Acute Bacterial Prostatitis

Updated: Jul 20, 2022
Author: Samuel G Deem, DO; Chief Editor: Edward David Kim, MD, FACS 


Practice Essentials

Although prostatitis is the most common urologic diagnosis in males younger than 50 years and the third most common diagnosis in men older than 50 years (after benign prostatic hyperplasia [BPH] and prostate cancer), acute prostatitis is rare. Acute prostatitis is easier to identify than chronic prostatitis, however, because of its more uniform clinical presentation.

Acute prostatitis presents as an acute urinary tract infection (UTI). It is usually associated with predisposing risk factors, including bladder outlet obstruction secondary to BPH or an immunosuppressed state.[1] Approximately 5% of cases of acute bacterial prostatitis (ABP) progress to chronic prostatitis.[2]

Pathologic definition of prostatitis

Pathologically, prostatitis is defined as an increased number of inflammatory cells within the prostate gland. The inflammatory process may be infectious or inflammatory in origin. The most common histologic pattern is a lymphocytic infiltrate in the stroma immediately adjacent to the prostatic acini (see the image below).[3]

Leukocytic infiltration of the stroma and glandula Leukocytic infiltration of the stroma and glandular lumina during acute bacterial prostatitis (ABP).

Prostatitis occurs in distinct forms that have separate causes, clinical features, and outcomes. Four clinical entities have been described: acute bacterial prostatitis, chronic bacterial prostatitis, nonbacterial or abacterial prostatitis, and prostatodynia.

NIH classification and definition of prostatitis

The National Institutes of Health (NIH) classification and definition of the categories of prostatitis are as follows:

  • Category I – Acute bacterial prostatitis (ie, acute infection of the prostate)

  • Category II – Chronic bacterial prostatitis (ie, recurrent urinary tract infection and/or chronic infection of the prostate)

  • Category III – Chronic abacterial prostatitis/chronic pelvic pain syndrome (ie, discomfort or pain in the pelvic region for at least 3 mo with variable voiding and sexual symptoms and/or no demonstrable infection; by definition, the syndrome becomes chronic after 3 mo)

  • Category IIIA – Inflammatory chronic pelvic pain syndrome (ie, white blood cells in semen and/or expressed prostatic secretions and/or third midstream bladder specimen)

  • Category IIIB – Noninflammatory chronic pelvic pain syndrome (ie, no white blood cells in semen and/or expressed prostatic secretions)

  • Category IV – Asymptomatic inflammatory prostatitis (ie, evidence of inflammation in biopsy samples, semen and/or expressed prostatic secretions, but no symptoms)

Historical and epidemiologic data

In 1978-1979, symptoms due to acute and chronic prostatitis accounted for 25% of outpatient urinary conditions in the United States. In 1985, according to Nickel, acute and chronic prostatitis accounted for more office visits than BPH or prostate cancer. Most of these visits were for chronic prostatitis. In the early 1990s, the diagnosis of prostatitis resulted in slightly more than 2 million office visits per year.[4]

The international prevalence rate of prostatitis is similar to that in the United States. In one report, of 600 men diagnosed with prostatitis, 5% had bacterial prostatitis, 64% had nonbacterial prostatitis, and 31% had pelvic-perineal pain syndrome or prostatodynia.

Relevant anatomy

The prostate is an extraperitoneal organ that encircles the neck of the bladder and urethra. In an adult, this organ is divided into four distinct zones or regions: periurethral, central, transitional, and peripheral. Prostate carcinoma arises more often in the peripheral zone than the other zones. However, the distribution of prostatic inflammation among the various zones is not clear.

A normal prostate gland is approximately 20 g in volume, 3 cm in length, 4 cm wide, and 2 cm in depth. As men get older, the prostate gland often enlarges because of BPH.

The gland is located posterior to the pubic symphysis, superior to the perineal membrane, inferior to the bladder, and anterior to the rectum. The base of the prostate is in continuity with the bladder and the prostate ends at the apex before becoming the striated external urethral sphincter. The sphincter is a vertically oriented tubular sheath that surrounds the membranous urethra and prostate.

See Prostate Anatomy for more information.

Additional Resources

For patient education information, see the Men's Health Center, as well as The Male Anatomy, and Prostate Infections (Prostatitis).

See also the following:


Theories regarding the pathogenesis of acute bacterial prostatitis include the following:

  • Intraprostatic urinary reflux
  • Ascending urethral infection
  • Direct invasion or lymphogenous spread from the rectum
  • Direct hematogenous infection

Intraprostatic urinary reflux is the most widely accepted theory. In this scenario, infected urine refluxes into the ejaculatory and prostatic ducts that empty into the posterior urethra. Because of the anatomy of the prostate gland, ducts that drain glands in the large peripheral zone are positioned more horizontally than other prostatic ducts and, thus, facilitate the reflux of urine into the prostate. Consequently, most infections occur in the peripheral zone.

In younger men, ascending urethral infection may occur following sexual intercourse. Meatal inoculation may occur during unprotected anal intercourse, instrumentation, and prolonged catheterization.


The organisms primarily responsible for acute bacterial prostatitis (ABP) are also those responsible for most urinary tract infections; these include gram-negative members of the Enterobacteriaceae family such as Escherichia coli, Proteus mirabilis, Klebsiella species, Enterobacter species, Pseudomonas aeruginosa, and Serratia species. Of these, E coli is involved most often and has been shown to increase biofilm formation.[5] Most prostatic infections (82%) involve only a single bacterial organism. In some cases, two or three strains of bacteria may be involved.

Obligate anaerobic bacteria and gram-positive bacteria other than enterococci rarely cause acute bacterial prostatitis. Enterococci account for 5-10% of documented prostate infections.[6] Staphylococcus aureus infection due to prolonged catheterization may occur in the hospital. Other occasional causative organisms include Neisseria gonorrhoeae,Mycobacterium tuberculosis,Salmonella species, Clostridium species, and parasitic or mycotic organisms. N gonorrhoeae should be suspected in sexually active men younger than 35 years.

If recurrent urinary tract infections are confirmed, patients need to be evaluated for any structural abnormality.

Prostate biopsy

Another source of acute prostatitis is following transrectal ultrasound-guided prostate needle biopsy. In this instance, the acute prostatitis is iatrogenic in nature but presents similarly and is treated as acute bacterial prostatitis. In a French study, acute bacterial prostatitis occurred 1–7 days after 21-core prostate biopsy in 20 of 3000 patients (0.67%). All the patients had received fluoroquinolone prophylaxis, but on antibiotic susceptibility testing, 95% of samples were resistant to fluroquinolones and amoxicillin. Escherichia coli was the only bacterium isolated.[7]

A study comparing the multiresistant ST131 E coli pathogen found after transrectal ultrasound-guided prostate biopsy to non-ST131 E coli from patients with spontaneous urosepsis showed that the ST131 E coli had fewer virulence-associated genes than the non-ST131 group. The finds suggest that antimicrobial resistance, rather than virulence genotype, is the most important trait associated with an increased risk of infection following transrectal biopsy.[8]

Risk factors

The following are risk factors for acute bacterial prostatitis (all allow bacterial colonization):

  • Intraprostatic ductal reflux
  • Phimosis and redundant foreskin
  • Specific blood groups [9]
  • Unprotected anal intercourse
  • Urinary tract infections
  • Acute epididymitis
  • Indwelling Foley catheter and condom catheter
  • Transurethral surgery
  • Altered prostatic secretions
  • Recent transrectal ultrasound-guided prostate needle biopsy

In the pediatric population, acute bacterial prostatitis has been associated with septicemic seeding, abnormal bladder dysfunction, congenital abnormalities of the ureter, and sexual abuse.  A case report describes acute bacterial prostatitis in an adolescent after blunt trauma to the lower abdomen.[10]


If the initial response to medical therapy for acute bacterial prostatitis is favorable, the patient's prognosis is very good. Decreased fertility has been reported, but only in cases of massive bacterial inoculation. Decreased sperm viability, including impaired motility and agglutination, has been reported in samples that contained more than 106 colony-forming units (CFU)/mL of bacteria.

Prostatic abscess is an uncommon but well-described complication of acute bacterial prostatitis. Although very rare, it usually occurs in patients who are immunocompromised, who have diabetes, who have urethral instrumentation or a prolonged indwelling urethral catheters, or who are on maintenance dialysis. Coliform bacteria, especially E coli, cause more than 70% of prostatic abscesses.

Other potential sequelae of acute bacterial prostatitis include progression to chronic prostatitis, septicemia, pyelonephritis, and epididymitis. Nearly 10% of patients with acute bacterial prostatitis develop chronic prostatitis and another 10% develop chronic pelvic pain syndrome.[11]




Acute bacterial prostatitis typically presents as an acute onset of fever, chills, malaise, dysuria, and perineal or rectal pain. One study cited that over 96% of patients present with a triad of pain, prostate enlargement, and failure to void and 92% present with fever.[12] It may also present as dysuria, urinary frequency, urinary urgency, and, occasionally, urinary retention. Acute bacterial prostatitis can be a complication of previous instrumentation, such as cystoscopy or prostate needle biopsy. Hematuria, although rare, can be in the presentation.

Physical Examination

In most cases, perineal tenderness alone is sufficient for a diagnosis. If a digital rectal examination is performed, it must be done cautiously, as palpation can be very painful. Measurement of vital signs is necessary, to exclude signs and symptoms of sepsis. Urinary retention is occasionally seen; these patients present with an inability to void and abdominal fullness.



Diagnostic Considerations

A prostatic abscess should be suspected when worsening clinical symptoms follow an initial favorable response to treatment of acute bacterial prostatitis or a fluctuant mass is palpable in the prostate gland.

Differential Diagnoses



Approach Considerations

The diagnosis of acute bacterial prostatitis (ABP) can be made on the basis of clinical findings and urine studies. Although prostatic secretions in patients with acute bacterial prostatitis contain large numbers of leukocytes and fat-laden macrophages, prostatic massage to obtain secretions should not be performed as it is rarely necessary for diagnosis.

Prostatitis may cause irritative and obstructive voiding symptoms that mimic other primary causes of those symptoms, and in such cases the use of urodynamics may possibly be helpful to avoid misdiagnosis. However, this is more the situation in chronic prostatitis; in acute prostatitis, this should not be necessary.

Acute bacterial prostatitis may be an incidental finding on a cross-sectional prostate imaging study.[13] However, imaging studies are not  needed in uncomplicated cases. The presence of a prostatic abscess is confirmed with transrectal ultrasonography and noncontrast computed tomography (CT) scanning of the pelvis.

Occasionally, blood culture results are positive.

Urine Studies

A urinalysis that shows leukocytes and a positive result on urine culture are essential for the diagnosis of acute bacterial prostatitis (ABP). To confirm the prostate as the site of involvement, the tests can be conducted on paired urine specimens collected before and after massage of the prostate; this is known as the two-glass test.[14]

If the patient is febrile or exhibits signs of acute bacterial prostatitis, only the midstream urine is collected for urine culture. The prostatic massage is contraindicated.

Urethral swab culture and postmassage urine culture as well as microscopic examination may be an alternative standard protocol to simplify the evaluation of prostatitis-like syndrome in clinical practice.[15]

The evaluation for chronic prostatitis may include first-voided urine, midstream urine, urine after prostatic massage, and expressed prostatic secretions to localize the nidus of infection, as described by Meares and Stamey.[16]

Serum PSA Levels

Serum prostate-specific antigen (PSA) levels are also increased in prostatitis but should not be used as a screening test for this condition. In the setting of acute bacterial prostatitis, PSA has little to no clinical value. If the PSA level is obtained and is found to be elevated, the study should be repeated 30-60 days after adequate treatment. Studies have shown that a 2- to 4-week treatment with antibiotics decreased the PSA levels in approximately half of patients with PSA levels in ray zone who did not have prostatitis symptoms.[17]

CT Scanning/Transrectal Ultrasonography

Imaging studies, including computed tomography (CT) scanning of the pelvis or transrectal ultrasonography, should be reserved for cases in which findings from laboratory analyses are equivocal or when no improvement is observed following medical therapy.

Ruling out complications of prostatitis (eg, prostatic abscess) is a strong indication to proceed to imaging studies. Transrectal ultrasonography and CT scanning of the pelvis can be very useful in diagnosing and draining prostatic abscesses.[18] However, transrectal ultrasonography should be performed as gently as possible to prevent bacteremia.


