Acute bacterial prostatitis

Author

Masahiro Matsumoto (Department of Urology, University of Occupational and Environmental Health, Fukuoka, Japan)

Shingo Yamamoto (Department of Urology, Hyogo College of Medicine, Hyogo, Japan)

Executive Summary

Epidemiology and pathogenesis

1. Prostatitis syndromes are a very common presentation in the clinical setting and tend to occur in young and middle-aged men.

Diagnosis

1. Patients with acute bacterial prostatitis (ABP) present with typical signs and symptoms of an acute urinary tract infection including irritative and/or obstructive voiding complaints, and have additional symptoms of systemic infections like malaise, nausea, vomiting, chills and fever, and sometimes present with signs of symptoms of urosepsis. They also complain of perineal and suprapubic pain due to a painful swollen prostate and may have associated pain or discomfort of the external genitalia (GR: B).

2. Digital rectal examination (DRE) reveals a hot, boggy, and exquisitely tender prostate gland (GR: B).

3. Prostatic massage for the expression of prostatic fluid is not indicated and perhaps even harmful because it could precipitate bacteremia or sepsis (GR: B).

4. A midstream urine specimen is sufficient and will show prominent leukocyturia and bacteriuria with typical uropathogens (GR: B).

5. The sonographic determination of residual volume is an important diagnostic procedure, because infravesical obstruction may play an important pathogenic role in ABP (GR: B).

6. Transrectal ultrasound (TRUS) does not need to be performed on every patient with suspected ABP (GR B), but can aid in the diagnosis or exclusion of a prostatic abscess (GR: B).

7. Computer tomography (CT) and magnetic resonance imaging (MRI) offer no advantage over TRUS, unless the abscess has penetrated the confines of the prostate gland or there are further abscess foci suspected (GR: B).

8. Prostate-specific antigen (PSA) is moderately to markedly elevated in a patient with ABP, but is not a diagnostic requirement (GR: C).

9. In patients with elevated PSA serial measurement is recommended as a useful tool for followup (GR: B).

10. Escherichia coli is the most common pathogen encountered in ABP (GR: B).

11. There is a significantly higher rate of mixed infection in prostatitis from prior manipulation as compared with spontaneous ABP (GR: B).

Treatment

1. Rapid initiation of broad-spectrum parenteral antibiotics and symptomatic support are mandatory for the patients with ABP (GR: B).

2. Supportive measures include i.v. hydration and catheter drainage if the patient cannot void (GR: B).

3. Insertion of a suprapubic cystotomy tube is the optimal therapy for relief from urinary obstruction (GR: B).

4. In-and-out catheterization to relieve the initial obstruction or short-term (< 12 hours) indwelling catheterization with a small-caliber Foley catheter is appropriate (GR: B).

5. The selection and course of antibiotics should be adjusted according to the pathogens isolated and the results of bacterial susceptibility testing (GR: B).

Prostatic abscess

1. Suspicion of a developing abscess is raised if there is no response to appropriate antibiotic therapy, and can be confirmed by TRUS (GR: B).

2. If prostatic abscess is discovered, initiation of broad-spectrum antibiotics and prompt surgical drainage is crucial (GR: B).

Introduction

ABP constitutes a urologic emergency. It is uncommon and usually occurs in concert with a urinary tract infection (UTI) but can have a dramatic presentation. Usually, many clinicians diagnose and treat the ABP empirically. A correct diagnosis has therapeutic implications since ABP may require a longer course of treatment than other forms of urinary tract infection and because the choice of antibiotic to complete treatment after fever subsides should be based on its ability to penetrate into prostatic tissue. Thus, it is of great necessity to define detailed and consensual diagnosis and treatment criteria for ABP.

Methodology

We surveyed the extensive literature regarding ABP available in Medline via Pubmed and also considered other relevant publications up to December 2020. We used terms: prostatitis, “bacterial prostatitis”, “acute bacterial prostatitis”, combined with the terms: diagnosis, evaluation, management or treatment, for the search strategy. For the purpose of this review a total of 78 possibly eligible publications were included into the analysis, which were screened by title and abstracts. The limitations for this literature search were English language. The papers were rated according to the level of evidence and the strength of recommendations according to ICUD standards ^[1][2].

Definition of the disease

Overview

ABP represents an acute infection of the prostate gland. It is a male UTI that has some features in common with lower UTI in females, including the etiological organisms involved and some of their urovirulence factors. The host response, however, is very different from simple cystitis and the treatment course is more complicated ^[3].

The prostatitis syndrome is a common healthcare issue affecting 10–14% of men of all ages and ethnicities. ABP is associated with severe, mainly Gram-negative infection ^[4].

In the 1999, NIH consensus statement on prostatitis, prostatitis and prostatitis-like symptoms were classified into four broad categories ^[5]. Type I prostatitis refers to ABP.

Epidemiology

Overall, prostatitis syndromes are a very common presentation in the clinical setting and tend to occur in young and middle-aged men. However, ABP accounts for the rarest category among the NIH classification. It is diagnosed in less than 0.02% of all patients seen for prostatitis ^[6]. However, the potential morbidity and mortality of ABP constitutes a true urologic emergency. It is characterized by an acute onset of pain combined with irritative and obstructive voiding symptoms in a patient with manifestations of a systemic febrile illness. The hospital admission rate for ABP in the USA in 1994 was 12.7 in 100,000 as the first, second or third principal diagnosis for hospital admission ^[7] (LE: 4).

Characterization

Etiology

ABP is the result of severe infection of mainly Gram-negative bacteria, which can be easily isolated from the urine. E. coli is the most common pathogen encountered in ABP, accounting for 50-87% of cases, other pathogens include Enterobacteriaceae (eg, Klebsiella species and Proteus species, which account for 10%–30% of cases), and nonfermenting gram-negative bacilli (eg, Pseudomonas species; 5-15% of cases), Enterococcus species (5-10% of cases) ^[8]-[15] (LE: 3). Commonly, infections are caused by a single organism, but occasionally by two or more ^[15]. Mixed cultures were isolated in 2.4% of the ABP ^[14] (LE: 3). In sexually active men, Neisseria gonorrhoeae and Chlamydia trachomatis should be considered ^[13][16][17] (LE: 4).

