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Ciprofloxacin resistance: a review of patients in East London undergoing prostate biopsy.

Transrectal ultrasound guided biopsy of the prostate remains the gold standard investigation to diagnose prostate cancer. Although post-biopsy complications are relatively rare, the risk of sepsis associated with the procedure means that prophylactic antibiotics are paramount. The most widely used antibiotic regimen includes a quinolone, such as ciprofloxacin. Resistance to quinolone antibiotics is rising. In this small pilot study, the incidence of quinolone resistance was 18% in our population of patients attending the prostate biopsy clinic.

Key Words: Prostate biopsy, infection, sepsis, quinolone resistance, ciprofloxacin.


Prostate cancer is diagnosed by using a combination of digital rectal examination, prostate-specific antigen (PSA), and prostate biopsy (Turner et al., 2011). Prostate biopsy is done transrectally, whereby a biopsy needle is passed through the rectal wall into the prostate to obtain samples for histological analysis. First described by Astraldi in 1937, transrectal ultrasound guided prostate biopsy (TRUS biopsy) allows tissue samples of the prostate to be obtained for histological analysis to confirm or exclude the presence of prostate cancer. TRUS biopsy is a common procedure in the urology department, and is performed by urologists, radiologists, physician assistants, and advanced nurse practitioners (Turner & Aslet, 2011; Turner & Pati, 2010).

The vast majority of patients with prostate cancer throughout the world are currently diagnosed following a TRUS biopsy. Recent advances with pre-biopsy multi-parametric MRI scan may increase the detection of prostate cancer (Dickinson et al., 2013). In addition, trans-perineal template biopsies may further improve detection. Prostate biopsies carry a risk of morbidity and mortality, the most serious complication being severe infection.

Literature Review

Significance of Quinolone Resistance

The rate of severe complications following TRUS biopsy are relatively low (Ecke et al., 2008; Mottet et al., 2015), with the most common complication being mild, such as self-limiting hematuria in 6.5% of cases, followed by dysuria in 6.0% of cases (Ecke et al., 2008). Urinary or clot retention is described in up to 4.6% of patients (Ecke et al., 2008; Mottet et al., 2015). Urinary tract infection affects up to 5% of patients (see Table 1) (Greene, Ased, Kinsella, & Turner, 2015).

Infective complications are considered the most significant, with a noted increase after TRUS biopsy in recent years (Greene et al., 2015; Lee, 2015; Turner et al., 2011). The rate of post-biopsy infection has been reported in up to 6.6% of patients (Djavan et al., 2001; Ecke et al., 2008). The risk of hospitalization for infectious complications in contemporary studies ranges from 0.6% to 4.1% (Nam et al., 2010). Severe postbiopsy infection was reported at less than 1%, but numbers have increased as a consequence of antibiotic resistance (Loeb et al., 2013). Other studies have shown that serious infection requiring hospitalization affects 1.6% to 3% of patients (Ecke et al., 2008; Greene et al., 2015). One study demonstrated a 30-day mortality rate of 0.09% for all complications post-TRUS biopsy (Nam et al., 2010). Serious rectal bleeding lasting more than two days affects 0.7% of patients.

Infective Complications And Prophylaxis

The rectum is host to numerous bacteria, the more common being Escherichia coli, Streptococcus faecalis, and Bacteroides (Patel & Rickards, 2002), which are introduced into the prostate and subsequently the bloodstream at the time of TRUS biopsy. It is thought that bacterial flora harbored in the rectum are introduced into the genitourinary system or systemically into the bloodstream following perforation of the rectal mucosa with the biopsy needle (Batura, Rao, & Nielson, 2010). Up to 75% of post-biopsy infections are reported to be a consequence of Escherichia coli (Carignan et al., 2012). The use of broad-spectrum antibiotics is common practice (Greene et al., 2015; Turner & Pati, 2010; Turner et al., 2011) because for many years, it has been demonstrated that the risk of post-biopsy infection is significantly increased if prophylactic antibiotics are omitted (Lindstedt, Lindstrom, Ljunggren, Wullt, & Grabe, 2006; Puig et al., 2006; Ruebush, McConville, & Calia, 1979). The type, route, duration, and dosage of antibiotics remains controversial (see Table 2) (Grabe et al., 2014; Turner & Pati, 2010). An older study (Taylor & Bingham, 1997) evaluating antibiotic prophylaxis practices in the United Kingdom reported finding 48 different regimens using 13 different antibiotics, including metronidazole (55%), ciprofloxacin (48%), gentamicin (48%), and trimethoprim (14%). Antibiotics were administered orally in 90% of cases; 58% of regimens included an intravenous antibiotic; 30% included intravenous, oral, and rectal administration; and 30% used only oral antibiotics (see Table 2).

