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The 4-Quinolones are known to induce the SOS response. This should also be the case with AZT (Zidovudine) which has the same bactericidal mechanism. SOS response might make the bacteria more sensitive or more resistant to subsequent doses of quinolones and AZT. NA (Nalidixic acid), the first quinolone of the early 1960s, sensitises a strain of E. coli isolated from the urine of patients with cystopyelitis and the E. coli AB1157 wild type strain which is a well-known SOS inducer. In this case, the SOS system is not involved but only the recombination repair mechanisms which make the bacteria more susceptible to further damage by NA. On the contrary, CPX (Ciprofloxacin) protects E. coli from further exposure to antibiotics. Therefore the SOS response induction assists the bacteria in recovering from the DNA damage caused by CPX. The SOS response induced by AZT in the tested E. coli strains does not seem to either contribute to the lethality of the drug or to be involved in protecting bacteria from the damage caused by AZT. In fact, the percentage of killing was the same for both pre-treated and non pre-treated bacteria (p = 0.5). On the contrary, it was found that in Salmonella typhimurium belonging to blood of a patient with recurrent bacteriaemia, the CPX added to pre-treated bacteria with AZT was less lethal than when it was added to non pre-treated bacteria. The SOS response, in this case, protects bacteria from the damage caused by AZT.

A total of 1,116 clinically isolated strains belonging to Staphylococcus aureus (200), Staphylococcus epidermidis (200), Streptococcus pneumoniae (20), Escherchia coli (200), Klebsiella spp. (177), Serratia marcescens (22), Pseudomonas aeruginosa (224), Haemophilus influenzae (35) and Salmonella (38) from the Department of Infectious Diseases, La Sapienza University in Rome (Italy) were tested against three fluoroquinolones (ofloxacin, ciprofloxacin and levofloxacin) and 10 other antibiotics (augmentin, ampicillin, cefaclor, cefixime, cefotaxime, cotrimoxazole, gentamicin, minocycline, oxacillin and vancomycin). Fluoroquinolones inhibited essentially about 100% of H. influenzae, Salmonella and S. pneumoniae, more than 75% of Staphylococcus including methicillin-resistant strains, and about 90% of Enterobacteriaceae and 50% of P. aeruginosa. Minimal inhibitory concentration values ranged from < 0.015 to > 32 micrograms/ml for Klebsiella, S. aureus and epidermidis, E. coli and P. aeruginosa; from < 0.015 to 2 micrograms/ml for Salmonella; from 0.03 to 16 micrograms/ml for Serratia; from < 0.015 to 1 microgram/ml for Haemophilus; and from 0.5 to 2 micrograms/ml for S. pneumoniae. Levofloxacin and to a lesser extent ofloxacin and ciprofloxacin, generally exhibited a greater activity than the other agents against both Gram-positive and Gram-negative bacteria. Regarding the distribution of resistant strains in Italy, we found a peculiar pattern of resistance as far as E. coli and P. aeruginosa were concerned. Quality control parameters are also summarized. S. epidermidis resulted as a new emergent pathogen especially in immunocompromised patients and its level of sensitivity has been modified over the last few years. In fact, the percentage of resistant strains to antibiotics or the percentage of methicillin-resistant isolates (in our study 35%), has gradually increased. Levofloxacin and ofloxacin showed good activity against staphylococcal strains compared with the majority of other antibiotics. These results suggest that the newer quinolones are promising antimicrobial agents for various infections.