What bacteria causes prostatitis?

Chronic bacterial prostatitis (CBP) is most often caused by Escherichia coli or other gram-negative Enterobacteriaceae, and typically affects men 36 to 50 years of age. After an episode of acute bacterial prostatitis, approximately 5% of patients may progress to CBP.

emedicine.medscape.com - Chronic Bacterial Prostatitis - Medscape Reference

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The recurrent UTIs in chronic bacterial prostatitis are secondary to uropathogens residing within the gland. The gram-negative Enterobacteriaceae family of bacteria are the most common causative organisms, with Escherichia coli the most common strain, found in around 80% of cases. [9, 10] Other bacteria of the Enterobacteriaceae family (ie, Pseudomonas aeruginosa, Serratia species, Klebsiella species, Proteus species, and Enterobacter aerogenes) make up another 10%-15% of infections. Enterococci are present in 5%-10% of prostate infections, but other gram-positive organisms have a questionable role as their localization in cultures in inconsistent. [11] The gram-positive organisms that typically colonize the anterior urethra (ie, Staphylococcus epidermitis, S saprophyticus, Streptococcus, Corynebacterium, and Bacteroides) may represent contamination when present in a culture specimen, and their role in prostatic inflammation remains unclear. Patients with these bacteria, even when localized to prostate specimens, are currently considered to have CPPS, but this may change as understanding of prostatic bacterial pathogenicity evolves. [1] Although Chlamydia trachomatis has been implicated as a cause of the condition, [12] the evidence is conflicting and unclear. Some studies have been able to isolate Chlamyida in specimens while other studies were unable to confirm Chlamydia as an etiologic agent using cultures and serologic tests. Treatment of presumed chlamydial prostate infections does not relieve symptoms in many cases and no definitive statement can be made about its prostatic origin and effect at this time. [1]

Uropathogens

See the list below:

E coli

Klebsiella pneumoniae

Pseudomonas aeruginosa

Proteus species

Enterococcus species

Trichomonas species

Chlamydia trachomatis

Ureaplasma urealyticum

Mycoplasma hominis

Other microorganisms

Candida and other mycotic infections have been identified in cases of prostatic inflammation, but mostly in patients who have systemic fungal infections or are immunosuppressed. Viruses have also been implicated, but their role in prostatitis has not been formally evaluated. [1] With limitations to culture techniques, some microorganisms may fail to be identified.

Bacterial virulence

Bacterial P-fimbriae facilitate colonization of the lower urinary tract by binding to urothelial receptors. E coli has mannose-sensitive fimbria with receptors that has been associated with the development of cystitis and prostatitis. Biofilm formation by bacteria allows the bacteria to persist despite antibiotic treatment. Biofilms are protective aggregates of bacteria that form in response to host defenses or antibiotic therapy; in prostatitis, they develop deep in the ducts of the prostate. [13] Patients with organisms persisting in biofilms or within obstructed ducts may have persistent symptoms despite sterile cultures. Hemolysin may also increase the ability of bacteria to persist as biofilms, as seen with certain strains of E coli causing CBP. [1] Even after bacteria have been eradicated, the virulence of the specific bacteria may influence the development of CPPS. [1]

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Risk factors

Risk factors for CBP include the following:

Intraprostatic ductal reflux and prostatic calculi

Other infections (eg, acute epididymitis, urinary tract infections)

Phimosis

Unprotected penetrative anal intercourse

Manipulation of the lower urinary tract

Secretory dysfunction of prostate gland

Intraprostatic ductal reflux and prostatic calculi

[14] The peripheral zone of the prostate is composed of a system of ducts with a poor drainage system, which prevents the dependent drainage of secretions and makes that zone the most susceptible to reflux. As the prostate enlarges with age, the poorly draining ducts can become obstructed and reflux. High-pressure dysfunctional voiding from anatomic or neurophysiologic obstruction may result in reflux in addition to contributing to symptoms of prostatitis with development of chronic pain. Pathogenic bacteria can directly enter the prostate via ascending urethral infection with refluxing urine and may exist as aggregates protected by prostatic calculi. Refluxing urine, even when sterile, may cause chemical irritation and initiate tubule fibrosis and prostatic stone formation, which then can lead to intraductal obstruction and stagnation of intraductal secretions. Prostatic stones and stagnant fluid can serve as a nidus for relapsing infections and prostatitis. Prostatic calculi are generally evidence of intraprostatic reflux because they are composed of substances only found in urine and not in secretions from the prostate. They serve as a source of bacterial colonization allowing bacterial to aggregate or form biofilms leading to recurrent UTIs despite adequate antimicrobial therapy. [15] Prostatic calculi are also common in men with chronic inflammatory prostatitis, compared with men without prostate inflammation.

Manipulation of the lower urinary tract

Treatments that increase risk include the following:

Indwelling urethral catheters or condom catheters

Transurethral surgery, especially in men with infected urine who have not been treated. [16] Prostate biopsy can irritate the prostate or cause an infection. Infections following prostate biopsy often involve organisms with different virulence and resistance than those from spontaneous acute infections of the prostate. Extended-spectrum β-lactamase (ESBL) E coli infection after prostate biopsy is a risk factor for chronic prostatitis.

Secretory dysfunction of prostate gland

Altered secretions can reduce the natural antibacterial nature of prostatic secretions. Findings in prostatic secretions during infections include a decrease in fructose, citric acid, acid phosphatase, zinc, magnesium, calcium, and prostatic antibacterial factor, as well as an increase in ceruloplasmin and complement C3. It is unclear whether the changes in prostatic fluid are a cause or consequence of inflammation, but they correlate with inflammation and are blamed for reducing the antibacterial nature of prostatic secretions.

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Alkaline pH (up to 8.0) of prostatic fluid is associated with inflammation and can also reduce its antibacterial properties, as well as limit diffusion of some basic antimicrobials into the prostate. Prostatic fluid is generally acidic, with a pH of 6.4 (compared with plasma pH of 7.4), thus creating a pH gradient that further inhibits diffusion of acidic antibiotics into the prostatic fluid. Basic antibiotics are able to dissociate and concentrate in the prostatic fluid because of ion trapping within the prostatic fluid due to the pH gradient. Therefore, the best antibiotics for use in prostatitis have high dissociation constants (ie, measure of acid strength), are basic instead of acidic, and are not tightly protein bound. This combination can allow up to a six-fold higher concentration of antibiotic in the prostatic fluid compared with plasma. Infection often persists because antibiotics do not easily penetrate the prostate and no active transport mechanism exists whereby antibiotics can enter the prostatic ducts. Therefore, antibiotics depend on passive diffusion to enter the epithelial-lined prostatic glandular acini. The epithelial cells do not allow the free passage of antibiotics unless they meet certain criteria (ie, non-ionized, lipid-soluble, not firmly protein bound).

Routes of infection

The actual routes of prostatic infection are unknown in most cases, but various possibilities exist. Ascending urethral infection is a known route because of the frequency of previous gonococcal prostatitis, as well as the finding of identical organisms in prostatic fluid and vaginal culture in many couples. Intraprostatic urinary reflux has been demonstrated in human cadavers and may play a role. Other possible routes of infection include hematogenous spread, migration of rectal bacteria via direct extension, and lymphogenous spread.

emedicine.medscape.com - Chronic Bacterial Prostatitis - Medscape Reference

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