Οξεία και χρόνια βακτηριακή προστατίτιδα παγκόσμιες οδηγίες

[aaa]

Acute and chronic bacterial prostatitis
Authors
Alain Meyrier, MD
Thomas Fekete, MD
Section Editor
Stephen B Calderwood, MD
Deputy Editor
Allyson Bloom, MD
Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: May 2012. |This topic last updated:Φεβ 1, 2012.
INTRODUCTION — The prostate is subject to various inflammatory disorders [1]. In one five-year survey of 58,955 ambulatory visits to clinicians by men over the age of 18 years, genitourinary tract symptoms accounted for 5 percent of all complaints [2]. Prostatitis was listed as a diagnosis in nearly two million encounters annually in the United States National Ambulatory Medical Care Surveys.
Prostatitis syndromes tend to occur in young and middle-aged men. The symptoms of prostatitis are common and often not recognized by clinicians. These symptoms include pain (in the perineum, lower abdomen, testicles, penis, and with ejaculation), bladder irritation, bladder outlet obstruction, and sometimes blood in the semen. Impotence is occasionally attributed to prostatitis; however, it occurs no more commonly than in men of a similar age without prostatitis [3]. In a large population-based Canadian questionnaire study, over 20 percent of the men had complaints compatible with chronic prostatitis, and 8 to 10 percent had moderate to severe symptoms [4]. The men with the most severe symptoms also had poorer general health and recurrent complaints.
Definitions of these syndromes, acute prostatitis, and chronic bacterial prostatitis, will be reviewed here. Chronic prostatitis/pelvic pain syndrome is discussed separately. (See "Chronic prostatitis/chronic pelvic pain syndrome".)
DEFINITIONS — Inflammatory or irritative conditions of the prostate were traditionally classified according to the following schema (table 1) [5]:
•   Acute prostatitis.
•   Chronic bacterial prostatitis.
•   Nonbacterial prostatitis, which presents with similar symptoms and signs as chronic prostatitis (including pyuria) except that cultures of urine and expressed prostatic secretions are negative.
•   Prostatodynia, which also presents with similar symptoms and signs as chronic prostatitis except that the cultures are negative and pyuria is absent.
A classification approach supported by the National Institutes of Health (NIH) to standardize definitions and facilitate research made the following recommendations [6]:
•   Adding an entity called asymptomatic inflammatory prostatitis.
•   Combining nonbacterial prostatitis and prostatodynia into an entity called chronic prostatitis/pelvic pain syndrome.
The inflammatory subset of this syndrome included patients with significant numbers of inflammatory cells in expressed prostatic secretions, post-prostate massage urine or seminal fluid. The noninflammatory chronic prostatitis/pelvic pain subset included the remainder of the patients with chronic prostatitis or pelvic pain. (See "Chronic prostatitis/chronic pelvic pain syndrome".)
Thus, the newer schema defined the following categories:
•   I. Acute prostatitis
•   II. Chronic bacterial prostatitis
•   IIIA. Chronic prostatitis/pelvic pain syndrome, inflammatory
•   IIIB. Chronic prostatitis/pelvic pain syndrome, noninflammatory
•   IV. Asymptomatic inflammatory prostatitis
Maneuvers performed in the urology office can help refine the categorization of patients. For example, including post-massage urine and seminal fluid for the assessment of inflammatory cells effectively doubles the number of people in the inflammatory subset (as compared with the older distinction using only purulent prostatic secretions) [7].
ACUTE PROSTATITIS — Entry of microorganisms into the prostate gland almost always occurs via the urethra. In most cases, bacteria migrate from the urethra or bladder through the prostatic ducts, with intraprostatic reflux of urine. As a result, there may be concomitant infection in the bladder or epididymis.
Risk factors for acute prostatitis are said to include trauma (eg, bicycle or horseback riding), dehydration, and sexual abstinence. However, these have not been established by well controlled studies. Prostatitis can also occur in patients with chronic indwelling bladder catheters and in those who perform intermittent catheterization [8]. A urethral stricture is a possible etiology that should be sought after the acute episode by means of contrast medium urethrography.
