BackgroundStaphylococcus aureus is a frequent cause of infections in both the community and hospital. Methicillin-resistant Staphylococcus aureus continues to be an important nosocomial pathogen and infections are often difficult to manage due to its resistance to multiple antibiotics. Healthcare workers are important source of nosocomial transmission of MRSA. This study aimed to determine the nasal carriage rate of S. aureus and MRSA among healthcare workers at Universal College of Medical Sciences and Teaching Hospital, Nepal and to determine antibiotic susceptibility pattern of the isolates.MethodsA cross-sectional study involving 204 healthcare workers was conducted. Nasal swabs were collected and cultured on Mannitol salt agar. Mannitol fermenting colonies which were gram positive cocci, catalase positive and coagulase positive were identified as S. aureus. Antibiotic susceptibility test was performed by modified Kirby-Bauer disc diffusion method. Methicillin resistance was detected using cefoxitin disc diffusion method.ResultsOf 204 healthcare workers, 32 (15.7 %) were nasal carriers of S. aureus and among them 7 (21.9 %) were carrier of MRSA. Overall nasal carriage rate of MRSA was 3.4 % (7/204). Highest MRSA nasal carriage rate of 7.8 % (4/51) was found among nurses. Healthcare workers of both surgical wards and operating room accounted for 28.6 % (2/7) of MRSA carriers each. Among MRSA isolates inducible clindamycin resistance was observed in 66.7 % (2/3) of erythromycin resistant isolates.ConclusionsHigh nasal carriage of S. aureus and MRSA among healthcare workers (especially in surgery ward and operating room) necessitates improved infection control measures to be employed to control MRSA transmission in our setting.

Chlamydia trachomatis is an obligate intracellular pathogen with global health and economic impact. Upon infection, C. trachomatis resides within a protective niche, the inclusion, wherein it replicates and usurps host cell machinery and resources. The inclusion membrane is the key host-pathogen interface that governs specific protein-protein interactions to manipulate host signaling pathways. At the conclusion of the infection cycle, C. trachomatis exits the host cell via lysis or extrusion. Extrusion depends on the phosphorylation state of myosin light chain 2 (MLC2); the extent of phosphorylation is determined by the ongoing opposing activities of myosin phosphatase (MYPT1) and myosin kinase (MLCK). Previously, it was shown that MYPT1 is recruited to the inclusion and interacts with CT228 for regulation of host cell egress. In this study, we generated a targeted chromosomal mutation of CT228 (L2-ΔCT228) using the TargeTron system and demonstrate a loss of MYPT1 recruitment and increase in extrusion production in vitro. Mutation of CT228 did not affect chlamydial growth in cell culture or recruitment of MLC2. Moreover, we document a delay in clearance of L2-ΔCT228 during murine intravaginal infection as well as a reduction in systemic humoral response, relative to L2-wild type. Taken together, the data suggest that loss of MYPT1 recruitment (as a result of CT228 disruption) regulates the degree of host cell exit via extrusion and affects the longevity of infection in vivo.

Objective: This study aimed to determine prevalence of inducible and constitutive clindamycin resistance among clinical S. aureus isolates and also study their association with methicillin resistance. Methods: A cross-sectional study including 140 non-duplicate isolates of S. aureus was done. Isolates were identified by standard microbiological methods and methicillin resistance was detected by cefoxitin disc diffusion method. Inducible clindamycin resistance was detected by D-test. Results: Prevalence of inducible and constitutive clindamycin resistance was 12.1% and 7.9% respectively. Constitutive and inducible resistance was associated with MRSA. An unusual phenotype, erythromycin sensitive and clindamycin resistance, was detected in 2 MRSA isolates. Conclusions: Inducible and constitutive clindamycin resistance is comparatively low in our setting. Constitutive and inducible resistance was higher among MRSA than MSSA. However the trends in resistance vary in different places. D-test reporting should be done routinely which will allow clinicians to opt for clindamycin judiciously and avoid potential treatment failure.

The reliance on antibiotics and antimicrobials to treat bacterial infectious diseases is threatened by the emergence of antibiotic resistance and multi-drug-resistant organisms, thus having the potential to greatly impact human health. Thus, the discovery and development of antimicrobials capable of acting on antibiotic-resistant bacteria is a major area of significance in scientific research. Herein, we present the development of a eumelanin-inspired antimicrobial capable of killing methicillin-resistant Staphylococcus aureus (MRSA). By ligating quaternary ammonium-functionalized "arms" to a eumelanin-inspired indole with intrinsic antimicrobial activity, an antimicrobial agent with enhanced activity was prepared. This resulting antimicrobial, EIPE-1, had a minimum inhibitory concentration of 16 μg/mL (17.1 μM) against a clinical isolate of MRSA obtained from an adult cystic fibrosis patient. The biocidal activity occurred within 30 min of exposure and resulted in changes to the bacterial cell surface as visualized with a scanning electron microscope. Taken together, these studies demonstrate that EIPE-1 is effective at killing MRSA.

Chlamydia species are causative agents of sexually transmitted infections, blinding trachoma, and animal infections with zoonotic potential. Being an obligate intracellular pathogen, Chlamydia relies on the host cell for its survival and development, subverting various host cell processes throughout the infection cycle. A key subset of host proteins utilized by Chlamydia include an assortment of host kinase signaling networks which are vital for many chlamydial processes including entry, nutrient acquisition, and suppression of host cell apoptosis. In this review, we summarize the recent advancements in our understanding of host kinase subversion by Chlamydia.