Prostatitis and chronic pelvic pain

• Prostatitis is an umbrella term. The most useful modern division, from the United States National Institutes of Health (NIH), separates confirmed or suspected infection (acute bacterial prostatitis, type I, and chronic bacterial prostatitis, type II) from chronic pelvic pain syndrome (type III), which has no proven infection or other obvious local pathology, plus the symptomless, incidental type IV. ^[1]
• Fewer than 1 in 10 men who receive a diagnosis of prostatitis have proven bacterial infection. ^[1]
• Acute bacterial prostatitis is a febrile, systemic illness: it presents abruptly with voiding symptoms, pelvic or perineal pain and often fever and malaise, and it is most often due to gut bacteria, especially Escherichia coli. ^[1]
• Chronic bacterial prostatitis is defined by symptoms lasting at least three months. ^[1] It is diagnosed by localising cultures (the two-glass or four-glass test), and is treated with a fluoroquinolone, or with azithromycin, doxycycline or metronidazole when the pathogen is atypical. ^[1]
• Chronic pelvic pain syndrome is now called primary prostate pain syndrome when the pain is perceived in the prostate. It is managed as a biopsychosocial pain condition using phenotype-guided, multimodal care rather than repeated or prolonged antibiotics. ^[2][3]
• Diagnosis rests on the story and simple bedside tests (dipstick, culture), plus localising cultures in chronic disease. Imaging is used to find complications (abscess, urinary retention), not to label the illness. ^[1]

By the end of this page you should be able to:

1. Use the NIH classification to place a patient with pelvic pain into acute bacterial, chronic bacterial, chronic pelvic pain syndrome or asymptomatic inflammatory prostatitis.
2. Explain why most cases of clinically labelled prostatitis are not bacterial, and why that changes management.
3. Take a focused history and examination, including digital rectal examination, and know when prostatic massage must be avoided.
4. Choose and interpret the right tests (dipstick, culture, two- or four-glass localising tests, imaging) for acute and chronic disease.
5. Treat acute bacterial prostatitis (empirical regimen, route, duration, complications) and chronic bacterial prostatitis (drug, atypical pathogen, duration).
6. Apply the current approach to chronic pelvic pain syndrome: assessment of psychological, sexual, pelvic floor and systemic features; when (and when not) to use antibiotics, alpha-blockers, anti-inflammatory drugs and other agents; and low-resource adaptations.
7. Cross-check prostatitis against urinary tract infection and avoid the common errors of over-diagnosing infection or over-treating pain with antibiotics.

The modern working definition is clinical: prostatitis is a syndrome, not a single disease. ^[1][2] Because the old label "prostatitis" was applied to almost any chronic pelvic pain in men, treatment failures and unnecessary antibiotic courses were common. The contemporary approach separates infections from pain syndromes. ^[1][2]

The most widely used classification is from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) of the United States National Institutes of Health (NIH), and the EAU guidelines recommend that clinicians use it. ^[1] It is:

The chronic pelvic pain guideline prefers the term primary prostate pain syndrome for the type III picture with pain perceived in the prostate, because ending the name in "itis" wrongly suggests infection or inflammation. ^[2] Under the older naming, type III was also called chronic non-bacterial prostatitis or chronic prostatitis.

Both sets of terms are still used in practice. Throughout this page, "chronic bacterial prostatitis" is reserved for the confirmed-infection form (NIH type II) and "chronic pelvic pain syndrome" for the non-infection form (NIH type III, also called primary prostate pain syndrome).

Prostatitis is one of the most common reasons for a man to see a urologist. ^[1] However, fewer than 1 in 10 men who receive the diagnosis have proven bacterial infection. ^[1] The clinical lesson is striking: if 10 men are told they have prostatitis, fewer than 1 of them is likely to benefit from an antibiotic.

