Molecular typing and analysis of antimicrobial resistance in clinical isolates of Streptococcus pneumoniae and Haemophilus influenzae

• Main Author: Bamarouf, Abdulaziz Omar
• Published: University of Edinburgh 2000
• Subjects: 616.9
• Online Access: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.641268

b-Lactams are widely used to treat <i>S. pneumoniae </i>and <i>H. influenzae</i> respiratory infections. However, resistance to b-lactams is increasing in the UK. To establish if this results from spread of a small number of resistant strains or from a wider emergence of resistance, the molecular type and mechanisms of resistance in <i>S. pneumoniae</i> and <i>H. influenzae </i>isolates, from throughout the UK, were determined. Resistance of <i>S. pneumoniae </i>to penicillin is due entirely to the development of altered forms of the high molecular weight penicillin binding proteins (PBPs) and decreased affinity of PBP 2x, 2b and 1a together give high-level penicillin resistance. Between 1995 and 1996, 80 isolates of <i>s. pneumoniae</i> were obtained from centres throughout the UK. Eighteen isolates were penicillin-resistant and these were typed by pulsed-field gel electrophoresis (PFGE). In addition, changes in penicillin binding proteins (PBPs) 2x, 2b and 1a were examined by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). Cluster analysis of patterns produced by PFGE of chromosomal DNA digested with <i>Sma1</i> revealed that penicillin resistance was not simply the result of clonal spread. Screening for changes in PBPs and RFLP of the amplified <i>pbp2x, 2b </i>and <i>1a</i> genes by <i>Hin</i>fI showed that there was a correlation between resistance and alteration in PBPs. The results indicate that penicillin resistance in <i>S. pneumoniae </i>in the UK is evolving in a variety of different strains and this raises cause for concern. b-Lactams resistance in <i>H. influenzae</i> is mainly mediated by the production of b-lactamases. b-lactamase-mediated resistance is associated with the production of TEM-1, ROB-1 and VAT-1 b-lactamase enzymes. Impermeability and alterations in PBPs are further mechanisms that mediate resistance to b-lactams. The epidemiology and mechanisms of resistance to amoxycillin and amoxycillin/clavulanic acid (co-amoxiclav) in <i>H. influenzae </i>isolates from the UK was examined. Between 1995 and 1996, 231 isolates of <i>H. influenzae</i> were obtained from centres throughout the UK. Twenty percent of isolates were amoxycillin-resistant and, of these, 19% were also resistant to co-amoxiclav.