Insertion Sequence-Dependent <i>OmpK</i>36 Mutation Associated Ertapenem Resistance in Clinical <i>Klebsiella pneumoniae</i>

Extended-spectrum β-lactamases (ESBLs) and/or AmpC enzymes combined with deficiency of porins OmpK35 and OmpK36 are important for the development of carbapenem-resistant Klebsiella pneumoniae. We characterized the clinical K. pneumoniae human isolates and investigated the effect of meropenem induction on the ompK35 and ompK36 mutation to develop carbapenem resistance from six carbapenem-susceptible ESBL-producing K. pneumoniae strains. 163 clinical K. pneumoniae isolates were grouped mostly into the ESBL + AmpC (44.2%) and ESBL (42.9%) phenotypes. The resistance rate differed between cephalosporins (52.1% for cefepime - 97.5% for cefotaxime) and carbapenems (16% for meropenem - 28.2% for imipenem) (P blaTEM, blaSHV, blaCTX-M-3-like, and blaCTX-M-14-like of AmpA β-lactamase genes and blaDHA and blaCMY of AmpC β-lactamase genes. Compared to all 163 clinical isolates, the 56 carbapenem-resistant isolates carried less frequently of blaTEM, blaCTXM-14-like, and blaCTXM-3-like and more frequently of blaDHA-1 and blaCMY-2. The carbapenem-resistant isolates differed in prevalence against imipenem, ertapenem, and meropenem and lacked OmpK35 more frequently than OmpK36, but abnormal PCR amplicons were detected fewer in the Omp K35-deficient group than in the OmpK36-deficient group (32.5% vs. 68.4%, respectively). The carbapenem-resistant isolate mostly carried blaDHA (91.1%) and three isolates carried blaKPC-2. Following induction with meropenem insertion sequences in ompK36, not ompK36, were identified as IS5 for KP08, IS1 for KP15, and IS903 for KP16 isolates. OmpK36 deficiency increased resistance to ertapenem, but not imipenem and meropenem. Clinical isolates belonged mainly to ESBL + AmpC group and ESBL group with difference in resistance to cephalosporins and carbapenems, the bla genes. Carbapenem resistant isolates lacked OmpK35 expression, than the OmpK36 expression, Meropenem induction developed the carbapenem resistant isolates with insertion of different insertion sequences in ompK36, not ompK35.

Cross-Sectional Study of Tuberculosis and HIV/AIDS Co-Infections among Patients Attending Directly Observed Treatment Centers in Bayelsa State, Nigeria

Introduction: Mycobacterium tuberculosis (TB) infects about one quarter of the global population and is transmitted via aerosols by coughing, sneezing, etc. Some socio-behavioral factors may predispose an individual to the disease. Methodology: The study used a cross-sectional design with random stratified sampling technique. Sputum samples from suspected TB patients totaling 600 were obtained from patients attending directly observed treatment (DOTs) centers from different local government areas in Bayelsa. The sputum samples were examined for tuberculosis using the Ziehl-Neelsen staining technique and Gene Xpert molecular method while HIV/AIDS tests were carried out with EDTA blood using the Alere HIV12 test kit and others. Results: The Prevalence of TB by Gene Xpert was 294 (49.0%) and by AFB 217 (36.1%), while TB/HIV co-infection was 94 (32.0%), RRMTB was 34 (11.9%) and HIV 249 (41.5%). Prevalence by age group showed the 20 - 39 years had the highest prevalence of TB 98 (47.0%), TB/HIV 35 (47.0%), RRMTB 17 (48.0%) and HIV 90 (57.0%). By gender the male had slightly higher prevalence of TB 109 (52.0%), TB/HIV 51 (54.0%), RRMTB 20 (56.0%) and HIV 126 (51.0%) than the female. Prevalence among smokers and alcoholics and subjects who engaged in both habits had high prevalence TB 109 (37.0%), TB/HIV 14 (40.0%), RRMTB 14 (40.0%) and HIV 72 (29.0%). For educational status those with tertiary and secondary education had similar high prevalence and for occupation, the self-employed and civil servants had similar elevated prevalence. The prevalence by local government area showed that Yenegoa had the highest with TB 235 (80.0%), TB/HIV 72 (76.6%), RRMTB 24 (68.5%) and HIV 202 (81.2%). Conclusion: An increase in the development of resistance by M. tuberculosis also contributes to the persistence of the disease as well as some socio-economic factors.

Clonal Dissemination of Genetically Diverse Fluoroquinolone-Resistant Extended-Spectrum Beta-Lactamase (ESBL)-Producing Escherichia coli ST131 in a Veterans Hospital in Southern Taiwan

Uropathogenic Escherichia coli is the common pathogen to cause urinary tract infections (UTIs) and have become multidrug-resistant (MDR) extended-spectrum β-lactamase (ESBL) producers. The differences in the antimicrobial susceptibility, 5 bla genes, 12 virulence genes of 87 clinical ESBL-producing E. coli isolates and genomic variations and sequence types of 18 recurrent and repeated isolates from 9 patients were investigated. The 87 MDR-ESBL isolates collected mainly from indwelling urinary catheters (IUCs) and UTIs were highly resistant to fluoroquinolones, with over 50% of the isolates being resistant to cefepime and piperacillin/tazobactam and a few being resistant to carbapenem. These isolates carried at least two of the five bla genes examined, with the highest prevalence (87.4%) found for blaCTX-M (blaCTX-M3-like and blaCTX-M14-like), followed by blaCMY-2 (80.5%) and blaSHV (56.3%). The predominant virulence genes were the fimbriae gene fimH and the toxin genes cnf1 and hlyA in blood isolates and the capsule gene kpsMTII in UTI and blood isolates. Over 80% of the isolates carried yersiniabactin and aerobactin of siderophores. In 18 isolates, the fluoroquinolone-resistant ST131 isolate of pulsotypes I and II with blaCTX-M-15 was clonally disseminated in the hospital. The genomic plasticity of these ST131 occurred mainly through the conjugative plasmids with differences in replicon types A/C, I1, FIA, FIB and Y, size and number. In conclusion, MDR ESBL-producing E. coli isolates differed in virulence genes of UPEC and antibiotic resistance associated with the sources. Plasmid acquisition and chromosomal variations increase the spread of fluoroquinolone-resistant UPEC ST131 worldwide.