Acute bacterial prostatitis and chronic bacterial prostatitis are a minority of the caseload. Chronic bacterial prostatitis and acute bacterial prostatitis are a minority of the caseload; the non-bacterial (inflammatory) form accounts for the large majority of cases. ^[1][2]

The microbiology differs between the two bacterial forms:

• Acute bacterial prostatitis is caused mainly by Enterobacterales, especially Escherichia coli. ^[1]
• Chronic bacterial prostatitis has a wider spectrum and may include atypical organisms such as Chlamydia trachomatis, Trichomonas vaginalis or Ureaplasma urealyticum; the significance of intracellular organisms is debated. ^[1]
• In one retrospective series of 1,442 men with the prostatitis syndrome, an infectious cause was found in 74.2% overall, but Escherichia coli accounted for only 6.6% of these cases, while Chlamydia trachomatis, Trichomonas vaginalis and Ureaplasma urealyticum were found in 37.2%, 10.5% and 5% respectively. ^[1] This is a reminder that in chronic disease, the ordinary urine pathogen is often not the organism.

HIV infection and other immunodeficiency states broaden the spectrum further: prostatitis may be caused by Mycobacterium tuberculosis, Candida species or fungi such as Coccidioides immitis, Blastomyces dermatitidis and Histoplasma capsulatum. ^[1]

A particular clinical trap is the young man with asymptomatic bacteriuria. In a premenopausal woman, asymptomatic bacteriuria is usually harmless; in a younger man it is uncommon enough that chronic bacterial prostatitis should be considered before it is dismissed. ^[1]

Escherichia coli and the other Enterobacterales are the predominant pathogens in acute bacterial prostatitis, usually arriving from the lower urinary tract by ascent through the urethra and into the prostatic ducts. ^[1] The infection is therefore best understood as the prostatic extension of the same process that causes pyelonephritis. This is why it counts as a systemic urinary tract infection in the EAU 2026 scheme. ^[1]

Risk factors that increase the chance or severity of an episode include recent instrumentation, transrectal prostate biopsy and pre-existing obstruction (benign prostatic enlargement, urethral stricture, prostate cancer). ^[1] Transrectal biopsy in particular increases the risk of acute bacterial prostatitis despite antibiotic prophylaxis and antiseptic preparation. ^[1]

The spectrum is wider. ^[1] Atypical and intracellular organisms (Chlamydia trachomatis, genital mycoplasmas) may be involved. ^[1] Levofloxacin did not demonstrate significant clearance of Chlamydia trachomatis in patients with chronic bacterial prostatitis, which is why macrolides or tetracyclines are chosen when these organisms are detected. ^[1]

This is not a bacterial illness. It is better understood as a multidimensional chronic pain syndrome in which low-grade inflammation and immune dysregulation, peripheral and central sensitisation (nerve sensitisation), microbiome disturbance, autonomic imbalance and psychosocial amplification each contribute. ^[2][3] The term "chronic prostatitis" continues to be equated with it, but the infection meaning is not the mechanism. ^[2]

Phenotypes vary between men. Suggestive features include pelvic or perineal pain worsened by ejaculation or micturition, lower urinary tract symptoms, sexual dysfunction, sleep disturbance and emotional distress. ^[3]

In acute bacterial prostatitis, bacteria ascend from the urethra into the prostate, multiply within the glandular ducts and elicit an intense inflammatory response. Pyogenic inflammation of a gland enclosed in a tight fibrous capsule raises tissue pressure; that is why pain is often severe, why fever is common, and why pus can form an abscess. ^[1]

The inflammatory process spreads the infection into the systemic circulation, producing the systemic illness picture. Urinary retention may occur both because of inflammatory swelling at the bladder neck and because pain makes the patient reluctant to void. ^[1]

Chronic bacterial prostatitis is best understood as a persistent reservoir of bacteria within the prostate. The gland itself is a pharmacological sanctuary: many antibiotics penetrate it poorly. This is the main reason treatment is prolonged and why recurrence is common. ^[1][2]

Here the problem is not persistent infection but a pain system that has become sensitised. ^[2][3] Peripheral nociceptors become hyperexcitable, so sensations that should be painless (bladder filling, straining at defaecation, ejaculation) become painful; central sensitisation in the spinal cord and brain spreads and prolongs the pain. ^[3] The result is a syndrome that behaves like a neuropathic pain condition, with flares, allodynia (pain from a touch that should not hurt) and pain extending into the lower abdomen, scrotum or perineum. ^[3]

