Diagnosis and Treatment of Prostatitis. Part 2
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Acute Bacterial Prostatitis
Acute bacterial prostatitis (ABP) is the least common of the prostate infections. It is usually accompanied by a urinary tract infection with positive cultures from prostatic secretions. It presents with a sudden onset of fever, chills, and low back and perianal pain. Patients often complain of obstructive (dysuria, nocturia, urgency, frequency, and burning) and irritative (hesitancy, straining, dribbling, weak stream, and incomplete emptying) urinary symptoms. Other constitutional symptoms include generalized malaise, arthralgias and myalgias. Physical examination reveals a warm, tender, swollen and indurated prostate.
The diagnosis of acute bacterial prostatitis can be made based on clinical signs and symptoms. Often, urinary cultures are positive and reveal Escherichia coli as the most prevalent pathogen. Other Gram-negative microorganisms from the Enterobacteriaceae class, such as Proteus sp. and Klebsiella sp., may also be present. In patients who present with a recent history of hospitalization and/or broad-spectrum antimicrobial use, a high index of suspicion for Pseudomonal, Enterococcal and Staphylococcal infections should be maintained.Other microorganisms implicated in prostatitis include Ureaplasma urealyticum, Chlamydia trachomatis, and Corynebacterium seminale. Occasionally, urinary cultures will be negative. Bacteria may be isolated from prostatic fluid by prostatic massage, although it is not recommended since vigorous manipulations can lead to bacteremia.
The mainstay of therapy in acute bacterial prostatitis is empiric antimicrobial therapy directed toward the most likely pathogens. Urinary cultures should be obtained prior to initiating antimicrobial therapy to allow for identification of the causative pathogen and subsequent streamlining of pharmacotherapy. Generally, antimicrobials penetrate poorly into the prostate gland due to the lipid solubility and pH of the prostate epithelial membrane. However, since inflammation is invariably present in acute prostatitis, most antimicrobials will readily diffuse into the prostate gland.
The most commonly prescribed antimicrobial for acute bacterial prostatitis is trimethoprim/sulfamethoxazole (TMP–SMX) due to its broad-spectrum activity against the most prevalent isolated pathogens. Trimethoprim inhibits bacterial dihydrofolate reductase; it works synergistically with sulfamethoxazole to interfere with microbial folic acid synthesis. Trimethoprim concentrations in prostatic fluid are two to three times that in serum, thus achieving adequate concentrations at the site of infection. The usual dose is 160 mg of trimethoprim and 800 mg of sulfamethoxazole, which is equivalent to one double-strength tablet (e.g., Septra DS, Bactrim DS) taken twice a day. TMP-SMX has a good safety profile, with most of the adverse effects limited to hypersensitivity reactions and gastrointestinal disturbances including nausea, vomiting, diarrhea, and anorexia. Other, more serious adverse effects such as leukopenia, thrombocytopenia and granulocytopenia are uncommon (they are prevalent, however, in the AIDS population).
The fluoroquinolones have gained popularity in the management of acute bacterial prostatitis due to their enhanced activity against many of the Gram-negative pathogens in urinary tract infections. The fluoroquinolones inhibit bacterial replication and transcription by blocking bacterial DNA gyrase and subsequent protein synthesis. Prostatic fluid contains lower fluoroquinolone concentrations than does serum; nevertheless, appreciable concentrations are achieved in prostatic tissues to eradicate the most common causative pathogens. Ciprofloxacin, ofloxacin, and norfloxacin are effective fluoroquinolones in the management of prostatitis; however, only ofloxacin and norfloxacin are FDA-approved. Adverse effects associated with the fluoroquinolones include nausea, vomiting and diarrhea; dizziness, lightheadedness, confusion, insomnia, hallucinations; tendonitis and tendon rupture; and photosensitivity reactions. Rash that may progress to an anaphylactoid reaction has occasionally been reported. Recent data have demonstrated higher eradication rates for the parenteral administration of fluoroquinolones (67%–91%) than for TMP–SMX (40%–71%); however, clinical efficacy with oral therapy in outpatients has been similar.
Rarely, patients who present acutely ill will require hospitalization with intravenous therapy (e.g., those who present with bacteremia or significant voiding difficulties). Generally an aminoglycoside in combination with ampicillin or parenteral TMP–SMX is initiated. The penicillins inhibit cell wall synthesis, and the aminoglycosides bind to bacterial ribosomes, inhibiting protein synthesis. The aminoglycosides and penicillins often yield a synergistic bactericidal effect. Patients requiring initial intravenous therapy should be switched based on culture and sensitivity reports to an oral antimicrobial once acute symptoms have resolved.
The duration of treatment for acute bacterial prostatitis is uncertain; however, most authorities suggest 4–6 weeks of therapy. Short-course therapy is not recommended due to the risk of relapse or progression to chronic bacterial prostatitis.
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