Bacterial Acute Prostatitis


Article Author:
Nathan Davis


Article Editor:
Michael Silberman


Editors In Chief:
Casey Ciresi


Managing Editors:
Avais Raja
Orawan Chaigasame
Khalid Alsayouri
Kyle Blair
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Navid Mahabadi
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Abbey Smiley
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beenish Sohail
Hajira Basit
Phillip Hynes
Sandeep Sekhon


Updated:
2/28/2019 10:08:08 PM

Introduction

Bacterial prostatitis (BP) is a bacterial infection of the prostate gland occurring in a bimodal distribution in younger and older men. It can be acute (ABP) or chronic (CBP) in nature and if not treated appropriately, can result in significant morbidity. As a result, the causes, pathophysiology, presentation, evaluation, and management of BP are important for providers to understand in an emergency and ambulatory settings.[1][2][3]

Etiology

BP is most commonly caused by infection from members of the Enterobacteriaceae family, but organisms from other families can be responsible and are more likely in certain high-risk populations. Escherichia coli is the most common isolate from urine cultures and is the causative agent in the majority (approximately 50% to 90%) of cases. Other common isolates include the species Proteus, Klebsiella, Enterobacter, Serratia, and Pseudomonas. Gram-positive organisms such as Enterococcus species and Staphylococcus species and sexually transmitted organisms such as Neisseria gonorrhoeae, Chlamydia trachomatis, Ureaplasma urealyticum are also sometimes implicated. Prostate manipulation from procedures such as transrectal prostate biopsy, transurethral prostate biopsy, cystoscopy, and catheterization appears to increase the risk of pseudomonasmixed organism, staphylococcal infectionsand treatment failure prostatitis. Special consideration should be given to immunocompromised patients as they are at higher risk of contracting BP from atypical organisms such as Salmonella species, Mycobacterium species, Staphylococcus speciesamong others. Though this article focuses on bacterial etiologies, fungal and viral etiologies should be strongly considered in these patient populations as well. Despite the fact that Enterobacteriaceae are the most common causative organisms in both ABP and CBP, gram-positive organisms and atypicals are more likely in CBP than in ABP; although, the role of gram-positive organisms in CBP is debated despite the fact they sometimes are isolated in culture.[4][5]

Epidemiology

Prostatitis has a bimodal distribution in young to middle-aged men and in senior men and has a prevalence of approximately 8% to 16%; however, it should be noted that only 5% to 10% cases of prostatitis are identified as bacterial in origin. As a result, the NIH has created four classifications for prostatitis: ABP, CBP, chronic prostatitis/chronic pelvic pain syndrome, and asymptomatic inflammatory prostatitis.  Bacterial prostatitis is relatively uncommon when compared to other causes of prostatitis. Men who have one episode of bacterial prostatitis are more likely to have subsequent episodes and progress to chronic bacterial and nonbacterial prostatitis. Risk factors for bacterial prostatitis include prostate manipulation, urethral stricture, benign prostatic hyperplasia (BPH), phimosis, urethritis, diabetes and other immune-compromising states, and a history of sexually transmitted infections (STIs), among others. Prostatitis also appears to increase the risk for developing BPH and possibly prostate cancer.[6][7]

Pathophysiology

The proposed mechanisms of BP all involve the infiltration of pathogenic organisms that are capable of overcoming the prostate gland's natural immune defenses. Most commonly, BP is secondary to ascending infection from urethritis, cystitis, and epididymal-bronchitis, but BP is also often caused by direct inoculation from prostate biopsy or manipulation. Less commonly, BP can be caused by hematogenous or lymphatic seeding from sepsis or other sources of infection in the body. The pathophysiology of CBP is less well understood but may involve the development of bacterial biofilms.[3]

History and Physical

ABP typically presents with abrupt signs and symptoms of infection while CBP often presents more subtly. Patients with ABP typically complain of fever, malaise, myalgias, dysuria, urinary frequency/hesitancy, and pelvic pain. On physical exam, the prostate is often enlarged and exquisitely tender to palpation. Vigorous manipulation of the prostate gland should not be performed in ABP as this may acutely exacerbate the patient's condition. The patient should also be evaluated for signs and symptoms of urinary retention, which may present with suprapubic tenderness and suprapubic fullness.  Patients suspected of having ABP should also be assessed for CVA tenderness, as pyelonephritis is an important differential. The symptoms of CBP are, by definition, chronic and recurring and are often less severe than acute prostatitis but can nevertheless significantly impact the quality of life. As with ABP, CBP can present with signs and symptoms of urinary tract infection, urinary retention, and pelvic pain; however, men with CBP do not typically appear acutely ill, and some men simply have chronic asymptomatic bacteriuria. The prostate is not acutely inflamed on the exam but may be tender to palpation. Men with CBP may also present with sexual dysfunction.

