CASE
A warehouse officer, aged 45 years, presented to his general practitioner with a three-day history of dysuria. Associated symptoms included slow urinary stream and increased frequency to 10 times daily, as well as fatigue, malaise and anorexia (patient reported lack of appetite in the preceding three days). He denied any new sexual partners, episodes of frank haematuria or dysorgasmia. He was alert and afebrile on examination.
Preceding this presentation, he was hospitalised 10 days prior for right upper front incisor periodontal abscess. This was managed through incision, drainage and intravenous antibiotic therapy. His past medical history included well-managed fatty liver.
Laboratory investigations revealed elevated prostate-specific antigen (PSA; 5.9 µg/L ) and C-reactive protein (CRP; 10.4 mg/L). The initial mid-stream urine (MSU) microscopy, culture and sensitivities (MCS) revealed sterile urine with nil pyuria (leukocytes 7 × 106/L). Because of the inconsistency with the clinical picture, a repeat MSU MCS was performed five days later, which revealed mild pyuria (leukocytes 20 × 106/L) and cephalexin-resistant enterococcus faecalis (>108 organisms).
Question 1
What is the provisional diagnosis for this presentation?
Question 2
How is acute bacterial prostatitis diagnosed?
Question 3
What are the risk factors for acute bacterial prostatitis?
Question 4
What is the management approach to acute bacterial prostatitis?
Question 5
What are the potential complications of acute bacterial prostatitis?
Question 6
Is the patient’s recent history of periodontal disease relevant to the development of acute bacterial prostatitis?
Answer 1
The symptoms are suggestive of a urinary tract infection (UTI) with prostatic involvement. In middle-aged men, this presentation is typical of acute bacterial prostatitis (ABP). Prostatitis refers to the condition of prostate gland inflammation, which is classified as per the internationally accepted National Institutes of Health Classification System detailed in Table 1.1 ABP is a subtype of prostatitis, characterised by rapid onset of symptomatic prostate inflammation caused by bacterial invasion.2–4
| Table 1. Subtypes of prostatitis |
| |
Type 1 |
Type 2 |
Type 3 |
Type 4 |
| Name1,3,4 |
Acute bacterial prostatitis |
Chronic bacterial prostatitis |
Chronic prostatitis or chronic pelvic pain syndrome |
Asymptomatic inflammatory prostatitis |
| Clinical features4 |
Acute development of irritative and obstructive urinary symptoms, systemic symptoms and pain |
Symptoms of ABP or remains asymptomatic. Infection persists beyond a 3-month period |
Obstructive urinary symptoms without any bacterial infection |
There are no urinary or systemic symptoms, despite prostate inflammation |
| Proportion of cases3,4 |
Up to 10% |
<5% |
>90% |
Rare |
| Causes |
UTI:
Majority of cases are caused by Gram-negative bacteria
- Escherichia coli (50–87%)2
- Entereobacterales (10–30%)2
Minority of cases are caused by Gram-positive bacteria
STI:
- Chlamydia trachomatis3
- Neisseria gonorrhoea3
|
ABP treated inadequately, which progresses to chronic infection, or a new bacterial infection triggers a state of chronic inflammation3 |
Cause unknown;4 proposed it is a neuropathic pain3 caused by peripheral nervous system sensitisation, which causes hyperalgesia and allodynia4 |
Cause and clinical significance unknown; typically an incidental finding (eg in prostate biopsy for exploration of infertility)4 |
| ABP, acute bacterial prostatitis; STI, sexually transmissible infection; UTI, urinary tract infection. |
Answer 2
ABP is a clinical diagnosis, based on the presence of key features, outlined in Table 2. It is imperative to recognise ABP because despite shared features with other pathologies including simple UTI and sexually transmitted infection (STI), the management approach and complication risks differ.