Risk factors

The mechanisms of ABP are reflux of infected urine into the ejaculatory and prostatic ducts, an ascending urethral infection from the distal urethra, meatus and bladder direct or lymphatic invasion from the rectum, and hematogenous infection ^[15][18] (LE: 4). Although many patients with ABP have no clear risk factors, underlying functional or anatomical anomalies that predispose to urogenital infections might affect the development of prostatitis. Prior manipulation of the lower urinary tract including chronic indwelling bladder catheterization, intermittent bladder catheterization, urodynamic study, transurethral surgery and transrectal prostate biopsy (TRPB) could be predisposing factors ^{[14][16][19]-[22]} (LE: 3). Patient populations who are at especially high risk of ABP include those with diabetes, cirrhosis, and suppressed immune systems ^[23] (LE: 4).

Clinical Evaluation/risk assessment

Diagnostic and staging procedures

ABP might be difficult to diagnose. Several conditions, such as benign prostatic hypertrophy, chronic bacterial prostatitis (CBP), chronic pelvic pain syndrome (CPPS), cystitis, diverticulitis, epididymitis, orchitis, proctitis, prostate cancer, present with similar symptoms and must be differentiated from ABP ^[16]. Patients with symptoms of ABP have to undergo urinalysis and culture of the urine. An initial imaging of the prostate is suggested to exclude prostatic abscess ^[24] (LE: 4).

Symptoms and signs

There are no common key symptoms of ABP. The NIH revised classification of prostatitis deals more with pathophysiology and laboratory diagnosis and describes the clinical features of ABP only briefly as "acute symptoms of a UTI" ^[5] (LE: 4). Irritative and/or obstructive voiding complaints including dysuria, urinary frequency and urgency are typical ^[5] (LE:4). Obstructive voiding complaints including hesitancy, poor interrupted stream, and even acute urinary retention are common. The patients complain of perineal and suprapubic pain and may have associated pain or discomfort of the external genitalia. The patients have a swollen prostate that is extremely painful when investigated. Patients with ABP are often acutely ill and distressed. Symptoms of systemic infection like malaise, nausea, vomiting, chills and fever may vary. These patients may even be systemically toxic, i.e. flushed, febrile, tachycardic, tachypnoic, hypotensive, and present even with all signs and symptoms of an urosepsis ^{[5][8][16][25][26]} (LE: 4).

DRE reveals a hot, boggy, exquisitely tender and tense prostate gland. Fluctuation during palpation is suspicious for prostatic abscess. Painful ejaculation, hematospermia, and painful defecation may be present as well ^[3][16]. Older patients also had fewer signs and symptoms (less burning micturition, less painful DRE, and less hematuria) ^[27] (LE: 4). Perineal pain and anal sphincter spasm may complicate the DRE ^[28][29] (LE: 4). Although a gentle rectal examination can be performed in patients who have suspected ABP, prostatic massage for the expression of prostatic fluid is not indicated and perhaps even harmful because it is painful for the patient and it could precipitate bacteremia or sepsis ^{[4][8][14][16][30]} (LE: 4).

Clinical findings

In patients presenting with ABP, a midstream urine specimen will show prominent leukocyturia and bacteriuria. Midstream urine culture is considered the only laboratory evaluation of the lower urinary tract and usually shows typical uropathogens ^[31](LE:4).

Blood culture and complete blood count are useful in ABP ^[30] (LE: 4). In particular, blood cultures should be collected before initiating antibiotics in patients with a body temperature greater than 38.4°C ^[32] (LE: 3), a possible hematogenous source of infection (e.g., endocarditis with Staphylococcus aureus), complicated infections (e.g., sepsis), or who are immunocompromised ^[16] (LE: 4).

Functional findings

The sonographic determination of residual volume is an essential diagnostic procedure, because intravesical obstruction may play an important pathogenic role in ABP ^[33] (LE: 3). And the difference in voiding problems may reflect age differences and the prostate volume. In addition, the frequency of voiding problems, particularly urinary retention, was remarkably higher in the group that underwent prior manipulation ^[22] (LE: 3). Some investigators suggested that bladder outlet obstruction might not be the main cause of ABP ^[14] (LE: 3). For this reason, more evidence is necessary to clarify the relationship between obstructive bladder dysfunction and ABP.

Imaging studies

There are only a few studies that describe ultrasonographic findings in non-abscessed ABP ^[34]-[37]. In a prospective study of 45 patients with a clinical diagnosis of ABP, TRUS was performed upon admission as well as one month after antibiotic therapy and the findings correlated with the clinical presentation of disease ^[38]. The authors conclude that TRUS does not need to be performed on every patient with suspected ABP (as only 47% had sonographically demonstrable lesions on admission and 61% had lesions improved or disappeared post treatment), but TRUS would be indicated to exclude the presence of prostatic abscess (LE: 2a, GR: B). In conclusion, carefully performed TRUS can aid in the diagnosis or exclusion of a prostatic abscess without increasing the risk for urosepsis ^[38] (LE: 2a, GR: B).

Some reports indicate that the more cost-intensive computer tomography (CT) and magnetic resonance imaging (MRI) offer no advantage over TRUS, unless the abscess has penetrated the confines of the prostate gland or there are further abscess foci suspected ^[3][39] (LE: 3).