Biopsy and Histology

Histologically, the normal prostate gland is composed of tubuloalveolar glands. The glandular spaces are lined by epithelium, which is composed of 2 layers of cells—a basal layer of low cuboidal epithelium covered by a layer of columnar mucus-secreting cells. The glands have a distinct basement membrane and are separated by a fibromuscular stroma.

Prostate biopsy is contraindicated in patients with suspected acute bacterial prostatitis because of the potential complication of seeding the bacterial infection in adjacent organs and the risk of gram-negative sepsis. Furthermore, prostate biopsy is extremely painful without a prostatic nerve block. The current practice is to anesthetize the area before core biopsy sampling.

In prostatitis, a stromal leukocytic infiltrate may be accompanied by increased prostatic secretion or leukocytic infiltration within gland spaces (see image below). When complicated by abscess formation, focal or larger areas of the prostate become necrotic.

Leukocytic infiltration of the stroma and glandula Leukocytic infiltration of the stroma and glandular lumina during acute bacterial prostatitis (ABP).


Approach Considerations

The intense inflammation in acute bacterial prostatitis (ABP) makes the prostate gland highly responsive to antibiotics, which otherwise penetrate poorly into the prostate. Consequently, outpatient therapy with oral antibiotics and supportive measures will suffice for most patients.[19] Antipyretics, analgesics, stool softeners, bed rest, and increased fluid intake provide supportive therapy. Hospitalization is required for patients in whom acute urinary retention develops and in those who require intravenous antimicrobial therapy.

A Foley catheter can be inserted gently for drainage if severe obstruction is suspected. A punch suprapubic tube can be used if a catheter cannot be passed easily or is not tolerated by the patient. The catheter can be removed 24-36 hours later.

Alpha-blocker therapy should also be considered for acute bacterial prostatitis. Because the bladder neck and prostate are rich in alpha-receptors, alpha blockade may improve outflow obstruction and diminish intraprostatic urinary reflux. Terazosin, 5 mg/d orally for 4-52 weeks, is the usual first choice.[20] Tamsulosin (Flomax), alfuzosin (Uroxatral), and doxazosin (Cardura) are acceptable alternative agents.

Medical management is often unsuccessful in cases of prostatic abscess. In such situations, transrectal or perineal aspiration or, less preferably, transurethral resection of the prostate and drainage of the cavity are possible surgical approaches.

Antibiotic Therapy

The choice of antibiotic for treatment of acute bacterial prostatitis (ABP) is based on the results of the initial culture and sensitivity. However, initial therapy should be directed at gram-negative enteric bacteria. Useful agents include fluoroquinolones, trimethoprim-sulfamethoxazole, and ampicillin with gentamicin. In sexually active men under 35 years of age and men over 35 years of age who practice high-risk sex, regimens covering Neisseria gonorrhoeae and Chlamydia trachomatis are recommended.[19, 21]

If the initial clinical response to therapy is satisfactory and the pathogen is susceptible to the chosen antibiotic, treatment is continued orally (PO) for 30 days to prevent sequelae such as chronic bacterial prostatitis and prostatic abscess formation.

The rapid rise in drug resistance, especially to fluoroquinolones, must be considered. Of particular concern, especially in patients undergoing transrectal ultrasound (TRUS)–guided prostate biopsy, are Gram-negative uropathogens such as extended-spectrum β-lactamase (ESBL)–producing Enterobacteriaceae and carbapenem-resistant Enterobacteriaceae.[22] Local resistance patterns and sensitivities should help guide initial treatment.[12]

In a study of 3000 men who received a prophylactic fluroquinolone-based regimen for 7 days to minimize the risk of iatrogenic acute prostatitis after undergoing TRUS-guided biopsy, fewer than 1% (n=20) developed acute bacterial prostatitis within a week of the procedure. In all 20 cases the only bacteria isolated was Escherichia coli.

