Mechanisms of beta-lactam resistance inHaemophilus influenzae

Abstract

Haemophilus influenzae has become increasingly resistant to beta-lactam antibiotics. Three major mechanisms, both enzymatic and non-enzymatic, are involved. Enzymatic resistance is mainly due to production of a TEM-1 plasmid-mediated beta-lactamase, and in some cases to a new enzyme ROB-1. Of the non-enzymatic mechanisms, decreased permeability due to alteration of outer membrane proteins seems to be rare in comparison to decreased affinity of penicillin-binding proteins for beta-lactam antibiotics. Enzymatic resistance is present in about 10-20% of clinical isolates, while non-enzymatic resistance is present only in 2-4%.

Distinct plasmid profiles of Pasteurella haemolytica serotypes and the characterization and amplification in Escherichia coli of ampicillin-resistance plasmids encoding ROB-1 -lactamase

“…Our data indicate little resistance to the cephalosporin class of P-lactams by the original and transconjugant P. haemolytica isolates, but higher resistance of E. coli transformants containing the ApR plasmids, particularly pPH843. The sensitivity and substrate profiles of the ROB-and TEM-type /Ilactamases have been reported to be similar (Guttmann et al, 1988) and this was confirmed in the present study (Tables 4 and 5). The ROB-1 P-lactamase has been differentiated from the TEM-1 enzyme by its higher PI and its ability to hydrolyse ampicillin more rapidly and cephaloridine more slowly (Rubin et al, 1981).…”

Susceptibility of Clinically Significant <i>Haemophilus influenzae</i> Strains to Oral Antimicrobial Agents Used in Saudi Arabia

“…There is evidence that there has been some increase in the occurrence in the UK of these strains, al though the prevalence generally remains low [14]. In France [22], non-enzymatic resistances have been found increasingly, occurring in about 2^f% of the H. influenzae strains. The most frequent non-enzymatic mechanism of resistance is based on an alteration of penicil lin-binding proteins 4 and 5 [22].…”

“…In France [22], non-enzymatic resistances have been found increasingly, occurring in about 2^f% of the H. influenzae strains. The most frequent non-enzymatic mechanism of resistance is based on an alteration of penicil lin-binding proteins 4 and 5 [22]. Decreased permeability by alteration of porins has been reported only rarely [22], Infections due to these strains are being reported more fre quently than before [8,23,24], It has been agreed that the different pre scription policies and treatment strategies em ployed in different regions might influence the resistance rates and patterns of resistance in H. infuienzae.…”

Susceptibility of Haemophilus Influenzae to Selected Antimicrobial Agents

“…5,13 Ampicillin resistance mostly recognized in type b strains is mainly due to the production of a ß-lactamase-type TEMI enzyme. 15 Nonenzymatic mechanisms of resistance to ampicillin and other ß-lactam antibiotics include decreased outer membrane permeability and alterations in penicillin-binding proteins 4 and 5. 15 Resistance to chloramphenicol is due to the production of a chloramphenicol acetyl-transferase enzyme and is usually related to tetracycline resistance.…”

“…15 Nonenzymatic mechanisms of resistance to ampicillin and other ß-lactam antibiotics include decreased outer membrane permeability and alterations in penicillin-binding proteins 4 and 5. 15 Resistance to chloramphenicol is due to the production of a chloramphenicol acetyl-transferase enzyme and is usually related to tetracycline resistance. 13 While resistance to ampicillin is usually plasmid mediated, 16 that of trimethoprim is mediated by a gene located on the chromosome.…”