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Ciprofloxacin Hydrochloride: Resistance

Resistance to ciprofloxacin can be produced in vitro in some organisms, including some strains of Enterobacteriaceae, Pseudomonas aeruginosa, Staphylococcus aureus, and Enterococcus faecalis (formerly Streptococcus faecalis), by serial passage in the presence of increasing concentrations of the drug. Ciprofloxacin resistance resulting from spontaneous mutation occurs rarely in vitro (i.e., with a frequency of 10-9 to 10-7).

Resistant strains of Ps. aeruginosa have emerged occasionally during therapy with the drug. Ciprofloxacin-resistant strains of S. aureus (including oxacillin-resistant strains; previously known as methicillin-resistant strains or MRSA) and S. epidermidis also have emerged during therapy with the drug. Strains of S. aureus, especially oxacillin-resistant S. aureus resistant to ciprofloxacin and other fluoroquinolones have been reported with increasing frequency, and such strains can emerge at relatively rapid rates (e.g., increasing within an institution from 0% of isolates prior to introduction of the drug to 80% 1 year later for oxacillin-resistant S. aureus).

Rapid emergence of resistance to fluoroquinolones in Campylobacter also has been reported and appears to be associated with widespread use or prolonged therapy with the drugs. Over a 10- to 12-year period in Finland, fluoroquinolone-resistant strains of C. jejuni and C. coli increased from 0-4% to 9-11%. A similar increase was observed over a 7-year period in Campylobacter isolates obtained from poultry and humans in the Netherlands; this increase in resistance was attributed to use of enrofloxacin in the poultry industry. In the US, fluoroquinolone-resistant isolates of Campylobacter have been obtained from raw turkey or chicken products in the retail market. Ciprofloxacin-resistant strains of initially susceptible Mycobacterium fortuitum have developed in a few patients who received ciprofloxacin alone or in conjunction with amikacin.

Resistance in Neisseria gonorrhoeae

Strains of Neisseria gonorrhoeae with decreased susceptibility to ciprofloxacin and other fluoroquinolones have been reported within the last several years. Until 1992, virtually all strains of N. gonorrhoeae tested were susceptible to ciprofloxacin in vitro; however, in vitro susceptibility of the organism to fluoroquinolones is changing. Strains of N. gonorrhoeae with decreased susceptibility to fluoroquinolones are endemic in many Asian countries and have been reported sporadically in other parts of the world, including North America, Australia, Africa, and Great Britain. In the US, strains with decreased susceptibility to fluoroquinolones have been isolated from patients in Hawaii, Ohio, Oregon, California, and Washington.

In some cases, these isolates appeared to have been introduced into the US by travelers returning from the Philippines; however, in Ohio, these strains appeared to have been transmitted locally and were not linked to travel outside the US.

The recent increase in ciprofloxacin-resistant N. gonorrhoeae in Hawaii also appears to be the result of endemic spread. The prevalence of quinolone-resistant N. gonorrhoeae (QRNG) in the US is being monitored by the CDC Gonococcal Isolate Surveillance Project (GISP). According to GISP data, about 6% of urethral isolates collected from samples of men at sexually transmitted diseases (STD) clinics in Cleveland, Ohio from January 1992 to June 1993 had decreased susceptibility to ciprofloxacin; expanded screening of all isolates from men at one clinic in Ohio during November and December 1993 revealed that about 14% of isolates had decreased susceptibility.

There is some evidence that strains of N. gonorrhoeae with reduced susceptibility to ciprofloxacin that were identified in Hawaii were different phenotypically than the strains identified in Ohio. The clinical importance of reduced susceptibility to fluoroquinolones has not been fully determined, and it is unclear whether uncomplicated gonococcal infections caused by these strains respond to currently recommended single-dose fluoroquinolone regimens.

Treatment failures have been reported with the currently recommended single-dose regimens; the likelihood of treatment failure seems greatest when the gonococcal strain has a ciprofloxacin MIC of 1 mcg/mL or greater. During 1996, less than 0.05% of clinical isolates collected by GISP in the US had ciprofloxacin MICs of 1 mcg/mL or greater.

If Hawaii is excluded, 0.2% of isolates collected by GISP in the US in 1999 were resistant to fluoroquinolones. GISP data collected during 2000 indicate that 0.4% of clinical isolates were resistant to ciprofloxacin (MICs 1 mcg/mL or greater); although QRNG made up 0.2% of samples collected from 25 cities within the continental US and Alaska, 14.% of isolates from the Honolulu GISP sample were QRNG. The CDC states that, as long as QRNG comprise less than 1% of all N. gonorrhoeae strains isolated at each of the cities included in the GISP sample, fluoroquinolone regimens recommended for treatment of gonorrhea can be used with confidence.

However, importation of QRNG will probably continue and the prevalence of these strains in the US could increase to the point that fluoroquinolones no longer reliably eradicate gonococcal infections. Strains ofN. gonorrhoeae with decreased susceptibility to ciprofloxacin also have decreased susceptibility to other fluoroquinolones (e.g., lomefloxacin, norfloxacin, ofloxacin), but may be susceptible to ceftriaxone, cefixime, and spectinomycin. A few strains with decreased susceptibility to ciprofloxacin also were resistant to tetracycline.

Neisseria gonorrhoeae

Resistance in Bacillus anthracis

Strains of Bacillus anthracis with natural resistance to ciprofloxacin have not been reported to date. There are published reports of B. anthracis strains that have been engineered to have tetracycline and penicillin resistance as well as resistance to other anti-infectives (e.g., macrolides, chloramphenicol, rifampin). In addition, reduced susceptibility to ofloxacin (4-fold increase in MICs from baseline) has been produced in vitro following sequential subculture of the Sterne strain of B. anthracis in subinhibitory concentrations of the fluoroquinolone.

Mechanisms of Fluoroquinolone Resistance

The mechanism(s) of resistance to fluoroquinolones, including ciprofloxacin, has not been fully elucidated but appears to involve mutations in the target DNA type II topoisomerase enzymes and mutations that result in alterations in membrane permeability and/or efflux pumps.


Cross-resistance can occur among the fluoroquinolones. Cross-resistance generally does not occur between ciprofloxacin and other anti-infectives, including aminoglycosides, b-lactam antibiotics, sulfonamides (including co-trimoxazole), macrolides, and tetracyclines. However, rare strains of Enterobacteriaceae and Ps. aeruginosa resistant to ciprofloxacin have also been resistant to aminoglycosides, b-lactam antibiotics, chloramphenicol, trimethoprim, and/or tetracyclines. Resistance in these organisms appears to be related to decreased permeability of the organism to the drug, principally because of alterations in outer-membrane porin proteins; however, other mechanisms that affect permeability may also be involved.

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