Prevalence Of Fluoroquinolone Resistance Research Articles

PREVALENCE OF FLUOROQUINOLONES RESISTANCE AMONG ESBL-PRODUCING ESCHERICHIA COLI ISOLATED FROM URINE SAMPLES

BACKGROUND
 Resistance among uropathogens has emerged as a growing concern necessitating re-evaluation of the efficacy of recommended empiric antimicrobial regimens. Misuse and overuse of various antibacterial agents in hospitals is a key cause of the emergence of anti-microbial resistance.
 Aims: To identify the prevalence of extended-spectrum beta-lactamase (ESBL) producing Escherichia coli from urine specimens and to know the prevalence of Fluoroquinolone resistance among ESBL-producing Escherichia coli (E. coli) isolates.
 Material and method: The study was conducted on 500 E. coli isolates from urine samples received in the Department of Microbiology, MMIMSR, Mullana, Ambala. The organism isolation and identification were done as per the standard procedures and antibiotic sensitivity testing was done following CLSI guidelines. All the strains were screened out for ESBL production as per CLSI guidelines. Ciprofloxacin, Norfloxacin, and Ofloxacin discs were used for the detection of fluoroquinolone resistance.
 Results: Out of the total 500 E. Coli isolates from urine samples received in our laboratory, 69% were found to be ESBL producers.
 Conclusion: We found a high level of quinolone resistance among ESBL-producing Escherichia coli strains isolated from patients with UTI. Because of the widespread use of fluoroquinolones in our country, there is a need for sensitive antibiotic stewardship. Further research is needed to ascertain the gravity of quinolone resistance and to swiftly act against its spread among other nosocomial pathogens.

Transmission of Fluoroquinolones Resistance among Multidrug-Resistant Tuberculosis in Shanghai, China: A Retrospective population-based Genomic Epidemiology Study

ABSTRACT Fluoroquinolones (FQ) are essential for the treatment of multidrug-resistant tuberculosis (MDR-TB). The FQ resistance (FQ-R) rate in MDR-TB in China and its risk factors remain poorly understood. We conducted a retrospective, population-based genomic epidemiology study of MDR-TB patients in Shanghai, China, from 2009 to 2018. A genomic cluster was defined as strains with genetic distances ≤ 12 single nucleotide polymorphisms. The transmitted FQ-R was defined as the same FQ resistance-conferring mutations shared by ≥ 2 strains in a genomic cluster. We used multivariable logistic regression analysis to identify the risk factors for drug resistance. Among the total 850 MDR-TB patients included in the study, 72.8% (619/850) were male, the median age was 39 (interquartile range 28, 55) years, 52.7% (448/850) were migrants, and 34.5% (293/850) were previously treated patients. Most of the MDR-TB strains belong to the Beijing lineage (91.7%, 779/850). Overall, the genotypic resistance rate of FQ was 34.7% (295/850), and 47.1% (139/295) FQ-R patients were in genomic clusters, of which 98 (33.2%, 98/295) were presumed as transmitted FQ-R. Patients with treatment-naïve (aOR = 1.84; 95% CI: 1.09, 3.16), diagnosed in a district-level hospital (aOR = 2.69; 95% CI: 1.56, 4.75), and streptomycin resistance (aOR = 3.69; 95% CI: 1.65, 9.42) were significantly associated with the transmission of FQ-R. In summary, the prevalence of FQ-R among MDR-TB patients was high in Shanghai, and at least one-third were transmitted. Enforced interventions including surveillance of FQ drug susceptibility testing and screening among MDR-TB before initiation of treatment were urgently needed.

High Burden of Intestinal Colonization With Antimicrobial-Resistant Bacteria in Chile: An Antibiotic Resistance in Communities and Hospitals (ARCH) Study.