The majority of studies support the use of a quinolone, such as ciprofloxacin for TRUS biopsy prophylaxis (Briffaux et al., 2009; Lindstedt et al., 2006; Schaeffer et al., 2007; Wagenlehener et al., 2013; Yamamoto, Ishitoya, Segawa, Kamoto, & Okumura, 2008). The American Urological Association (AUA) (2008) best practice policy statement on urological surgery suggests the use of quinolone antibiotics as a first choice for TRUS biopsy prophylaxis.


The bactericidal action of ciprofloxacin results from the inhibition of both type II topoisomerase (DNA-gyrase) and topoisomerase IV, required for bacterial DNA replication, transcription, repair, and recombination (Electronic Medicines Compendium [EMC], 2014), and thus, affect bacterial DNA replication and packaging (Yassin & Dawson, 2007). Following oral administration, ciprofloxacin is rapidly and extensively absorbed from the small intestine, with peak serum concentrations 1 to 2 hours following ingestion. Ciprofloxacin is so well absorbed orally that intravenous administration is rarely required unless the patient is unable to tolerate oral medication (Yassin & Dawson, 2007). Ciprofloxacin reaches high concentrations in a variety of tissues, including the urogenital tract (urine, prostate, endometrium), where total concentrations exceeding those of plasma concentrations are reached (EMC, 2014). Quinolones as a group of agents have high bioavailability within prostate tissue (Patel et al., 2012), and their concentrations in prostatic fluid, prostatic tissue, and seminal fluid are relatively high in comparison to corresponding plasma concentrations (Naber, 1991). Ciprofloxacin is largely excreted unchanged both renally, and to a smaller extent, fecally. The serum elimination half-life is approximately 4 to 7 hours (EMC, 2014).

Until recently, these agents have also had a good range of coverage across the colonic flora (e.g., Escherichia coli), but quino-lone-resistant bacteria are increasing (Lugg, Lettieri, Stass, & Agarwal, 2008; Patel et al., 2012).

Risk Factors for Post-Biopsy Infection

The most common risk factor for post-TRUS biopsy infection appears to be exposure to antimicrobials within six months prior to biopsy (AUA, 2008). One study noted that men treated with three weeks of fluoroquinolone antibiotics for elevated PSA with suspected prostatitis who subsequently underwent prostate biopsy showed a three-fold increase in sepsis compared to those who had not received antibiotics (Akduman et al., 2011). Patel and colleagues (2012) reported a fourfold relative risk for infection in patients recently exposed to antimicrobials, while two other studies found a three-fold or greater incidence of acute prostatitis among men with quinolone exposure within six months prior to TRUS biopsy (Mosharafa, Torky, Said, & Meshref, 2011; Shigehara, Miyagi, Nakashima, & Shimamura, 2008).

Quinolone-resistant E. coli strains in the fecal flora are a significant risk factor for post-biopsy infection (Liss et al., 2011; Steensels et al., 2011). Additionally, the use of fluoroquinolones in the six months prior to TRUS biopsy is associated with an increased risk of detecting resistant bacteria in the fecal flora. These findings may explain why recent fluoroquinolone exposure may increase the risk for infectious complications after TRUS biopsy (AUA, 2008). Hospital staff and their family members appear to be at higher risk of infection and often demonstrate multi-drug-resistant bacteria on culture (Carlson, Bell, Lawen, & Rendon, 2010; Kamdar, Moopan, Gulmi, & Kim, 2008). Travel is also a risk factor, with one study noting a 2.7-fold relative risk for infection after TRUS biopsy among those who had recently returned from abroad (Patel et al., 2012). Prior TRUS biopsy also appears to be a risk factor for an infectious complication, but most studies attribute this to previous antimicrobial exposure (AUA, 2008). The rate of complications is independent of the number of biopsy cores obtained (Berger et al., 2004; Rodriquez & Terris, 1998).

