Prostatitis

• Acute bacterial prostatitis (category I): fever, rigors, perineal and low back pain, dysuria and obstructive symptoms, with an exquisitely tender, boggy prostate. Usually Escherichia coli and other Enterobacterales; in younger sexually active men consider Neisseria gonorrhoeae and Chlamydia trachomatis. Vigorous prostatic massage is avoided because it can precipitate bacteraemia.
• Chronic bacterial prostatitis (category II): recurrent urinary tract infections with the same organism, since the prostate acts as a reservoir; antibiotic courses must be long because penetration is poor.
• Chronic prostatitis / chronic pelvic pain syndrome (category III): much the most common form, with pelvic pain and voiding symptoms but no demonstrable infection.
• Asymptomatic inflammatory prostatitis (category IV): found incidentally on biopsy or semen analysis, and a cause of a raised PSA without cancer.

Uropathogen ascent (categories I and II)

• Enterobacterales: Escherichia coli causes the majority of culture-positive cases; Klebsiella, Proteus, Enterobacter, Serratia and Pseudomonas follow. Enterococci are the main gram-positive isolate.
• Sexually transmitted organisms: Neisseria gonorrhoeae and Chlamydia trachomatis in men under ~35 or with a new partner; the stem gives urethral discharge or recent unprotected intercourse.
• Atypical/opportunistic: Mycobacterium tuberculosis, Candida and Cryptococcus in advanced HIV or other immunosuppression; disseminated BCG after intravesical therapy for bladder cancer.

Modifiable / iatrogenic risk factors (the ones examiners plant)

• Transrectal prostate biopsy: seeds rectal flora directly into the gland and is the classic setup for **fluoroquinolone-resistant *E. coli*** sepsis.
• Urethral instrumentation and indwelling catheters: cystoscopy, TURP, urodynamics, chronic catheterisation.
• Unprotected insertive anal intercourse: exposure to rectal flora.
• Poorly controlled diabetes and immunosuppression: impaired neutrophil function, higher abscess risk.
• Untreated STI or urethritis and incomplete treatment of a prior UTI (fosters a prostatic reservoir).

Non-modifiable / structural

• Bladder outlet obstruction from BPH, urethral stricture, or a neurogenic bladder: high-pressure voiding drives intraprostatic urinary reflux.
• Age: acute bacterial disease peaks in middle age and again after 60 with BPH; chronic pelvic pain syndrome clusters in men aged 20–50.
• Prior episode of prostatitis and prostatic calculi, which harbour biofilm.

• Route of entry: the prostatic and ejaculatory ducts drain into the posterior urethra, so organisms colonising the urethra or refluxing from an infected bladder enter the gland directly. Turbulent, high-pressure voiding against an obstructed outlet forces urine retrogradely into these ducts — intraprostatic urinary reflux — the reason BPH, stricture and dysfunctional voiding predispose. Haematogenous and direct rectal spread (post-biopsy) are less common.
• Acute inflammatory phase: bacterial invasion of the ductal epithelium triggers neutrophil influx, cytokine release and glandular oedema. The prostate becomes engorged, warm and boggy, and stretch of its non-distensible capsule produces the perineal, suprapubic and low back pain. Periurethral swelling narrows the prostatic urethra, generating hesitancy, poor stream and sometimes frank retention.
• Barrier disruption explains two exam points: acute inflammation breaks down the normally tight prostatic epithelial barrier, which (1) lets antibiotics that would otherwise be excluded reach therapeutic concentrations, and (2) allows PSA to leak into serum, so PSA rises with inflammation and is not interpretable during or shortly after an episode. The same inflamed, hyperaemic gland is why vigorous prostatic massage can force organisms into the bloodstream and precipitate bacteraemia.
• Chronic bacterial phase: once inflammation subsides, the intact lipid epithelial barrier and the ion gradient across it re-form. Prostatic fluid is relatively acidic, so lipophilic weak bases (trimethoprim, fluoroquinolones, macrolides) are ion-trapped and concentrate, while hydrophilic beta-lactams and nitrofurantoin penetrate poorly. Residual bacteria persist in ducts and around prostatic calculi within biofilm, seeding the bladder intermittently — hence recurrent UTIs with the identical organism and the need for prolonged therapy.
• CP/CPPS: without demonstrable infection, pain is attributed to pelvic floor muscle spasm, neurogenic inflammation and central sensitisation, which is why symptoms outlast any antimicrobial course.