Microbiology — The flora of acute prostatitis reflects the spectrum of agents causing urethritis, urinary tract infection, and deeper genital infection. Gram-negative infections, especially with Enterobacteriaceae (typically Escherichia coli or Proteus spp), are most common [9]. Rarely, organisms, such as Burkholderia pseudomallei, have been reported to cause acute prostatitis and prostatic abscess in association with bacteremia [10]. Recurrent infection after completion of therapy is usually caused by the same organism that was found in the original infection [11].
Clinical presentation — The typical signs and symptoms of acute prostatitis include spiking fever, chills, malaise, myalgia, dysuria, pelvic or perineal pain, and cloudy urine. With the exception of fever and chills, these symptoms are similar to those of lower urinary tract infection; it is important to appreciate, however, that isolated acute cystitis does not commonly occur in men, in whom virtually all lower UTIs are due to prostatitis [12,13]. Men with acute cystitis often have a functional or anatomic abnormality, with prostatic hypertrophy and genitourinary instrumentation being the major predispositions to these complicated UTIs.
Swelling of the acutely inflamed prostate can cause obstructive symptoms, ranging from dribbling and hesitancy to acute urinary retention. Rarely, patients lack these local symptoms, and present with the clinical picture of a constitutional or flu-like illness. Clearly, the diagnosis of prostatitis is challenging in this setting.
Early diagnosis and treatment of acute prostatitis are important for both symptom control and the prevention of secondary problems, such as gram-negative sepsis, prostatic abscess, or metastatic infection (eg, spinal or sacroiliac infection) [14].
Diagnosis — Clinical symptoms, together with an edematous and tender prostate on physical examination, should prompt a presumptive diagnosis of acute prostatitis. Digital rectal examination should be performed gently; vigorous prostate massage should be avoided since it is uncomfortable, allows no additional diagnostic or therapeutic benefit, and increases risk for bacteremia.
A urine Gram stain and culture should be obtained in all men suspected of having acute prostatitis. Gram stain of the urine, if positive, can be used as a guide to initial therapy. Confirmatory laboratory findings include pyuria, peripheral leukocytosis, and occasionally, positive blood cultures.
An elevated serum prostate specific antigen (PSA) level is also potentially consistent with a diagnosis of acute prostatitis, although a PSA should not be considered to be a standard diagnostic test for prostatitis. Elective serum PSA for prostate cancer screening should be deferred for one month following acute prostatitis [15]. (See "Measurement of prostate specific antigen".)
Treatment — A variety of antimicrobials may be used for treatment of acute prostatitis. The barrier between the microcirculation and the prostate gland stroma limits drug entry to passive diffusion, which only permits non-protein-bound, lipophilic antimicrobial agents to reach therapeutic levels within the gland. In addition, the low pH of prostatic fluid permits antibiotics with alkaline pKas (such as quinolones and sulfonamides) to achieve high concentrations in prostatic tissue more readily than antibiotics with acidic pKas. However, antibiotic prostatic penetration in the setting of inflammation occurs more readily [16].
Patients with acute bacterial prostatitis may need to be hospitalized for parenteral antibiotic therapy if they cannot tolerate oral medication or if they demonstrate signs of sepsis, such as hypotension or altered mental status. In such cases, shock due to gram-negative bacteremia may occur abruptly and be life threatening.
In general, antibiotic coverage should be administered empirically pending the culture results. A Gram stain of the urine may be helpful in choosing empiric antibiotic coverage. Regional patterns of resistance to various antimicrobials can help in the initial selection of empiric therapy, but clinical response and culture reports will be useful in guiding therapeutic changes.
•   Patients with gram-negative rods should be treated with trimethoprim-sulfamethoxazole (TMP-SMX or cotrimoxazole; one double-strength tab PO every 12 hours) or a fluoroquinolone (ciprofloxacin 500 mg PO every 12 hours or levofloxacin 500 mg PO once daily) if oral therapy is indicated. Other agents with good to excellent penetration into prostatic fluid and tissue include tetracyclines, macrolides, sulfonamides, and nitrofurantoin [17]. For patients who need parenteral therapy, an aminoglycoside (gentamicin or tobramycin 5 mg/kg daily) may be combined with intravenous levofloxacin or ciprofloxacin.
If a urine Gram stain is not performed, the patient should be treated as if infected with gram-negative rods until additional culture data are available.