Quinolone-Resistant Bacteria

Increased quinolone resistance (Cuevas et al., 2011) is associated with a rise in severe post-biopsy infection (Loeb, Carter, Berndt, Ricker, & Schaeffer, 2011). One study has demonstrated that over 50% of patients with infective complications after a prostate biopsy have ciprofloxacin-resistant pathogens (Carignan et al., 2012). In a North American cohort, 2.77% of cases developed infection after biopsy, of which 55% had fluoroquinolone-resistant infection (Zaytoun et al., 2011). In an Australian study that analyzed E. coli bacteremia after TRUS-biopsy, 62% of patients were fluoroquinolone-resistant (Williamson et al., 2012).

The normal colonic flora is part of a dynamic environment, continually harmonizing with the local conditions. Hospitalization, travel, and recent antibiotic use are recognized causes of change in the intestinal commensals (Patel et al., 2012). Fluoroquinolone resistance has been observed frequently for extended-spectrum [beta]-lactamase-producing strains of E. coli and K. pneumoniae, and has been reported as a concern since 2001 (Lautenbach et al., 2001).

A number of mechanisms of antimicrobial resistance exist. Aldred, Kerns, and Osheroff (2014) discuss three mechanisms that decrease the sensitivity of bacterial cells to quinolones. The first is target-mediated resistance, which is the most common and clinically significant form of resistance. It is caused by specific mutations in gyrase and topoisomerase IV that weaken interactions between quinolones and these enzymes. The second is plasmid-mediated resistance, which results from extrachromosomal elements that encode proteins that disrupt quinoloneenzyme interactions, alter drug metabolism, or increase quinolone efflux. The third is chromosome-mediated resistance, which results from the under-expression of porins or the over-expression of cellular efflux pumps, both of which decrease cellular concentrations of quinolones (Aldred et ah, 2014). Antimicrobial resistance is becoming a grave concern, especially gramnegative bacterial resistance. The English Surveillance Programme for Antimicrobial Utilization and Resistance (ESPAUR) was established by Public Health England (PHE), and the first report was published in 2014. ESPAUR's key aims were to develop surveillance systems to measure both antimicrobial utilization and resistance and to measure the impact of antimicrobial utilisation on resistance and patient/ public safety (PHE, 2014).

Purpose of the Study

Homerton University Hospital NHS Foundation Trust is situated in the London Borough of Hackney, east London, the second most deprived local authority in England. It is described as the sixth most diverse borough in London. Hackney is a young borough, with only 15% of the population over 55 years of age. According to the 2011 Census, 35% of people in Hackney described themselves as white British; black Africans and black Caribbeans accounted for 11.4% and 7.8% of the population, respectively. Other significantly sized communities include Charedi Jews (7.4%), Turkish and Kurdish (4.5%), Indian (3.1%), Bangladeshi (2.5%), and Chinese (1.4%). The main causes of premature death are cancer, especially breast, prostate, lung, and bowel cancers; coronary heart disease; and stroke (London Borough of Hackney, 2016).

A small pilot study of patients attending Homerton University Hospital's urology nurse consultant-led TRUS biopsy clinic was undertaken to ascertain the rate of ciprofloxacin-resistant bacteria in this population.

Standard clinic practice included administration of a single dose of oral ciprofloxacin 500 mg one hour prior to biopsy, 1 gram of metronidazole rectally one hour prior to biopsy, and gentamicin 3 mg/kg intravenously immediately before the procedure. Ciprofloxacin 500 mg twice a day for seven days was prescribed post-biopsy for diabetic patients.



Over a one-month period, male patients attending the nurse consultant urology TRUS biopsy clinic who required a rectal examination to assess the prostate were asked to participate in the study. The pilot study was registered as a clinical review/ audit at Homerton University Hospital. Patients were asked if they were willing to have a rectal swab taken before a digital rectal examination was performed to assess for ciprofloxacin-resistant bacteria.

