BackgroundMethicillin resistant Staphylococcus aureus (MRSA) is a major human pathogen associated with nosocomial and community infections. Panton Valentine leukocidin (PVL) is considered one of the important virulence factors of S. aureus responsible for destruction of white blood cells, necrosis and apoptosis and as a marker of community acquired MRSA. This study was aimed to determine the prevalence of PVL genes among MRSA isolates and to check the reliability of PVL as marker of community acquired MRSA isolates from Western Nepal.MethodsA total of 400 strains of S. aureus were collected from clinical specimens and various units (Operation Theater, Intensive Care Units) of the hospital and 139 of these had been confirmed as MRSA by previous study. Multiplex PCR was used to detect mecA and PVL genes. Clinical data as well as antimicrobial susceptibility data was analyzed and compared among PVL positive and negative MRSA isolates.ResultsOut of 139 MRSA isolates, 79 (56.8 %) were PVL positive. The majority of the community acquired MRSA (90.4 %) were PVL positive (Positive predictive value: 94.9 % and negative predictive value: 86.6 %), while PVL was detected only in 4 (7.1 %) hospital associated MRSA strains. None of the MRSA isolates from hospital environment was found positive for the PVL genes. The majority of the PVL positive strains (75.5 %) were isolated from pus samples. Antibiotic resistance among PVL negative MRSA isolates was found higher as compared to PVL positive MRSA.ConclusionOur study showed high prevalence of PVL among community acquired MRSA isolates. Absence of PVL among MRSA isolates from hospital environment indicates its poor association with hospital acquired MRSA and therefore, PVL may be used a marker for community acquired MRSA. This is first study from Nepal, to test PVL among MRSA isolates from hospital environment.Electronic supplementary materialThe online version of this article (doi:10.1186/s12879-016-1531-1) contains supplementary material, which is available to authorized users.
In this study, we present long-term near-surface measurements of sulfur dioxide (SO 2 ), oxides of nitrogen (NO x ), carbon monoxide (CO), and ozone (O 3 ) carried out at an urban location, Kanpur (26.46°N, 80.33°E, 125 m amsl), in Northern India from June 2009 to May 2013. The mean concentrations of SO 2 , NO x , CO, and O 3 over the entire study period were 3.0, 5.7, 721, and 27.9 ppb, respectively. SO 2 , NO x and CO concentrations were highest during the winter season, whereas O 3 concentration peaked during summer. The former could be attributed mainly to the near-surface anthropogenic sources (e.g. automobiles, residential cooking, brick kilns, coal-burning power plants, agricultural land-clearing, and biomass burning) and low mixing height in winter, whereas the latter was clearly due to enhanced chemical production of O 3 during the pre-monsoon (i.e. summer) season. The lowest concentration of all trace gases were observed during the monsoon season, due to efficient wet scavenging by precipitation. The averaged diurnal patterns also showed similar seasonal variation. NO x and CO showed peaks during morning and evening traffic hours and a valley in the afternoon irrespective of the seasons, clearly linked to the boundary layer height evolution. Contrarily, O 3 depicted a reverse pattern with highest concentrations during afternoon hours and lowest in the morning hours. The mean rate of change of O 3 concentrations (dO 3 /dt) during the morning hours (08:00 to 11:00 h) and evening hours (17:00 to 19:00 h) at Kanpur were 3.3 ppb h −1 and −2.6 ppb h −1 , respectively. O 3 followed a positive linear relationship with temperature, except in post-monsoon season while the strong negative with the relative humidity in all seasons. The ventilation coefficient was found to be highest in the pre-monsoon season (15,622 m 2 s −1 ) and lowest during winter (2564 m 2 s −1 ), indicative of excellent pollution dispersion efficiency during the pre-monsoon season. However, the low ventilation coefficient during winter and post-monsoon seasons indicated that the highpollution potential occurs at this site.
Background-The de novo occurrence of sustained ventricular tachycardia (VT) after CABG has been described, but the incidence, mortality rate, long-term follow-up, and mechanism are not well defined. Methods and Results-This prospective study enrolled consecutive patients undergoing CABG at a single institution.Patients were followed up for the development of sustained VT, and a detailed analysis of clinical, angiographic, and surgical variables associated with the occurrence of VT was performed. A total of 382 patients participated, and 12 patients (3.1%) experienced Ն1 episode of sustained VT 4.1Ϯ4.8 days after CABG. In 11 of 12 patients, no postoperative complication explained the VT; 1 patient had a perioperative myocardial infarction. The in-hospital mortality rate was 25%. Patients with VT were more likely to have prior myocardial infarction (92% versus 50%, PϽ0.01), severe congestive heart failure (56% versus 21%, PϽ0.01), and ejection fraction Ͻ0.40 (70% versus 29%, PϽ0.01). When all 3 factors were present, the risk of VT was 30%, a 14-fold increase. Patients with VT had more noncollateralized totally occluded vessels on angiogram (1.4Ϯ0.97 versus 0.54Ϯ0.7, PϽ0.01), a bypass graft across a noncollateralized occluded vessel (1.50Ϯ1.0 versus 0.42Ϯ0.62, PϽ0.01), and a bypass graft across a noncollateralized occluded vessel to an infarct zone (1.50Ϯ1.0 versus 0.17Ϯ0.38, PϽ0.01). By multivariate analysis, the number of bypass grafts across a noncollateralized occluded vessel to an infarct zone was the only independent factor predicting VT. Conclusions-The first presentation of sustained monomorphic VT in the recovery period after CABG is uncommon, but the incidence is high in specific clinical subsets. Placement of a bypass graft across a noncollateralized total occlusion in a vessel supplying an infarct zone was strongly and independently associated with the development of VT. (Circulation. 1999;99:903-908.)
This study clearly suggests that paper currency can serve as a carrier for the spread of resistant bacterial pathogens.
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