| Table 2. Features of acute bacterial prostatitis |
| Symptoms/signs |
Features |
| Genitourinary |
- Cloudy urine3
- Digital rectal examination – prostate gland is tender, hot and boggy2
- Dysorgasmia1
- Dysuria1
- Haematuria1
- Increased urinary frequency1
- Increased urinary urgency1
- Oliguria or anuria, distended abdomen (acute urinary retention)4
- Poorly localised pain – perineal, external genitalia, tip of penis, rectum, suprapubic region to lower back3
- Poor urinary stream2
|
| Systemic3 |
- Fever
- Malaise
- Myalgia
- Nausea
- Vomiting
Severe/sepsis:
- Tachycardia
- Hypotension
- Tachypnoea
|
| Investigation findings |
- CRP – low specificity for ABP; however, this is useful in indicating presence of infection or inflammation1
- First void urine specimen (PCR) – Chlamydia trachomatis or Neisseria gonorrhoea, in a ABP caused by an STI3
- PPMT – note that this test is contraindicated in the investigation of suspected ABP because of the risk of bacteraemia; this is reserved only for investigation of suspected chronic bacterial prostatitis (refer to Table 4)4
- PSA – not a diagnostic criterion for ABP, rather it is useful to indicate prostatic involvement, which might aid in excluding other differentials.1 PSA is elevated (>4 µg/L) in 70% of ABP cases1
- Urine culture – shows growth of bacterial species in ABP caused by a UTI.1 If growth occurs, subsequent susceptibility testing should be performed to determine which antimicrobial agents the species is sensitive or resistant to1
- Urinary dipstick, midstream urinalysis and full blood count – leukocytosis1
- Transrectal or bladder ultrasound – indicated only if acute urinary retention is suspected to determine whether bladder emptying is incomplete4
|
| ABP, acute bacterial prostatitis; CRP, C-reactive protein; PCR, polymerase chain reaction; PPMT, pre- and post-prostate massage test; PSA, prostate-specific antigen; STI, sexually transmissible infection; UTI, urinary tract infection. |
Answer 3
ABP can develop through any mechanism that allows bacteria to reach the prostate gland.2 Known mechanisms and their respective risk factors are outlined in Table 3.
| Table 3. Risk factors of acute bacterial prostatitis |
| Mechanism |
Associated risk factors |
| Reflux of infected urine2 |
- Malignant tumours5
- Phimosis6
- Prostate enlargement6
- Urethral stricture6
- Urinary tract stones5
|
| Ascending urethral infection2 |
- Lower urinary tract intervention – indwelling catheter2
- Transurethral surgery – infection likely to be from Pseudomonas species4
- Urethritis6
|
| Lymphatic invasion from rectum2 |
- Prostate manipulation6
- Transrectal prostate biopsy2
|
| Haematogenous infection2 |
- Cirrhosis2
- Diabetes mellitus2
- Immune system suppression (eg HIV/AIDS) – more likely to be infected with Cryptococcus, Salmonella or Candida species4
|
Answer 4
ABP can be managed safely in the community if the patient is haemodynamically stable without signs of severe infection (Table 2), with Trimethoprim 300 mg orally daily for 14 days, as first-line therapy.7 However, the choice of antibiotic should be guided by susceptibility testing and account for patient factors including allergies. Urgent hospital referral should be made for patients who meet any of the following indications for intravenous antimicrobial therapy:7
- severely unwell or have signs of sepsis – refer to Table 23,5
- recent transrectal or transurethral prostatic manipulation2
- urinary retention – will additionally require catheterisation5
- inability to tolerate oral antibiotics2
- antibiotic resistance.5
Upon completion of the initial antibiotic course, healthcare practitioners should review the response to treatment. An additional 2–4 weeks of antimicrobial therapy should be prescribed if:
7
- genitourinary or systemic
- symptoms persist
- repeat urine cultures display bacterial growth
- PSA levels remain elevated.
Supportive therapies can also be recommended to aid in symptomatic relief, including:
2
- antipyretics
- anti-inflammatories
- alpha-blockers
- stool softeners.
Preliminary research has been conducted on direct antibiotic injection of Amikacin into the prostate gland, demonstrating superior bacterial eradication rates (33.3% direct vs 5% IM, P<0.05) for ABP because of enhanced antibiotic concentration within the prostate gland.5 As direct injection also reduces treatment duration and antibiotic resistance, it is emerging as a future treatment option for ABP.
