Characterization of rpoB mutations in rifampin-resistant clinical Mycobacterium tuberculosis isolates from Kuwait and Dubai.
Ahmad S, Mokaddas E, Fares E.

Department of Microbiology, Faculty of Medicine, Kuwait University.

Mutations conferring resistance to rifampin in rifampin-resistant clinical Mycobacterium tuberculosis isolates occur mostly in the 81 bp rifampin-resistance-determining region (RRDR) of the rpoB gene. In this study, 29 rifampin-resistant and 12 -susceptible clinical M. tuberculosis isolates were tested for characterization of mutations in the rpoB gene by line probe (INNO-LiPA Rif. TB) assay and the results were confirmed and extended by DNA sequencing of the PCR amplified target DNA. The line probe assay identified all 12 susceptible strains as rifampin-sensitive and the DNA sequence of RRDR in the amplified rpoB gene from two isolates matched perfectly with the wild-type sequence. The line probe assay identified 28 resistant isolates as rifampin-resistant with specific detection of mutation in 22 isolates including one isolate that exhibited hetro-resistance containing both the wild-type pattern as well as a specific mutation within RRDR while one of the rifampin-resistant strain was identified as rifampin-susceptible. DNA sequencing confirmed these results and, in addition, led to the specific detection of mutations in 5 rifampin-resistant isolates in which specific base changes within RRDR could not be determined by the line probe assay. These analyses identified 8 different mutations within RRDR of the rpoB gene including one novel mutation (S522W) that has not been reported so far. The genotyping performed on the isolates carrying similar mutations showed that majority of these isolates were unique as they exhibited varying DNA banding patterns. Correlating the ethnic origin of the infected TB patients with the occurrence of specific mutations at three main codon positions (516, 526 and 531) in the rpoB gene showed that most patients (11 of 15) from South Asian region contained mutations at codon 526 while majority of isolates from patients (6 of 11) of Middle Eastern origin contained mutations at codon 531.

 

Septicaemia after burn injury: a comparative study.

Bang RL, Sharma PN, Sanyal SC, Al Najjadah I.

Al-Babtain Centre for Plastic Surgery and Burns, Kuwait.

Seventy-nine (8.4%) patients during June 1992-May 1996 (Group-1) and 68 (7.2%) patients from June 1996 to May 2000 (Group-2) who developed septicaemia at the Burns Unit of Al-Babtain Centre for Plastic Surgery and Burns, Kuwait, were retrospectively studied and compared. The mean age of 26 years, male predominance, flame burns as main aetiology and mean burn percentage of >or=40% was observed in both the groups. Both groups revealed extensive flame burn, inhalation injury, intubation and difficult resuscitation as the risk factors. The proportion of satisfactory resuscitation increased significantly (P<0.001) in Group-2. The septicaemia commonly occurred within 2 weeks postburn but the number of episodes during 5 days postburn was less in Group-2. The surface wound was found to be the likely source of entry of the organisms into the blood stream in both the groups. The gram positive organisms were dominant aetiologic factor in both groups but an increase frequency of Acinetobacter was found in Group-2. The proportion of MRSE and Pseudomonas septicaemia was significantly higher (P<0.01) in the Group-1. The rate of survivors, in both the groups was higher among operated patients but it was significantly higher (P<0.001) in the Group-1. A mortality rate 20.6% in Group-2 decreased against Group-1, which can be attributed to better resuscitation, nutritional care, early detection of septicaemia, appropriate antibiotics and early wound excision and skin grafting. MOF was the cause of death of 60.9% in Group-1 and 85.7% in Group-2. There was no role of prophylactic antibiotic in burn patients in the incidence of septicaemia and mortality.

 

In vitro activity of 15 antimicrobial agents against clinical isolates of Clostridium difficile in Kuwait.

Jamal WY, Mokaddas EM, Verghese TL, Rotimi VO.
Department of Microbiology, Faculty of Medicine, Kuwait University and Mubarak Al-Kabeer Teaching Hospital, Kuwait.

A total of 73 clinical isolates of Clostridium difficile isolated from stool/rectal swabs of patients admitted to the intensive care units at Mubarak Hospital, Ibn Sina Hospital Burn unit and Haematology wards at the Kuwait Cancer Control Centre, were investigated for their susceptibility to 15 antibiotics using the Etest. Amoxycillin-clavulanic acid, ampicillin, meropenem, metronidazole, penicillin, piperacillin, piperacillin/tazobactam, teicoplanin and vancomycin had excellent activities with MIC(90)s of 0.38, 0.5, 1, 0.19, 1.5, 2, 3, 0.25 and 0.75 mg/l, respectively. Of the 73 C. difficile isolates, 86% were resistant to imipenem (MIC(90) >32 mg/l) and almost 97% were resistant to trovafloxacin (MIC(90)>256 mg/l). Forty eight percent of the isolates were resistant to clindamycin. A total of 18 isolates were highly clindamycin-resistant with an MIC of >256 mg/l; 10 of these were toxin producers. Multiple antibiotic resistance (two or more antibiotics) was noted in 63 isolates. These were more common among the toxigenic strains than the non-toxigenic strains by a ratio of 2.5:1.

 

Antibiotic resistance of Enterococci isolated at a teaching hospital in Kuwait.
Udo EE, Al-Sweih N, John P, Chugh TD.

Department of Microbiology, Faculty of Medicine, Kuwait University, Safat, Kuwait.

Enterococci isolated in a teaching hospital were studied for their resistance to different antibiotics. Minimum inhibitory concentrations to high-level aminoglycosides and glycopeptide antibiotics were determined by agar dilution and E-test methods respectively. Genes encoding aminoglycoside-modifying enzymes were detected by the polymerase chain reaction (PCR). 195 enterococci were isolated from urines (54.3%), wounds (16.4%), blood (10.2%), and miscellaneous sources (18.9%). They consisted of E. faecalis (88.7%), E. faecium (9.2%), E. casseliflavus (1.5%) and E. bovis (0.5%). None of the Enterococci produced penicillinase but 3.5% of them were resistant to ampicillin. They were also resistant to high-level gentamicin (15.9%), kanamycin (22.0%), streptomycin (21.0%), tetracycline (65.1%), erythromycin (62.6%), ciprofloxacin (36.1%), chloramphenicol (26.1%), vancomycin (3.0%) and teicoplanin (2.0%). Most of the high-level aminoglycoside-resistant isolates contained genes coding the bifunctional aminoglycoside modifying enzymes AAC(6')-APH(2"), APH(3') and ANT(6') but not the ANT(4') enzyme. The results demonstrated a low prevalence of vancomycin resistance among Enterococci in this hospital.

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