Antimicrobial resistance is a global threat, heavily impacting low- and middle-income countries. This study estimated antimicrobial-resistant gram-negative bacteria (GNB) fecal colonization prevalence in hospitalized and community-dwelling adults in Chile before the coronavirus disease 2019 pandemic. From December 2018 to May 2019, we enrolled hospitalized adults in 4 public hospitals and community dwellers from central Chile, who provided fecal specimens and epidemiological information. Samples were plated onto MacConkey agar with ciprofloxacin or ceftazidime added. All recovered morphotypes were identified and characterized according to the following phenotypes: fluoroquinolone-resistant (FQR), extended-spectrum cephalosporin-resistant (ESCR), carbapenem-resistant (CR), or multidrug-resistant (MDR; as per Centers for Disease Control and Prevention criteria) GNB. Categories were not mutually exclusive. A total of 775 hospitalized adults and 357 community dwellers were enrolled. Among hospitalized subjects, the prevalence of colonization with FQR, ESCR, CR, or MDR-GNB was 46.4% (95% confidence interval [CI], 42.9-50.0), 41.2% (95% CI, 37.7-44.6), 14.5% (95% CI, 12.0-16.9), and 26.3% (95% CI, 23.2-29.4). In the community, the prevalence of FQR, ESCR, CR, and MDR-GNB colonization was 39.5% (95% CI, 34.4-44.6), 28.9% (95% CI, 24.2-33.6), 5.6% (95% CI, 3.2-8.0), and 4.8% (95% CI, 2.6-7.0), respectively. A high burden of antimicrobial-resistant GNB colonization was observed in this sample of hospitalized and community-dwelling adults, suggesting that the community is a relevant source of antibiotic resistance. Efforts are needed to understand the relatedness between resistant strains circulating in the community and hospitals.

Concentrations of Ciprofloxacin in the World's Rivers Are Associated with the Prevalence of Fluoroquinolone Resistance in Escherichia coli: A Global Ecological Analysis.

Background: Extremely low concentrations of ciprofloxacin may select for antimicrobial resistance. A recent global survey found that ciprofloxacin concentrations exceeded safe levels at 64 sites. In this study, I assessed if national median ciprofloxacin concentrations in rivers were associated with fluoroquinolone resistance in Escherichia coli. Methods: Spearman’s regression was used to assess the country-level association between the national prevalence of fluoroquinolone resistance in E. coli and the median ciprofloxacin concentration in the country’s rivers. Results: The prevalence of fluoroquinolone resistance in E. coli was positively correlated with the concentration of ciprofloxacin in rivers (ρ = 0.36; p = 0.011; n = 48). Discussion: Steps to reducing the concentrations of fluoroquinolones in rivers may help prevent the emergence of resistance in E. coli and other bacterial species.

Association of fluoroquinolone resistance and ESBL production in hypervirulent Klebsiella pneumoniae ST11 and ST893 in Iran.

The spread of multidrug resistance in Klebsiella pneumoniae is a serious threat to the public health. In this study, the prevalence of fluoroquinolone resistance and virulence determinants among ESBL-producing K. pneumoniae isolates was investigated. A total of 50 third-generation cephalosporin resistant K. pneumoniae strains were collected from patients' clinical cultures between September 1st, 2019 and February 30th, 2020. Clonal relatedness of clinical isolates was determined by multilocus sequence typing. All 50 isolates were multidrug-resistant (MDR) and carried at least one of the ESBL resistance determinants. The bla CTX-M-15 gene was the major ESBL determinant found in K. pneumoniae (88%), followed by bla SHV (86%) and bla TEM (78%). PMQR was detected in 96% of the isolates and aac(6')-Ib-cr was the most common (78%) as well as multiple mutations in gyrA (S83I, D87G) and parC (S80I) were found. Selected isolates were assigned to seven sequence types (STs) (ST11, ST893, ST147, ST16, ST377, ST13, and ST392). Overall, hypervirulent phenotypes were identified in 26 (52%) of the isolates. Among the 50 isolates, 28 (56%) were positive for ybt, 23 (46%) for rmpA, 17 (34%) for iroB, 15 (30%) for magA, 4 (8%) for alls and 3 (6%) for iucA genes. The K1 capsular type was the most prevalent (11/50; 22%) among isolates. The emergence of hypervirulent K. pneumoniae (hvKp) ST11 and ST893, which co-carried ESBL, PMQR determinants and different virulence genes has become a threat to the treatment of inpatients in the clinical setting.