The bladder and prostate are usually structurally normal at cystoscopy and imaging, which helps to explain why repeated investigations find nothing and why "prostate-centred" treatment fails. ^[2][3]

In the patient's own words, acute bacterial prostatitis declares itself suddenly. Typical features: ^[1]

• dysuria and a burning feeling on passing urine
• urinary frequency and urgency, with small volumes
• pelvic, perineal or suprapubic pain, often poorly localised and severe
• low back or flank pain in some men
• fever, chills, rigors and malaise
• nausea or vomiting when the infection is severe

The patient usually looks unwell.

On examination, the prostate is swollen and exquisitely tender on digital rectal examination. ^[1] Because prostatic massage can force bacteria into the bloodstream and precipitate septicaemia, it must be avoided in acute bacterial prostatitis. ^[1]

Who is at risk: men with recent urological instrumentation or transrectal biopsy, with obstruction from benign prostatic enlargement, stricture, or prostate cancer, and men with an indwelling catheter. ^[1]

Pain must have been present for at least three months. ^[1] Typical features: ^[1]

• pain at various sites: perineum, scrotum, penis, inner thigh, lower back, lower abdomen, or tip of the penis
• lower urinary tract symptoms of the irritative type: frequency, urgency, dysuria
• occasional haematuria or haemospermia, especially after ejaculation
• symptoms that recur with fresh urine infection

The clinical picture is dominated by pain, not fever. The patient does not usually look unwell between episodes. Symptoms may improve with antibiotics and then relapse when the course stops. ^[1]

Digital rectal examination is usually non-diagnostic in chronic disease: the prostate may feel normal, boggy or only slightly tender. The important work is diagnostic, not examination-based.

This is diagnosed by the absence of proven infection or other obvious local pathology, with pain perceived in the prostate region for at least three months. ^[2] It is reproduced convincingly by palpation of the prostate. ^[2] Associated features are: ^[2][3]

• lower urinary tract symptoms
• sexual dysfunction (erectile difficulty, ejaculatory pain)
• sleep disturbance and fatigue
• anxiety or depressed mood
• pelvic floor muscle tenderness

A 32 year old man who has had 4 months of perineal ache that flares after ejaculation, with no fever and repeated negative urine cultures, has chronic pelvic pain syndrome, not chronic bacterial prostatitis, and will not benefit from repeated antibiotic courses. ^[2] The diagnostic label itself is useful: studies show that naming the condition helps the patient accept it as chronic and engage with stepped care. ^[2]

The pain of prostatitis is non-specific and easily mistaken for other pelvic, anorectal and urological conditions. The common confusions and the clues that separate them:

Note: links to other MedGrasp topics are shown as plain text here: benign prostatic hyperplasia, urinary tract infection, prostate cancer, interstitial cystitis and bladder pain syndrome, sepsis.

The work-up is intentionally limited. The aim is to confirm or refute infection, to find atypical organisms in chronic disease, and to exclude complications.

• Midstream urine dipstick for nitrite and leukocytes has a reported positive predictive value of 95% and a negative predictive value of 70%. ^[1]
• Urine culture is the most important investigation. ^[1]
• Blood culture and full blood count are useful, because bacteraemia is common. ^[1]
• Imaging (transrectal ultrasound, and cross-sectional imaging when an abscess is suspected) is used to detect a suspected prostatic abscess or to rule it out. ^[1]
• Uroflowmetry or urethrography when bladder outflow obstruction is suspected.
• Digital rectal examination if safe. Do not perform prostatic massage. ^[1]
• PSA testing is best avoided in acute prostatitis. ^[1] Levels rise in about 60% of men with acute bacterial prostatitis and fall after treatment, so a result taken during an episode cannot be compared with screening values; recheck later if cancer screening is otherwise indicated. ^[1]

