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Aims@#Maternal vaginal Group B Streptococcus (GBS) colonization is considered a risk factor for preterm delivery and, consequently, neonatal infections. Previous studies have portrayed the important roles of these virulence factors, including hemolytic pigment, hyaluronidase (HylB), serine-rich protein (Srr) and bacterial surface adhesion of GBS (BsaB) in mediating GBS colonization and intrauterine ascending infection, causing preterm delivery. This study aimed to investigate the association between mRNA expression of virulence genes in GBS isolates obtained from symptomatic pregnant women and preterm delivery.@*Methodology and results@#GBS isolates were obtained from high vaginal swabs of 40 symptomatic pregnant women of gestational age of less than 37 weeks. RNA was extracted from these GBS isolates and RT-qPCR was performed to determine the relative mRNA expression of GBS virulence genes, including CylE (encode enzyme required for the biosynthesis of the hemolytic pigment), HylB, Srr-1 and BsaB. Socio-demographic details and obstetric history were not found to be associated with the delivery outcomes of these women. The GBS isolates from symptomatic pregnant women who delivered prematurely showed a higher expression of CylE gene and a trend towards an elevated expression of HylB gene compared to women with term delivery. Meanwhile the expression of both Srr-1 and BsaB genes was similar between symptomatic pregnant women who had term or preterm delivery.@*Conclusion, significance and impact of study@#The results suggest that following vaginal colonization, both CylE and HylB genes are likely to contribute to intrauterine ascending infection and inflammation, leading to preterm delivery in humans. These virulence factors may be targeted for the pre-clinical stages of vaccine development or therapeutic intervention.
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Background: To assess antimicrobial susceptibility of extended-spectrum β-lactamase- (ESBL-) producing Klebsiella pneumoniae and Escherichia coli isolates from Hospital Tengku Ampuan Afzan (HTAA), as well as to identify ESBL genes. Methods: Non-duplicate K. pneumoniae and E. coli isolates were recovered from various clinical samples. Isolates were screened for antimicrobial resistance by disc diffusion method. Isolates resistant to oxyimino-cephalosporins were subjected to phenotypic ESBL production. Detection of resistance genes was then performed using primers specific for ESBL genes (blaCTX-M, blaSHV and blaTEM). Results: Piperacillin/tazobactam and carbapenems remained the active β-lactam antibiotic against K. pneumoniae and E. coli. ESBLs were detected among 35.5% (39/110) of K. pneumoniae and 18.8% (28/149) of E. coli isolates. CTX-M β-lactamase was detected in 90% of all ESBL-positive isolates, whereas blaSHV and blaTEM genes were found among 56% and 52% of them, respectively. Twenty-eight percent (28%) of the total ESBL-positive isolates harboured the three ESBL genes, while 50% carried two of the tested ESBL genes. Conclusion: ESBLs encoded by at least one ESBL genes are frequently isolated among K. pneumoniae and E. coli in HTAA. The significant proportion rate of these resistant determinants is alarming, thus monitoring their transmission and dissemination is essential to control it at an early phase.