Emergence of Plasmid-mediated Quinolone-Resistant Salmonella Typhi Clinical Isolates from Punjab, Pakistan

The present study evaluated the prevalence of fluoroquinolone resistance and the underlying mechanisms among Salmonella Typhi clinical strains from Punjab, Pakistan. A total of 174 Salmonella Typhi strains were isolated from the blood culture samples. The strains identification was done by using the API 20E system and VITEK®, while serovar validation was done by agglutination assays using antisera. Molecular characterization was done by PCR using the primers targeting the fliC-d gene of Salmonellaenterica serovar Typhi. Antimicrobial susceptibility testing was performed by disc diffusion procedure and the minimum inhibitory concentration using the broth microdilution technique. Moreover,plasmid-mediated quinolone resistance genes were amplified through a polymerase chain reaction. Alarming rate of ciprofloxacin resistance (90.8%) were observed with high MICs ranging from <0.06 µg/mL to > 2.0 µg/mL.Overall, the qnrS gene was detected among every ciprofloxacin-resistant isolate, of which maximum frequency of qnrS genes was detected among isolates showing MICs <1.0 µg/mL, while 14 qnrSgene-positive isolates were showing very high MICs values 2.0 µg/mL.Moreover, the ciprofloxacin-resistantisolates, as well as the ten isolates showing intermediate resistance (MIC; 0.5 µg/mL), were negative for qnrA and qnrB genes. This study highlights that the quinolone resistance among S. Typhiis at a critical level that necessitates the need for alternative therapeutic measures and the development of new antibiotics.

Positive Association between the Use of Quinolones in Food Animals and the Prevalence of Fluoroquinolone Resistance in E. coli and K. pneumoniae, A. baumannii and P. aeruginosa: A Global Ecological Analysis.

(1) Background: It is unclear what underpins the large global variations in the prevalence of fluoroquinolone resistance in Gram-negative bacteria. We tested the hypothesis that different intensities in the use of quinolones for food-animals play a role. (2) Methods: We used Spearman’s correlation to assess if the country-level prevalence of fluoroquinolone resistance in human infections with Acinetobacter baumannii, Escherichia coli, Klebsiella pneumoniae and Pseudomonas aeruginosa was correlated with the use of quinolones for food producing animals. Linear regression was used to assess the relative contributions of country-level quinolone consumption for food-animals and humans on fluoroquinolone resistance in these 4 species. (3) Results: The prevalence of fluoroquinolone resistance in each species was positively associated with quinolone use for food-producing animals (E. coli [ρ = 0.55; p < 0.001], K. pneumoniae [ρ = 0.58; p < 0.001]; A. baumanii [ρ = 0.54; p = 0.004]; P. aeruginosa [ρ = 0.48; p = 0.008]). Linear regression revealed that both quinolone consumption in humans and food animals were independently associated with fluoroquinolone resistance in E. coli and A. baumanii. (4) Conclusions: Besides the prudent use of quinolones in humans, reducing quinolone use in food-producing animals may help retard the spread of fluoroquinolone resistance in various Gram-negative bacterial species.

High Prevalence of Fluoroquinolone Resistance among Non-Multidrug-Resistant Pulmonary Tuberculosis Patients Attending a Tertiary Care Hospital: An Imminent Threat

High Prevalence of Fluoroquinolone Resistance among Non-Multidrug-Resistant Pulmonary Tuberculosis Patients Attending a Tertiary Care Hospital: An Imminent Threat

Epidemic and molecular characterization of fluoroquinolone-resistant Shigella dysenteriae 1 isolates from calves with diarrhea