Acute bacterial prostatitis (category I) — the stem is a febrile man with obstructive voiding

• Systemic sepsis physiology: fever, rigors, malaise, myalgia, tachycardia — reflecting bacteraemic seeding from an inflamed gland.
• Pain from capsular distension: perineal, suprapubic, low back and rectal pain; painful ejaculation; pain on defecation because the inflamed gland abuts the rectum.
• Irritative and obstructive LUTS: dysuria, frequency, urgency (urethral mucosal inflammation) plus hesitancy, weak stream, straining and possible acute urinary retention (periurethral oedema).
• Digital rectal exam: an exquisitely tender, warm, oedematous, boggy prostate — the single most cited physical finding. Examine gently; do not massage.
• Labs commonly show leukocytosis and pyuria; a spuriously elevated PSA may appear as a distractor.

Chronic bacterial prostatitis (category II)

• Afebrile man with recurrent UTIs caused by the same organism, punctuated by pelvic discomfort, dysuria and postvoid dribbling; between flares the exam and even the urine may be normal. The prostate is usually non-tender or only mildly so.

CP/CPPS (category III) — by far the commonest presentation

• ≥3 months of urogenital pain in the perineum, suprapubic area, penis, testes or during/after ejaculation, with variable voiding symptoms and sexual dysfunction, but no fever and no positive culture. Typical stem: a man aged 20–50, often with prior negative antibiotic courses, tender pelvic floor musculature on exam.

Acute bacterial prostatitis — clinical diagnosis, confirmed microbiologically

• First step: urinalysis and midstream urine culture with susceptibilities in every case; pyuria, bacteriuria and positive nitrite are typical. Culture guides the long course that follows, so obtain it before antibiotics.
• Blood cultures if febrile, rigoring or haemodynamically unstable; CBC shows leukocytosis.
• Gentle DRE to elicit tenderness and exclude a fluctuant mass. Prostatic massage and the Meares–Stamey test are contraindicated in the acute setting because of bacteraemia risk.
• **NAAT for N. gonorrhoeae and *C. trachomatis*** on first-void urine in sexually active men under ~35 or with urethral discharge, per CDC STI Treatment Guidelines.
• PSA is not a diagnostic test here — it is elevated by inflammation and should be deferred for several weeks after resolution.
• Imaging: reserve for failure to defervesce within roughly 48–72 hours of appropriate antibiotics, or for suspected retention. Transrectal ultrasound or contrast CT/MRI of the pelvis identifies prostatic abscess; bladder ultrasound quantifies postvoid residual.

Chronic bacterial prostatitis — localisation studies

• Meares–Stamey four-glass test is the named gold standard: VB1 (urethral), VB2 (bladder), EPS after prostatic massage, and VB3 (post-massage void). Diagnostic pattern is a bacterial colony count in EPS/VB3 that is at least tenfold higher than in VB1/VB2, with leukocytes in EPS.
• The two-glass pre- and post-massage test (PPMT) is the practical substitute used in most US clinics.

CP/CPPS (category III)

• Diagnosis of exclusion: ≥3 months of pelvic pain with negative localisation cultures. Subtype IIIa (inflammatory) has leukocytes in EPS/semen; IIIb (non-inflammatory) does not.
• Symptom severity and treatment response are quantified with the NIH Chronic Prostatitis Symptom Index (NIH-CPSI), scoring pain, urinary symptoms and quality of life.
• Exclude mimics: urethritis, bladder cancer (cystoscopy/cytology if haematuria or smoking history), stone disease, and inguinal or anorectal pathology.

Immediate assessment (category I)

• Assess for sepsis and retention. Hospitalise and give IV antibiotics with fluid resuscitation if the patient is toxic, hypotensive, immunocompromised, diabetic with instability, or unable to tolerate oral intake.
• Acute urinary retention: drain the bladder, but prefer a suprapubic catheter or a fine, gently placed urethral catheter — transurethral instrumentation of an acutely inflamed gland is best minimised.
• Do not perform vigorous prostatic massage.

First-line antimicrobials (outpatient, culture pending)

• Fluoroquinolones: ciprofloxacin or levofloxacin — excellent prostatic penetration and Enterobacterales coverage.
• Trimethoprim–sulfamethoxazole: acceptable alternative when local resistance permits.
• Total duration is prolonged — on the order of 4–6 weeks — to eradicate organisms from prostatic tissue and prevent progression to category II.

Inpatient/severe or post-biopsy disease

• IV broad-spectrum beta-lactam: ceftriaxone, or an antipseudomonal agent such as piperacillin–tazobactam or a carbapenem when ESBL or recent fluoroquinolone exposure is suspected, ± an aminoglycoside; then de-escalate to a culture-directed oral agent to complete the course.