•   Gram-positive cocci in chains usually indicate enterococcal infection, which should be treated with amoxicillin 500 mg PO every eight hours. If parenteral therapy is necessary, ampicillin can be given at a dose of 2 g IV every six hours.
•   Gram-positive cocci in clusters are most often due to Staphylococcus aureus or coagulase-negative staphylococci (eg, S. epidermidis), which should be treated with a cephalosporin (eg, cephalexin 500 mg PO every six hours) or a penicillinase-resistant penicillin (eg, dicloxacillin 500 mg PO every six hours). Choices for parenteral therapy include cefazolin (1 g IV every eight hours), nafcillin (2 g IV every four to six hours), or for methicillin-resistant S. aureus, vancomycin (30 mg/kg/d in two divided doses with adjustments made for renal insufficiency).
When S. aureus is recovered from a urine culture, it is important to perform blood cultures to be certain the bacteriuria reflects local infection and not seeding of the urine in association with bacteremia. (See "Complications of Staphylococcus aureus bacteremia".)
Nonsteroidal antiinflammatory drugs (NSAIDs) can be given to relieve pain, speed the clearing of inflammation, and liquefy prostatic secretions [18]. Rarely, acute urinary retention develops during an episode of acute prostatitis. In this setting, bladder drainage must be done by suprapubic catheterization. Passage of a catheter through the inflamed urethra into the bladder is contraindicated in patients with acute prostatitis.
Patients initiated on parenteral antibiotics may be switched to oral antibiotics following improvement in fever and clinical symptoms. Antibiotics should be administered for four to six weeks to ensure eradication of the infection [19]. Prolonged therapy is required because of limited antimicrobial penetration into the prostate and the development of protected microcolonies deep within the inflamed gland that are difficult to reach with antimicrobials.
Clinical course — In most cases, fever abates and dysuria disappears within two to six days after the start of therapy. Acute phase reactants (eg, sedimentation rate, C reactive protein) and the PSA, if obtained, return to normal more gradually [15]. Clinical studies using a fluoroquinolone suggest that a negative urine culture at seven days following initiation of therapy predicts cure at the conclusion of the full four to six week course of therapy [20]. If the urine culture is still positive at seven days,

[aaa]

alternative therapy should be considered, based upon in vitro susceptibility tests of the most recent isolate.
Complications — Although most patients with acute prostatitis respond well to antibiotic therapy, a variety of complications can occur, including bacteremia, epididymitis, chronic bacterial prostatitis (see below), and prostatic abscess. Prostatic abscess should be suspected when clinical and laboratory abnormalities persist despite appropriate antimicrobial therapy. The diagnosis of abscess is made by prostate ultrasonography or by computed tomography (CT) scan [21]. Transrectal prostatic ultrasonography is only indicated in acute prostatitis if prostatic abscess is suspected [22].
Although the clinical presentation of prostatic abscess can be confused with other diseases of the prostate, the incidence of prostatic abscess is currently low with the use of appropriate antibiotic therapy. Published case series of prostatic abscess since 1976 have fewer than five patients each, as compared with literature from the 1960s, which included dozens of patients in each of several studies [23]. Urology referral for surgical drainage is indicated if an abscess is persistent after one week or more of therapy.
Bacterial prostatitis and HIV infection — Bacterial prostatitis occurs more frequently in patients with HIV infection than in the general population [24]. Why this occurs is not clear. Anal sex does not seem to be the main triggering factor, since heterosexual men with HIV infection caused by drug abuse are similarly affected.
Signs and symptoms of acute prostatitis in these patients are identical to those described above. There are, however, some differences from the disease seen in non-HIV infected individuals:
•   Various gram-negative organisms have been identified, but some cases are due to unusual organisms, such as Haemophilus parainfluenzae [25].
•   Prostate abscess formation, though rare, appears to be more common in HIV-infected men [26]. It is seldom diagnosed until the patient has failed a trial of antimicrobial therapy.
•   Acute episodes respond favorably to antibiotics, but relapses occur frequently after discontinuation.
The prostate may serve as an asymptomatic reservoir for recurrent infection by certain organisms, such as Cryptococcus neoformans. In one series of AIDS patients, cryptococci were isolated from prostatic secretions at a time when they were not retrieved from blood or cerebrospinal fluid [27].
