The emergence of multidrug-resistant (MDR) and extended-spectrum beta-lactamase (ESBL)-producing Klebsiella pneumoniae poses a serious antibiotic management problem as resistance genes are easily transferred from one organism to another. Fifty-one strains of K. pneumoniae isolated from sporadic cases in various hospitals throughout Malaysia were analysed by antimicrobial susceptibility testing, PCR detection of ESBL-encoding genes and DNA fingerprinting. Although 27 of the 51 K. pneumoniae strains were MDR (i.e. resistant to three or more classes of antibiotics), the majority of the strains (98 %) were sensitive to imipenem. PCR detection using ESBL gene-specific primers showed that 46 of the K. pneumoniae strains harboured bla(SHV), 19 harboured bla(CTX-M), 5 harboured bla(OXA-1) and 4 harboured bla(TEM-1). Class 1 integron-encoded intI1 integrase was detected in 21 of the 51 K. pneumoniae strains and amplification of the integron 5'CS region showed the presence of several known antibiotic resistance gene cassettes of various sizes. Results of conjugation and transformation experiments indicated that some of the ESBL-encoding genes (i.e. bla(SHV), bla(CTX-M) and bla(TEM-1)) were transmissible and were likely plasmid-encoded. DNA fingerprinting using PFGE and PCR-based methods indicated that the 51 K. pneumoniae strains were genetically diverse and heterogeneous.
Streptococcus pneumoniae is an epidemiologically important bacterial pathogen. Recently, we reported the antibiotic susceptibility patterns of a limited collection of pneumococcal isolates in Malaysia with a high prevalence of erythromycin resistant strains. In the present study, 55 of the pneumococcal isolates of serotype 19F were further analysed by pulsed field gel electrophoresis (PFGE) and multilocus sequence typing (MLST). The generated genotypic patterns were then correlated with the antibiograms previously reported. Forty-seven different PFGE profiles (PTs) were obtained, showing that the isolates were genetically diverse. MLST identified 16 sequence types (STs) with ST-236 being predominant (58.2%), followed by ST-81 (10.3%). Among the ST-236 isolates, 22 were erythromycin resistant S. pneumoniae (ERSP) and 15 were trimethoprim/sulfamethoxazole (TMP/SMX) resistant, while among ST-81, four isolates were ERSP and two were TMP/SMX resistant. The high prevalence of erythromycin resistant serotype 19F isolates of ST-236 in this study has also been reported in other North and South East Asian countries.
The in vitro activities of 6 antimicrobial agents against clinical isolates of Streptococcus pneumoniae (pneumococci) were investigated and the erythromycin minimum inhibitory concentrations (MICs) were correlated with the two major macrolide resistance determinants, mef(A) and erm(B). MICs of commonly used antibiotics as well as the presence of macrolide resistance determinant genes in all isolates were tested. Seventy one pneumococcal isolates collected at Institute for Medical Research (IMR) were included in this study. Phenotypic characterization, MIC determination using E-test strips and polymerase chain reactions for antibiotic resistance determination were included. Among the isolates, 25 (35.2%) isolates were erythromycin susceptible, 3 (4.2%) were intermediate and 42 (60.6%) were resistant. Fifty three isolates (74.7%) were found with mef(A) alone, 15 (21.1%) isolates with erm(B) + mef(A) combination and 3 (4.2%) isolates with none of the two genes. The in vitro activity of penicillin, amoxicillin clavulanic acid, ceftriaxone and cefotaxime is superior to trimethoprim-sulfamethoxazole and erythromycin. In conclusion, pneumococcal isolates in this study were highly susceptible to penicillin with very low MICs. However, a very high prevalence rate of erythromycin resistance was observed. Erythromycin resistant S. pneumoniae isolates with both mef(A) and erm(B) showed very high MICs ≥256 μg/mL.
The availability of molecular genetic testing for retinoblastoma (RB) in Malaysia has enabled patients with a heritable predisposition to the disease to be identified, which thus improves the clinical management of these patients and their families. In this paper, we presented our strategy for performing molecular genetic testing of the RB1 gene and the findings from our first 2 years of starting this service.