Carbapenem-resistant Acinetobacter (A.) baumannii were further characterized by resistance gene sequencing, PCR-based bacterial strain typing, pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing (MLST "Oxford scheme"). A. baumanni was detected in wound infections of 45 patients (15%); 22 isolates were carbapenem-resistant. Carbapenemases NDM-1 and/or OXA-23 were detected in all isolates; two isolates harboured additionally OXA-420. PFGE and MLST analyses confirmed the presence of one A. baumannii strain in 17 patients that was assigned to the worldwide spread sequence type ST231 and carried NDM-1 and OXA-23. Furthermore, two new A. baumannii STs (ST2145 and ST2146) were detected in two and three patients, respectively. Within three years the prevalence of carbapenem-resistant A. baumannii increased dramatically in the hospital. The early detection of multidrug-resistant bacteria and prevention of their further spread are only possible if continuous surveillance and molecular typing will be implemented.
ABSTRACT
Wound infections are an emerging medical problem worldwide, frequently neglected in under-resourced countries. Bacterial culture and antimicrobial drug resistance testing of infected wounds in patients in a rural hospital in Ghana identified no methicillin-resistant Staphylococcus aureus or carbapenem-resistant Enterobacteriaceae but identified high combined resistance of Enterobacteriaceae against third-generation cephalosporins and fluoroquinolones.
Subject(s)
Anti-Bacterial Agents/pharmacology , Bacteria/drug effects , Wound Infection/microbiology , Drug Resistance, Bacterial , Ghana/epidemiology , Humans , Wound Infection/epidemiologyABSTRACT
Traumatic brain injury causes progressive brain atrophy and cognitive decline. Surprisingly, an early treatment with erythropoietin (EPO) prevents these consequences of secondary neurodegeneration, but the mechanisms have remained obscure. Here we show by advanced imaging and innovative analytical tools that recombinant human EPO, a clinically established and neuroprotective growth factor, dampens microglial activity, as visualized also in vivo by a strongly attenuated injury-induced cellular motility.
Subject(s)
Cell Movement/drug effects , Erythropoietin/pharmacology , Microglia/metabolism , Neuroprotective Agents/pharmacology , Brain Injuries/drug therapy , Brain Injuries/metabolism , Brain Injuries/pathology , Cells, Cultured , Humans , Recombinant Proteins/pharmacologyABSTRACT
In a first genome-wide association study (GWAS) approach to anti-Borrelia seropositivity, we identified two significant single nucleotide polymorphisms (SNPs) (rs17850869, P = 4.17E-09; rs41289586, P = 7.18E-08). Both markers, located on chromosomes 16 and 3, respectively, are within or close to genes previously connected to spinocerebellar ataxia. The risk SNP rs41289586 represents a missense variant (R263H) of anoctamin 10 (ANO10), a member of a protein family encoding Cl(-) channels and phospholipid scramblases. ANO10 augments volume-regulated Cl(-) currents (IHypo) in Xenopus oocytes, HEK293 cells, lymphocytes and macrophages and controls volume regulation by enhancing regulatory volume decrease (RVD). ANO10 supports migration of macrophages and phagocytosis of spirochetes. The R263H variant is inhibitory on IHypo, RVD and intracellular Ca(2+) signals, which may delay spirochete clearance, thereby sensitizing adaptive immunity. Our data demonstrate for the first time that ANO10 has a central role in innate immune defense against Borrelia infection.