Answer 5
If bacterial eradication is not achieved during ABP treatment, patients are at risk of the complications outlined in Table 4.
| Table 4. Complications of acute bacterial prostatitis |
| Complication |
Clinical features |
Further investigations |
Treatment |
Other notes |
| Chronic bacterial prostatitis1 |
Symptoms of ABP persist, or patient is asymptomatic |
PPMT – leukocytosis in post-prostatic massage urine specimen, positive culture |
Antibiotics for 6 weeks |
There is lower tissue penetration of antibiotic therapy because of less inflammation compared to ABP |
| Chronic pelvic pain syndrome1 |
Penile pain, inguinal pain, pudendal discomfort, prostate hyperplasia, bladder outlet obstruction |
PPMT – no bacteraemia detected |
Alpha-1 blockers, phosphodiesterase type 5 inhibitors |
Can impact mental health and functioning causing insomnia and depression |
| Epididymitis1 |
Urethral damage, genital swelling, tenderness |
Ultrasound – to rule out testicular torsion |
Oral quinolone for 14–21 days |
If untreated it can narrow the passage sperm must pass and contribute to infertility |
| Prostate abscess |
Elevated inflammation markers despite antibiotic treatment3 |
Transrectal ultrasound6 |
If >1 cm, perform surgical drain (TURP)6 |
Typically caused by Escherichia coli and MSSA.1 Has an incidence of 2–18%.2 Risk of prostate abscess increases in immune-suppressed patients2 |
| Sepsis3,5 |
Tachycardia, hypotension, pyrexia, tachypnoea, neutrophilia or neutropenia |
Blood cultures, platelets, bilirubin, creatinine |
Intravenous antibiotics, vasopressors, fluids, oxygen |
Prostatic massage contraindicated when performing DRE for ABP patients |
| ABP, acute bacterial prostatitis; DRE, digital rectal examination; MSSA, methicillin-sensitive Staphylococcus aureus; PPMT, pre- and post-prostate massage test; TURP, transurethral, percutaneous or open. |
Answer 6
The literature suggests that periodontal disease and prostatitis are correlated through the theorised mechanisms outlined in Table 5. As there is no evidence to demonstrate that increased periodontal disease incidence increases the incidence of prostatitis, further research is imperative in clarifying the significance of the proposed correlation and the implications for clinical practice.8
| Table 5. Proposed prostatitis and periodontal disease correlation |
| Proposed mechanism |
Evidence |
| Hematogenous spread of pathogens from the periodontium to the prostate gland8 |
There are common pathogens in periodontal disease and prostatitis, including: Escherichia coli, Porphyromona gingivalis, Fusobacterium nucleatum and Actinomyces actinomycetemcomitans8 |
| Systemic inflammatory cytokines (IL-6, TNF-α, IL-1) released during periodontitis predispose patients to prostatitis because of chronic inflammation and endothelial dysfunction8,9 |
Inflammatory cytokines are found in the serum of prostatitis patients10 |
| The periodontium as a site of PSA generation elevated distant PSA levels8,10 |
The prostate gland has inflammatory reactions to elevated PSA levels8 |
| All of the above |
Clinical evidence supports the proposed correlation, as a cohort of periodontitis patients followed over a 15-year study period were found to have an 11% rate of prostate disorder and a 4.6-fold increase in prostatitis risk (P=0.001)9 |
| IL, interleukin; PSA, prostate-specific antigen; TNF, tumour necrosis factor. |
Case continued
This patient was treated for ABP with a course of Trimethoprim 300 mg orally daily for seven days after shared decision making between the patient and general practitioner. Post-treatment consultation confirmed full resolution of symptoms. Repeat tests demonstrated regression of pyuria with no subsequent bacterial growth, reduction of PSA to 0.64 g/L (within normal range) and reduction of CRP to 0.4 mg/L (within normal range). The patient experienced no further complications of ABP.
Key points
- It is important to consider ABP in male patients presenting with UTI or STI.
- Patients should be reviewed. post-treatment to confirm resolution of symptoms, no further culture growth and a normal PSA level.
- There is a possible, yet inconclusive correlation between prostatitis and periodontitis.