BERKELEY, CA (UroToday.com) - Transrectal ultrasound (TRUS)-guided prostate biopsy is the standard urologic procedure for prostate cancer detection. Although TRUS-guided biopsy is a safe and well-tolerated procedure, complications occasionally arise, and the incidence of infectious complications after TRUS-guided biopsy is recently on the rise. The emergence of antimicrobial-resistant strains of bacteria and production of extended spectrum beta-lactamase (ESBL) are considered as a major cause of the increase in the hospital admission rate. In this study, we aimed to provide an overview of the incidence, bacteriologic characteristics of urine and blood cultures, and antimicrobial resistance of acute prostatitis after TRUS-guided biopsy according to time period, with a focus on quinolone-resistant E. coli and the ESBL-producing strain.
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We retrospectively reviewed the medical records of 9 568 patients who underwent TRUS-guided biopsy between March 1995 and May 2013. A total of 11 345 cases of TRUS-guided biopsy were performed. For prophylactic treatment, rectal preparation (bisacodyl suppository) was performed and patients received oral quinolone and/or cephalosporin before and continually for a total of 7 days after the biopsy, and aminoglycoside was administered intramuscularly just before the biopsy.
Acute prostatitis was diagnosed by a body temperature over 38° C, increased leukocytes in urine sediment, and pathologic clinical findings by DRE. Patients who developed acute prostatitis returned to the hospital, and blood and urine samples were collected before starting antimicrobial treatment. The whole time period was divided into two parts, based on emergence of an ESBL-producing strain. Changes in the incidence and proportion of antimicrobial resistance in acute prostatitis after TRUS-guided biopsy were accessed.
Acute prostatitis was detected in 103 (0.91%) cases over the whole period. Although the incidence of acute prostatitis was low, the incidence of acute prostatitis increased more than three times over the last 10 years. Of the 103 cases involving acute prostatitis, blood and/or urine culture was positive in 63 (61.1%) cases. The most frequent etiologic organism was E. coli, which was isolated from 47 of 49 (95.9%) cases in blood and from 39 of 41 (95.1%) cases in urine. Among patients with E. coli isolated from culture, the incidence of resistance to quinolone was 44 (93.6%) cases in blood and 36 (92.3%) cases in urine. ESBL-producing E. coli were found in 12 patients (10 blood and 8 urine cultures). ESBL-producing E. coli were not detected from 1995 to 2007, but have been detected continuously since 2008. All patients with ESBL-producing E. coli infection showed resistance to quinolone.
When the incidence of antimicrobial resistance of E. coli isolated from blood and urine was analyzed according to time period, E. coli were highly resistant to quinolone and ampicillin early on, and were even more resistant recently, with a resistance rate of about 90%. Imipenem and amikacin resistance of E. coli was less than 10%, but resistance of E. coli to trimethoprim/sulfamethoxazole and cefepime increased steeply across the time periods.
In addition to quinolone-resistant E. coli, the emergence of an ESBL-producing strain is another concern. In our study, ESBL-producing E. coli were present in 20% of patients with post-biopsy infection. Moreover, all ESBL-producing E. coli isolated from blood and/or urine showed quinolone resistance. Bacteremia caused by ESBL-producing E. coli has a higher mortality rate than that caused by non-ESBL-producing E. coli. Therefore the recommended antibiotic treatment is intravenous carbapenems. However, carbapenems are recommended to treat severe infections and are not indicated as prophylactic antibiotics because such use would increase the rate of multidrug-resistant organisms. The cause of acute prostatitis after TRUS-guided biopsy is suggested to be the direct inoculation of bacteria from the rectal mucosa to the prostate which spread into the blood or urinary tract. Thus, rectal swab screening before TRUS-guided biopsy may provide information about the presence of quinolone resistance or ESBL-producing strains, if acute prostatitis develops. However, presence of quinolone-resistant organisms in rectal swabs does not always result in clinical infection. Therefore, we suggest rectal swab screening in high-risk patients who are older and who have repeat biopsy, a previous history of acute prostatitis, or previous use of quinolones within 3 months.
Our study had several limitations. First, the incidence of acute prostatitis after TRUS-guided biopsy was determined only for patients who returned to our hospital; thus, the incidence was possibly underestimated. Second, we did not evaluate comorbidities such as benign prostatic hyperplasia (BPH) and diabetes that could have affected the infection rate. Finally, the geographic variability in antibiotic susceptibility patterns should be considered when generalizing our results.
In conclusion, with the increase in antimicrobial-resistant E. coli and the emergence of an ESBL-producing strain, treatment of infectious complications after TRUS-guided biopsy has become more complicated. Quinolone is not an effective antimicrobial for the treatment of acute prostatitis after TRUS-guided biopsy due to the high rate of quinolone resistance. Instead, the types of pathogens and their antimicrobial resistance should be taken into account to treat acute prostatitis after TRUS-guided biopsy. Further investigations are required to verify the utility of pre-biopsy rectal swab screening for quinolone-resistant E. coli and ESBL-producing strains.
Wan Song and Hwang Gyun Jeon as part of Beyond the Abstract on UroToday.com. This initiative offers a method of publishing for the professional urology community. Authors are given an opportunity to expand on the circumstances, limitations etc... of their research by referencing the published abstract.
Department of Urology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea