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Radiographic Examination

Posted by admin on June 21st, 2011 No Comments

Radiographic examination of patients with chronic bacterial prostatitis and prostatitis inflammatory syndromes is usually unnecessary and findings are nondiagnostic. While patients with tuberculosis prostatitis and granulomatous prostatitis may undergo radiographic examination with diagnostic findings, the majority of patients can be evaluated and treated without imaging studies. In patients who have chronic bacterial prostatitis and are undergoing transrectal ultrasound for elevated prostate-specific antigen levels, lesions may be identified, including prostatic calcifications, hypoechoic lesions in the peripheral zone, periprostatic venous engorgement, and abnormalities in size, symmetry, and consistency of the seminal vesicles. Hypoechoic lesions are frequently multifocal, often occurring in the peripheral zone and usually without changes in the overlying prostatic capsule.

Prostatic calcifications are a more common abnormality in imaging studies of patients with recurrent chronic bacterial prostatitis. These calcifications are visible on transrectal ultrasound as multifocal or unifocal, with or without acoustical shadowing, and are often associated with calcifications throughout the prostate and verumontanum. Such calculi can also be seen on plain pelvic film, IVP, or Computed tomography scan. Prostatic calculi are more common in patients with chronic bacterial prostatitis than in those with other inflammatory conditions of the prostate.

Perisprostatic venous engorgement on transrectal ultrasound has been associated with the diagnosis of chronic bacterial prostatitis as well as of benign prostatic hyperplasia. Thin reported eight patients in whom transrectal ultrasound for symptoms of prostatitis revealed prostatic cysts. The prostatic cyst aspiration was associated with relief of symptoms in the small group of patients. Seminal vesicles may also be abnormal, with engorgement, obstructive appearance, or calcifications. Christiansen and Purvis suggest that unilateral seminal vesicle dilatation, loculation and septal thickening of seminal vesicle, and calcifications of the seminal vesicle are more common in patients with chronic bacterial prostatitis. Seminal vesicle asymmetry occurs more than twice as often in patients with chronic bacterial prostatitis than in those with prostastodynia. The use of color Doppler flow techniques in differentiating normal prostates from chronic bacterial prostatitis has been suggested but the nonspecific nature of findings of increased blood flow has not been reproducible. The value of color Doppler flow in distinguishing prostatitis from prostatic malignancy or normal tissue warrants further investigation.

While Computed tomography scan may demonstrate prostatic calcifications, its use in differentiating benign prostatic diseases is neither cost effective nor accurate. Computed tomography scanning appears to be an inappropriate method for evaluating patients with chronic bacterial prostatitis. Magnetic resonance imaging may be helpful in some rare conditions where transrectal ultrasound and Computed tomography are not diagnostic.

Elevations in prostate-specific antigen levels are frequently associated with chronic bacterial prostatitis. Differentiation of patients with prostate-specific antigen level elevations caused by prostatitis or other benign disease must be considered. If prostate-specific antigen level elevations are persistent, transrectal ultrasound and biopsy for suspicion of prostatic malignancy must be carried out. Patients with elevated prostate-specific antigen levels who are in the younger age group or in whom acute elevation of prostate-specific antigen level is associated with tender prostates should be treated with antibiotics. Their prostate-specific antigen level should be determined again to eliminate the possibility of prostatic inflammation as a cause. The use of a fluoroquinolone for 2 to 3 weeks prior to repeat prostate-specific antigen screening will help differentiate those patients with benign and malignant disease. Similarly, free and total prostate-specific antigen ratios may be helpful to further pinpoint those patients who have benign inflammatory prostatic disease.

The use of videourodynamics in evaluating patients who fail standard treatment algorithms for prostatitis has been suggested by Kaplan and associates. Using videourodynamics studies in 43 men aged 23 to 50 who had chronic voiding dysfunction associated with prostatitis, pseudodyssynergia was diagnosed based on brief intermittent closing of the membranous urethra during voiding in the absence of obstructive uropathy or abdominal straining. No patients had positive expressed prostatic secretions or bacteruria. Alpha-adrenergic blocking agents were unsuccessful in these patients and many of them had elevated American Urological Association symptom scores suggestive of lower urinary tract symptoms. Eighty-three percent of patients so diagnosed responded successfully to behavior modification and biofeedback techniques.