CHRONIC BACTERIAL PROSTATITIS — Chronic bacterial prostatitis may present as a complication of acute prostatitis, or in the absence of previously recognized initial infection. The diagnosis should be considered in men who have dysuria and frequency in the absence of the signs of acute prostatitis, in those with recurrent urinary tract infections in the absence of bladder catheterization, and in the setting of incidental bacteriuria. In a study of 38 men with recurrent UTIs, for example, about one-half had evidence of infection localized to the prostate (demonstrated by comparing cultures of urine and expressed prostatic secretions) [11].
Gram-negative rods are the most common etiologic agent, with Escherichia coli causing approximately 75 to 80 percent of episodes [28]. Other organisms, including enterococci, gram-negative rods (other than E. coli), and Chlamydia trachomatis have also been associated with chronic infection. Fastidious organisms also play an important role in chronic prostatitis. In a series of 597 patients with chronic prostatitis, for example, Ureaplasma urealyticum was detected using quantitative determination of expressed prostatic secretions and urine voided after prostatic massage from 13 percent of patients. Rarely, fungi or Mycobacterium tuberculosis may be involved [29].
Clinical presentation — Chronic bacterial prostatitis has more subtle clinical findings than acute prostatitis. Patients may be asymptomatic or have complaints typical of a lower urinary tract infection, such as frequency, dysuria, urgency, perineal discomfort, and perhaps a low-grade fever. In some cases, the diagnosis may be suspected by the incidental finding of bacteriuria. Sexual dysfunction may accompany chronic bacterial prostatitis [30]. Rectal examination may demonstrate prostatic hypertrophy, tenderness, and edema, but is frequently normal.
Diagnosis — The diagnosis of chronic prostatitis can be made by analyzing specimens obtained following prostatic massage for leukocytes and bacteria. The periurethral area is cleaned and four samples are taken -- the so-called four-glass test [28]. The initial 5 to 10 mL (VB1) and a midstream specimen (VB2) are obtained for quantitative culture. The patient should stop voiding before the bladder is empty and the prostate should then be massaged. Any prostatic secretions that are expressed (EPS) should be cultured and have a leukocyte count performed, as well as the first 5 to 10 mL of subsequently voided urine (VB3) (figure 1). (See "Urine sampling and culture in the diagnosis of urinary tract infection in adults".)
For the test to be interpretable, the colony count in VB2 must be less than 103/mL, since bladder bacteriuria prevents identification of the frequently small number of organisms from the prostate. Chronic prostatitis is suspected when VB3 has more than 12 leukocytes per high power field; more than 20 leukocytes per high power field is almost diagnostic unless leukocytes were also present in VB2 [12].
Cultures of urine or expressed prostatic secretions are almost always positive in chronic bacterial prostatitis (table 1). However, negative cultures do not necessarily exclude the possibility of bacterial prostatitis. One study found that some patients with chronic bacterial prostatitis had positive cultures of prostate tissue despite negative cultures of expressed prostatic fluid [31].
Although the four-glass test is described extensively in the literature, it is not clear that it is frequently used in practice. In one survey of urologists in which 64 percent responded, 33 and 47 percent, respectively, said that they never or rarely performed the four-glass test [32]. Furthermore, the results of the test apparently did not influence the use of antibiotics, since urologists who used the test routinely did not differ in antibiotic prescribing from others who used it less often.
Ultrasonography may also be useful for evaluation of prostatitis sequelae, including prostatic abscess (see 'Complications' above) and prostatic calcification [33].
Chlamydia infection — Although it has not been clearly established that Chlamydia trachomatis can cause chronic bacterial prostatitis, it is thought to be a possible cause in cases in which routine cultures are negative. Chlamydial genital infections are common and may involve the epididymis and the urethra. C. trachomatis has been isolated from the prostate, and there is some evidence that it resides in prostate tissue rather than being brought along with other urethral contaminants [34,35]. Cultures for Chlamydia or other unusual pathogens are seldom obtained until a thorough diagnostic workup has been completed. Culturing for C. trachomatis is beyond the capacity of most laboratories because of the technical demands involved. On the other hand, diagnostic tests to look for chlamydial antigens or nucleic acids have been developed and these tests can easily be done on genital secretions or urine. Because these tests are highly sensitive and specific, they may be able to settle the question of whether C. trachomatis causes prostatitis if the tests can be performed on prostate tissue and show positive results when Chlamydia are not found in urine or other genital secretions. (See "Genital Chlamydia trachomatis infections in men".)