• Meares and Stamey localising cultures (the four-glass test): quantitative bacteriological culture of the first-void urine, midstream urine, expressed prostatic secretion (EPS) and a post-massage urine specimen. This is the optimum test for categorising chronic bacterial prostatitis. ^[1]
• The two-glass test (pre- and post-massage urine) has shown similar diagnostic sensitivity and is simpler. ^[1]
• Microscopy of EPS for white cells divides the "non-bacterial" type III into inflammatory (IIIA) and non-inflammatory (IIIB), although the distinction changes little in practice.
• Semen culture improves the diagnostic yield of the four-glass test but is more often positive than expected in men with non-bacterial prostatitis; sensitivity is around 50%, so it is not routine. ^[1]
• Testing for atypical pathogens (Chlamydia trachomatis, Mycoplasma species) by nucleic acid amplification on first-void urine. ^[1]
• Transrectal ultrasound is unreliable as a diagnostic tool for prostatitis and is reserved for suspected abscess or calcification. ^[1]
• PSA is raised in about 20% of men with chronic bacterial prostatitis and adds no practical diagnostic information. ^[1]
• Prostate biopsy cannot be recommended in routine work-up and is not advisable in untreated bacterial prostatitis because of the risk of sepsis. ^[1]

There is no single test that diagnoses either bacterial prostatitis or chronic pelvic pain syndrome. The diagnosis is clinical, supported by the tests above.

• Acute bacterial prostatitis: sudden onset voiding and pelvic pain symptoms in a systemically unwell man, with a tender prostate on digital rectal examination and supportive urinalysis and culture. ^[1]
• Chronic bacterial prostatitis: symptoms (pain with or without voiding symptoms) for at least three months with a localised culture showing the same organism in post-massage or expressed prostatic secretion at higher counts than in pre-massage urine, as in the Meares and Stamey method. ^[1]
• Chronic pelvic pain syndrome / primary prostate pain syndrome: at least three months of pelvic pain, reproduced by prostate palpation, with no proven infection or other obvious local pathology; often associated with urinary, sexual, bowel, pelvic floor or gynaecological dysfunction and with negative cognitive, behavioural, sexual or emotional consequences. ^[2]

Severity measurement. For chronic disease the National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI) is a widely used research and clinical tool; it quantifies pain, urinary symptoms and quality of life. A fall of at least 6 points in the total score is commonly taken as clinically meaningful. ^[3]

The treatment approach is that of a systemic urinary tract infection with prostatic involvement. ^[1]

Immediate care.

• Empirical parenteral therapy with broad-spectrum bactericidal antimicrobials: a broad-spectrum penicillin, a third-generation cephalosporin or a fluoroquinolone, with the option of adding an aminoglycoside. ^[1]
• Adequate fluid intake and urine drainage. About 1 in 10 men with acute bacterial prostatitis develop urinary retention, which can be managed by urethral or suprapubic catheterisation; in recent evidence suprapubic drainage reduces the later development of chronic bacterial prostatitis. ^[1]
• Supportive care and analgesia; the EAU 2026 systemic UTI recommendations should be followed for complicated cases, including cross-sectional imaging when the patient is severely ill or remains unwell after 48 to 72 hours of appropriate treatment. ^[1]

Step-down. After normalisation of infection markers, oral therapy can be substituted and continued for a total of two to four weeks. ^[1]

Cross-checking with urinary tract infection: the standard systemic urinary tract infection regimens are repurposed here. Typical oral outpatient regimens for systemic urinary tract infection include ciprofloxacin 500 to 750 mg by mouth twice daily for 7 days and levofloxacin 500 mg once daily (standard) or 500 mg twice daily (high dose) for 5 days; parenteral step-down often uses ceftriaxone 2 g intravenously once daily (standard) or 2 g intravenously twice daily (high dose). ^[1] In men with systemic urinary tract infection, seven days of treatment is inferior to fourteen days; cross this caution onto any man whose prostatitis includes the whole urinary tract. ^[1]

Complications to act on. Prostatic abscess: conservative treatment succeeds when abscess cavities are smaller than 1 cm in diameter, while larger collections are better managed by single aspiration or continuous drainage. ^[1]