Color Doppler sonography is a useful tool in monitoring response to treatment and in predicting clinical outcome ^[40] (LE: 3). In some papers, the investigators stated that intraprostatic color flow in patients with ABP was greater than in the normal prostate, or those with chronic inflammation or carcinoma ^[41] (LE: 3). According to the study, in most of the patients, the vascularity of the prostate was increased in the acute phase of inflammation (15-spot scale). With recovery from infection color flow in the prostate decreased to 15 spots, the pattern in healthy men ^[42] (LE: 3).

Hypoechoic areas in the peripheral zone of the prostate can persist for a long time in patients with ABP. Color doppler ultrasonography of these areas can helps to differentiate them from those with carcinoma ^[43].

There are also two interesting imaging studies – one performed with prostatic Indium-labeled leukocyte scintigraphy and one performed with a combination of PSA levels and TRUS-provided evidence supporting a frequent involvement of the prostate in male UTI ^[27][44][45] (LE: 2a).

The former was carried out to determine whether indium-111 (111In)-labelled leukocytes (ILLs) accumulated in the infected tissue and whether uptake responded to treatment ^[46]. Scintigraphs prior to antibiotic treatment showed uptake in prostates of all patients with ABP; after treatment no uptake was noted in nine out of 10 patients, and one out of 10 had markedly decreased uptake. In the patients with UTI, if there was no involvement in the prostate, no uptake occurred in prostates. ILLs could be useful for detecting ABP in the future ^[31].

The latter showed the prostate is concurrently involved in men with febrile UTI with a transient increase in prostate volume and serum PSA during the acute stage of disease ^[34][35] (LE: 3). With these two concepts, the presence of an inflammatory reaction within the prostate can inform us of ABP when the diagnosis is not clear ^[27].

Serum PSA

Although PSA levels are not a mainstay of diagnosis, they are generally moderately to markedly elevated in the setting of ABP ^[47]-[49] (LE:3). The role of serum PSA in the differential diagnosis and evaluation of ABP is not clear. But elevated levels of PSA have been described in 70% of men with ABP ^[50] (LE: 3) as a consequence of increased vascular permeability and disrupted epithelium of the gland.

In a prospective study of 39 men with pyrexia (>38.3°C), serum PSA levels were used to categorize patients according to an initial diagnosis of ABP, pyelonephritis, urogenital infection or fever of unknown origin. All of the 20 cases with pyrexia and elevated PSA were diagnosed and treated as ABP ^[47].

Gamé et al. demonstrated a decreased free-to-total (f/t) PSA ratio up to 30 days following adequate antimicrobial therapy, indicating the significance of increased bound PSA in ABP ^[51] (LE: 3). The decrease of f/t PSA ratio has been correlated to systemic inflammation as measured by serum C reactive protein (CRP) levels. In a prospective study of 70 men with febrile UTI with prostatic involvement as measured by tPSA, this marker has been proven useful to assess prostatic infection. Effective treatment with antibiotics resulted in significantly reduced serum PSA. A decline of tPSA levels in patients after appropriate antimicrobial treatment has been suggested to indicate a healing process ^[34] (LE: 3).

So the authors recommend PSA as a concise, accurate, rapid and cost-effective tool for identifying ABP and for follow-up ^[31] (GR: B).

Principles of management and treatment

Hospitalization criteria

Management of ABP should be based on severity of symptoms, risk factors (benign prostatic hypertrophy, genitourinary infections, high-risk sexual behavior, history of sexually transmitted diseases, immunocompromised states, phimosis, prostate manipulation, and urethral stricture), and local antibiotic resistance patterns ^[16]. Most patients can be treated with outpatient antibiotics; fewer than one in six patients will require hospitalization ^[14][16]. Hospitalization should be considered in the following situations: failed outpatient management, inability to tolerate oral intake, resistance risk factors, recent fluoroquinolone use, recent transurethral or transrectal prostatic manipulation, systemically ill or septicemia, urinary retention ^[16] (LE: 4).

Use of antibiotics

There has been no randomized controlled trial on antibiotic selection and the duration of antibiotic use ^[52]. The treatment regimen for ABP is based on clinical experience and a number of uncontrolled clinical studies. For systemically ill patients with ABP, parenteral antibiotic therapy is preferable ^[30][53] (LE: 4).

Appropriate management of ABP includes rapid initiation of broad-spectrum parenteral antibiotics and symptomatic support. Current guidelines for the treatment of ABP have been worked out by the European Association of Urology (EAU), the Korean Society of Infectious Diseases/Korean Society for Chemotherapy (KSID/KSC), the National Institute for Health and Care Excellence (NICE), the Japanese Association for Infectious Disease/Japanese Society of Chemotherapy (JAID/JSC) ^{[30][52]-[54]}.

Pharmacologic penetration of antibiotics in the acutely inflamed prostatic tissue is considered to be sufficient in the case of susceptible bacteria. In severe cases, parenteral administration of high doses of bactericidal antibiotics, such as a broad-spectrum penicillin derivative, a third-generation cephalosporin with or without aminoglycosides, or a fluoroquinolone, is required until fever and other parameters of acute infection are normalized. It can be performed alone or in combination with supportive measures including i.v. hydration and catheter drainage if the patient cannot void ^[16][55][56] (LE: 4).

In less severe cases, an oral fluoroquinolone for 10 days may be sufficient ^[33] (LE: 4). The selection and course of antibiotics can be adjusted according to the pathogens isolated and the results of bacterial susceptibility testing ^{[16][30][52][53]}.

In most cases the fever resolves in 36–48 h ^[43][57] (LE: 2a-4). After successful initial therapy, switching to an oral regimen such as a fluoroquinolone is appropriate. The oral antibiotic therapy should be continued at least for a total of 2 to 4 weeks ^{[16][30][52]-[54]} (LE: 4) although currently there is no consensus on the optimal treatment duration.