Ethical Considerations

Homerton University Hospital's audit department reviewed the proposed pilot study and granted permission. Men were informed participation was completely voluntary and that nonparticipation would not affect their care. The questionnaire was completely anonymized except for an identifying number known only to the nurse consultant undertaking the audit.

Data Collection

In total, 40 patients were asked to participate in the pilot study, of which 38 (95%) agreed. These men were then asked a series of questions using a questionnaire designed to identify potential risk factors for quinolone-resistant bacteria (see Appendix 1). The questionnaire was administered to the patient in the clinic when the rectal swab was taken.

The rectal swab was taken immediately before performing a digital rectal examination when the patient was already undressed and optimally positioned. The swab was inserted just beyond the anus into the rectum and sent for microscopy, culture, and sensitivity. The specimen was labeled "? ciprofloxacin resistance," which alerted the laboratory staff that this formed part of the study.

The results of the questionnaire and of the swab were held in a Microsoft Excel[R] spreadsheet; only the nurse consultant had access. Other members of the team were able to access the anonymized data.


Thirty-eight patients were included in the pilot study. Sixteen (42%) patients had knowingly used a quinolone antibiotic previously; 22 (58%) did not know or were certain they had not used a quinolone antibiotic (see Figure 1). Of the 38 participants, 13 (34%) were diabetic, and one patient (2.7%) reportedly had a suppressed immune system (was taking methotrexate).

Of the 38 rectal swabs taken, seven patients were found to have ciprofloxacin-resistant bacteria, demonstrating an 18.4% rate of ciprofloxacin-resistant bacteria in our patient population (see Figure 2). Antibiotic resistance and sensitivities of the patients with ciprofloxacin-resistant bacteria are demonstrated in Table 3.

Of patients with ciprofloxacin-resistant bacteria, two were born in Nigeria, two in Monserrat, one in Turkey, one in Guyana, and one in India. Of these patients, the Turkish national had lived in the United Kingdom for three years, but the others all lived in the United Kingdom for more than 30 years. Of the 38 patients who participated in the study, eight (21%) were born in the United Kingdom, none of whom were colonized with quinolone-resistant bacteria (see Figure 3).

One (14%) patient had been a hospital inpatient in the preceding three months and had been given antibiotics. He was the only patient with ciprofloxacin-resistant bacteria who had received antibiotics in the preceding three months. Two (28.5%) patients with quinolone-resistant bacteria had diabetes mellitus, and neither (0%) reported being immunocompromised or were taking drugs that affect the immune system. Both patients with diabetes mellitus had ciprofloxacin-resistant bacteria.

One (14%) patient reported travel to Morocco in the preceding 12 months, and one (14%) had travelled to Nigeria in the preceding 12 months. Interestingly, both patients who had been out of the country harbored ciprofloxacin-resistant bacteria. None of the patients with quinolone-resistant bacteria had been employed as healthcare workers in their lifetime.

Of the patients with ciprofloxacin-resistant bacteria, four (57%) proceeded to prostate biopsy and none developed post biopsy sepsis. All four patients had gentamicin sensitive bacteria (gentamicin was also administered intravenously immediately before prostate biopsy).


Ciprofloxacin resistance is a concern because it is an independent risk factor for mortality in patients with E. coli bacteremia (Laupland et al., 2008). Rates of antibiotic resistance in the general population are causing concern among healthcare professionals worldwide.

While this pilot study was small, it demonstrated a relatively high level of colonization with ciprofloxacin-resistant bacteria (18.4%) in the population served by Homerton University Hospital's Urology service. Those with recent travel may have had an increased risk from some destinations (Nigeria and Morocco). This supports findings in a study by Patel et al. (2012) that men with a history of recent international travel or antibiotic use had up to four times greater risk of septicemia and hospitalization after undergoing prostate biopsy. Infections that occur are most often due to multi-drug resistant E. coli, and require aggressive and early treatment.

Of the 18.4% of patients colonized with ciprofloxacin-resistant bacteria, 57% had a TRUS biopsy, with no subsequent episodes of sepsis; the remaining 43% did not require a biopsy. While this may suggest that gentamicin and metronidazole afforded these patients additional protection, microbiology experts disagreed and felt this antibiotic regimen would be inadequate (Dr. A. Claxton, personal communication, September 2015).