Posted in Prostatitis

Chronic Bacterial Prostatitis in the Elderly

Posted by admin on May 5th, 2011 No Comments

Chronic bacterial prostatitis is now recognized as an important cause of relapses of urinary tract infection in elderly men. It is most commonly caused by E. coli, but Klebsiella-Enterobacter, P. mirabilis, and enterococci are also common causes. S. epidermidis, S. aureus, and diphtheroids have been frequent isolates in some series. Many individuals with chronic infection of the prostate are totally asymptomatic. However, some have perineal discomfort, low back pain, or dysuria. Symptoms of acute urinary tract infection may periodically appear. In fact, chronic bacterial prostatitis is probably the most common cause of relapsing urinary tract infection in men. Fever, if present, tends to be low grade unless pyelonephritis occurs. Rectal examination and intravenous pyelograms are unremarkable unless the patient also has an enlarged prostate from benign prostatic hypertrophy or carcinoma.

Because of the focal nature of chronic bacterial prostatitis, needle biopsy of the prostate gland for culture of tissue is unreliable. Demonstration of leukocytes in prostatic fluid is not specific for bacterial prostatitis. There is a quantitative localization technique for making the bacteriologic diagnosis. Because bacteria present in the urethra can contaminate prostatic secretions obtained by prostatic massage, accurate diagnosis requires simultaneous quantitative cultures of urethral urine, midstream urine, prostatic secretions expressed by massage, and the urine voided after massage. An ejaculate is probably preferable to expressed secretions.

Specimens must be cultured immediately after collection, and methods of quantitating small numbers of bacteria must be used. The study should be done at a time the patient has no significant bacteriuria. If bacteriuria is present, ampicillin, cephalexin, or nitrofurantoin should be given for two to three days to sterilize the urine; these agents will not affect prostatic bacterial counts in chronic bacterial prostatitis. If chronic bacterial prostatitis is present, the number of bacteria in the expressed secretions or ejaculate will exceed those in urethral or midstream urine by at least 10-fold. If no secretions or ejaculate can be obtained, the bacterial counts in the postmassage specimen should be at least 10-fold higher than the urethral or midstream samples.

Chronic bacterial prostatitis is very difficult to cure because few antimicrobial agents penetrate the noninflamed prostate. Further, the nidus of infection in some patients may be small prostatic calculi that presumably are difficult to sterilize. Chronic bacterial prostatitis is therefore likely to persist and cause relapsing urinary tract infection. Unlike classical urinary tract infection, relapses may occur after long periods without bacteriuria (e.g., months). Transurethral prostatectomy is curative only if all the infected tissue is removed; about one third of patients will be cured by this procedure. Total prostatectomy is contraindicated because of the complications of sexual impotence and incontinence.

Until recently, medical therapy for patients who have chronic bacterial prostatitis consisted of treatment for bacteriuria followed by daily low dose suppressive antibacterial therapy. With these regimens, most patients remain relatively asymptomatic. However, the pathogen persists in the prostatic fluid cultures, and cessation of antibiotic therapy eventually results in relapse of urinary tract infection. Trimethoprim-sulfamethoxazole now appears to be the most effective therapy available for chronic bacterial prostatitis. Approximately one third of patients can be cured with prolonged therapy with this agent (i.e., two tablets given twice daily for 12 weeks). If this regimen fails, the patient should be managed either by treating acute exacerbations of urinary tract infection or by chronic suppressive therapy using low daily doses (e.g., half normal doses) of an antimicrobial agent.

Posted in Prostatitis

Diagnosis and Treatment of Prostatitis. Part 5

Posted by admin on May 4th, 2011 No Comments

Nonbacterial Prostatitis

Nonbacterial prostatitis (NBP) is the most common type of prostatitis, and occurs eight times more frequently than bacterial prostatitis. Nonbacterial prostatitis presents with the same signs and symptoms as bacterial prostatitis; however, prostatic fluid cultures are negative for presence of bacteria. Inflammation is evident upon prostatic fluid analysis, and can be identified by a minimum of 10 to 15 white blood cells per high power field on microscopic examination. Although controversial, implicated pathogens include Chlamydia trachomatis, Ureaplasma urealyticum, and Trichomonas vaginalis. Minocycline 100 mg twice daily, doxycycline 100 mg twice daily, or erythromycin 500 mg four times daily have been utilized in order to eradicate the suspected pathogens. Erythromycin’s antimicrobial activity is significantly enhanced in the presence of the alkaline pH in prostatic fluid, thus, it achieves high cure rates of prostatic infections. Treatment duration is approximately 2 to 4 weeks. Prolonged therapy after treatment failure is not indicated, since nonbacterial prostatitis is generally self-limiting. Adjunctive recommendations may include sitz baths, normal sexual activity, and analgesics for painful urinary symptoms.

