The burden of hospital acquired infections and antimicrobial resistance.

The burden of Hospital care-associated infections (HCAIs) is becoming a global concern. This is compounded by the emergence of virulent and high-risk bacterial strains such as "ESKAPE" pathogens - (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa and Enterobacter species), especially within Intensive care units (ICUs) that house high-risk and immunocompromised patients. In this review, we discuss the contributions of AMR pathogens to the increasing burden of HCAIs and provide insights into AMR mechanisms, with a particular focus on last-resort antibiotics like polymyxins. We extensively discuss how structural modifications of surface-membrane lipopolysaccharides and cationic interactions influence and inform AMR, and subsequent severity of HCAIs. We highlight some bacterial phenotypic survival mechanisms against polymyxins. Lastly, we discuss the emergence of plasmid-mediated resistance as a phenomenon making mitigation of AMR difficult, especially within the ICUs. This review provides a balanced perspective on the burden of HCAIs, associated pathogens, implication of AMR and factors influencing emerging AMR mechanisms.

Expression profiles of sporulation genes in multidrug-resistant Bacillus species isolated from intensive care units of Ghanaian hospital.

Sporulating bacteria such as Bacillus spp. have contributed to severity of opportunistic hospital acquired infections, including postoperative wounds and respiratory tract infections. This study determines the expression profiles of sporulation markers in multidrug-resistant Bacillus spp. isolated from Ghanaian hospital environments. Antimicrobial resistance (AMR) profiles of the bacteria were determined with disk diffusion and broth microdilution. Primer-specific polymerase chain reaction (PCR) amplification was used to profile the sporulation markers, and quantitative reverse transcription polymerase chain reaction (RT-qPCR) was used for the expression of the sporulation markers at different antibiotic concentrations. The strains are multidrug resistant (70-100%) to at least two of the eight classes of the antibiotics tested including cephalosporins, penicillin, aminoglycosides, and glycopeptide. The strains showed different resistance patterns to all the tested antibiotics, which might indicate diverse resistance mechanisms. Common (spoVK spoVE, spoJ, and sigF) and not commonly (sigJ, soJ, yrbC, and yjcE) reported sporulation markers were detected in the strains. The study showed an association of the sporulation markers with AMR as indicated by their expression profiles.

Profiling Mycobacterium ulcerans: sporulation, survival strategy and response to environmental factors.

Mycobacterium ulcerans is the causative agent of Buruli ulcer - a necrotizing skin infection. As an environmental pathogen, it has developed stress response mechanisms for survival. Similar to endospore formation in M. marinum, it is likely that M. ulcerans employs sporulation mechanisms for its survival and transmission. In this review, we modeled possible transmission routes and patterns of M. ulcerans from the environment to its host. We provided insights into the evolution of M. ulcerans and its genomic profiles. We discuss reservoirs of M. ulcerans as an environmental pathogen and its environmental survival. We comprehensively discuss sporulation as a possible stress response mechanism and modelled endospore formation in M. ulcerans. At last, we highlighted sporulation associated markers, which upon expression trigger endospore formation.

Buruli ulcer is an infectious disease characterized by extensive sores on the skin and soft body tissues. The disease is caused by a bacterium called Mycobacterium ulcerans and is mainly found in tropical countries. Over the years, several attempts to understand the means by which humans get into contact with this bug as well as how it thrives in its host remain futile. In this review, we describe a possible survival strategy, known as sporulation, that is adopted by the pathogen for dispersal and survival.

Calcium Potentiated Carbapenem Effectiveness Against Resistant Enterobacter Species.

Background: Antimicrobial resistance (AMR) remains a global health challenge, as bacteria display increasing resistance to last-resort antibiotics such as carbapenems. Enterobacter cloacae are evolving and developing high level of resistance to carbapenems. With increasing AMR, availability of antibiotics for treatment dwindles, hence a need to complement antibiotics to enhance activity or reduce the level of resistance. This study explored the use of calcium ions in attenuating bacterial resistance to carbapenems. Method: E. cloacae strains isolated from hospital fomites and air were subjected to antimicrobial susceptibility testing with carbapenem antibiotics (imipenem, meropenem, doripenem and ertapenem) using the disc diffusion (E. coli ATCC 25922 as control). Growth profile, Ca-Adjusted assay and time-kill curve of the strains was determined in the presence and absence of carbapenem antibiotics following a calcium stress assay. Results: Growth profile showed that all the E. cloacae strains grew markedly well at 37°C relative to ATCC 25922 and all strains displayed 80% to 100% level of resistance to tested antibiotics. The growth rate of the strains in the presence of the antibiotics was comparable to the growth rate in the absence of carbapenems. Conditional growth stress with calcium ions showed a 50% reduction in the level of resistance with doripenem displaying the lowest level of reduction and ertapenem, the highest. Discussion: The study showed that E. cloacae strains displayed high levels of resistance to carbapenems, increasing the possibility of treatment failure. Challenging strains with calcium prior to antibiotic treatment led to a significant reduction in level of resistance, indicating that calcium ions could affect bacterial strains during antibiotic activity leading to reduction in level of resistance. Conclusion: Calcium supplement could potentiate carbapenem effectiveness and reduce bacterial AMR.