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Aim of study: This study aimed to detected the presence of the plasmid mediated quinolone resistance genes in quinolone resistant Klebsiella pneumoniae isolates in clinical and environmental hospital samples. Methodology: A total of 195 clinical samples of different sources and 50 environmental hospital samples were collected of three main hospitals in Al-Najaf city .K. pneumoniae was identified depending on cultural and traditional biochemical tests, then confirmed by API 20E system. Phenotype detecting of quinolone resistance in K. pneumoniae isolates were carried out by growing on MacConkey agar supplemented with 10µg/ml Ciprofloxacin. Antibiotic susceptibility performed by disk diffusion. Quinolones resistant isolates were selected for molecular study for detecting aac (6 ')-Ib-cr, qepA, qnrS and qnrB as plasmid mediated resistance genes using Multiplex polymerase chain reaction Results: Eighty-nine isolates were identified as .K. pneumoniae. Thirty-four (38%) resist ciprofloxacin (10µg/ml ) and were resistant to at least fourteen antibiotics to which they are tested. Hence, all isolates were considered to be multidrug resistant (MDR). The results of detection the plasmod mediated antibiotic resistance genes revealed the widely distribution aac (6 ')-Ib-cr gene alone or combined with qnrS gene in 14 (41.18%) isolates, or with qepA (2.94%) and 8.82% of bacterial isolates carried aac (6 ')-Ib-cr, qepA and qnrS whereas only one isolates (29.41%) that caused wound infection showed the presence of qnrB gene. Conclusions :High prevalence MDR K. pneumoniae harbouring PMQR mediated by aac(6`)-Ib-cr and qnrS . This study is the first trail to detect PMQR genes in clinical and environmental isolates of K. pneumoniae in Iraq. Recommendations: Further studies are necessary to understand the dissemination of plasmid mediated genes (qnr, aac (6`)-Ib-cr and qepA gene) and chromosomal resistance among K. pneumoniae and other common pathogenic bacteria.

Disruption in the epigenetic mechanisms is one of the causes of cancer; particularly in the gut. It has been elucidated that multiple genetic and epigenetic alterations during this process caused by chronic inflammation play a crucial role in the cancer progress. DNA methylation impairment as a leading change is caused during the proliferation of Helicobacter pylori. It has been unraveled that numerous tumor suppressor genes are regulated by related promoter methylation, justifying environmental factors inducing gastric carcinoma. H. pylori infection affects various cells through inflammation, changes in apoptosis, proliferation and differentiation of epithelial cells into oncogenic cells. This is exerted through intracellular pathways in epithelial cells such as mitogen-activated protein kinase, Nuclear factor κB, activator protein, Wnt/β-catenin, Phosphoinositide 3-kinase pathways, signal transducers and transcriptional activators. The accumulations of cytosine methylation free radicals damage the DNA; hence nitric oxide (NO) alters the DNA-methylating enzymes function. Accordingly, gastritis due to H. pylori infection results in the inflammation and triggers signaling pathways mostly inducing gastrointestinal cancer. Noticeably, H. pylori-induced microRNAs exert epigenetic changes influencing various processes most of which including immune responses, autophagy, cell cycle and apoptosis. These mechanisms also stimulate gastric cancer progress. It is noteworthy that gene expression regulation through epigenetic mechanisms, including DNA methylation and micro-RNAs include major cellular pathways regulators. These epigenetic alterations represent prominent candidates for describing environmental factors roles in the genomic and cellular function enhancing the gastrointestinal carcinoma by H. pylori.

The current study was performed to identify the genotypes related to Klebsiella pneumonia isolated from urinary tract infection (UTI) of humans and pneumonia (PMN) of sheep in Al-Qadisiyah province, Iraq. 140 samples of (80 UTI and 60 post-mortems identified PMN) were collected and processed using traditional and molecular techniques. Following isolation of the microorganism, pure colonies were introduced into steps of a polymerase chain reaction (PCR) confirming method that targeted the 16S rRNA and the virulence-related capsular (magA and k2A) genes and partial gene sequencing (PGS) which focused on the 16S rRNA gene only. Primary results of the traditional techniques (TTs) highly revealed the presence of K. pneumonia in 11 (13.75%) and 18 (30%) of the UTI and the PMN samples, respectively. However, rest samples showed the presence of different bacteria with no bacterial growth in others. This was confirmed by PCR results that strongly uncovered the identity of the K. pneumoniae in the positive samples. Using specific primers for Maga and k2A genes, PCR results revealed full percentage based presence of the k2A gene in the UTI and the PMN samples with less, 3/7 (43%) and 4 (100%) in the UTI and the PMN samples, respectively, presence of the magic gene. Moreover, PGS findings confirmed the accuracy of the TT and the PCR results plus recognized specific local strain identities that differently aligned with some of the worlds isolates on a phylogenetic tree. Current findings provide valuable information about virulence status of the K. pneumoniae isolates. in Al-Qadisiyah province, Iraq.