Treatment — Selection of agents for and duration of therapy for chronic prostatitis have not been studied using comparative trials. In case series, there has been a general sense that various fluoroquinolone regimens (eg, ciprofloxacin 500 mg PO every 12 hours or levofloxacin 500 mg PO daily) have a satisfactory outcome in about two-thirds of patients who can tolerate them for four weeks or longer. Failures of therapy appear to be related to underlying prostate disease, infecting agent, incomplete adherence, drug interactions that reduce fluoroquinolone bioavailability, or to some other less understood component. (See "Fluoroquinolones", section on 'Drug interactions'.)
Recurrences of chronic bacterial prostatitis are common and are generally treated with a second course of antibiotics. If the first course was less than six weeks, a longer second course is recommended, preferably with an antibiotic from a different class with efficacy against usual pathogens responsible for prostatitis (eg, trimethoprim-sulfamethoxazole); in some cases, a second course of a fluoroquinolone can be given. Courses exceeding four weeks should also be considered in patients who have previously failed treatment, who have a relatively difficult to treat organism, or who cannot tolerate first line therapy and need other agents. In patients requiring an extended course of antibiotics due to relapse or failure to respond to a course of a fluoroquinolone, causes of impaired bioavailability of the fluoroquinolone should be sought (see "Fluoroquinolones", section on 'Drug interactions'). Tendinitis and tendon rupture are important adverse effects that have been reported in patients requiring prolonged fluoroquinolone therapy, especially in patients >60 years of age [36]. Among patients in this age group, those receiving glucocorticoids are at the highest risk. (see "Fluoroquinolones", section on 'Tendinopathy and tendon rupture'). In patients with pelvic pain syndromes in whom there is no evidence of prostatic inflammation or infection, the success rate of any antimicrobial therapy is much lower.
C. trachomatis infection can be treated with doxycycline, minocycline, or azithromycin [37,38], but use of these drugs in prostatic infections is not reported separately. One study compared azithromycin (500 mg daily for three days each week for three weeks) with ciprofloxacin (500 mg twice daily for 20 days) in 89 patients with chronic prostatitis and laboratory evidence of C. trachomatis infection [39]. The rate of bacterial eradication and clinical cure was significantly higher among the patients treated with azithromycin.
Chronic bacterial prostatitis often recurs and is usually treated with a second course of antibiotics. A fluoroquinolone is once again the treatment of choice. One report, for example, evaluated 33 patients with chronic bacterial prostatitis who had failed therapy with trimethoprim, TMP-SMX, or norfloxacin; the patients were retreated with ciprofloxacin (500 mg twice daily) for two to four weeks [40]. The following results were noted:
•   Of 26 patients with E. coli as the pathogen, 17 were cured at greater than one year follow-up. In another two, a second treatment course with ciprofloxacin was successful. Two patients withdrew from therapy due to adverse drug reactions.
•   Therapy was successful in two of five with pathogens other than E. coli.
In another report, 15 patients refractory to TMP-SMX and/or carbenicillin were treated with norfloxacin (400 mg twice daily) for 28 days. Of the 14 patients followed for at least six months, nine (64 percent) infected with E. coli were cured [41]. Similar results have been noted in other studies [42].
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
•   Basics topic (see "Patient information: Prostatitis (The Basics)")
ALTERNATIVE PERSPECTIVE ON THE TREATMENT OF BACTERIAL PROSTATITIS — As noted above, it is frequently difficult to distinguish which patients with chronic symptoms actually have chronic bacterial prostatitis. A group of urologists in Canada utilized leukocyte counts, cultures, and antibody determinations for common uropathogens before and after prostatic massage to try to differentiate among these patients and then treated all with ofloxacin (300 mg PO twice daily for 12 weeks) [43]. Fifty-seven percent of the 102 patients reported a moderate to marked improvement in symptoms which did not correlate with any of the measures of bacterial infection. The authors

[aaa]

concluded that placebo-controlled studies are required to assess the role of antibiotic therapy and suggested that these studies might best be performed in a mixed group of patients with chronic prostatitis.
