PMID- 9158769
OWN - NLM
STAT- MEDLINE
DCOM- 19970617
LR  - 20051116
IS  - 1076-6294 (Print)
IS  - 1076-6294 (Linking)
VI  - 2
IP  - 2
DP  - 1996 Summer
TI  - Borderline susceptibility to methicillin in Staphylococcus aureus: a new 
      mechanism of resistance?
PG  - 257-60
AB  - Staphylococcus aureus strains with borderline levels of susceptibility or 
      resistance to antistaphylococcal penicillinase-resistant penicillins (PRPs) were 
      initially reported as neither heteroresistant nor multiply resistant organisms, 
      producing large amounts of beta-lactamase, and becoming fully susceptible to PRPs 
      in the presence of beta-lactamase inhibitors. This borderline susceptibility or 
      low-level resistance was suggested to be due to beta-lactamase hyperproduction: 
      according to this hypothesis, the staphylococcal beta-lactamase, when 
      hyperproduced, would succeed in partially hydrolyzing methicillin and related 
      PRPs. However, later studies demonstrated that borderline PRP susceptibility 
      cannot be explained soley on this basis, beta-lactamase hyperproduction being 
      neither sufficient nor necessary to determine the borderline phenotype. Intrinsic 
      mechanisms have also been reported to be associated with some borderline PRP 
      susceptible S. aureus strains. The more recent discovery of a PRP-hydrolyzing 
      beta-lactamase (methicillinase) produced, in addition to the conventional 
      penicillinase, by borderline S. aureus strains suggests that this second, more 
      specific beta-lactamase is more likely to be responsible for the borderline 
      phenotype than an increased amount of the penicillinase. The slow kinetics of PRP 
      hydrolysis by methicillinase is consistent with its association with reduced 
      susceptibility rather than true resistance to PRPs. The combined effect of 
      methicillinase plus penicillinase on some common substrates might explain the 
      increased beta-lactamase activity often observed in borderline S. aureus strains.
FAU - Montanari, M P
AU  - Montanari MP
AD  - Institute of Microbiology, University of Ancona Medical School, Italy.
FAU - Massidda, O
AU  - Massidda O
FAU - Mingoia, M
AU  - Mingoia M
FAU - Varaldo, P E
AU  - Varaldo PE
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Microb Drug Resist
JT  - Microbial drug resistance (Larchmont, N.Y.)
JID - 9508567
SB  - IM
MH  - Methicillin Resistance/*genetics/*physiology
MH  - Phenotype
MH  - Staphylococcus aureus/*drug effects/*genetics
RF  - 27
EDAT- 1996/07/01 00:00
MHDA- 2000/03/18 09:00
CRDT- 1996/07/01 00:00
PHST- 1996/07/01 00:00 [pubmed]
PHST- 2000/03/18 09:00 [medline]
PHST- 1996/07/01 00:00 [entrez]
AID - 10.1089/mdr.1996.2.257 [doi]
PST - ppublish
SO  - Microb Drug Resist. 1996 Summer;2(2):257-60. doi: 10.1089/mdr.1996.2.257.