BackgroundThe widespread distribution of antimicrobial-resistant Shigella has become a recurrent challenge in many parts of the developing world. Previous studies indicate that the host of Shigella has expanded from humans to animals. This study aimed to investigate the prevalence of fluoroquinolone resistance and associated molecular characterization of S. dysenteriae 1 isolated from calves.ResultsAll 38 unduplicated S. dysenteriae 1 isolates were collected from calves in Gansu Province from October 2014 to December 2016. According to MLST and PFGE analysis, these isolates were separated into 4 and 28 genotypes, respectively. The most common STs identified were ST228 (34.21%, 13/38) and ST229 (39.47%, 15/38), which were first found in the present study. All isolates harbored virulence genes, and the incidence of the seven virulence genes were ipaH (100%), ipaBCD (92.11%), stx (73.68%), ial (57.89%), sen (28.95%), set1A and set1B (0%). According to the results of antimicrobial susceptibilities, 76.32% (29/38) were resistant to fluoroquinolone and showed multidrug resistance. In a study on the polymorphism of quinolone resistance–determining region (QRDR) of gyrA/B and parC/E genes, we identified two mutations in gyrA (Ser83 → Leu and Asp87 → Asn) and parC (Ser80 → Ile and Ser83 → Leu), respectively. Among them, 55.17% (16/29) of resistant strains had the gyrA point mutations (Ser83 → Leu) and parC point mutation (Ser83 → Leu). Moreover, 41.38% (12/29) of isolates had all five point mutations of gyrA and parC. In addition, the prevalence of the plasmid-mediated quinolone resistance (PMQR) determinant genes was also investigated. All 29 fluoroquinolone-resistant isolates were positive for the aac (6′)-Ib-cr gene but negative for qepA, except for SD001. In addition, only 6 (20.69%, 6/29) isolates harbored the qnr gene, including two with qnrB (6.90%, 2/29) and four with qnrS (13.79%, 4/29).ConclusionGiven the increased common emergence of multidrug resistant isolates, uninterrupted surveillance will be necessary to understand the actual epidemic burden and control this infection.

Prevalence of fluoroquinolone resistance and mutations in the gyrA, parC and parE genes of Riemerella anatipestifer isolated from ducks in China

BackgroundRiemerella anatipestifer is one of the most serious infectious disease-causing pathogens in the duck industry. Drug administration is an important method for prevention and treatment of infection in duck production, leading to widespread drug resistance in R. anatipestifer.MethodsFor a total of 162 isolates of R. anatipestifer, the MICs were determined for a quinolone antimicrobial agent, namely, nalidixic acid, and three fluoroquinolones, namely, ciprofloxacin, enrofloxacin and ofloxacin. The gyrA, parC, and parE gene fragments were amplified by PCR to identify the mutation sites in these strains. Site-directed mutants with mutations that were detected at a high frequency in vivo were constructed (hereafter referred to as site-directed in vivo mutants), and the MICs of these four drugs for these strains were determined.ResultsIn total, 100, 97.8, 99.3 and 97.8% of the 137 R. anatipestifer strains isolated between 2013 and 2018 showed resistance to nalidixic acid, ciprofloxacin, enrofloxacin, and ofloxacin, respectively. The high-frequency mutation sites were detected in a total of 162 R. anatipestifer strains, such as Ser83Ile and Ser83Arg, which are two types of substitution mutations of amino acid 83 in GyrA; Val799Ala and Ile811Val in ParC; and Val357Ile, His358Tyr, and Arg541Lys in ParE. MIC analysis results for the site-directed in vivo mutants showed that the strains with only the Ser83Ile mutation in GyrA exhibited an 8–16-fold increase in MIC values, and all mutants showed resistance to ampicillin and ceftiofur.ConclusionsThe resistance of R. anatipestifer to quinolone agents is a serious problem. Amino acid 83 in GyrA is the major target mutation site for the fluoroquinolone resistance mechanism of R. anatipestifer.

Prevalence and mechanism of fluoroquinolone resistance in clinical isolates of Proteus mirabilis in Japan