Spicy foods, caffeine, and alcohol should be avoided; they may cause bladder irritation and spasms culminating in reflux of urine into prostatic ducts, thus exacerbating nonbacterial prostatitis symptoms. If symptomatology persists patients should be referred to a urologist for evaluation of serious conditions such as urinary bladder carcinoma and interstitial cystitis.

Conclusion

As the most accessible health care professional, the pharmacist often encounters patients with prostatitis. Treatment of prostatitis is associated with high failure rates; therefore it is paramount that pharmacists counsel patients regarding prostatitis and its treatment. Since prostatitis tends to require prolonged therapy, patients must understand the importance of compliance. Pharmacists must carefully screen for drug interactions that may decrease compliance and efficacy. Furthermore, pharmacists play a vital role in referring patients who are unresponsive to therapy for evaluation of serious underlying conditions.

Posted in Prostatitis

Research and Treatments Ahead for Prostatitis

Posted by admin on January 8th, 2010 No Comments

Every year, men make over two million visits to the doctor because of prostatitis, a condition that causes chronic pelvic pain, urinary problems and often pain during ejaculation. While experts still don’t know for sure what causes this disease, or how to cure it, great strides have been made in the past few years.

“It’s really unknown whether [the cause] is a small microbial agent such as a bacterium or virus, cytokines or autoimmune factors, toxins in the urine or some kind of oxidative stress. But there’s evidence of all of these, particularly psychological and immunological [factors],” according to Dr. Mark Samuel Litwin of the University of California at Los Angeles. Dr. Litwin addressed an audience of urologists at the annual meeting of the American Urological Association in Atlanta last week.

Litwin pointed out that “there is a tremendous psychological burden associated with this chronic condition.” Prostatitis can affect men of any age, but is most common among those between 35 and 50.

In the past, men with prostatitis were usually treated with antibiotics because it was assumed that the condition was the result of an often-unidentified bacterial infection. But Litwin explained that most cases are not caused by infection although sometimes signs of bacteria can be found if a urologist looks hard enough.

Antibiotics are less likely to be prescribed today, says Litwin, and there are other treatment options: alpha-blockers (such as Cardura, used to treat benign prostatic hyperplasia (BPH) and high blood pressure), non-steroidal anti-inflammatory drugs (NSAIDs), finasteride (Proscar — used to treat BPH), microwave therapy and even the drug allopurinol, used to treat urinary stones and gout.

Current practice involves a more thorough evaluation at diagnosis to look for any source of infection, Litwin stated. A urologist will massage the prostate and take a sample of the milky fluid it produces, and it will be examined for bacteria and for white blood cells. If signs of infection are present, antibiotics are prescribed. In most cases, though, there’s no sign of infection, and patients are prescribed NSAIDs and/or alpha-blockers as well as counseling and stress management training.

Litwin also noted that current research is looking into the usefulness of the new COX-2 inhibitors and bioflavonoids in treating prostatitis. In addition, the National Institutes of Health has recently funded a large collaborative study at six North American centers that will focus on basic research to understand prostatitis as well as clinical research to evaluate treatments.

Posted in Prostatitis

Trimethoprim-sulfamethoxazole in the treatment of chronic prostatitis. Part 3

Posted by admin on December 6th, 2009 No Comments

Results

Of the 40 patients who received trimethoprim-sulfamethoxazole for 6 weeks, 9 were classed as failures. These either had no response or relapsed during therapy or relapsed after therapy with unchanged severity of symptoms.

Eleven were considered improved on the basis of continued symptomatic improvement or because of a good initial response followed by relapse with symptoms less severe than before treatment. Included in the “improved” group are two patients who initially relapsed but who have since remained asymptomatic on long-term therapy.

The 20 patients who have had continued satisfactory relief of symptoms are classified as having good results.