A network meta-analysis of treatment for chronic prostatitis/chronic pelvic pain syndrome found little evidence that a single strategy is likely to succeed in most patients, but there is some evidence that alpha-blockers, antibiotics, anti-inflammatories, finasteride, and physical therapy might all play a role [44]. Unfortunately, the quality and number of studies looking at these interventions is low and there could also be publication bias (especially with alpha-blockers). This review found only three studies comparing antibiotics to placebo and the total number of patients in both arms of these studies was about 200.
SUMMARY AND RECOMMENDATIONS
•   Prostatitis can be divided into the following categories:
•   I. Acute prostatitis
•   II. Chronic bacterial prostatitis
•   IIIA. Chronic prostatitis/pelvic pain syndrome, inflammatory
•   IIIB. Chronic prostatitis/pelvic pain syndrome, noninflammatory
•   IV. Asymptomatic inflammatory prostatitis (See 'Definitions' above.)
Acute prostatitis
•   Acute prostatitis is generally caused by the same organisms that cause urinary tract infections and urethritis. Gram-negative infections, especially with Enterobacteriaceae (typically Escherichia coli or Proteus spp), are most common. (See 'Microbiology' above.)
•   The most common symptoms of acute prostatitis are fevers, chills, dysuria, pelvic or perineal pain, and cloudy urine; obstructive symptoms, such as dribbling of urine, can also occur. (See 'Clinical presentation' above.)
•   Early diagnosis and treatment of acute prostatitis are important for both symptom control and the prevention of secondary problems, such as gram-negative sepsis, prostatic abscess, or metastatic infection (eg, spinal or sacroiliac infection). (See 'Clinical presentation' above.)
•   A combination of symptoms and a tender prostate on rectal examination makes the diagnosis. Digital rectal examination should be performed gently; vigorous prostate massage should be avoided since it is uncomfortable, allows no additional diagnostic or therapeutic benefit, and increases risk for bacteremia. (See 'Diagnosis' above.)
•   A urine Gram stain and culture should be obtained in all men suspected of having acute prostatitis. Gram stain of the urine, if positive, can be used as a guide to initial therapy. (See 'Diagnosis' above.)
•   Initial antibiotic treatment should cover gram-negative organisms (eg, trimethoprim-sulfamethoxazole or a fluoroquinolone) until cultures return. If parenteral therapy is required due to the toxic appearance of the patient, an aminoglycoside is frequently combined with a fluoroquinolone. Oral therapy can be initiated after the patient has been afebrile for 24 to 48 hours. (See 'Treatment' above.)
•   The total duration of antibiotics is four to six weeks to ensure eradication of the organisms. (See 'Treatment' above.)
Chronic bacterial prostatitis
•   Chronic bacterial prostatitis has more subtle clinical findings than acute prostatitis. Chronic bacterial prostatitis should be considered in men with dysuria and frequency who do not have symptoms of acute prostatitis or in those with recurrent UTIs in the absence of a bladder catheter. The infection is usually caused by gram-negative rods. (See 'Chronic bacterial prostatitis' above.)
•   The four-glass test is a method for collecting urine and prostatic secretions for quantitative analysis of leukocytes and bacteria (figure 1), but this test is not usually performed in clinical practice. Cultures of urine or expressed prostatic secretions are almost always positive in chronic bacterial prostatitis (table 1). (See 'Diagnosis' above.)
•   Chlamydia trachomatis should be considered in patients with clinical evidence of chronic prostatitis and negative results of urine and prostatic secretion cultures. (See 'Chlamydia infection' above.)
•   The fluoroquinolones are the most common antibiotics used in treatment of chronic bacterial prostatitis since they penetrate the less inflamed prostate well. The duration of treatment for chronic bacterial prostatitis is commonly four weeks. Courses exceeding four weeks should be considered only in patients who have previously failed treatment, who have a relatively difficult to treat organism, or who cannot tolerate first line therapy and need other agents. (See 'Treatment' above.)
•   C. trachomatis infection can be treated with doxycycline, minocycline, or azithromycin. (See 'Treatment' above.)
