[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address Please contact the publisher to request reinstatement.
[Skip to Content Landing]
January 1996

Emerging Antibiotic Resistance: Real and Relative

Author Affiliations

Houston, Tex

Arch Ophthalmol. 1996;114(1):91-92. doi:10.1001/archopht.1996.01100130087016

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.


Emergence of antibiotic resistance is a global crisis.1,2 Approximately 2 million nosocomial infections occur in the United States each year, of which one half are caused by antibiotic-resistant organisms. Treatment failure owing to antibiotic resistance adds approximately $4.5 billion annually to health care costs in this country.

Bacteria acquire resistance through clever mechanisms of genetic engineering to survive increasing selection pressure of antibiotic use. Methicillin resistance in Staphylococcus aureus is due to the mecA gene that encodes for a surrogate penicillin-binding protein (PBP), PBP2a, which has a low affinity for β-lactam antibiotics.3 The PBP2a functions as a transpeptidase to maintain cell wall synthesis, thereby preventing β-lactams from blocking the production of peptidoglycans. All methicillin-resistant Staphylococcus aureus (MRSA) possess the mecA gene, which also conveys methicillin resistance in coagulase-negative staphylococci (CNS). MRSA first appeared in 1960, one year after introduction of β-lactamase-resistant penicillins, and now accounts for 40% of

American Society for Microbiology.  Report of the ASM Task Force on Antibiotic Resistance . Antimicrob Agents Chemother . 1995( (suppl) ):1-23.
Tomasz A.  Multiple-antibiotic-resistant pathogenic bacteria; a report on the Rockefeller University Workshop . N Engl J Med . 1994;330:1247-1251.Article
de Lencastre H, de Jonge BLM, Matthews PR, Tomasz A.  Molecular aspects of methicillin resistance in Staphylococcus aureus . J Antimicrob Chemother . 1994;33:7-24.Article
Spratt BG.  Resistance to antibiotics mediated by target alterations . Science . 1994;264:388-393.Article
Wiedemann B, Heisig P.  Mechanisms of quinolone resistance . Infection . 1994;22( (suppl 2) ):S73-S79.Article
Centers For Disease Control and Prevention.  Fluoroquinolone resistance in Neisseria gonorrhoeae—Colorado and Washington . MMWR Morb Mortal Wkly Rep . 1995;44:761-764.
Woodford N, Johnson AP, Morrison D, Speller DCE.  Current perspectives on glycopeptide resistance . Clin Microbiol Rev . 1995;8:585-615.
Courvalin P.  Transfer of antibiotic resistance genes between gram-positive and gram-negative bacteria . Antimicrob Agents Chemother . 1994;38:1447-1451.Article
Davis J.  Inactivation of antibiotics and the dissemination of resistance genes . Science . 1994;264:375-382.Article
Stratton CV IV.  In vitro testing: correlations between bacterial susceptibility, body fluid levels, and effectiveness of antibacterial therapy . In: Lorian V, ed. Antibiotics in Laboratory Medicine . Baltimore, Md: Williams & Wilkins; 1991:849-879.
Kowalski RP, Karenchak LM, Eller AW.  The role of ciprofloxacin in endophthalmitis therapy . Am J Ophthalmol . 1993;116:695-699.
Diamond JP, White L, Leeming JP, et al.  Topical 0.3% ciprofloxacin, norfloxacin, and ofloxacin in treatment of bacterial keratitis: a new method for comparative evaluation of ocular drug penetration . Br J Ophthalmol . 1995;79:606-609.Article