The duration of therapy for ABP has not been well studied. If the patient is responding clinically and the pathogen is sensitive to treatment, most experts recommend that antibiotic therapy be continued for 3 to 4 weeks to prevent relapse, although a longer course is sometimes necessary ^[57] (LE: 4, GR: C). A patient with ABP must be over-treated rather than under-treated ^[58] (LE: 4, GR: C). Kravchick et al. reported that three months after the end of a 6-week therapy, expressed prostatic secretion (EPS) cultures were still positive in a third of the men.

Prolonged therapy (at least 6 weeks) and subsequent follow-up with Stamey’s test at the three-monthly visits are required to prevent early recurrence ^[43] (GR: B).

Antibiotic resistance

In recent guidelines for antibiotic treatment of ABP, the administration of cephalosporins or a quinolone alone or in combination with an aminoglycoside has been recommended ^{[30][52]-[54]} (LE: 4). For patients with ABP requiring hospitalization, or if the resistance of the causative bacteria to fluoroquinolone is considered, third-generation cephalosporins, a broad-spectrum beta lactam/beta lactamase inhibitor (BLI), or carbapenem are recommended ^[52] (LE: 4).

The susceptibility to ciprofloxacin of E. coli was shown to be relatively low (76.2%) for ABP in some Korean areas between 2001 and 2005 ^[55] (LE: 3). A result as such probably reflects the increase in resistant bacteria owing to the excessive use of ciprofloxacin at that local area.

As in the previous report, ciprofloxacin alone may be an inadequate choice, especially in patients with prior manipulation of the urinary tract. Considering the very low susceptibility to cephalosporins (< 60%) in pathogens other than E. coli, and the relative high isolation rates (>40%) of pathogens other than E. coli, cephalosporins as single therapeutic agents may have limited use in this community. Most commonly, antibiotic combination therapy for ABP includes a cephalosporin and an aminoglycoside. The second- and third-generation cephalosporins have been prescribed relatively frequently for this purpose. Administration of an aminoglycoside must be confined to the group of patients without prior manipulation owing to their susceptibility. In the group of patients with prior manipulation in which pathogens other than E. coli constitute a substantial number of isolates, a combination of a cephalosporin and amikacin should be recommended for empirical therapy ^[55] (GR: B).

The use of levofloxacin could be a risk factor for ABP after TRPB, due to an increase in fluoroquinolone-resistant E. coli in the rectum. Treatment with cephalosporin or carbapenem is recommended for patients with ABP after prostate biopsy ^[59] (GR: C).

History of prior urologic manipulation was an independent risk factor for ciprofloxacin-resistant and Extended spectrum beta-lactamase (ESBL)-producing microbes. Advanced age (over 60 years) was an independent risk factor for ciprofloxacin-resistant microbes 60 (LE: 4).

For ABP in single Korean institution between 2006 and 2015, the ciprofloxacin susceptibility for E. coli in groups without prior manipulation was documented 85.7%. For groups with prior manipulation, the susceptibility was 10.0% ^[60] (LE: 4).

For ABP in single Korean institution between 2006 and 2015, incidence of ESBL-producing microbes by pathogen was 3.8% for E. coli and 1.0% for Klebsiella pneumonia in the absence of manipulation group, and 20% and 33.3% in the presence of manipulation group, respectively ^[60] (LE: 4). Initial treatment of ABP must consider patient's age and the possibility of prior manipulation to optimize patient treatment. With the high rate of resistance to fluoroquinolone, cephalosporins with amikacin, or carbapenems, or extended-spectrum penicillin with beta lactamase inhibitor should be considered as the preferred empirical ABP treatment in the patients with history of prior urologic manipulation ^[60] (LE: 4).

Pseudomonas species were much more dominant pathogens in the group by transurethral manipulation than transrectal manipulation group. The susceptibilities to second-, third- and fourth-generation cephalosporins, amikacin, carbapenem and aztreonam were shown to be very low in the transurethral manipulation group ^[61] (LE: 3).

For ABP in single Korean institution between 2004 and 2013, ESBL-producing bacteria accounted for 64.7% of culture-positive patients in the biopsy-related ABP compared to 13.3% in the spontaneous ABP. Biopsy-related ABP showed a higher incidence of septicemia and antibiotic-resistant bacteria than the spontaneous ABP. These results have important implications for the management and antimicrobial treatment of biopsy-related ABP, which may well deserve to be considered a distinct prostatitis category ^[62] (LE: 4).

For ABP in Korean institutions between 2005 and 2014, the ABP following TRPB group (59.1%) showed a higher bacteremia prevalence than the community-acquired ABP group (13.2%). Significant differences in the antibiotic sensitivity to E. coli between the two groups were observed for fluoroquinolone, cephalothin, and gentamicin. The antibiotic sensitivity of fluoroquinolone in the ABP following TRPB group was only 27.3%. Amikacin, imipenem, meropenem, amoxicillin/clavulanic acid, and piperacillin/tazobactam showed more than 95% antibiotic sensitivity in both groups. ABP following TRPB was an independent predictive factor for bacteremia by multivariate analysis. Carbapenem may be a treatment of choice for patients suspected of having sepsis ^[63] (LE: 3).

Treatment for ABP

Initial empiric antimicrobials should be based on risk factors of drug resistant bacterium and clinical characteristics. Antimicrobials should be adjusted based on the results of culture testing of the initial urine sample and antimicrobial susceptibility testing. Table 1 shows summary of treatment for ABP according to the guidelines and previous studies of ABP.

Table 1. Summary of treatment for ABP

Additional points to be considered

Another supportive treatment options like alpha-blockers, antipyretics or anti-inflammatory agents may be beneficial, although current data are insufficient. There is only one animal study investigating the effects of levofloxacin on tamsulosin for ABP. In the prostatic tissues, tamsulosin increased the Cmax, prolonged the t1/2 and decreased the clearance rate of levofloxacin. These results indicate that tamsulosin may enhance the effect of levofloxacin in the treatment of bacterial prostatitis without changing the drug concentration in the liver and kidney ^[64] (LE: 3). Stool softeners are also recommended ^[26] (GR: C).