Testing revealed resistance to the following antibiotics: fluroquinolone and amoxicillin (95%), amoxicillin-clavulanate and trimethoprim/sulfamethoxazole (70%), third-generation cephalosporin (25%) and amikacin (5%). No resistance to imipenem was reported. The investigators concluded that fluroquinolone-based prophylaxis remains effective in minimizing the risk of acute prostatitis secondary to prostate biopsy.[23]

A review of acute prostatitis after TRUS-guided biopsy in Korean patients found that ESBL-producing E coli had been detected continuously since 2008; those E coli were susceptible to imipenem, amikacin, and cefoxitin but resistant to fluoroquinolones. These authors concluded that fluoroquinolones are not an effective antimicrobial of choice for the treatment of acute prostatitis after TRUS-guided biopsy.[24]

An increase in infection rates after transrectal prostate biopsy due to fluoroquinolone-resistant bacteria in feces has been reported. Targeted prophylaxis after rectal flora swabbing has been shown to be efficacious compared with empirical antibiotic prophylaxis. Use of a perineal prostate biopsy has only limited data support and further study is needed.[25]

Some resistant strains may require prolonged intravenous (IV) therapy. For IV therapy, use trimethoprim/sulfamethoxazole, 8-10 mg/kg/d (based on the trimethoprim component) in 2-4 doses two to four times daily until the culture and sensitivity results are known. An alternative regimen is gentamicin, 3-5 mg/kg/d IV in three divided doses, plus ampicillin 2 g in four divided doses. In addition, two approved β-lactam/β-lactamase inhibitor combinations, ceftolozane/tazobactam and ceftazidime/avibactam, have promising activity against multidrug-resistant Gram-negative organisms.[26]

For prostatitis from ESBL-producing multidrug-resistant E coli, off-label treatment with oral fosfomycin has proved effective. The usual regimen is 3 g/24 hr for 1 week followed by 3 g/48 hr, for a total treatment duration of 6-12 weeks.[27, 28]

After the patient is afebrile for 24 hours, an appropriate oral agent can be substituted for an additional 30 days. For oral therapy, use double-strength trimethoprim/sulfamethoxazole twice daily for 30 days. Alternatives for oral therapy include the following:

  • Levofloxacin 500-750 mg daily
  • Ciprofloxacin, 500 mg twice daily
  • Norfloxacin, 400 mg twice daily
  • Ofloxacin, 400 mg twice daily
  • Enoxacin, 400 mg twice daily

If an abscess is diagnosed, anaerobic antimicrobial therapy should be added to the treatment regimen. Clindamycin 600-900 mg IV or 150-450 mg orally every 8 hours is a good choice. Medical management is often unsuccessful, however, in which case surgical drainage is required. Transrectal or perineal aspiration of the abscess is preferred and is often effective, especially if symptoms do not improve after 1 week of medical therapy.

Surgical Intervention

A potential indication for surgery is a prostatic abscess, which is an uncommon but well-described complication of acute bacterial prostatitis. Medical management of prostatic abscess is often unsuccessful. Thus, surgical drainage via either transrectal or perineal aspiration, transurethral resection, or transrectal ultrasound–guided placement of a transrectal drainage tube may be considered.[2]

Transrectal or perineal aspiration of the abscess is preferred and is often effective, especially in patients whose symptoms have not improved after 1 week of medical therapy. Transurethral resection of the prostate (TURP) and drainage of the cavity is another approach, but is less desirable because of the potential hematogenous spread of bacteria.

However, TURP may be an effective treatment for recurrent acute bacterial prostatitis. In a retrospective analysis, Decaestecker and Oosterlinck reported that 12 of 21 patients who underwent TURP for treatment of refractory recurrent acute bacterial prostatitis were symptom free during a median followup of 44 months. No incontinence or bladder neck contracture were reported.[29]

Prostatic abscesses should be allowed to drain, or some type of drainage should be performed if the abscess is larger than 1 cm.[30, 31] Monitor the abscess closely if a spontaneous rupture occurs into the urethra. Recurrent abscesses are rare.

Because of the potential for systemic infection and bacteremia, urethral instrumentation should be avoided in patients with acute bacterial prostatitis, especially if the patient is clinically unstable or is already showing signs of sepsis, although placement of a small drainage catheter is safe in experienced hands. Pretreatment with appropriate antibiotics is mandatory.