•   Recurrences of chronic bacterial prostatitis are common and are generally treated with a second course of antibiotics. If the first course was less than six weeks, a longer second course is recommended, preferably with an antibiotic from a different class with efficacy against usual pathogens responsible for prostatitis (eg, trimethoprim-sulfamethoxazole); in some cases, a second course of a fluoroquinolone can be given. (See 'Treatment' above.)
Use of UpToDate is subject to the Subscription and License Agreement.
REFERENCES
1.   Pontari MA, Joyce GF, Wise M, et al. Prostatitis. J Urol 2007; 177:2050.
2.   Collins MM, Stafford RS, O'Leary MP, Barry MJ. How common is prostatitis? A national survey of physician visits. J Urol 1998; 159:1224.
3.   Krieger JN, Egan KJ, Ross SO, et al. Chronic pelvic pains represent the most prominent urogenital symptoms of "chronic prostatitis". Urology 1996; 48:715.
4.   Nickel JC, Downey J, Hunter D, Clark J. Prevalence of prostatitis-like symptoms in a population based study using the National Institutes of Health chronic prostatitis symptom index. J Urol 2001; 165:842.
5.   Leigh DA. Prostatitis--an increasing clinical problem for diagnosis and management. J Antimicrob Chemother 1993; 32 Suppl A:1.
6.   Krieger JN, Nyberg L Jr, Nickel JC. NIH consensus definition and classification of prostatitis. JAMA 1999; 282:236.
7.   Krieger JN, Jacobs RR, Ross SO. Does the chronic prostatitis/pelvic pain syndrome differ from nonbacterial prostatitis and prostatodynia? J Urol 2000; 164:1554.
8.   Wyndaele JJ. Complications of intermittent catheterization: their prevention and treatment. Spinal Cord 2002; 40:536.
9.   Cornia PB, Takahashi TA, Lipsky BA. The microbiology of bacteriuria in men: a 5-year study at a Veterans' Affairs hospital. Diagn Microbiol Infect Dis 2006; 56:25.
10.   Heyse AM, Dierick J, Vanhouteghem H, et al. A case of imported melioidosis presenting as prostatitis. Infection 2003; 31:60.
11.   Smith JW, Jones SR, Reed WP, et al. Recurrent urinary tract infections in men. Characteristics and response to therapy. Ann Intern Med 1979; 91:544.
12.   Orland SM, Hanno PM, Wein AJ. Prostatitis, prostatosis, and prostatodynia. Urology 1985; 25:439.
13.   Lipsky BA. Urinary tract infections in men. Epidemiology, pathophysiology, diagnosis, and treatment. Ann Intern Med 1989; 110:138.
14.   Siroky MB, Moylan R, Austen G Jr, Olsson CA. Metastatic infection secondary to genitourinary tract sepsis. Am J Med 1976; 61:351.
15.   Gamé X, Vincendeau S, Palascak R, et al. Total and free serum prostate specific antigen levels during the first month of acute prostatitis. Eur Urol 2003; 43:702.
16.   Aagaard J, Madsen PO. Bacterial prostatitis: new methods of treatment. Urology 1991; 37:4.
17.   Charalabopoulos K, Karachalios G, Baltogiannis D, et al. Penetration of antimicrobial agents into the prostate. Chemotherapy 2003; 49:269.
18.   Canale D, Turchi P, Giorgi PM, et al. Treatment of abacterial prostato-vesiculitis with nimesulide. Drugs 1993; 46 Suppl 1:147.
19.   Wagenlehner FM, Weidner W, Naber KG. Therapy for prostatitis, with emphasis on bacterial prostatitis. Expert Opin Pharmacother 2007; 8:1667.
20.   Arakawa S, Kamidono S. Assessment of the UTI criteria for bacterial prostatitis in Japan. Infection 1992; 20 Suppl 3:S232.
21.   Chia JK, Longfield RN, Cook DH, Flax BL. Computed axial tomography in the early diagnosis of prostatic abscess. Am J Med 1986; 81:942.
22.   Horcajada JP, Vilana R, Moreno-Martínez A, et al. Transrectal prostatic ultrasonography in acute bacterial prostatitis: findings and clinical implications. Scand J Infect Dis 2003; 35:114.