Gentamicin is administered intravenously prior to biopsy, necessitating intravenous cannulation, which is time-consuming, and increases cost and patient discomfort. It may be an unnecessary adjunct in patients who do not have ciprofloxacin-resistant bacteria but would be important when a patient's rectal screening swab result was not available; results from this study indicate the prevalence of bacteria resistant to both ciprofloxacin and gentamicin in the local population is 0%. In patients with ciprofloxacin-sensitive bacteria, it may be possible to omit the gentamicin.

The high level of ciprofloxacin-resistant bacteria is concerning because post-biopsy sepsis is a serious complication and can lead to prolonged hospitalization or death. In addition, it is costly in terms of morbidity, bed occupancy, and direct hospital costs with one study suggesting that the average cost of U.S. hospital admission due to infection after prostate biopsy was $5,900 (Adibi, Pearle, & Lotan, 2011).

We recommend that patients have a rectal swab to assess for ciprofloxacin sensitivity status so patients with quinolone-resistant bacteria can be given appropriate alternative antibiotics as recommended by the microbiology department. All patients in our department have a multi-parametric MRI scan of the prostate prior to prostate biopsy; therefore, all patients return at a later date to have the biopsy performed after initial assessment by the nurse consultant or urologist. This affords time for rectal swab analysis and does not slow down the patient pathway.

We acknowledge limitations to our study. The small sample size is not generalizable to the population as a whole. More study is needed on the practice of rectal swab for antibiotic resistance pre-TRUS biopsy. It is also important to acknowledge that the population served by Homerton University Hospital is not generalizable to the United Kingdom population as a whole.


This small study revealed an 18% ciprofloxacin-resistant bacteria rate in men attending a nurse consultant-led TRUS biopsy clinic at Homerton University Hospital. None of the patients with ciprofloxacin resistance were born in the United Kingdom, although many had lived in the United Kingdom for more than 30 years. None of the patients with ciprofloxacin-resistant bacteria developed post-biopsy infection, possibly due to additional coverage with gentamicin and metronidazole.

As quinolones remain the antibiotic of choice for TRUS biopsy, we suggest performing rectal swabs on all patients prior to undertaking TRUS biopsy, which may afford the patient extra protection from post-biopsy infective episodes. We also suggest that alternative antibiotic choice should be microbiology-guided to ensure the patient receives the most effective alternative antibiotic.


Research Summary


The risk of post-prostate biopsy infection is well known. With increasing rates of ciprofloxacin-resistant bacteria, it is thought the risk of serious post-biopsy infection is increasing. We assessed the level of ciprofloxacin-resistant bacteria in our population.


To assess the rate of ciprofloxacin-resistant bacteria in men with elevated prostate-specific antigen (PSA) attending a hospital nurse consultant urology clinic.


Patients were asked to participate in a pilot study whereby a rectal swab was taken and sent for antibiotic sensitivity analysis. The patient was asked to complete a questionnaire regarding risk factors for harboring ciprofloxacin-resistant bacteria.


Thirty-eight (38) out of 40 patients who were asked agreed to participate in the pilot study. A significant number of patients (18.4%) were found to have quinolone-resistant bacteria.


This small study revealed an 18% ciprofloxacin-resistant bacteria rate in men attending a nurse consultant-led transrectal ultrasound (TRUS) biopsy clinic at Homerton University Hospital in London, England, United Kingdom. None of the patients with ciprofloxacin resistance were born in the United Kingdom, although many had lived in the United Kingdom for more than 30 years. None of the patients with ciprofloxacin-resistant bacteria developed post-biopsy infection.

Level of Evidence--Level VI

(Polit & Beck, 2012)
Appendix 1.

Questionnaire for Transrectal Biopsies of the Prostate

1. Have you been admitted to hospital in the last 3 months? If so,
why? --

Did you require antibiotics?

[] No

[] Yes: I was admitted but no antibiotics

[] Yes: I was admitted and received antibiotics

2. Have you taken any antibiotics in the last 3 months?

[] Yes [] No

If yes--Do you know the name/s? --

3. Have you previously taken quinolone antibiotics (e.g.
ciprofloxacin, ofloxacin)? These drugs are often used for recurrent
urine infections, chlamydia, and prostatitis.