Drug choice. Culture the organism and treat to sensitivities where possible. ^[1] Empirical first-line treatment is a fluoroquinolone, chosen for its penetration into prostatic tissue, its Gram-negative activity and its activity against Chlamydia trachomatis. ^[1]

Duration. Antimicrobials should be given for four to six weeks after initial diagnosis. ^[1] Fluoroquinolone treatment must continue for at least fourteen days; azithromycin and doxycycline for at least three to four weeks. ^[1]

Pathogen-specific choices (from the EAU Table 10): ^[1]

Practical points.

• If intracellular bacteria have been detected, macrolides or tetracyclines should be used. ^[1]
• Increasing resistance among uropathogens is a concern; consider local resistance patterns when choosing an antibiotic. ^[1]
• Intravenous or intraprostatic injection of antimicrobials has not been evaluated in controlled trials and is not recommended. ^[1]
• Intraprostatic and herbal or phytotherapeutic adjuncts should not replace targeted therapy.
• If symptoms persist with repeated positive microbiological results for sexually transmitted pathogens, screen the partner(s). ^[1]
• Treatment can be repeated with a more prolonged course, a higher dose or a different compound. ^[1]
• Nitrofurantoin should only be used once prostatic involvement has been reliably excluded; it is not a dependable choice for bacterial prostatitis. ^[1]

The management of the pain syndrome is not antibiotic management. ^[2][3] It is multidisciplinary, biopsychosocial and phenotype-guided.

Assessment first. Phenotype the patient before treating. The EAU chronic pelvic pain guideline points urologists toward a measurable tool, and the widely described UPOINT framework captures six domains: Urinary, Psychosocial, Organ-specific, Infection, Neurologic/systemic and Tenderness of muscles. ^[2][3] A newer sexual domain is often added. ^[2] UPOINT is deliberately dynamic: it maps the dominant drivers so that treatment can be matched to them rather than to the syndrome name. ^[3]

The evidence for this framework is supportive: UPOINT-guided multimodal interventions can help a substantial proportion of patients to reach a clinically meaningful fall (at least 6 points) in the NIH-CPSI within six months. ^[3]

Management options, matched to phenotype. ^[2][3]

• Alpha-blockers (terazosin, alfuzosin, doxazosin, tamsulosin, silodosin) have widespread use on the back of positive randomised trials and a meta-analysis that reported moderate, significant benefit in total symptoms, pain, voiding and quality of life, with a higher favourable-response rate than placebo (relative risk 1.4; 95% confidence interval 1.1 to 1.8; p = 0.013). ^[2] Effects are less convincing in long-standing disease and in a 2019 Cochrane review the treatment effect on symptoms was described as uncertain. ^[2] Expect moderate benefit and stop if there is none after a reasonable trial.
• Anti-inflammatory drugs (NSAIDs, and a single short trial of celecoxib) showed a pain and quality-of-life benefit in one randomised trial, and across pooled studies anti-inflammatory drugs were 80% more likely than placebo to produce a favourable response. ^[2] A Cochrane review concluded that they may reduce symptoms compared with placebo. ^[2] They are a reasonable short-term option, limited by long-term side effects (gastrointestinal, renal, cardiovascular).
• Antibiotics are widely used empirically, and some men improve, but the cultures and leukocyte status of prostatic specimens do not predict response. The few good placebo-controlled trials used oral ciprofloxacin or levofloxacin for 6 weeks, or tetracycline for 12 weeks. ^[2] A Cochrane review concluded that antibiotics may reduce symptoms compared with placebo, but direct meta-analysis did not reach significance and the improvement was often below clinical significance. Combination of an antibiotic with an alpha-blocker outperformed the antibiotic alone in network meta-analysis. ^[2] If an antibiotic is tried, it should be one six-week course of a quinolone or tetracycline; if it fails, move on to other therapies rather than repeating it. ^[2]
• 5-alpha-reductase inhibitors (finasteride, dutasteride) cannot be recommended in general for the pain syndrome, although a Cochrane review concluded that finasteride probably reduces symptoms, and symptom scores fell in an older subgroup of men with an elevated prostate-specific antigen in one large prevention trial. ^[2]
• Phytotherapy such as pollen extract (Cernilton, DEPROX 500) and quercetin has produced clinically meaningful symptom improvement in several small randomised trials; saw palmetto improved the NIH-CPSI in a larger trial. ^[2]
• Pregabalin did not significantly reduce the total NIH-CPSI in an adequately powered trial, though it may help selected patients. ^[2]
• Pentosan polysulphate at high oral dose improved clinical global assessment and quality of life in one trial. ^[2]
• Pelvic floor physical therapy is prioritised for the tenderness phenotype; muscle relaxants and botulinum toxin have been used with mixed evidence, and intraprostatic injection of any drug has no controlled-trial support. ^[2][3]
• Psychological support, sleep management, neuromodulators should be addressed for the psychosocial and neurologic/systemic domains. ^[2][3]