Discussion

An earlier controlled study compared the results of treatment with sulfamethoxazole with those from the use of trimethoprim-sulfamethoxazole. Only after 6 weeks of treatment was a significant response obtained and this influenced the choice of 6 weeks as the treatment period. A longer period of treatment (12 weeks) produced better results when trimethoprim-sulfamethoxazole (TMP-SMX) was used after a course of sulfamethoxazole. The late results, however, showed no significant differences according to the sequence in which the agents were given. In this later survey a similar success rate was obtained, namely 50% in patients with the clinical manifestations of chronic prostatitis.

When we disregarded bacterial counts of less than 3000/ml, which is standard practice, only one of the patients was reported as having a growth of Escherichia coli. This is in contrast with the earlier report, in which meticulous bacteriologic investigation, including use of anaerobic culture, showed that 66% of patients had pathogens in their prostatic fluid.

It is concluded from our results in this small series that there is justification for use of trimethoprim-sulfamethoxazole in patients with chronic prostatitis where proof of bacterial etiology is lacking. The desirability of meticulous bacteriologic studies is not disputed.

Posted in Prostatitis

Trimethoprim-sulfamethoxazole in the treatment of chronic prostatitis. Part 2

Posted by admin on December 6th, 2009 No Comments

Treatment

Antibiotic therapy with appropriate agents, even in well documented infections, rarely proved successful in the past because the diffusion of most antibacterial drugs from plasma into prostatic fluid provided too low a concentration to be effective. Of many drugs tested for diffusion across the prostatic epithelium only the basic macrolides (erythromycin and oleandomycin) achieved significant concentrations in the prostatic fluid. These drugs are ineffective against the common gram-negative organisms cultured from prostatic fluid. Trimethoprim has been shown in both dogs and man to reach higher concentrations in the prostatic fluid than in serum at the normal pH of prostatic fluid. The concentrations attained in the diseased prostate may be lower, since in prostatitis the prostatic fluid pH may be elevated, but are probably still effective. When trimethoprim is combined with a sulfonamide, synergistic antibacterial activity results, with both a bactericidal effect and delayed emergence of resistant strains. Because of a similar half-life, sulfamethoxazole has been used in the combined drug. Sulfamethoxazole attains a concentration in the prostatic fluid that is only 10% of that in the serum, but this concentration is sufficient to bring about the synergistic effects of trimethoprim-sulfamethoxazole, which has a wide range of activity against both gram-negative and gram-positive organisms.

Trimethoprim-sulfamethoxazole has previously been shown to be effective in treating chronic prostatitis. The present study was a further clinical assessment of the usefulness of this combination in clinically diagnosed chronic prostatitis.

Methods and materials

The 40 subjects in this study were patients who satisfied the criteria of clinical diagnosis, who completed a 6-week course of trimethoprim-sulfamethoxazole (two tablets twice daily) and were available for review at 6 months or later. Clinical data on these patients are set forth in Table 2. All cultures of midstream urines and cultures for tubercle bacilli were negative. Serum acid phosphatase values were normal in all. Intravenous urograms were normal and no patient had a significant amount of residual urine. Those examined by cystourethroscopy showed only changes compatible with chronic prostatitis. None of the needle biopsies of the prostate was significantly abnormal.

Table 2 — Clinical data on 40 patients with chronic prostatitis
Average age, 37.9 years. Range, 22 to 65 years
Average length of history, 2.4 years. Range 6 months to 15 years
Manifestations:

Pain

36
  • Perineum

9

  • Groin

10

  • Testis

13

  • Suprapubic

7

  • Back

12

  • Penis

11

Urinary symptoms

32
Prostatic signs

35
Previous epididymitis

7

Patients were reviewed 2 weeks after completion of treatment and again at 6 months or later. Routine bacteriologic examination of midstream urines, expressed prostatic fluid (when obtained) and postmassage urines was carried out.

Assessment was based on clinical signs and symptoms and the appraisal was made by one observer.