[] Yes [] No

If yes, please provide details: --

4. Do you have diabetes mellitus? Do you take tablets or use

[] Yes [] No

If yes, which treatment: --

5. Are you taking any medication that affects your immune system or
do you have any condition which affects your immune system? (E.g.
steroids, methotrexate, antiretrovirals for HIV infection, HIV
infection, splenectomy)

[] Yes [] No

If yes please give details: --

6. Have you had any foreign travel in the last 12 months? [] Yes []

If so, where? --

7. In which country were you born? --

8. How many years have you lived in the UK? --

9. Have you ever been a healthcare worker? (e.g., nurse, doctor,
healthcare assistant, caregiver)

[] Yes [] No

If yes please give details: --

Source: [c] Copyright B. Turner and J.S.A. Green. Reprinted with


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Bruce Turner, BN (Hons), MSc, RN, is a Consultant Nurse, Uro-Oncology/Urology, Homerton University Hospital NHS Foundation Trust, London, United Kingdom; and a Nurse Practitoner, Bart's Health NHS Trust, London, England, United Kingdom.

Jhumur Pati, FRCS, FRCS (Urol), is a Consultant Urological Surgeon, Homerton University Hospital NHS Foundation Trust, London, England, United Kingdom.

Vinod Nargund, PhD, FRCS, Urol., is a Consultant Urological Surgeon, Homerton University Hospital NHS Foundation Trust, London, England, United Kingdom.

Alleyna Claxton, MB, BS, MRCP, MSc (Micro), MSc (Epi), DLSHTM, FRCPath, is a Consultant Microbiologist and Director of Infection and Prevention Control, Homerton University Hospital, NHS Foundation Trust, London, England, United Kingdom.

Victoria Longstaff, MSc, RN, is a Consultant Nurse, Infection and Prevention Control, and Deputy Director of Infection and Prevention Control, Homerton University Hospital, NHS Foundation Trust, London, England, United Kingdom.

Somita Sarkar, MBChB, MRCS, is a Specialty Registrar in Urology, Whipps Cross University Hospital, London, England, United Kingdom.

James Green, LLM, FRCS (Urol), is a Consultant Urological Surgeon, Whipps Cross University Hospital, London, England, United Kingdom.

Acknowledgement: The authors would like to thank Kaye K. Gaines, FNP-BC, CUNP, for her assistance and guidance in creating this manuscript.
Table 1.
Complications Associated with Prostate Biopsy

Post-biopsy complications                                          %

Hematospermia                                                    37.4
Hematuria > 1 day                                                14.5
Rectal bleeding < 2 days                                          2.2
Prostatitis                                                       1.0
Fever > 38.5[degrees]C                                            0.8
Epididymitis                                                      0.7
Rectal bleeding > 2 days (+/- requiring surgical intervention)    0.7
Urinary retention                                                 0.2
Other complications requiring hospitalization                     0.3

Source: Adapted from Mottet et al., 2015.

Table 2.
Selection of Studies Analyzing Antibiotic Prophylaxis in Prostate

                                       % with    % with       % with
Study             Antibiotic(s)        Fever   Bacteriuria  Bacteraemia

Aron, Rajecv, &   Placebo                5         14            2
Gupta (2000)      Cipro/tinidazole x1    2          4            0
                  Cipro/tinidazole x6    2          6            1

Brewster,         Cefuroxime             3         3.5           2
MacGowan, &       Tazocin               4.5         5            0
Gingell (1995)

Crawford,         Placebo                48        36           16
Haynes, Story,    Carbenicillin          17         9           22
& Borden (1982)

Fong, Struther,   Cotrimoxazole          --         2           37
Honey, Simbul, &  Netilmycin/            --        17           28
Boisseau (1991)   metronidazole

Roach,            Ciprofloxacin          --         9            3
Riguerora,        Gentamicin             --         5           18
George, & Neal

Ruebush,          Placebo                18        21           70
McConville, &     Cotrimoxazole          --         0           59
Calia (1979)

Taylor &          Ciprofloxacin          --        --            7
Bingham (1997)    Gentamicin             --        --           37

Batura, Rao, &    Cip/Aug/Mz             --        2.5          2.5
Nielson (2010)    Cip/Aug/Mz/Ami         --        1.2          0.4
                  Cip/Mz/Ami             --         0            0

Efesoy, Bozlu,    Ciprofloxacin         4.7        6.1          0.5
Cayan, & Akbay

Cormio et al.     Ciprofloxacin         1.5        4.5          --
(2002)            Piperacillin/          0         2.8          --

Notes: Cip = ciprofloxacin, Aug = augmentin, Mz = metronidazole,
Ami = amikacin.