Follow-up and monitoring

Although the role of serum PSA in the differential diagnostic evaluation of ABP is not finally proven, elevated PSA is common. Effective treatment with antibiotics results in significantly reduced serum PSA. Therefore, some authors recommend PSA as a concise, accurate, rapid and cost-effective tool for identifying ABP and for the follow-up ^[31][65] (LE: 4).

After antibiotic treatment, the long-term response is unclear. A prospective study found that the total serum PSA level was elevated up to 3 months after the episode of ABP in 39% patients ^[43] (LE: 2a). Therefore, prolonged therapy of fluoroquinolones for 6 weeks and reevaluation after that has been recommended ^[43] (GR: B). In this manner, patients with ABP tend to have persistent infection. ABP tends to persist and bacterial localization cultures should be taken at subsequent follow-up visits for at least 3 months ^[43]. According to another prospective study, PSA levels could be high even up to 6 months after an acute episode ^[66] (GR: B).

Morote et al. ^[67] showed that acute inflammation contributed to PSA increases but did not influence the percentage of free PSA in patients with cancer-free biopsies (LE: 3). Moreover, some patients with carcinoma could be missed during the acute phase of inflammation. Therefore, PSA and TRUS monitoring are strongly recommended (GR: B).

According to a retrospective analysis, of the 437 ABP patients, 1.3% progressed to CBP and 10.5% progressed to inflammatory CPPS ^[11] (LE: 3). The patients who developed to chronic infection were higher in alcohol consumption rate, diabetes, voiding symptoms, prior manipulation rate, enlarged prostate volume, catheterization history rate and short duration of antibiotic treatment.

Relief from obstruction

In ABP, urinary obstruction is a very common symptom. Because patients can have significant obstruction from an acutely inflamed prostate, bladder scanning for postvoid residual urine is recommended. If the residual urine is less than 100 mL, the patient should be initiated on alpha blocker therapy; if the residual is large, consideration should be given to placement of a small urethral catheter if short-term drainage is required or a suprapubic catheter if longer-term drainage is required ^[6][25] (GR: B).

Traditionally, it has been suggested that the insertion of a suprapubic cystotomy tube is the optimal therapy because an indwelling Foley catheter may further obstruct urethral ducts, resulting in the potential to develop prostatic abscesses ^[67]-[69] (LE: 4). In most patients, however, an in-and-out catheterization to relieve the initial obstruction or short-term (<12 hours) indwelling catheterization with a small-caliber Foley catheter is appropriate ^[29] (GR: C).

Special considerations

Prostatic abscess

Prostatic abscesses are uncommon but potentially serious manifestations of acute infection of the prostate and demand prompt treatment. It represents a severe complication of acute bacterial prostatits with an estimated incidence of 2–18% ^[70] (LE: 3) and a mortality rate of 3–16% ^[71] (LE: 3).

Antibiotic treatment of ABP is simple but abscess formation is well described and may have devastating sequelae. Its clinical diagnosis is somewhat difficult and suspicion of a developing abscess is raised if there is no response to appropriate antibiotic therapy, and can be confirmed by TRUS ^[38][39] (LE: 4). TRUS should not be postponed for > 48 h in patients who do not respond to appropriate antibiotic therapy ^[43] (GR B). CT and MRI are helpful when it is difficult to diagnose prostatic abscesses with TRUS, or when TRUS cannot be performed due to the pain or discomfort.

Patients who are immunocompromised, especially patients who have HIV/AIDS, seem to be more susceptible to the development of ABP and to the occurrence of a potentially life-threatening prostatic abscess. The incidence rate rises to roughly 14% in those who have developed AIDS ^[68] (LE: 3). If a prostatic abscess is discovered, initiation of broad-spectrum antibiotics and prompt surgical drainage is crucial ^[6][69] (GR: C).

Microbiology of prostatic abscess

E. coli and Staphylococcus species are the most commonly isolated pathogens in prostatic abscess, although other pathogens, such as Mycobacterium tuberculosis, Actinomyces, Citrobacter, Bacteroides fragilis, Aeromonas aerophyla, and K. pneumonia have been reported ^{[10][39][71]-[76]} (LE: 3). Burkholderia pseudomallei overwhelmingly predominates in the Thai population ^[75]. Increasing cases as a result of methicillin-resistant Staphylococcus aureus (MRSA), both nosocomial and community-acquired, are a growing concern, with >30 cases of prostatic abscess as a result of S. aureus (methicillin-resistant and -sensitive) reported in the literature ^[71].

How to treat the prostatic abscess

Recommended treatment of prostatic abscess consists of broad-spectrum antibiotic coverage and, in most cases, drainage of the abscess. Several surgical procedures have been described to relieve abscess formation. Transurethral incision or resection, suprapubic adenectomy, perineal incision and transrectal or transperineal prostatic puncture and drainage under sonographic guidance have been applied according to location and extension of the abscess ^[3][39] (GR: C &B).

Transperineal incision and drainage ^[77] must be considered when the abscess has penetrated beyond the prostatic capsule or penetrated through the levator ani muscle ^[28][29] (GR: C).

Although transurethral unroofing and perineal drainage were once the mainstays of surgical drainage, TRUS-guided aspiration of prostatic abscesses has been increasingly used as an effective means of drainage that may avoid the potential morbidity associated with transurethral drainage ^[72][78] (GR: B). Some authors also support urinary diversion with a suprapubic catheter ^[39][73]. The follow-up requires regular TRUS controls ^[3][39] (GR: C & B).