What not to do. Avoid repeated or prolonged antibiotic courses in the absence of a target organism, avoid routine prostate biopsy in active prostatitis, and avoid invasive prostatic procedures in unstable pain syndromes. ^[1][2]

• Urinary retention, in about 1 in 10 men with acute bacterial prostatitis. ^[1]
• Prostatic abscess, particularly in diabetes, immunosuppression, catheterised patients and severe disease. ^[1]
• Urosepsis from an ascending infection; acute bacterial prostatitis is a systemic urinary tract infection and is managed accordingly. ^[1]
• Progression from acute to chronic bacterial prostatitis, especially when obstruction or drainage is not addressed; suprapubic rather than urethral drainage may reduce this risk. ^[1]
• Needless antibiotic exposure, harm from mislabelling chronic pelvic pain as infection: resistance, side effects (fluoroquinolone restrictions in Europe) and prolonged psychological distress. ^[1][2]
• Missed prostate cancer, if a raised prostate-specific antigen sampled during active inflammation is either over-interpreted during the episode or ignored afterwards. ^[1]

• Acute bacterial prostatitis managed with appropriate parenteral then oral therapy settles in the majority, provided drainage and obstruction are addressed. ^[1]
• Chronic bacterial prostatitis is a relapsing condition; even with optimal fluoroquinolone courses relapses are common, and treatment is repeated with prolonged courses or different compounds. ^[1]
• Chronic pelvic pain syndrome tends to run a chronic, fluctuating course. It is not life-threatening but reduces quality of life substantially. ^[2] Phenotype-guided multimodal care improves outcomes for a substantial proportion of men within six months, and many continue to improve with sustained, stepped management. ^[3]
• Asymptomatic inflammatory prostatitis requires no treatment but should be recognised when it is found incidentally, because it can raise PSA and mimic cancer on biopsy. ^[1]

• Avoid unnecessary transrectal biopsy where possible; when biopsy is required, recognise the increased risk of acute bacterial prostatitis. ^[1]
• Resolve or bypass obstruction (benign prostatic enlargement, stricture, stone) to reduce recurrent infection. ^[1]
• Do not treat catheterised or asymptomatic patients with antibiotics for "prostate infection" without evidence. ^[1]
• Correctly label chronic pelvic pain so that patients are not exposed to repeated antibiotics and are channelled into multimodal care. ^[2][3]
• Prostate-specific antigen should not be measured during an episode; if screening is relevant, retest once inflammation has resolved. ^[1]

• Younger men with asymptomatic bacteriuria. Always consider chronic bacterial prostatitis before dismissing the finding. ^[1]
• Immunocompromised or HIV-positive men. Think beyond the ordinary bacterial pathogens (tuberculosis, Candida and systemic fungi). ^[1]
• Older men with chronic pelvic pain. The same multimodal strategies apply; 5-alpha-reductase inhibitors may have more benefit when an enlarged prostate and elevated PSA are present. ^[2]
• Men with sexual dysfunction. Address this directly as part of chronic pelvic pain management; sexual dysfunction is common and is associated with anxiety and family disharmony. ^[3]
• Diabetes and indwelling catheters predispose to severe acute bacterial prostatitis and to abscess formation. ^[1]