Fluoroquinolone (FQ) and cephalosporin (CEP) resistance among Enterobacteriaceae has been increasingly reported. FQ resistance occurs primarily through mutations in DNA gyrase (gyrA and gyrB) and topoisomerase IV (parC and parE). CEP resistance in Enterobacteriaceae is mainly due to the production of CTX-M type extended-spectrum β-lactamases. Although prevalence and mechanisms of FQ and CEP resistance in Enterobacteriaceae such as Escherichia coli have been well studied, little is known about Proteus mirabilis in Japan. In this study, we assessed the prevalence and mechanism of FQ resistance in Japanese clinical isolates of P. mirabilis. We collected 5845 P. mirabilis isolates from eight hospitals between 2000 and 2013. Prevalence of FQ resistance was calculated as the annual average percentage of all P. mirabilis isolates. We selected 50 isolates exhibiting susceptibility, intermediate resistance, or resistance to levofloxacin (LVX) and identified amino acid substitutions in GyrA, GyrB, ParC, and ParE. The prevalence of FQ-resistant P. mirabilis gradually increased from 2001 to 2004, reaching 16.6% in 2005, and has remained relatively high (13.3–17.5%) since then. Low-level LVX-resistant strains (MIC, 8–16 mg/L) showed significant changes in GyrB (S464Y or -I, or E466D). High-level LVX-resistant strains (MIC, 32–128 mg/L) displayed significant changes in GyrA (E87K) and ParE (D420N). The highest-level LVX-resistant strains (MIC, ≥ 256 mg/L) presented significant changes in GyrA (E87K or -G), GyrB (S464I or -F), and ParE (D420N). Our findings suggest that substitutions in GyrA (E87) and ParE (D420) have played an important role in the emergence of high-level LVX-resistant P. mirabilis isolates (MIC, ≥ 32 mg/L) in Japan.

Review on strategies to minimize the appearance of multi-drug resistant organism

Background: The use of antibiotic drugs (ABX) in hospitals, and especially in intensive care units (ICU), is widespread. The early administration of ABX therapy can improve survival rates. The influence and impact of the ABX are observed in the patients who receive them (clinical response, course) and in the ecosystem surrounding the patient (hospital flora). Aim of the review: The objective of this review is to identify strategies that reduce or limit the appearance and transmission of multidrug-resistant microorganisms. This identification can then develop a rational use of the ABX plan in the ICU. Method: The following databases were queried; Medline, Embase, The Cochrane Library, and the Centre for Reviews and Dissemination (University of York), asking the questions in PICO format to evaluate the efficacy and safety of several interventions: A) Therapeutic de-escalation; B) Cycling of ABX and; C) Early antibiotic treatment. Results: A) In therapeutic de-escalation of 98 studies identified, three studies that met the inclusion criteria were analyzed. B) Two studies comparing antibiotic cycling versus other interventions were selected. C) No studies have been found with sufficiently robust methodological designs that address the ABX early treatment. There is no strong evidence to indicate which of the different antibiotic interventions (therapeutic de-escalation, cycling of ABX and preemptive treatment) is more effective in reducing antibiotic resistance in ICU patients. There is insufficient evidence that de-escalation of antimicrobial agents is effective against resistance. In patients admitted to the ICU with a low prevalence of fluoroquinolones resistance, increased exposure to this class of antibiotics, using antibiotic cycling, increases the emergence of resistant strains. Conclusion: Despite the fact that no prospective studies were identified in this SR, rationale and day-to-day clinical practice experience suggest that multidisciplinary participation of different specialists in ABX's Infection and Policy Commission (or the ABX Commission), or the Pharmacy and Therapeutics Committee, might improve the development and application of these strategies.

Trend of multidrug and fluoroquinolone resistance in Mycobacterium tuberculosis isolates from 2010 to 2014 in Korea: a multicenter study.

Background/AimsThis study was conducted to evaluate the recent prevalence and trend of anti-tuberculosis (TB) drug resistance with a focus on multidrug-resistance (MDR) and fluoroquinolone resistance in South Korea.MethodsWe retrospectively reviewed the drug susceptibility testing results of culture-confirmed Mycobacterium tuberculosis isolates collected from 2010 to 2014 at seven tertiary hospitals in South Korea.ResultsA total of 5,599 cases were included: 4,927 (88.0%) were new cases and 672 (12.0%) were previously treated cases. The MDR rate has significantly decreased from 6.0% in 2010 to 3.0% in 2014 among new cases, and from 28.6% in 2010 to 18.4% in 2014 among previously treated cases (p < 0.001 and p = 0.027, respectively). The resistance rate to any fluoroquinolone was 0.8% (43/5,221) in non-MDR-TB patients, as compared to 26.2% (99/378) in MDR-TB patients (p < 0.001). There was no significant change in the trend of fluoroquinolone resistance among both nonMDR-TB and MDR-TB patients. Among the 43 non-MDR-TB patients with fluoroquinolone resistance, 38 (88.4%) had fluoroquinolone mono-resistant isolates.ConclusionsThe prevalence of MDR-TB has significantly decreased from 2010 to 2014. The prevalence of fluoroquinolone resistance among non-MDR-TB patients was low, but the existence of fluoroquinolone mono-resistant TB may be a warning on the widespread use of fluoroquinolone in the community.

