This work assessed the impact of tailored antibiotic treatment on PBI-development based on patient classification into PBI-risk groups before TRPBx.
During the last decade, an increase in febrile UTIs after TRPBx, ranging from 4.2 to 17.5%, with 0.8–6.3% of patients needing hospital admission was observed [11]. The prevalence of Fluoroquinolone-resistant bacteria in the rectal flora, which ranges between 20–50%, is a major concern and is associated with increased PBIs (6.6% versus 1.6%) and hospital admission rates (4.4% versus 0.9%) [12]. Increasing age, recent antimicrobial use, and non-Caucasian race are independent predictors of Fluoroquinolone resistance in the rectal vault [10]. Furthermore, the continuously rising prevalence of ESBL-producing bacteria is of utmost importance in promoting PBI [13]. Generally, there are diverse views regarding the effectiveness of different antibiotic prophylaxes before TRPBx [14]. Given that there is insufficient evidence of augmented prophylaxis's superiority, monoprophylaxis with 3rd-generation Cephalosporins has proven equally efficient in preventing PBIs when compared to Fluoroquinolones [15].
In our cohort however, PBIs after Ciprofloxacin prophylaxis – even though rarely administered - were high when compared to the treatment with Ceftriaxone, ranging between 5.6% (1/18) for standard-risk, 22.2% (2/9) for urine culture targeted and 50% (1/2) for high-risk patients.
The transition from Cefuroxime to Ceftriaxone for standard-risk patients in 2020 due to peaking PBIs with Cefuroxime significantly reduced PBI rates without any sepsis from 2020 onwards (PBI-rates Ceftriaxone vs. Cefuroxime: 0.24% vs. 8.1%). E. coli was commonly cultured for patients who were treated with Cefuroxime and experienced PBI (12/16, 75%). This suggests a distinct superiority of 3rd - over 2nd -generation Cephalosporines in preventing E. coli-associated PBIs within this risk group. With Ceftriaxone as the actual standard for the standard-risk group, we observed persisting low PBI rates which are comparable to the TPPBx [3, 16] and results from one of the largest available multicenter studies (n = 12240) with < 1% PBI rates following TRPBx [17].
Among high-risk patients, the cumulative PBI rate was 5.6%. On an antibiotic level, only 1.7% (1/58) of patients correctly treated with Ertapenem developed PBI. However, 15.5% (11/71) of high-risk patients were erroneously treated with Ceftriaxone due to missing rectal swab results at the biopsy appointment. Two out of eleven (18.2%) of these patients developed PBI, with ESBL E. coli detected in blood cultures in one case. The considerable difference in PBI rates between standard and high-risk patients treated with Ceftriaxone (0.24% vs. 18.2%) underscores the crucial role of rectal-swab-based identification and Carbapenem based treatment of high-risk patients which is of paramount importance in preventing PBIs within this risk-group [9, 16, 18, 19]. Importantly, rectal ESBL/MRGN prevalence in our cohort was only 6.3% which is considerably lower than in other large population-based studies with prevalences close to 20% [13].
Further, we obtained urine cultures as an additional tool in PBI-risk stratification before TRPBx for all patients with targeted antibiotic therapy in case of culture-positive results. Of all patients, 4.1% (48/1182) had positive urine cultures and 6.8% (3/44) of patients who received culture-targeted treatment developed PBI. Two of these patients were treated with Ciprofloxacin due to sensitivity on initial urine cultures, however developed PBI with growth of Ciprofloxacin resistant E. coli (n = 1) and Pseudomonas (n = 1) on culture results during infection.
Moreover, apart from the choice of antibiotic treatment, increasing prostate volume was associated with increased PBI risk (OR 1.01, 95%-CI: 1.00-1.03, p = 0.033) on MLRA in our study. Interestingly, this finding is supported by only little evidence in the literature and could be associated with chronical intraprostatic infection [20].
Compared to the TRPBx, the TPPBx is undoubtedly a safe way to reduce infection rates, as rectal bacteria prostatic inoculation is avoided. Recorded PBI-rates after TPPBx have been lower than 1% [3, 21], and hospital readmissions have been extremely uncommon [4, 22]. TPPBx can be carried out safely and effectively under local anesthesia [21, 23] and without antibiotics, even in a semi-sterile environment [5, 6, 21, 24]. Nevertheless, high-quality evidence proving the superiority of TPPBx over TRPBx has been missing [25] and actual randomized-controlled trials failed to demonstrate significant differences in PBIs between the different techniques [26–28]. The significance of rectal swab-based targeted prophylaxis for TRPBx was also highlighted by recent evidence of the PREVENT trial in which biopsy-naïve patients were recruited to either undergo TPPBx without antibiotic prophylaxis or TRPBx with targeted prophylaxis. No significant difference in PBI was demonstrated (0 vs 1.4%; difference − 1.4%; 95%-CI: 3.2%-0.3%; p = 0.059) despite a Fluoroquinolone resistance rate of 23% in the site of the highest study enrollment with antibiograms demonstrating cross-resistance to Sulfamethoxazole-trimethoprim, Ceftriaxone, and Gentamicin at 53%, 37%, and 18% [26].
Alternative strategies to decrease PBI rates are reducing the biopsy core number and prebiopsy rectal cleansing with povidone-iodine [16, 29, 30]. A recent metanalysis demonstrated that the use of a rectal povidone-iodine in addition to antimicrobial prophylaxis resulted in a significantly lower rate of PBIs (RR 0.47, 95%-CI: 0.36–0.61, p < 0.000001) [16]. In this study, we did not perform rectal cleansing, and a relatively high rectal bacterial load may have influenced PBI development. Furthermore, additional formalin disinfection of the needle tip before each puncture together with povidone-iodine cleansing has shown to lead to a significant decrease in PBI rates following TRPBx (3.9% vs. 6.4%, p = 0.049) [30]. Additional factors like needle guide type (disposable vs. reusable), needle type (coaxial vs. non-coaxial), needle size (large vs. small), and number of injections for peri-prostatic nerve block (standard vs. extended) do not seem to have an impact on PBI development[16].
Some of this study’s limitations should be considered. First, the study is retrospective. Second, we did not uniformly assess patient-related risk factors like diabetes mellitus, immunosuppression, adiposity, prior antibiotics, or the presence of transurethral catheters. Third, even though patients were advised to present to our outpatient clinic in case of infectious symptoms, it cannot be fully excluded that patients presented at different institutions. Finally, no direct comparison with TPPBx was performed.