• The diagnosis of acute bacterial prostatitis is clinical: a febrile, systemically unwell man with pelvic pain and a tender prostate needs immediate antibiotic treatment without waiting for culture results. The EAU pathway is to treat as a systemic urinary tract infection. ^[1]
• If culture is unavailable, use simple empiric broad-spectrum parenteral therapy (third-generation cephalosporin, or a fluoroquinolone, or broad-spectrum penicillin, with an aminoglycoside when safe) followed by oral therapy for a total of two to four weeks, guided by the systemic urinary tract infection regimens quoted above. ^[1]
• Where transrectal ultrasound is unavailable, a suspected abscess should be referred; an acutely tender, fluctuant prostate with persistent fever despite 48 to 72 hours of antibiotics should be assumed to be abscess until proven otherwise.
• Chronic bacterial prostatitis is harder to investigate without localising culture facilities. In practice, a man with three months or more of pelvic pain, dysuria and recurrent positive midstream urine warrants a trial of a fluoroquinolone for four to six weeks, after which progress is reassessed. ^[1]
• For chronic pelvic pain syndrome, the core of care costs very little: education, validation, pelvic floor relaxation, sleep and stress management, and analgesia. Concentrate resources where the evidence is strongest and avoid prolonged antibiotics without a target organism. ^[2][3]

• The NIH classification is the practical map: type I acute bacterial, type II chronic bacterial, type III chronic pelvic pain syndrome (now also called primary prostate pain syndrome), type IV asymptomatic inflammatory. ^[1][2]
• Fewer than 1 in 10 men labelled with prostatitis have proven bacterial infection; most have chronic pelvic pain syndrome. ^[1]
• Acute bacterial prostatitis is a systemic urinary tract infection: febrile, sudden, usually Escherichia coli, and potentially serious (abscess, retention, urosepsis). Treat with parenteral broad-spectrum agents then oral therapy for two to four weeks, with adequate drainage. ^[1]
• Never perform prostatic massage in acute bacterial prostatitis. It can cause bacteraemia and sepsis. ^[1]
• Chronic bacterial prostatitis is pain for at least three months with a localised culture. Diagnosis with the Meares and Stamey two- or four-glass test; treat with a fluoroquinolone for four to six weeks, or pathogen-specific agents for atypical organisms. ^[1]
• Metronidazole 500 mg three times daily for fourteen days eradicates Trichomonas vaginalis in about 93.3% of patients. ^[1]
• Chronic pelvic pain syndrome is not an infection. Treat it with phenotype-guided multimodal care (UPOINT domains: Urinary, Psychosocial, Organ-specific, Infection, Neurologic/systemic, Tenderness), reserving a single short antibiotic trial for selected men and stopping it if it fails. ^[2][3]
• UPOINT-guided multimodal care can help a substantial proportion of men reach a clinically meaningful (6 point) fall in the NIH-CPSI within six months. ^[3]
• Alpha-blockers give moderate symptomatic benefit; anti-inflammatories may reduce symptoms; 5-alpha-reductase inhibitors are not generally recommended for the pain syndrome; pregabalin did not show benefit; phytotherapy evidence is encouraging but small. ^[2]
• Cross-check with urinary tract infection: male systemic urinary tract infection needs at least fourteen days of therapy; acute prostatitis and prostatitis-related infection are managed within the systemic urinary tract infection pathway. ^[1]
• Prostate-specific antigen rises in about 60% of acute and 20% of chronic bacterial prostatitis; do not sample it during an episode and reconfirm once inflammation has resolved. ^[1]
• Avoid routine prostate biopsy in active prostatitis because of the risk of sepsis. ^[1]

Plain text (topics are linked elsewhere by the site): urinary tract infection; benign prostatic hyperplasia; prostate cancer; acute kidney injury; sepsis; interstitial cystitis and bladder pain syndrome; antimicrobial stewardship; overactive bladder; nocturia.