23.   Weinberger M, Cytron S, Servadio C, et al. Prostatic abscess in the antibiotic era. Rev Infect Dis 1988; 10:239.
24.   Leport C, Rousseau F, Perronne C, et al. Bacterial prostatitis in patients infected with the human immunodeficiency virus. J Urol 1989; 141:334.
25.   Clairmont GJ, Zon LI, Groopman JE. Hemophilus parainfluenzae prostatitis in a homosexual man with chronic lymphadenopathy syndrome and HTLV-III infection. Am J Med 1987; 82:175.
26.   Trauzzi SJ, Kay CJ, Kaufman DG, Lowe FC. Management of prostatic abscess in patients with human immunodeficiency syndrome. Urology 1994; 43:629.
27.   Larsen RA, Bozzette S, McCutchan JA, et al. Persistent Cryptococcus neoformans infection of the prostate after successful treatment of meningitis. California Collaborative Treatment Group. Ann Intern Med 1989; 111:125.
28.   Schaeffer AJ. Clinical practice. Chronic prostatitis and the chronic pelvic pain syndrome. N Engl J Med 2006; 355:1690.
29.   Meares, EM Jr. Prostatitis: A review. Urol Clin North Am 1975; 2:3.
30.   Müller A, Mulhall JP. Sexual dysfunction in the patient with prostatitis. Curr Opin Urol 2005; 15:404.
31.   Nickel JC, Costerton JW. Bacterial localization in antibiotic-refractory chronic bacterial prostatitis. Prostate 1993; 23:107.
32.   McNaughton Collins M, Fowler FJ Jr, Elliott DB, et al. Diagnosing and treating chronic prostatitis: do urologists use the four-glass test? Urology 2000; 55:403.
33.   Shoskes DA, Lee CT, Murphy D, et al. Incidence and significance of prostatic stones in men with chronic prostatitis/chronic pelvic pain syndrome. Urology 2007; 70:235.
34.   Bruce AW, Reid G. Prostatitis associated with Chlamydia trachomatis in 6 patients. J Urol 1989; 142:1006.
35.   Poletti F, Medici MC, Alinovi A, et al. Isolation of Chlamydia trachomatis from the prostatic cells in patients affected by nonacute abacterial prostatitis. J Urol 1985; 134:691.
36.   van der Linden PD, Sturkenboom MC, Herings RM, et al. Fluoroquinolones and risk of Achilles tendon disorders: case-control study. BMJ 2002; 324:1306.
37.   Martin DH, Mroczkowski TF, Dalu ZA, et al. A controlled trial of a single dose of azithromycin for the treatment of chlamydial urethritis and cervicitis. The Azithromycin for Chlamydial Infections Study Group. N Engl J Med 1992; 327:921.
38.   Chiarini F, Mansi A, Tomao P, et al. Chlamydia trachomatis genitourinary infections: laboratory diagnosis and therapeutic aspects. Evaluation of in vitro and in vivo effectiveness of azithromycin. J Chemother 1994; 6:238.
39.   Skerk V, Schönwald S, Krhen I, et al. Comparative analysis of azithromycin and ciprofloxacin in the treatment of chronic prostatitis caused by Chlamydia trachomatis. Int J Antimicrob Agents 2003; 21:457.
40.   Weidner W, Schiefer HG. Chronic bacterial prostatitis: therapeutic experience with ciprofloxacin. Infection 1991; 19 Suppl 3:S165.
41.   Schaeffer AJ, Darras FS. The efficacy of norfloxacin in the treatment of chronic bacterial prostatitis refractory to trimethoprim-sulfamethoxazole and/or carbenicillin. J Urol 1990; 144:690.
42.   Weidner W, Schiefer HG, Brähler E. Refractory chronic bacterial prostatitis: a re-evaluation of ciprofloxacin treatment after a median followup of 30 months. J Urol 1991; 146:350.
43.   Nickel JC, Downey J, Johnston B, et al. Predictors of patient response to antibiotic therapy for the chronic prostatitis/chronic pelvic pain syndrome: a prospective multicenter clinical trial. J Urol 2001; 165:1539.
44.   Anothaisintawee T, Attia J, Nickel JC, et al. Management of chronic prostatitis/chronic pelvic pain syndrome: a systematic review and network meta-analysis. JAMA 2011; 305:78.