Transurethral or perineal surgical approaches in the treatment of a prostatic abscess should be undertaken with caution and are currently not advised unless other drainage techniques have failed. Perineal incision can cause impotence due to nerve injury, and transurethral resection can facilitate hematogenous spread of bacteria, leading to sepsis.[32]

In patients with sepsis, transurethral resection may be lifesaving and should be considered if their condition is not responding to conservative therapy.

In patients with acute urinary retention, insertion of a Foley catheter may be attempted first, as tolerated by the patient; however, this may cause extreme discomfort. In some cases, the transurethral catheter may obstruct drainage of an acutely inflamed prostate and cause bacteremia or prostatic abscess. If the catheter cannot be passed easily, a suprapubic punch cystostomy is indicated.


Prevention of Prostate Biopsy Infection

A number of strategies have been used to prevent acute bacterial prostatitis following post-transrectal prostate biopsy. These include antibiotic prophylaxis and rectal preparation with an enema, povidone-iodine, or chlorhexidine.[33, 34, 35]

Guidelines from major urology and infectious disease societies currently lack agreement regarding antibiotic prophylaxis for prostate biopsy, mainly due to differences in drug resistance and availability of medication.[33] A meta-analysis of different antibiotic regimens recommended a minimum of a full 1-day administration of fluoroquinolones for antibiotic prophylaxis. Targeted therapy was advised in cases of fluoroquinolone resistance. Fosfomycin was the best alternative in countries where fluoroquinolones are unavailable.[34]

A meta-analysis of nonantibiotic prevention found that a transperineal biopsy approach significantly reduced infectious complications compared with a transrectal approach (relative risk 0.55, 95% CI 0.33-0.92, P=0.02).  If a transrectal approach was used, preparation with povidone-iodine reduced both infections and hospitalizations following biopsy.[35] ​

Future and Controversies

Despite the fact that prostatitis syndromes are common urologic disease processes, little is known about prostatitis and the factors associated with the condition. Several important questions need to be answered, including the following:

  • Is prostatitis associated with prostate cancer?
  • What are the natural history and the epidemiology of prostatitis?
  • What is the best way to elucidate the exact etiology, diagnosis, and management of prostatitis?

Prostatitis, BPH, and prostate cancer

The first question is important, considering efforts in recent years to find the most accurate and most expedient method of diagnosing and treating prostate cancer. Prostatitis is more common in younger men, whereas benign prostatic hyperplasia (BPH) and prostate cancer are more common in men older than 50 years. An important research question is whether prostatitis in younger men leads to BPH or prostate cancer later in life, because approximately 5% of acute bacterial prostatitis cases lead to chronic prostatitis.

Although one study reported that nearly 50% of prostate specimens resected for prostate cancer showed evidence of prostatitis, no causal association has been demonstrated.[36] A meta-analysis found statistically significant evidence of an association between prostatitis and prostate cancer, but most of the studies included did not provide separate classification of acute and chronic prostatitis.[37]

Public health burden

The exact public health burden of prostatitis should also be addressed. Most urologists agree about the ever-growing need for both community-based cross-sectional and longitudinal epidemiologic prostatitis studies. Active research and a more aggressive effort are needed to generate hypotheses regarding the etiology of prostatitis.

Elucidating risk factors

Formulating risk factors associated with prostatitis is important. For example, the incidence of prostatitis in men with a history of a prostatic biopsy requires investigation. With increased screening for prostate cancer, more men are undergoing biopsy based on elevated serum prostate-specific antigen (PSA) levels. These biopsies may trigger an inflammatory response in the prostate, leading to prostatitis, or, alternatively, a biopsy may introduce organisms into the prostate gland.

The above examples outline potential research directions in the field of prostatitis. Results of these and other studies could promote an increased awareness of prostatitis and increase the knowledge about the disease. This research should improve diagnosis and treatment, promote an appropriate allocation of resources to the management of the disease, and reduce the incidence and public health burden of prostatitis.



Medication Summary

The goals of pharmacotherapy are to eradicate the infection, reduce morbidity, and prevent complications. Antibiotics are given empirically until results of urine culture and sensitivity become available. Alpha-blocker therapy should also be considered.


Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Trimethoprim-sulfamethoxazole (Bactrim DS, Septra DS)

This agent inhibits bacterial growth by inhibiting the synthesis of dihydrofolic acid.


