“Prostatitis” is the term used to describe a variety of conditions, syndromes, and diseases. Sometimes it is used precisely to describe histologic findings or microbiologic findings in prostatic fluid and/or urine, but all too frequently, prostatitis refers to a vague constellation of pelvic pain and voiding symptoms. Over the past 10-15 years, efforts have been made to redefine and better characterize the condition.
Classes of prostatitis
In 1995, the National Institute of Diabetes and Digestive Kidney Diseases (NIDDK) convened a seminar to address this condition. A classification based on patients’ symptoms and microscopic and bacteriologic assessment of prostatic fluid was conceived.
The four classes of prostatitis include acute bacterial prostatitis; chronic bacterial prostatitis; chronic pelvic pain syndrome (CPPS), formerly known as chronic nonbacterial prostatitis; and asymptomatic inflammatory prostatitis (Table 1).
Bacterial prostatitis can be an acute infection of the prostate or a chronic infectious process characterized by recurrent UTIs that emanate from the prostate. CPPS is characterized by discomfort or pain in the pelvic region, generally for at least three months, with variable voiding and sexual symptoms. This syndrome was further categorized into two types: Type IIIa CPPS is characterized by evidence of inflammation in expressed prostatic secretions (EPS) or voided bladder urine (VB) collected after prostatic massage, while type IIIb demonstrates no evidence of inflammation. It’s important to note that the significance of inflammatory cells in EPS has been questioned because studies have demonstrated that healthy men can have WBCs in their prostatic fluid.
Moreover, the number of WBCs is not correlated with the severity of symptoms in men with CPPS. Although semen assessment for WBCs was also included in the diagnostic criteria, most investigators do not use semen to define or categorize patients with CPPS. Last, a group of patients, particularly those with elevated PSA, may undergo assessment of prostatic fluid to determine if there is evidence of WBCs. This is based on the concept that inflammation is thought to–and probably does—raise PSA levels to those consistent with prostate cancer.
The epidemiology of prostatitis is difficult to assess, in large part because the kinds of patients with the condition and the database codes used to identify them are quite varied. Nevertheless, it is estimated that approximately 10%-15% of men worldwide have some form of prostatitis. The vast majority appear to be in the class III CPPS group. In the United States alone, “prostatitis” accounts for at least 2 million office visits per year; 8% of urologist office visits and 15% of primary-care physician office visits are associated with this diagnosis. Because of the vagaries of diagnosis and the difficulty in treating the condition, patients frequently return for subsequent visits, leading to a direct overall cost of care of approximately $4,000 per patient per year.
Approximately 10% of patients with prostatitis have bacterial prostatitis. The risk factors for bacterial prostatitis are not known, but they presumably include those for UTIs in men, e.g., urinary tract obstruction, urethral catheterization or instrumentation, sexual transmission (particularly through rectal intercourse), and perhaps transrectal biopsy of the prostate for prostate cancer.
Bacteria associated with this condition are the same as those associated with UTI in men, most commonly Escherichia coli and less commonly other gram-negative organisms, including Klebsiella, Enterobacter, Proteus, and Pseudomonas. Gram-positive bacteria, such as Streptococcus faecalis, are infrequently identified. Other gram-positive organisms, such as staphylococci, probably play a very minimal role. The false assumption that those organisms are frequently involved is based on inappropriate cultures of prostatic fluid that has been contaminated with bacteria from the foreskin or urethra.
Acute bacterial prostatitis is a distinct, toxic disease associated with UTI and sepsis. Patients present with fever, chills, irritative voiding, and musculoskeletal pain. Examination reveals a tender, swollen, warm prostate; in these patients, it is important to avoid prostatic massage, as undue pressure on the prostate will exacerbate the prostatitis.
Some patients experience urinary retention; a decision should be made whether to insert a small-caliber urethral catheter or a suprapubic catheter. The patient must be well-hydrated, and analgesics and stool softeners should be provided. Urinalysis demonstrates pyuria or bacteriuria. Cultures of the urine and blood will reveal one of the aforementioned bacteria.
Initiation of antimicrobial therapy must be prompt as failure to treat may lead to extension of the infection and even death. If the patient’s condition is severe enough to warrant inpatient management, a broad-spectrum aminoglycoside plus either ampicillin or a third-generation cephalosporin should be considered.
IV fluoroquinolones are also an attractive option. Because of the rapid emergence of organisms resistant to a variety of antimicrobials, including fluoroquinolones, response to therapy must be monitored. It may be necessary to switch antimicrobial agents if the patient’s clinical condition deteriorates on empiric therapy.
When the identification and susceptibility of the infecting bacteria are available, the patient should be treated with specific oral therapy for two to four weeks. Despite the severity of the condition, up to 95% of patients will be cured. This is partially because the severity of the infection ironically weakens the barrier between the serum and the prostate tissue, making it easier for a variety of antimicrobials to penetrate. If the patient’s response to therapy is poor, prostatic abscess is a consideration and CT or ultrasound imaging is warranted. A large abscess should be drained transurethrally or transperineally, as prolonged therapy usually does not lead to resolution of the abscess.
Chronic bacterial prostatitis refers to a disease in which bacteria are sequestered within the prostate and emerge periodically to cause acute recurrent UTIs. Between episodes, patients are relatively asymptomatic and physical findings are minimal.
Since many patients present with prostatitis and fewer than 5% have chronic bacterial prostatitis, it is important to determine by urine culture if the patient’s symptoms are associated with UTIs. If urine cultures repeatedly show infections with the same bacterial strain, chronic bacterial prostatitis is a possibility. Any patient who has negative cultures has CPPS by definition.
All UTIs in men should be considered complicated until proven otherwise and, therefore, the urinary tract should be evaluated for structural or functional abnormalities. A CT scan and determination of postvoid residual urine comprise the minimum testing requirements; 20%-25% of patients will have some significant abnormality deserving urologic evaluation and treatment.
If the urologic workup is negative and urine cultures repeatedly demonstrate the presence of the same bacterial strain, then lower urinary tract localization studies should be performed to determine if the prostate is the source of sequestered bacteria.
The Meares-Stamey 4-glass urine test involves the collection of four samples. The first 10 mL of urine (VB1) will reveal evidence of inflammation in the urethra, e.g., WBCs, while the mid-stream catch provides similar information about the bladder (VB2). One minute of prostatic massage will produce EPS and 10 mL of urine (VB3) within two to three minutes; these samples will give an indication of inflammation in the prostate.
Microscopic analysis of the samples will reveal whether there is evidence of inflammation of the urethra, bladder, or prostate. Only if VB1 and VB2 show no inflammation can one conclude that the prostatic fluid is the source of inflammation. Similarly with cultures, bacteria in VB1 and VB2 negate the validity of the EPS or VB3 assessment. On the other hand, if bacteria are found only in the EPS and VB3 or if the numbers of bacteria are significantly higher than those found in the urethra, chronic bacterial prostatitis is confirmed.
Effective treatment for chronic bacterial prostatitis is shown in Table 2. Follow-up urine cultures should be performed if symptoms occur or at six months. Response rates of approximately 75% have been observed following fluoroquinolone therapy for susceptible bacteria.
Some bacteria that may be sequestered in the prostate, such as Pseudomonas, are susceptible to an antimicrobial in vitro, but therapy is ineffective. In this situation, low-dose suppressive therapy with a drug that is effective against the pathogen should be utilized. The dose and frequency of administration can be tapered to prevent symptoms of recurrent bacteriuria.