Table 3.
Sensitivities of Patients with Ciprofloxacin-Resistant Bacteria

Identifier   Sensitivities

4            Culture:
             1) Growth of Escherichia coli
             2) Growth of Escherichia coli type 2

                               1)    2)

             Co-amoxiclav      R     S
             Ciprofloxacin     R     S
             Cefuroxime        S
             Gentamicin        S     S
             Ertapenem         S
             Amikacin          S
             Ceftazidime       S
             Ceftriaxone       S
             Pip/Tazobactam    S
             Tigecycline       S
             Trimethoprim      R     R
             Nitrofurantoin    S     R
             Amoxicillin       R     R
             Cephalexin        S

12           1) Growth of Escherichia coli

             Co-amoxiclav      S
             Ciprofloxacin     R
             Gentamicin        S
             Cephalexin        S
             Trimethoprim      S
             Nitrofurantoin    S
             Fosfomycin        S
             Pip/Tazobactam    S
             Ceftazidime       S
             Temocillin        S
             Amikacin          S
             Ertapenem         S
             Amoxicillin       R

15           1) Growth of Escherichia coli

             Co-amoxiclav      R
             Ciprofloxacin     R
             Gentamicin        S
             Cephalexin        S
             Trimethoprim      S
             Nitrofurantoin    S
             Pip/Tazobactam    S
             Fosfomycin        S
             Amikacin          S
             Ertapenem         S
             Ceftazidime       S
             Temocillin        S
             Amoxicillin       S

16           1) Growth of Escherichia coli

             Ciprofloxacin     R
             Gentamicin        S
             Ertapenem         S
             Trimethoprim      S
             Cephalexin        R
             Tazobactam        S
             Temocillin        S
             Amikacin          S
             Ceftazidime       S
             Fosfomycin        S
             Amoxicillin       W

27           1) Growth of Escherichia coli

             Co-amoxiclav      R
             Ciprofloxacin     R
             Gentamicin        S
             Nitrofurantoin    S
             Trimethoprim      S
             Ertapenem         S
             Ceftazidime       R
             Tazobactam        S
             Amikacin          S
             Temocillin        S
             Fosfomycin        S
             Amoxicillin       R

35           1) Growth of Escherichia coli

             Ciprofloxacin     R
             Gentamicin        S
             Ertapenem         S
             Nitrofurantoin    S
             Trimethoprim      R
             Cephalexin        S
             Fosfomycin        S
             Ceftazidime       S
             Amikacin          S
             Pip/Tazobactam    S
             Temocillin        S

38           1) Moderate growth of Escherichia coli

             Co-amoxiclav      S
             Ciprofloxacin     R
             Gentamicin        S
             Amoxicillin       W

Figure 1.

Previous Exposure to Quinolone Antibiotics

Number of Patients

Quinolone Exposure

Previous Quinolone                   16
Unknown or No Previous Quinolone     22

Note: Table made from bar graph.

Figure 2.
Patients Found to Have Ciprofoxacin-Resistant Bacteria
on Transrectal Swab Analysis

Number of Patients

Resistant/No Resistant Bacteria

No Ciprofloxacin Resistance         31
Ciprofloxacin Resistance             7

Note: Table made from bar graph.

Figure 3.
Country of Birth of Patients with Ciprofoxacin-Resistant Bacteria

Number of Patients

Country of Birth

Nigeria     2
Monserrat   2
Turkey      1
Guyaria     1
India       1

Note: Table made from bar graph.
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Title Annotation:Research/Quality Improvement Project
Author:Turner, Bruce; Pati, Jhumur; Nargund, Vinod; Claxton, Alleyna; Longstaff, Victoria; Sarkar, Somita;
Publication:Urologic Nursing
Article Type:Report
Date:Jul 1, 2016
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