Gentamicin is an aminoglycoside antibiotic for gram-negative coverage, including pseudomonal species. It is synergistic with beta-lactamase against enterococci. It interferes with bacterial protein synthesis by binding to the 30S and 50S ribosomal subunits.

Dosing regimens are numerous and are adjusted based on creatine clearance and changes in the volume of distribution, as well as body space into which the agent needs to distribute. Gentamicin may be given IV or IM. Each regimen must be followed by at least a trough level drawn on the third or fourth dose, 0.5 hour before dosing; the peak level may be drawn 0.5 hour after the 30-min infusion.


Ampicillin is a broad-spectrum penicillin. It interferes with bacterial cell wall synthesis during active replication, causing bactericidal activity against susceptible organisms. It is an alternative to amoxicillin when the patient is unable to take medication orally.

Levofloxacin (Levaquin)

Levofloxacin is indicated for chronic bacterial prostatitis due to E coli, E faecalis, or S epidermidis. It is a second-generation quinolone that acts by interfering with DNA gyrase in bacterial cells.


Ofloxacin penetrates the prostate well and is effective against N gonorrhea and C trachomatis. It is a pyridine carboxylic acid derivative with a broad spectrum of bactericidal effect.

Norfloxacin (Noroxin)

Norfloxacin is a fluoroquinolone with activity against pseudomonads, streptococci, MRSA, S epidermidis, and most gram-negative organisms, but it has no activity against anaerobes. It inhibits bacterial DNA synthesis and, consequently, growth.

Clindamycin (Cleocin)

Clindamycin is a semisynthetic antibiotic produced by a 7(S)-chloro-substitution of 7(R)-hydroxyl group of the parent compound lincomycin. It inhibits bacterial growth, possibly by blocking the dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. It widely distributes in the body, without penetration of the CNS. Clindamycin is protein bound and excreted by the liver and kidneys.

It is effective against gram-positive aerobic and anaerobic bacteria (except enterococci).


Questions & Answers


What is acute bacterial prostatitis?

What is the pathologic definition of prostatitis?

What is the NIH classification of prostatitis?

What is the historical epidemiologic data on prostatitis?

What anatomy is relevant in acute bacterial prostatitis?

Where can more information on acute bacterial prostatitis be found?

What theories of the pathogenesis of acute bacterial prostatitis have been proposed?

What organisms are primarily responsible for acute bacterial prostatitis?

What is the role of prostate biopsy in the etiology of acute bacterial prostatitis?

What are the risk factors for acute bacterial prostatitis?

What is the prognosis of acute bacterial prostatitis?


What are the signs and symptoms of acute bacterial prostatitis?

How is acute bacterial prostatitis diagnosed on physical exam?


When should prostatic abscess be suspected during an evaluation for acute bacterial prostatitis?

What are the differential diagnoses for Acute Bacterial Prostatitis?


How is acute bacterial prostatitis diagnosed?

What is the role of urine studies in the workup of acute bacterial prostatitis?

What is the role of serum prostate-specific antigen (PSA) testing in the workup of acute bacterial prostatitis?

What is the role of imaging studies in the workup of acute bacterial prostatitis?

Which histologic findings suggest acute bacterial prostatitis?


What are treatment options for acute bacterial prostatitis?

What is the choice of antibiotic determined in the treatment of acute bacterial prostatitis?

What is the duration of antibiotic therapy for acute bacterial prostatitis?

How is antibiotic drug resistance managed in the treatment of acute bacterial prostatitis?

What are oral medication options for acute bacterial prostatitis?

What is the role of anaerobic antimicrobial therapy for acute bacterial prostatitis?

When is surgery indicated in the treatment of acute bacterial prostatitis?

Which surgical procedures are preferred in the treatment of acute bacterial prostatitis?

When is drainage of prostatic abscess indicated in the treatment of acute bacterial prostatitis?

How is surgery performed in patients with acute bacterial prostatitis?

What is still unknown about prostatitis that requires additional study?

Why is prostatic biopsy a risk factor for acute bacterial prostatitis?


What are the goals of drug treatment in acute bacterial prostatitis?

Which medications in the drug class Antibiotics are used in the treatment of Acute Bacterial Prostatitis?