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Prostatitis

Commonly used label or diagnosis which can refer to broad spectrum of conditions.

Only 10 % of cases labelled as prostatitis have demonstrable bacterial infection.

NIH/NIDDK classification:

1

Acute bacterial prostatitis

2

Chronic bacterial prostatitis

3

Chronic non bacterial prostatitis

Chronic pelvic pain syndrome

3a

Inflammatory CPPS – white cells in semen, EPS or VB3

3b

Non inflammatory CPPS – no white cells

4

Asymptomatic inflammatory prostatitis (histological prostatitis)

Acute bacterial prostatitis

Generally younger men aged 20 – 40s, but with a second peak over 60.

Many potential causes – ascending infection thought to be common, direct seeding from prostate biopsy/instrumentation, possible intra-prostatic duct reflux of urine, or haematogenous infection/seeding (TB, melioid)

Presenting symptoms:

  • UTI – frequency, dysuria, urgency
  • Pelvic pain, or non specific lower abdominal, lower back, perineal pain
  • Fever / malaise and signs of sepsis
  • Urinary retention
  • Tender, boggy prostate on examination

Risk factors:

  • Phimosis
  • Unprotected anal sex
  • Catheterisation or condom catheter
  • Instrumentation / prostate biopsy
  • STIs
  • Epididymo-orchitis
  • Immunosuppression including DM
  • BPH
  • Urethral stricture

Most commonly E.coli – can also be pseudomonas or other common urinary pathogens.

Management of acute bacterial prostatitis:

  • Work up as above
  • Manage according to CCrISP algorithm.
  • Early broad spectrum antibiotics – IV piptaz or amp/gent.
  • IV fluid resuscitation.
  • Involvement of ID/ICU as needed.
  • Exclude or treat abscess, esp if very unwell or poor response.
  • If in retention – catheter – consider SPC over IDC – some evidence suggests urethral catheterisation increases risk of CPPS.
  • Oral antibiotics – I use 2 to 4 weeks of ciprofloxacin 500 mg BD. Alternative is trimethoprim but does not cover pseudomonas.

Antibiotics for the prostate

  • The prostate capillary bed lacks active transport for antibiotics – penetration is dependent on passive transport
  • 3 factors which determine ability for antimicrobials to penetrate the prostate – lipid solubility; pKa and protein binding
  • Most beta-lactams penetrate poorly into prostatic tissue due to low pKa and poor lipid solubility
  • Fluoroquinolones have the most favourable pharmacokinetic properties for penetrating the alkaline prostatic fluid. Trimethoprim is the next best alternative.

Chronic bacterial prostatitis

Classically characterised by recurrent UTIs with the same organism, suggesting a chronic prostatic source or nidus.

Typically the symptoms (dysuria/pain) will respond to antibiotic treatment and be relatively asymptomatic between episodes, cf. NIH type 3 prostatitis

Commonly caused by E.coli, pseudomonas, proteus, klebsiella or enterococcus. Research into specific isolates causing prostatitis show higher degree of virulence factors, in particular biofilms – making treatment and culture more challenging.

There is also potentially a common role of chlamydia.

Typically defined as symptoms > 3 months.

Diagnosis can be made with two glass test which has comparable sensitivity and specificity to the traditional 4 glass test (Meares-Stamey).

  • Two glass test – mid stream urine culture (VB2) -> prostate massage -> first catch urine culture (VB3)
  • Traditional four glass test:
    • First catch urine culture (VB1 urethral) -> mid stream urine culture (VB2 bladder) -> prostate massage -> secretions (EPS) -> first catch urine culture (VB3 prostate)
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Treatment is generally recommended to be 4 – 6 weeks of fluoroquinolone antibiotics, favoured for their pharmacokinetic properties. Consider adding azithromycin or doxycycline if concerns for atypicals like chlamydia or ureaplasma.

  • Think about alternate/underlying diagnoses – urethral stricture, TB, chronic urinary retention.
  • TURP can be considered in refractory cases.
  • +/- add in other therapies as per CPPS management strategies.

Granulomatous prostatitis

  • Histological finding of epithelioid granulomas with or without inflammatory cells.
  • Often found incidentally. Most commonly seen after intravesical BCG.

Can be categorised:

  • Specific or infectious – TB, BCG etc
  • Non specific
  • “Allergic” or secondary to systemic granulomatous disease – sarcoidosis, rheumatoid, Wegener’s granulomatosis
  • Post-surgical

Stony hard prostate on exam may mimic malignancy.

Also may mimic malignancy on MRI.