"Low prevalence of fluoroquinolone resistance among patients with tuberculosis in the Philippines: results of a national survey." Dodge R. Lim, Anna S. Dean, Mary Rosary Taguinod-Santiago, Angeli Borbe-Reyes, Andrea Maurizio Cabibbe, Matteo Zignol, Ramon P. Basilio, Anna Marie Celina Garfin and Maria Cecilia G. Ama. Eur Respir J 2018; 51: 1702571.

"Low prevalence of fluoroquinolone resistance among patients with tuberculosis in the Philippines: results of a national survey." Dodge R. Lim, Anna S. Dean, Mary Rosary Taguinod-Santiago, Angeli Borbe-Reyes, Andrea Maurizio Cabibbe, Matteo Zignol, Ramon P. Basilio, Anna Marie Celina Garfin and Maria Cecilia G. Ama. Eur Respir J 2018; 51: 1702571.

Acquisition of double mutation in gyrA caused high resistance to sitafloxacin in Helicobacter pylori after unsuccessful eradication with sitafloxacin-containing regimens.

Although sitafloxacin (STFX)-containing regimens are effective rescue treatments for Helicobacter pylori infection, prevalence of fluoroquinolone resistance in H. pylori has increased rapidly worldwide. The change in resistance levels and gyrA mutations, a major cause of fluoroquinolone resistance, after unsuccessful STFX-containing treatment has not been investigated. We conducted a retrospective, non-randomized study to compare the minimum inhibitory concentrations (MICs) of STFX and the location of gyrA mutations in H. pylori before and after unsuccessful eradication with STFX-containing regimens at Keio University Hospital between December 2011 and March 2015. A total of 266 patients treated with STFX-containing regimens for third-line H. pylori eradication were evaluated. Double mutations in gyrA were acquired by 20.8% of strains that exhibited seven-fold increased STFX MICs, compared to pre-treatment MICs. The STFX MICs did not increase, however, when the location of the gyrA mutations did not change after treatment. Double mutations in gyrA developed in 60.0% of the strains in which eradication failed, which exhibited a baseline mutation at position D91, and in 11.1% of strains with baseline mutations at position N87. Acquisition of double mutations in gyrA evoked high-level resistance to STFX in H. pylori after unsuccessful eradication with STFX-containing regimens.

Prevalence and Mechanism of Fluoroquinolone Resistance in Escherichia coli Isolated from Swine Feces in Korea

In this study, we investigated the prevalence and fluoroquinolone (FQ) resistance mechanisms in Escherichia coli isolated from swine fecal samples. E. coli isolates were collected from 171 (72.2%) of 237 swine fecal samples. Of these, 59 isolates (34.5%) were confirmed as FQ-resistant E. coli by the disk diffusion method. Of the FQ-resistant isolates, three major FQ resistance mechanisms were investigated. Of the 59 isolates, plasmid-mediated quinolone resistance genes were detected in 9 isolates (15.3%). Efflux pump activity was found in 56 isolates (94.9%); however, this was not correlated with the increased FQ resistance measured by determining the MIC. Point mutations in quinolone resistance-determining regions were the main cause of FQ resistance. All 59 ciprofloxacin-resistant isolates had mutations in quinolone resistance-determining regions; of these 59 isolates, all (100%) had mutations in gyrA, 58 (98.3%) had mutations in parC, 22 (37.3%) had mutations in parE, and none had mutations in gyrB. The predominant mutation type was double mutation in gyrA (Ser83Leu plus mutation in aspartic acid 87), and all FQ-resistant isolates (except one) that had mutations in parC or parE also had double mutations in gyrA. Importantly, the frequencies of multidrug-resistant and extended-spectrum β-lactamase-producing E. coli were significantly higher in the high ciprofloxacin MIC group in this study. Compared with previous studies in Korea, the prevalence of FQ resistance and plasmid-mediated quinolone resistance genes had increased considerably in swine. Although the use of FQ as a feed additive is prohibited in Korea, use for self-treatment and therapeutic purposes has been increasing, which may be responsible for the higher FQ resistance rate observed in this study. Therefore, prudent use of FQ on animal farms is warranted to reduce the evolution of FQ-resistant bacteria in the animal industry.