In small abscesses, patients may be treated conservatively by the administration of antibiotic agents together with the placement of a suprapubic catheter. According to a multicenter retrospective cohort study, patients with abscesses <20 mm in size did not undergo surgery and were cured without any complications. In contrast, patients with abscesses >20 mm who underwent transurethral resection had a shorter duration of antibiotic treatment than did those who did not have surgery. Early diagnosis is beneficial because prostatic abscesses require prolonged treatment protocols, or even require surgical drainage. Surgical drainage procedures such as transurethral resection of the prostate were not necessary in all patients with prostate abscesses. However, surgical intervention may have potential merits that reduce the antibiotic exposure period and enhance voiding function in patients with prostatic abscess ^[10] (LE: 3).

Abbreviation

ABP: acute bacterial prostatitis, BLI: beta lactamase inhibitor, CBP: chronic bacterial prostatitis, CPPS: chronic pelvic pain syndrome, CRP: C reactive protein, CT: Computer tomography, DRE: Digital rectal examination, EPS: expressed prostatic secretion, ESBL: Extended spectrum beta-lactamase, MRI: magnetic resonance imaging, MRSA: methicillin-resistant Staphylococcus aureus, PSA: prostate-specific antigen, TRPB: transrectal prostate biopsy, TRUS: transrectal ultrasound, UTI: urinary tract infection

References

1. Abrams, P., S. Khoury, and A. Grant, Evidence--based medicine overview of the main steps for developing and grading guideline recommendations. Prog Urol, 2007; 17(3): 681-684.

2. U.S. Department of Health and Human Services Public Health Service Agency for Health Care Policy and Research, 1992; 115-127.

3. Ludwig, M., Diagnosis and therapy of acute prostatitis, epididymitis and orchitis. Andrologia, 2008; 40(2): 76-80.

4. Naber, K.G., Management of bacterial prostatitis: what's new? BJU Int, 2008; 101 Suppl 3: 7-10.

5. Krieger, J.N., L. Nyberg, Jr., and J.C. Nickel, NIH consensus definition and classification of prostatitis. Jama, 1999; 282(3): 236-237.

6. Benway, B.M. and T.D. Moon, Bacterial prostatitis. Urol Clin North Am, 2008; 35(1): 23-32; v.

7. US Department of Health and Human Services Public Health Service, National Center for Health Statistics. National Hospital Discharge Survey Public Use Data Tape Documentation 1994. 1996, Hyattsville, MD: Centers for Disease Control and Prevention.

8. Nickel, J.C., Inflammatory and Pain Conditions of the Male Genitourinary Tract: Prostatitis and Related Pain Conditions, Orchitis, and Epididymitis. In Campbell-Walsh Urology 11th ed., Wein, A.J., Kavoussi, L.R., Partin, A.W., Peters, C.A., editors. 2016; 304-333, ELSEVIER, Philadelphia, PA.

9. Lipsky B. A., Byren I., Hoey C. T. Treatment of bacterial prostatitis. Clin Infect Dis. 2010; 50(12): 1641-1652.

10. Lee D. S., Choe H. S., Kim H. Y., Kim S. W., Bae S. R., Yoon B. I., Lee S. J. Acute bacterial prostatitis and abscess formation. BMC Urol. 2016; 16(1): 38.

11. Yoon B. I., Han D. S., Ha U. S., Lee S. J., Sohn D. W., Kim H. W., Han C. H., Cho Y. H. Clinical courses following acute bacterial prostatitis. Prostate international. 2013; 1(2): 89-93.

12. Nagy V., Kubej D. Acute bacterial prostatitis in humans: current microbiological spectrum, sensitivity to antibiotics and clinical findings. Urologia internationalis. 2012; 89(4): 445-450.

13. Etienne M., Chavanet P., Sibert L., Michel F., Levesque H., Lorcerie B., Doucet J., Pfitzenmeyer P., Caron F. Acute bacterial prostatitis: heterogeneity in diagnostic criteria and management. Retrospective multicentric analysis of 371 patients diagnosed with acute prostatitis. BMC infectious diseases. 2008; 8: 12.

14. Millan-Rodriguez F., Palou J., Bujons-Tur A., Musquera-Felip M., Sevilla-Cecilia C., Serrallach-Orejas M., Baez-Angles C., Villavicencio-Mavrich H. Acute bacterial prostatitis: two different sub-categories according to a previous manipulation of the lower urinary tract. World journal of urology. 2006; 24(1): 45-50.

15. Roberts R. O., Lieber M. M., Bostwick D. G., Jacobsen S. J. A review of clinical and pathological prostatitis syndromes. Urology. 1997; 49(6): 809-821.

16. Coker T. J., Dierfeldt D. M. Acute Bacterial Prostatitis: Diagnosis and Management. American family physician. 2016; 93(2): 114-120.

17. Videcnik Zorman J., Maticic M., Jeverica S., Smrkolj T. Diagnosis and treatment of bacterial prostatitis. Acta dermatovenerologica Alpina, Pannonica, et Adriatica. 2015; 24(2): 25-29.

18. Kirby R. S., Lowe D., Bultitude M. I., Shuttleworth K. E. Intra-prostatic urinary reflux: an aetiological factor in abacterial prostatitis. British journal of urology. 1982; 54(6): 729-731.

19. Wyndaele J. J. Complications of intermittent catheterization: their prevention and treatment. Spinal cord. 2002; 40(10): 536-541.

20. Mosharafa A. A., Torky M. H., El Said W. M., Meshref A. Rising incidence of acute prostatitis following prostate biopsy: fluoroquinolone resistance and exposure is a significant risk factor. Urology. 2011; 78(3): 511-514.

21. Ozden E., Bostanci Y., Yakupoglu K. Y., Akdeniz E., Yilmaz A. F., Tulek N., Sarikaya S. Incidence of acute prostatitis caused by extended-spectrum beta-lactamase-producing Escherichia coli after transrectal prostate biopsy. Urology. 2009; 74(1): 119-123.

22. Ha U. S., Kim M. E., Kim C. S., Shim B. S., Han C. H., Lee S. D., Cho Y. H. Acute bacterial prostatitis in Korea: clinical outcome, including symptoms, management, microbiology and course of disease. Int J Antimicrob Agents. 2008; 31 Suppl 1: S96-101.

