ABSTRACT
Biofilm formation on indwelling urinary catheters is a leading cause of Urinary tract infection [UTI]. Presence of biofilm is associated with increased bacterial resistance to antimicrobial therapy and resultant treatment failure. The study detected a reliable method for diagnosis of biofilm formation by comparing scanning electron microscopy [SEM] and tissue culture plate method [TCP]. The work was conducted on 20 urinary catheters from patients ranging from 1.5 to 85 years with catheters that remained in situ for a period of 3 to 20 days. Samples of catheters for culture and SEM and samples of urine were taken at the same time. The correlation between renal conditions and biofilm formation was not significant [p=0.336]. No significant correlation [p =0.836, 0.163 respectively] was found between predisposing conditions [DM, renal insufficiency, diarrhea and impaired immunity] and development of Catheter associated urinary tract infection [CAUTI] and biofilm formation. Biofilm formation increased with duration of catheter in situ, but no significant correlation was found [p=0,095]. This could be due to small number of specimens. 9/20[45%] urine samples, 12/20[60%] catheter samples were positive by culture and 14/20[70%] catheters showed biofilm on SEM. 4/12[33.33%] organisms isolated from catheter culture produced biofilm by TCP method. 9 isolates were recovered from 9 positive urine cultures. The microorganisms isolated were non Candida albicans [3/9], E. coli [2/9], C. albicans [2/9] and Acenitobacter [2/9]. 14 isolates were recovered from 12 culture positive catheters. The organisms isolated were E. coli [3/14], non-Candida albicans [3/14], C. albicans [2/14], C tropicalis [2/14], Acenitobacter [2/14], Klebsiella [1/14] and Enterococcus [1/14]. Reduction in microbial diversity with antimicrobial use was noticed but the correlation was insignificant [p=0.317]. The correlation between urine culture results as well as catheter culture results and biofilm formation by SEM were both significant [p 0.008 and 0.000 respectively]. The correlation between urine culture and TCP assay was insignificant [p=237]. Using SEM as the gold standard method for the detection of biofilm, the sensitivity, specificity, total accuracy, PPV and NPV of urine culture and catheter culture were, 64.30%, 100%, 75%, 100%, 54% and 85.70%, 100%, 90%,100%,.75% respectively
ABSTRACT
The prevalence of methicillin-resistant Staphyloccoccus aureus [MRSA] strains has presented a new challenge in antimicrobial medication. Linezolid is a new drug with potent activity on Grampositive pathogens such as MRSA. The aim of the study was to investigate the in vitro activity of linezolid alone and in combination with imipenem, vancomycin or rifampicin to determine the most active therapy against MRSA strains. Twenty clinical MRSA strains were isolated from patients admitted to inpatient departments and outpatient clinics of Theodor Bilharz Research Institute. Standard strain MRSA ATCC 43300 was included as a control. The MICs of MRSA strains to linezolid, vancomycin, imipenem and rifampicin were evaluated using E test. Time-kill curve were used to assess the in vitro activity of linezolid [at 8x MIC] alone and in combination with imipenem [at 32x MIC], vancomycin or rifampicin [at 8x MIC]. Scanning and transmission electron microscopy were performed to compare bacterial morphological alterations owing to the different combinations. Time-kill studies showed synergistic effect when linezolid combined with imipenem was tested against all the MRSA strains. Linezolid plus vancomycin or rifampicin combinations did not display any synergism or antagonism. Scanning and transmission electron microscopy observations confirmed the interactions observed in time kill experiments. Linezolid in combination with subinhibitory concentrations of imipenem can be bactericidal against MRSA strains and appears to be a promising combination for the treatment of MRSA infections. No synergistic activity was seen when the linezolid and vancomycin or rifampicin were combined. Linezolid could prevent the emergence of mutants resistant to rifampicin