Posted in Prostatitis

Trimethoprim-sulfamethoxazole in the treatment of chronic prostatitis. Part 1

Posted by admin on December 6th, 2009 No Comments

Chronic prostatitis is a common condition occurring in younger men which presents problems of diagnosis and treatment. In some patients a bacterial population of known pathogens can be identified in the prostatic fluid. In many others proof of bacterial etiology is lacking. There has therefore been an acceptance of two common forms of the disease, namely chronic bacterial prostatitis and a condition that has been variously termed chronic abacterial prostatitis, nonspecific prostatitis, prostatosis and prostatic neurosis. Despite the refinements of methods of collection and bacteriologic processing of prostatic fluid, certainty of bacterial recovery cannot be assumed. The sample obtained may fail to include fluid from all parts of the gland or, in particular, from the inflamed parts of the gland. The inconsistency of recovery of bacteria from known cases of bacterial prostatitis lends support to this thesis and suggests that the segregation of chronic prostatitis into bacterial and nonbacterial groups is by no means certain. Where episodes of recurrent genitourinary infection such as cystitis, epididymitis and, less commonly, pyelonephritis occur, bacterial etiology is more likely to be established but otherwise the distinction between differing clinical entities is not obvious.

Diagnosis

The common clinical features of chronic prostatitis are summarized in Table 1. A variety of complaints, singly or in various combinations, may be elicited, the most common being urinary symptoms and discomfort and pain in various sites. Less common symptoms include hemospermia, perineal discomfort or pain after ejaculation. Others relating to sexual function are sometimes emphasized but are probably coincidental. There is considerable variation between patients in severity of symptoms but the clinical pattern appears to be consistent for individual patients.

Table 1 — Signs and symptoms of chronic prostatitis
1. Urinary

  • Irritative: dysuria, frequency, urgency
  • Obstructive: slowness, dribbling
  • Urethral discharge
2. Pain at various sites (see Table 2)
3. Prostatic changes

  • Changes in consistence
  • Irregularity
  • Tenderness

Changes are commonly detectable on rectal examination of the prostate although normal palpatory findings may be encountered. These changes include variations in:

(1) size;

(2) consistence, such as areas of softening or bogginess with or without areas of induration;

(3) contour, with irregularity of the surface; and

(4) amount of discomfort or pain on palpation.

Assessment of these changes lacks the precision of bacteriologic quantitation but, provided the limitations are recognized, may still be valuable in diagnosis and assessment of therapy in chronic prostatitis.

The number of pus cells in prostatic fluid shows such variation from day to day in individual patients, unrelated to clinical course, that this feature lacks value in diagnosis or review.

Cystourethroscopy may show typical changes in the prostatic urethra but the importance of these has been largely discounted because to a minor degree they may be seen in asymptomatic patients. Apart from illustrating some typical prostatic changes, this examination is useful in excluding other pathologic conditions of the prostate and bladder. Trabeculation of the bladder in young men with prostatitis is seen frequently enough to suggest a relationship with dysfunctional voiding.

Radiologic studies including intravenous urograms serve to exclude other causes of urinary tract infection. Prostatic calculi may be demonstrated.

Needle biopsy of the prostate has been generally unrewarding either in demonstrating pathological changes or in isolating bacteria.

Bacteriologic diagnosis in chronic prostatitis was considerably advanced by the refined techniques introduced by Meares and Stamey. Their studies indicated the value of taking samples of urine from the first voided specimen (VB1), from a midstream specimen (VB2) and a voided specimen immediately after prostatic massage (VB3). Prostatic massage usually produces a specimen of prostatic fluid (EPS) for bacteriologic examination. Localization of the source of the infection may therefore be possible, although it must be remembered that all urine sampled passes through the prostatic urethra. In using these methods very sensitive bacteriologic culture techniques must be used to ensure counting of as few as 10 organisms per ml, because in chronic prostatitis there are often only small numbers of bacteria in the prostatic secretion (EPS) or urine after massage (VB3). This is the reason that routine bacteriologic studies of prostatic fluid or postmassage urine rarely show positive results.

Etiologic factors in chronic prostatitis are rarely obvious but include urethral stricture, previous urethritis (gonococcal or nonspecific), previous instrumentation or catheterization and previous episodes of acute prostatitis.

