Effect of low concentrations of quinolone antibiotics on bacterial virulence mechanisms

Sonstein, Stephen A.; Burnham, Jeffrey C.

doi:10.1016/0732-8893(93)90078-l

Cited by 45 publications

(33 citation statements)

References 28 publications

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“…Ciprofloxacin inhibits DNA gyrase and therefore disrupts the process of maintaining the proper DNA topology. By this process, it may interfere in the regulatory mechanisms that control extracellular enzyme production (30). Fluoroquinolones at a level even below the MIC are still capable of affecting these topological characteristics of DNA (4).…”

Section: Discussionmentioning

confidence: 99%

Secretion of Proteases by Pseudomonas aeruginosa Biofilms Exposed to Ciprofloxacin

Ołdak

Trafny

2005

Antimicrob Agents Chemother

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Pseudomonas aeruginosa proteases are considered important virulence factors which damage host tissues and interfere with host antibacterial defense mechanisms. P. aeruginosa biofilm cells are not completely killed by antibacterials, and therefore this study addresses the question whether ciprofloxacin attenuates the virulence of biofilm communities by abolishing their secretion of proteases. The surviving cells of the colony biofilms studied, despite their cyclical exposure to four doses of ciprofloxacin at bactericidal concentrations (one dose a day), still secreted active proteases to the environment surrounding the biofilms. The biofilm cells secreted elastase B (LasB) over the duration of the experiments as confirmed by Western immunoblot analysis. The colony biofilms did not secrete LasA-a protease with staphylolytic activity. The same profiles on zymogram gels with gelatin were observed for the proteases secreted by both ciprofloxacin-exposed and unexposed (control) biofilms. Total proteolytic activities of the colony biofilms studied were significantly reduced after exposure to ciprofloxacin at bactericidal concentrations-after 96 h of exposure they dropped to 38% for the strain intermediate resistant to ciprofloxacin and to 65% for the strain highly resistant to the antibiotic, relative to the control biofilms. The surviving cells of the colony biofilms after their release into a fresh medium displayed transient increased resistance to ciprofloxacin compared to their planktonic counterparts.Pseudomonas aeruginosa is an opportunistic pathogen. However, serious pneumonias and sepsis due to an infection with this organism may be life threatening for patients with burns or cystic fibrosis and also for immunocompromised individuals. In patients with persistent lung infections, P. aeruginosa has been shown to grow as a biofilm (19).The reduced susceptibility to antibiotics displayed by P. aeruginosa biofilms, compared with that exhibited by the bacterial cells in liquid cultures, is a well-known phenomenon (9,11,12). A complete characterization of the cells from many bacterial species that survived treatment with an antibiotic has not yet been accomplished. In particular, it has not been answered, until now, whether the surviving cells are in a dormant state (31) or, quite the reverse, whether the metabolic processes of survivors have not been arrested upon their exposure to antibiotic (14), and these organisms display other physiological features that enable them to persist in the presence of antibiotic.Some antibiotics in concentrations below the MIC for the organisms also affect the synthesis of proteins (4). The production of some of the proteins may even be upregulated in the presence of ciprofloxacin at sublethal concentrations (3). Assuming that the physiology of the surviving cells is not somehow changed by ciprofloxacin to that of a completely nonvirulent phenotype, the proteases secreted by P. aeruginosa biofilms, despite the antimicrobial treatment, may still damage mammalian matrix proteins. Hence,...

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Section: Discussionmentioning

confidence: 99%

Secretion of Proteases by Pseudomonas aeruginosa Biofilms Exposed to Ciprofloxacin

Ołdak

Trafny

2005

Antimicrob Agents Chemother

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“…50 Indeed, in rats with experimental cirrhosis, Guarner et al 52 have recently observed that a certain level of intestinal overgrowth is a prerequisite for a bacterium to translocate to mesenteric lymph nodes. Another possibility is that the exposure of fecal bacteria to norfloxacin below the minimal inhibitory concentration would result in interference with bacterial virulence factors, 53 these bacteria being less likely to translocate and cause SBP.…”

Section: Discussionmentioning

confidence: 99%

Infections Caused By Escherichia Coli Resistant to Norfloxacin in Hospitalized Cirrhotic Patients