CP/CPPS (category III): multimodal, phenotype-directed (UPOINT) rather than antibiotic-driven — pelvic floor physical therapy, alpha-blockers, NSAIDs, neuromodulators (amitriptyline, gabapentinoids), and cognitive-behavioural/stress management. Category IV requires no treatment.

Avoid

• Nitrofurantoin and fosfomycin — inadequate prostatic tissue penetration despite treating cystitis.
• Repeated empiric antibiotic courses in culture-negative CPPS.
• Note fluoroquinolone FDA boxed warnings (tendinopathy, aortic aneurysm/dissection, neuropathy, QT effects) before prolonged use.

Emergencies

• Bacteraemia and urosepsis: organisms escape the inflamed gland into prostatic venous plexuses; signalled by rigors, hypotension, tachypnoea and lactataemia. Highest risk after transrectal biopsy and after vigorous prostatic massage — the reason massage is avoided in acute disease. Requires resuscitation and IV antibiotics.
• Prostatic abscess: suspect when fever and pain persist beyond ~48–72 hours of appropriate therapy, or when DRE reveals a fluctuant area. Diagnosed by transrectal ultrasound or CT/MRI; managed with drainage (transrectal ultrasound-guided aspiration or transurethral unroofing) plus antibiotics. Diabetics and immunocompromised patients are over-represented.
• Acute urinary retention: periurethral oedema obstructs the prostatic urethra; presents with suprapubic pain and a palpable bladder. Needs prompt drainage, preferably suprapubic.

Later or chronic sequelae

• Progression to chronic bacterial prostatitis: inadequate duration or poor-penetration antibiotics leave a ductal reservoir → recurrent UTIs with the same organism.
• Epididymo-orchitis from retrograde spread along the vas; unilateral scrotal pain with relief on elevation (Prehn sign).
• Chronic pelvic pain, sexual dysfunction and infertility: persistent inflammation alters semen quality (leukocytospermia, reduced motility); erectile dysfunction and painful ejaculation are common in CP/CPPS.
• Elevated PSA persisting for weeks after infection — a source of unnecessary biopsy if PSA is checked too soon.
• Rare: prostatic fistula, bladder neck fibrosis, seeding of prosthetic joints or heart valves.

Treatment-related

• Fluoroquinolones: tendinopathy and tendon rupture, aortic aneurysm/dissection, peripheral neuropathy, CNS effects, QT prolongation, dysglycaemia, and Clostridioides difficile colitis — all amplified by the multi-week courses prostatitis requires.
• TMP-SMX: hyperkalaemia, rise in creatinine, hypersensitivity including Stevens–Johnson syndrome, marrow suppression.
• Alpha-blockers: orthostatic hypotension, retrograde ejaculation, intraoperative floppy iris syndrome at cataract surgery.

• **Fever + rigors + an *exquisitely tender, boggy prostate* on gentle DRE is acute bacterial prostatitis until proven otherwise. Best next step: urinalysis with urine culture (plus blood cultures if febrile), then start a fluoroquinolone or TMP-SMX** — not imaging, not PSA.
• The classic trap: prostatic massage. Vigorous massage of an acutely inflamed gland can precipitate bacteraemia, so the Meares–Stamey four-glass test belongs to chronic disease only.
• The antibiotic distractor: nitrofurantoin (or fosfomycin). It treats cystitis but does not penetrate prostatic tissue. Choose an agent that concentrates in the prostate and treat for weeks, not days — short courses breed category II disease.
• Same organism, recurrent UTIs, afebrile man = chronic bacterial prostatitis; the prostate is the reservoir.
• Age drives the organism: E. coli and other Enterobacterales overall, but in a younger sexually active man with urethral discharge think N. gonorrhoeae and C. trachomatis and treat per CDC with ceftriaxone 500 mg IM plus doxycycline.
• Recent transrectal prostate biopsy in the stem points to **fluoroquinolone-resistant *E. coli***; escalate to a broad-spectrum IV beta-lactam.
• Prostatitis raises PSA. Category IV (asymptomatic inflammatory) prostatitis is a benign cause of an elevated PSA; defer PSA measurement until well after the episode rather than proceeding straight to biopsy.
• Persistent fever after 48–72 hours of appropriate antibiotics = prostatic abscess — image and drain.
• Category III (CP/CPPS) is the most common form and the most commonly mismanaged: ≥3 months of pelvic pain with negative cultures, graded by the NIH-CPSI, treated with pelvic floor physical therapy, alpha-blockers and neuromodulators — not another antibiotic course.