Posted in Prostatitis

Diagnosis and Treatment of Prostatitis. Part 4

Posted by admin on December 2nd, 2009 No Comments
Antimicrobial Regimens for the Treatment of Acute and Chronic Bacterial Prostatitis
Drug class Dose* and Route Common Side Effects Comments
Trimethoprim/
sulfamethoxazole		 160 mg TMP–800 mg SMX PO BID Nausea, vomiting, diarrhea, photosensitivity May be used for suppressive therapy as one single-strength tablet given once a day
Fluoroquinolones
ofloxacin
 200 mg–400 mg PO BID Nausea, vomiting, dizziness, insomnia, photosensitivity Drug-drug interactions with theophylline, caffeine, warfarin and other drugs metabolized by the cytochrome p450 system. Drug-nutrient interactions with di– and trivalent cations (e.g., Mg, Al, Ca, Fe, Zn, and Cr)
norfloxacin
 400 mg PO BID
ciprofloxacin
 250 mg–500 mg PO BID
Aminopenicillins
ampicillin
 2 gm IV Q6h Diarrhea, rash, hypersensitivity reactions Contraindicated in patients with a history of penicillin anaphylaxis
amoxicillin
 500 mg PO Q8h
Aminoglycosides
gentamicin
 1 mg/kg–2 mg/kg Q8h Nephrotoxicity, vestibular and auditory toxicity Serum concentrations need to be monitored for efficacy and toxicity
tobramycin
 1 mg/kg–2 mg/kg Q8h
* Doses of all agents must be adjusted based on age, weight, and hepatic and renal function.
ABP = Acute bacterial prostatitis, CBP = Chronic bacterial prostatitis

U.S. Food and Drug Administration:

Active Ingredients: Sulfamethoxazole and Trimethoprim
Drug Name: Bactrim, Cotrim, Polytrim, Septra, Sulfamethoprim, Sulfatrim, Sulmeprim, Uroplus

Active Ingredients: Trimethoprim
Drug Name: Primsol, Proloprim, Trimethoprim, Trimpex

Active Ingredients: Sulfamethoxazole
Drug Name: Gantanol, Sulfamethoxazole, Urobak

Posted in Prostatitis

Diagnosis and Treatment of Prostatitis. Part 3

Posted by admin on December 2nd, 2009 No Comments

Chronic Bacterial Prostatitis

Chronic bacterial prostatitis (CBP) occurs when acute bacterial prostatitis is treated inadequately due to resistance, relapse, short-course therapy or because the ductal anatomy of the peripheral zone of the prostate may have blocked drainage of secretions from the prostate. Rarely will some patients be found who have not had a previous bout of acute prostatitis. The most common clinical feature of chronic bacterial prostatitis is recurrent urinary tract infections. Subsequently, patients will complain of obstructive and irritative urinary symptoms. Physical exam reveals a palpable, tender prostate. However, patients often present asymptomatic, with a normal prostate gland exam.

Localizing bacteria from the prostate is paramount in order to diagnose chronic bacterial prostatitis. The Stamy–Meares test is a collection of segmented urine samples from the urethra, bladder, and prostate; it is considered the gold standard for diagnosis. The patient voids and collects the first 5–10 mL of urinary stream (VB1), then collects a midstream specimen of 10–20 mL (VB2), and is administered a prostate exam and massage to express prostatic fluid (EPS). This is immediately followed by collection of a final urinary specimen with the first 10 mL of urine (VB3). The specimens are then analyzed for bacteria and leukocyte count. In CBP, large numbers of leukocytes are present in the EPS and VB3. However, these results have to be correlated with VB1 and VB2 results, since an active urinary tract infection will cause variable results.

The Gram-negative pathogens implicated in acute bacterial prostatitis have also been implicated in chronic bacterial prostatitis. Most clinicians discount Gram-positive bacteria as causative pathogens in chronic bacterial prostatitis. Fluoroquinolones and TMP/SMX are first- and second-line therapy in the management of chronic bacterial prostatitis, respectively. Other antimicrobials include doxycycline, minocycline, carbenicillin indanyl sodium, and erythromycin; however, these agents have shown variable results. Chronic prostatitis warrants at least 10 to 12 weeks of therapy. Usually, the bacteria remain susceptible to commonly used antimicrobials despite frequent, long-term use. However, poor clinical outcomes have been observed due to poor diffusion of antimicrobials into the prostate. As a result, long-term suppressive therapy may be needed. Long-term suppressive therapy may be initiated with TMP–SMX given as a single-strength tablet daily, trimethoprim 100 mg daily, sulfamethoxazole 500 mg daily, norfloxacin 200 mg daily, or nitrofurantoin 100 mg daily. Surgery may be an alternative in recurrent cases that are caused by infected calculi.

Posted in Prostatitis

Diagnosis and Treatment of Prostatitis. Part 2

Posted by admin on December 1st, 2009 No Comments

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.

Posted in Prostatitis
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