Antimicrobial Resistant Streptococcus pneumoniae: Prevalence, Mechanisms, and Clinical Implications.

Streptococcus pneumoniae is a major cause of pneumonia, meningitis, sepsis, bacteremia, and otitis media. S. pneumoniae has developed increased resistance to multiple classes of antibiotics. Systematic literature review of prevalence, mechanisms, and clinical implications in S. pneumoniae resistance. Since S. pneumoniae resistance to penicillin was first reported with subsequent development of resistance to other classes of drugs, selection of appropriate antibiotic treatment is challenging. We searched PubMed (English language) for citations to antibiotic resistance in S. pneumoniae published before March 1, 2016. We present a review of S. pneumoniae resistance to beta-lactams, macrolides, lincosamides, fluoroquinolones, tetracyclines, and trimethoprim-sulfamethoxazole (TMP-SMX). There has been a steady decline in susceptibility of S. pneumoniae to commonly used beta-lactams. Phenotypic expression of penicillin resistance occurs as a result of a genetic structural modification in penicillin-binding proteins. Between 20% and 40% of S. pneumoniae isolates are resistant to macrolides. Macrolide resistance mechanisms include ribosomal target site alteration, alteration in antibiotic transport, and modification of the antibiotic. Approximately 22% of S. pneumoniae isolates are resistant to clindamycin. Similar to macrolide resistance, clindamycin involves a target site alteration. The prevalence of fluoroquinolone resistance is low, although increasing. S. pneumoniae resistance to fluoroquinolones occurs by accumulated mutations within the bacterial genome, increased efflux, or acquisition of plasmid-encoded genes. S. pneumoniae resistance has also increased for the tetracyclines. The primary mechanism is mediated by 2 genes that confer ribosomal protection. The prevalence of TMP-SMX resistance is around 35%. As with fluoroquinolones, resistance to TMP-SMX is secondary to mutations in the bacterial genome. Effective treatment of resistant S. pneumoniae is a growing concern. New classes of drugs, newer formulations of older drugs, combination antibiotic therapy, nonantibiotic modalities, better oversight of antibiotic usage, and enhanced preventive measures hold promise.

Novel mutations in quinolone resistance-determining regions of gyrA, gyrB, parC and parE in Shigella flexneri clinical isolates from eastern Chinese populations between 2001 and 2011.

The aim of this study was to evaluate the prevalence of fluoroquinolone resistance and mechanisms of selected fluoroquinolone resistance in Shigella flexneri isolates. A total of 624 S. flexneri strains isolated between 2001 and 2011 in Jiangsu Province of China were analysed for their fluoroquinolone susceptibility. The quinolone resistance-determining region of gyrA, gyrB, parC and parE were amplified and sequenced. In general, 90.5% of S. flexneri exhibited resistance to nalidixic acid. The mean norfloxacin resistance rate was 22.4% during the 11years from 2001 to 2011 (6.4% from 2001 to 2005 and 36.8% from 2006 to 2011). Sequencing of gyrA, gyrB, parC and parE genes of all S. flexneri isolates showed that the mutation rate was as high as 93.9%. In addition, 91.8% and 92.3% of S. flexneri harboured mutations in gyrA and parC, respectively. About 35.2% of S. flexneri isolates susceptible to nalidixic acid contained mutations. Meanwhile, mutations were detected in 91.2% of norfloxacin-susceptible strains, and almost all S. flexneri isolates resistant to fluoroquinolone contained mutations. To the best of our knowledge, this is the first study reporting the occurrence of point mutations Asn57Lys and His80Pro in gyrA and Ala85Thr, Asp111His and Ser129Pro in parC. Emerging fluoroquinolone resistance with a significantly high mutation rate of the gyrA and parC genes in S. flexneri in Jiangsu Province deserves attention, and monitoring antibiotic susceptibility is important for the effective management of S. flexneri infections.