23. Brede C. M., Shoskes D. A. The etiology and management of acute prostatitis. Nature reviews Urology. 2011; 8(4): 207-212.

24. Weidner W., Anderson R. U. Evaluation of acute and chronic bacterial prostatitis and diagnostic management of chronic prostatitis/chronic pelvic pain syndrome with special reference to infection/inflammation. Int J Antimicrob Agents. 2008; 31 Suppl 1: S91-95.

25. Wagenlehner, F.M., et al., The role of antibiotics in chronic bacterial prostatitis. Int J Antimicrob Agents, 2005; 26(1): 1-7.

26. Roberts, R.O., et al., A review of clinical and pathological prostatitis syndromes. Urology, 1997; 49(6): 809-821.

27. Etienne, M., et al., Acute bacterial prostatitis: heterogeneity in diagnostic criteria and management. Retrospective multicentric analysis of 371 patients diagnosed with acute prostatitis. BMC Infect Dis, 2008; 8: 12.

28. Nickel, J.C., Lower urinary tract evaluation. Prostatitis and related conditions, in Campbell's urology, P.C. Walsh, Editor. 2002, Saunders: Philadelphia ; London. p.4 v. (xl, 3954 p.).

29. Nickel, J.C., Lower urinary tract evaluation. Prostatitis and related conditions, in Campbell's urology, M.F. Campbell, P.C. Walsh, and A.B. Retik, Editors. 2002, Saunders: Philadelphia, PA.

30. Bonkat G, Bartoletti RR, Bruyère F, et al：EAU Guidelines on Urological Infections. European Association of Urology 2019. [Access date November 2020] https://uroweb.org/guideline/urological-infections

31. Weidner, W. and R.U. Anderson, Evaluation of acute and chronic bacterial prostatitis and diagnostic management of chronic prostatitis/chronic pelvic pain syndrome with special reference to infection/inflammation. Int J Antimicrob Agents, 2008; 31 Suppl 1: S91-95.

32. Etienne M., Pestel-Caron M., Chapuzet C., Bourgeois I., Chavanet P., Caron F. Should blood cultures be performed for patients with acute prostatitis? J Clin Microbiol. 2010; 48(5): 1935-1938.

33. Ludwig M. Diagnosis and therapy of acute prostatitis, epididymitis and orchitis. Andrologia. 2008; 40(2): 76-80.

34. Ulleryd, P., et al., Prostatic involvement in men with febrile urinary tract infection as measured by serum prostate-specific antigen and transrectal ultrasonography. BJU Int, 1999; 84(4): 470-474.

35. Resnick, M.I., Ultrasonic evaluation of the prostate and bladder. Semin Ultrasound, 1980(1): 69.

36. Millan Rodriguez, F., et al., [Management of acute prostatitis: experience with 84 patients]. Arch Esp Urol, 1995; 48(2): 129-136.

37. Rifkin, M.D. and Resnick ML, Ultrasonography of the prostate, in Ultrasonography of the urinary tract, M.I. Resnick and M.D. Rifkin, Editors. 1991, Williams & Wilkins: Baltimore, Md. p. xviii, 502 p.

38. Horcajada, J.P., et al., Transrectal prostatic ultrasonography in acute bacterial prostatitis:findings and clinical implications. Scand J Infect Dis, 2003; 35(2): 114-120.

39. Ludwig, M., et al., Diagnosis and therapeutic management of 18 patients with prostatic abscess. Urology, 1999; 53(2): 340-345.

40. Palmas A. S., Coelho M. F., Fonseca J. F. Color Doppler ultrasonographic scanning in acute bacterial prostatitis. Archivio italiano di urologia, andrologia : organo ufficiale [di] Societa italiana di ecografia urologica e nefrologica. 2010; 82(4): 271-274.

41. Veneziano, S., P. Pavlica, and D. Mannini, Color Doppler ultrasonographic scanning in prostatitis: clinical correlation. Eur Urol, 1995; 28(1): 6-9.

42. Cho, I.R., et al., Prostate blood flow characteristics in the chronic prostatitis/pelvic pain syndrome. J Urol, 2000; 163(4): 1130-1133.

43. Kravchick, S., et al., Acute prostatitis in middle-aged men: a prospective study. BJU Int, 2004; 93(1): 93-96.

44. Velasco, M., et al., Accurate topographical diagnosis of urinary tract infection in male patients with (111)indium-labelled leukocyte scintigraphy. Eur J Intern Med, 2004; 15(3): 157-161.

45. Ulleryd, P., et al., Selective urological evaluation in men with febrile urinary tract infection. BJU Int, 2001; 88(1): 15-20.

46. Mateos, J.J., et al., 111Indium labelled leukocyte scintigraphy in the detection of acute prostatitis. Nucl Med Commun, 2002; 23(11): 1137-1142.

47. Hara, N., et al., Application of serum PSA to identify acute bacterial prostatitis in patients with fever of unknown origin or symptoms of acute pyelonephritis. Prostate, 2004; 60(4): 282-288.

48. Schaeffer, A.J., et al., Treatment of chronic bacterial prostatitis with levofloxacin and ciprofloxacin lowers serum prostate specific antigen. J Urol, 2005; 174(1): 161-164.

49. Neal, D.E., Jr., et al., Prostate specific antigen and prostatitis. I. Effect of prostatitis on serum PSA in the human and nonhuman primate. Prostate, 1992; 20(2): 105-111.

50. Pansadoro, V., et al., Prostate-specific antigen and prostatitis in men under fifty. Eur Urol, 1996; 30(1): 24-27.

51. Gamé, X., et al., Total and free serum prostate specific antigen levels during the first month of acute prostatitis. Eur Urol, 2003; 43(6): 702-705.