Ortiz¹,

Vila²,

Soriano³

et al. 1999

Hepatology

112

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Selective intestinal decontamination with norfloxacin is useful to prevent bacterial infections in several groups of cirrhotic patients at high risk of infection. However, the emergence of infections caused by Escherichia coli resistant to quinolones has recently been observed in cirrhotic patients undergoing prophylactic norfloxacin. Our aim is to determine the characteristics of the infections caused by E. coli resistant to norfloxacin in hospitalized cirrhotic patients. One hundred and six infections caused by E. coli in 99 hospitalized cirrhotic patients were analyzed and distributed into two groups: group I (n ‫؍‬ 67), infections caused by E. coli sensitive to norfloxacin, and group II (n ‫؍‬ 39), infections caused by E. coli resistant to norfloxacin. The clinical and analytical characteristics at diagnosis of the infection were similar in both groups. Previous prophylaxis with norfloxacin was more frequent in group II (15/67, 22.4% vs. 32/39, 82%, P F .0001), as a result of a higher number of patients submitted to continuous long-term prophylaxis in this group, whereas previous short-term prophylaxis was similar in both groups. Infections were more frequently nosocomial-acquired in group II than in group I (17/67, 25.3% vs. 20/39, 51.2%, P ‫؍‬ .01). The type of infections was similar in both groups: urinary tract infections 38 in group I and 24 in group II, spontaneous bacterial peritonitis 8 and 2, spontaneous bacteremia 4 and 4, and bacterascites 1 and 0, respectively (pNS). Mortality during hospitalization was similar in the two groups (4/67, 5.9% vs. 5/39, 12.8%, pNS). None of the E. coli resistant to norfloxacin were also resistant to cefotaxime and only one of them was resistant to amoxicillin-clavulanic acid. Prophylaxis with norfloxacin, usually continuous long-term prophylaxis, favors the development of infections caused by norfloxacin-resistant E. coli. Long-term antibiotic prophylaxis should therefore be restricted to highly selected groups of cirrhotic patients at high-risk of infection. Infections caused by E. coli resistant to norfloxacin show a severity similar to those caused by sensitive E. coli. No significant associated resistance between norfloxacin and the antibiotics most frequently used in the treatment of bacterial infections in cirrhotic patients has been observed.

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“…centrations of quinolones has been described in some cases (62,361). In contrast, ciprofloxacin and other SOS-inducing antimicrobial agents cause Shiga toxin-encoding bacteriophage induction and enhanced Shiga toxin production from E. coli O157:H7 both in vitro and in animal models (187,424).…”

Section: Antibiotics As Effectors Of Bacterial Virulencementioning

confidence: 99%

Interactions among Strategies Associated with Bacterial Infection: Pathogenicity, Epidemicity, and Antibiotic Resistance

2002

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SUMMARY Infections have been the major cause of disease throughout the history of human populations. With the introduction of antibiotics, it was thought that this problem should disappear. However, bacteria have been able to evolve to become antibiotic resistant. Nowadays, a proficient pathogen must be virulent, epidemic, and resistant to antibiotics. Analysis of the interplay among these features of bacterial populations is needed to predict the future of infectious diseases. In this regard, we have reviewed the genetic linkage of antibiotic resistance and bacterial virulence in the same genetic determinants as well as the cross talk between antibiotic resistance and virulence regulatory circuits with the aim of understanding the effect of acquisition of resistance on bacterial virulence. We also discuss the possibility that antibiotic resistance and bacterial virulence might prevail as linked phenotypes in the future. The novel situation brought about by the worldwide use of antibiotics is undoubtedly changing bacterial populations. These changes might alter the properties of not only bacterial pathogens, but also the normal host microbiota. The evolutionary consequences of the release of antibiotics into the environment are largely unknown, but most probably restoration of the microbiota from the preantibiotic era is beyond our current abilities.

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Effect of low concentrations of quinolone antibiotics on bacterial virulence mechanisms

Cited by 45 publications

References 28 publications

Secretion of Proteases by Pseudomonas aeruginosa Biofilms Exposed to Ciprofloxacin

Secretion of Proteases by Pseudomonas aeruginosa Biofilms Exposed to Ciprofloxacin

Infections Caused By Escherichia Coli Resistant to Norfloxacin in Hospitalized Cirrhotic Patients

Interactions among Strategies Associated with Bacterial Infection: Pathogenicity, Epidemicity, and Antibiotic Resistance

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