Fluoroquinolone resistance colonization from initial to repeat prostate biopsy

Purpose: Fluoroquinolone (FQ) resistant (FQR) bacteria are a major cause of infection after transrectal prostate biopsy (TRPB). We determined the prevalence of FQR in initial and subsequent rectal cultures from men undergoing repeat prostate biopsies. Materials and methods: After IRB approval, men presenting for TRPB at the San Diego Veterans Affairs Medical Center between January 1, 2010, and February 6, 2014, underwent pre-TRPB rectal culture. The rectal swab was collected from the patient immediately prior to TRPB. Rectal swabs were streaked onto locally prepared ciprofloxacin-supplemented (4 mg/L) MacConkey agar plates. A representative colony was selected for identification and susceptibility testing. Results: Of 617 patients who had rectal cultures done, 7% (43/617) had a repeat rectal culture performed in relation to a second prostate biopsy. All cipro-resistant bacteria isolated were Escherichia coli. The median time and interquartile range between first and second biopsy was 2.3 years (range 1.2–3.6 years). On first biopsy, 16.3% (7/43) had FQR, which was not statistically different from the 18.6% of patients who had FQR on their second biopsy ( p=0.78). Overall, 74% (32/43) of patients tested absent for FQR at both prostate biopsies, and 9.3% (4/43) tested present at both ( p=0.015). However, 9.3% (4/43) converted from absent to present FQR, and 7.0% (3/43) converted from present FQR to absent ( p=0.69). Seventy percent of the FQR E. coli were also resistant to gentamicin, and 22% were resistant to cefepime. Conclusions: Patients undergoing prostate biopsy should be examined for FQR prior to each individual biopsy because prior culture results do not always predict whether a patient will be colonized with FQR E. coli.

Optimizing prophylactic antibiotic regimen in patients admitted fortransrectal ultrasound-guided prostate biopsies: A prospective randomized study.

BackgroundTransrectal ultrasound-guided prostate biopsies (TRUSBx), in spite of being one of the most frequently performed urological office procedures, are associated with a spectrum of complications, most significantly including infection. The aim of the study is to evaluate the prevalence of fluoroquinolone-resistant bacteria in rectal swabs from our local population prior to TRUSBx and to identify risk factors among a patient population harboring fluoroquinolone-resistant organisms.MethodsWe prospectively included 541 men who were submitted for TRUSBx in our center from March 2011 to June 2015. The indications for TRUSBx were an elevated prostate-specific antigen level and/or abnormal digital rectal exam. All patients were randomly divided into two groups: Group 1 (n = 279 cases) who received standard empirical prophylactic antibiotics and Group 2 who received targeted prophylaxis based on a rectal swab culture and susceptibility result. Differences in risk factors between quinolone-resistant and nonresistant patients were compared. Univariate and multivariate analyses were performed to identify independent potential risk factors associated with fluoroquinolone-resistant rectal flora.ResultsSixteen out of 271 men developed infectious complications after TRUSBx in the group receiving standard empirical prophylaxis (5.7%). No men in the group who received targeted prophylactic antibiotic guided by rectal swab developed infectious complications. Among the 262 patients who underwent prebiopsy rectal swab cultures, 76 men (29%) displayed fluoroquinolone-resistant rectal flora (29%). In the multivariate analysis, a history of antibiotic exposure before prostate biopsy was the only independent factor associated with an increased risk of fluoroquinolone resistance.ConclusionDetermining the prevalence of fluoroquinolone resistance in rectal flora has important implications in the selection of targeted prophylactic antibiotic regimens. Antimicrobial profiles guided by rectal swabs may prove useful to optimize prophylaxis prior to TRUSBx; this strategy is effective at reducing the rates of infectious complications, including sepsis, especially in men at higher risk of infectious complications.