52. Kang C. I., Kim J., Park D. W., Kim B. N., Ha U. S., Lee S. J., Yeo J. K., Min S. K., Lee H., Wie S. H. Clinical Practice Guidelines for the Antibiotic Treatment of Community-Acquired Urinary Tract Infections. Infection & chemotherapy. 2018; 50(1): 67-100.

53. Yamamoto S., Ishikawa K., Hayami H., Nakamura T., Miyairi I., Hoshino T., Hasui M., Tanaka K., Kiyota H., Arakawa S. JAID/JSC Guidelines for Clinical Management of Infectious Disease 2015 - Urinary tract infection/male genital infection. J Infect Chemother. 2017; 23(11): 733-751.

54. NICE guideline [NG110], Prostatitis (acute): antimicrobial prescribing. Published date: 31 October 2018. The National Institute for Health and Care Excellence. [Access date November 2020] https://www.nice.org.uk/guidance/ng110

55. Ha, U.S., et al., Acute bacterial prostatitis in Korea: clinical outcome, including symptoms, management, microbiology and course of disease. Int J Antimicrob Agents, 2008; 31 Suppl1: S96-101.

56. Schaeffer, A.J., Diagnosis and treatment of prostatic infections. Urology, 1990; 36(5 Suppl): 13-17.

57. Nickel, J.C., Prostatitis: evolving management strategies. Urol Clin North Am, 1999; 26(4): 737-751.

58. Stevermer, J.J. and S.K. Easley, Treatment of prostatitis. Am Fam Physician, 2000; 61(10): 3015-3022, 3025-3026.

59. Shigehara K., Miyagi T., Nakashima T., Shimamura M. Acute bacterial prostatitis after transrectal prostate needle biopsy: clinical analysis. J Infect Chemother. 2008; 14(1): 40-43.

60. Lee Y., Lee D. G., Lee S. H., Yoo K. H. Risk Factor Analysis of Ciprofloxacin-Resistant and Extended Spectrum Beta-Lactamases Pathogen-Induced Acute Bacterial Prostatitis in Korea. Journal of Korean medical science. 2016; 31(11): 1808-1813.

61. Kim S. H., Ha U. S., Yoon B. I., Kim S. W., Sohn D. W., Kim H. W., Cho S. Y., Cho Y. H. Microbiological and clinical characteristics in acute bacterial prostatitis according to lower urinary tract manipulation procedure. J Infect Chemother. 2014; 20(1): 38-42.

62. Kim J. W., Oh M. M., Bae J. H., Kang S. H., Park H. S., Moon du G. Clinical and microbiological characteristics of spontaneous acute prostatitis and transrectal prostate biopsy-related acute prostatitis: Is transrectal prostate biopsy-related acute prostatitis a distinct acute prostatitis category? J Infect Chemother. 2015; 21(6): 434-437.

63. Park M. G., Cho M. C., Cho S. Y., Lee J. W. Comparison of antibiotic susceptibility of Escherichia coli between community-acquired and post-prostate biopsy acute bacterial prostatitis. Archivos espanoles de urologia. 2019; 72(10): 1018-1025.

64. Qin G. D., Xiao M. Z., Zhou Y. D., Yang J., He H. X., He Y., Zeng Y. Tamsulosin alters levofloxacin pharmacokinetics in prostates derived from rats with acute bacterial prostatitis. Asian journal of andrology. 2013; 15(2): 254-260.

65. Weidner, W., et al., Acute bacterial prostatitis and chronic prostatitis/chronic pelvic pain syndrome: andrological implications. Andrologia, 2008; 40(2): 105-112.

66. Zackrisson B., Ulleryd P., Aus G., Lilja H., Sandberg T., Hugosson J. Evolution of free, complexed, and total serum prostate-specific antigen and their ratios during 1 year of follow-up of men with febrile urinary tract infection. Urology. 2003; 62(2): 278-281.

67. Morote, J., et al., Effect of inflammation and benign prostatic enlargement on total and percent free serum prostatic specific antigen. Eur Urol, 2000; 37(5): 537-540.

68. Leport, C., et al., Bacterial prostatitis in patients infected with the human immunodeficiency virus. J Urol, 1989; 141(2): 334-336.

69. Santillo, V.M. and F.C. Lowe, The management of chronic prostatitis in men with HIV. Curr Urol Rep, 2006; 7(4): 313-319.

70. Millan-Rodriguez, F., et al., Acute bacterial prostatitis: two different sub-categories according to a previous manipulation of the lower urinary tract. World J Urol, 2006; 24(1): 45-50.

71. Ackerman A. L., Parameshwar P. S., Anger J. T. Diagnosis and treatment of patients with prostatic abscess in the post-antibiotic era. Int J Urol. 2018; 25(2): 103-110.

72. Chou, Y.H., et al., Prostatic abscess: transrectal color Doppler ultrasonic diagnosis and minimally invasive therapeutic management. Ultrasound Med Biol, 2004; 30(6): 719-724.

73. Varkarakis, J., et al., Three-dimensional ultrasound guidance for percutaneous drainage of prostatic abscesses. Urology, 2004; 63(6): 1017-1020; discussion 1020.

74. Oliveira, P., et al., Diagnosis and treatment of prostatic abscess. Int Braz J Urol, 2003; 29(1): 30-34.

75. Aphinives, C., et al., Prostatic abscesses: radiographic findings and treatment. J Med Assoc Thai, 2004; 87(7): 810-815.

76. Tai, H.C., Emphysematous prostatic abscess: a case report and review of literature. J Infect,2007; 54(1): e51-54.

77. Granados, E.A., et al., Prostatic abscess: diagnosis and treatment. J Urol, 1992; 148(1): 80-82.

78. Gogus, C., et al., The value of transrectal ultrasound guided needle aspiration in treatment of prostatic abscess. Eur J Radiol, 2004; 52(1): 94-98.