Evaluation

The evaluation of ABP depends largely on individual patient characteristics and suspicion for ABP complications, while the evaluation of CBP is most appropriately performed by a urologist or in close consultation with a urologist. At a minimum, once ABP is suspected based on history and physical, the patient should be evaluated with midstream urinalysis and urine culture. If the patient meets sepsis criteria or has significant medical comorbidities, blood cultures, lactic acid, metabolic panel, and complete blood count should be obtained. While imaging is not required in all cases, it should be strongly considered in the form of CT or TRUS to evaluate for a prostatic abscess in patients who are immunocompromised or predisposed to bacteremia or embolic bacterial seeding. It should also be strongly considered in patients who are clinically worsening despite appropriate treatment. Urology should be consulted for possible suprapubic catheterization when patients present with acute urinary retention in the setting of ABP, as the passage of a transurethral urinary catheter may worsen the patient's condition. PSA and inflammatory markers such as CRP and ESR are of limited utility in ABP due to lack of specificity. If STI is suspected or if the urethral discharge is present, N. gonorrhea and C. trachomatis testing should be performed. Diagnosis of chronic prostatitis is best performed by a specialist utilizing either the Meares and Stamey four-glass test or the simpler two-glass pre-massage and post-massage test and possibly semen sample with culture and urodynamic studies. The four-glass test, as its name implies, is a test of four different samples: initially voided urine, mid-stream urine, expressed prostatic secretions, and post-prostate massage urine. The 2-glass test is performed by obtaining pre-massage and post-prostate massage urine samples. The 4-glass test is not performed often as it is difficult to carry out for the patient and the provider and has poor supporting evidence.[8][9]

Treatment / Management

Management of BP involves both choosing appropriate spectrum antibiotics that have good prostate tissue penetration and managing the complications and sequelae of the disease. The prostate does have some unique structural and biochemical characteristics that render certain antibiotics less effective. The prostate gland tends to be alkaline, and its capillaries are not as permeable as many other tissue capillaries. Therefore, antibiotics with a high pKa and good fat solubility achieve higher tissue concentrations. Fluoroquinolones, tetracyclines, macrolides, and trimethoprim (but not sulfamethoxazole) generally have these characteristics. However, acutely inflamed prostate tissue is penetrated by most antibiotics (except nitrofurantoin), which gives the clinician several options in treating ABP. Treatment of CBP should be guided by culture results and should be done with antibiotics that achieve therapeutic prostate concentrates, as initiating antibiotic treatment emergently is not warranted and can wait on culture results. CPB treatment is 2 to 6 weeks in duration. As mentioned above, Enterobacteriaceae organisms are the most common cause of BP, so empiric treatment in ABP should aim to cover these organisms. Patients with ABP who are not severely ill and have none of those above risk factors for treatment failure from antibiotic resistance and/or atypical organisms can be discharged on oral fluoroquinolones or Bactrim for 2 to 4 weeks with follow-up culture to ensure resolution. Patients who are suspected of a sexually transmitted cause of prostatitis should be treated with a single dose of IM Rocephin followed by 2 weeks of doxycycline. Patients who meet sepsis criteria, have urinary retention, or have risk factors for treatment failure and/or resistant organisms should be admitted to the hospital and started on parenteral antibiotics. Initial choices may include a fluoroquinolone plus an aminoglycoside or an antipseudomonal penicillin or cephalosporin. As mentioned earlier, imaging should be strongly considered with TRUS or CT in patients who have failed treatment or who are at risk for bacterial seeding to evaluate for prostatic abscess which may require surgical drainage. Urology should be consulted for urinary retention in the setting of ABP for possible suprapubic catheter placement. Patients who are admitted for ABP should ultimately be discharged on oral antibiotics selected based on culture results and with those above favorable biochemical properties.[10][11][12]

Differential Diagnosis

  • Urethritis
  • Prostate cancer
  • Urinary tract infection

Complications

  • Sepsis
  • Epididymitis
  • Abscess
  • Chronic prostatitis
  • Chronic pelvic pain 

Pearls and Other Issues

A small, albeit significant proportion (approximately 5% to 10%) of patients with ABP will progress to CBP. Several risk factors for progression to CBP have been identified and include alcohol abuse, diabetes mellitus, large prostate volume, and history of prostate manipulation. Protective factors against progression to CPB appear to include cystostomy in ABP and prolonged antibiotic therapy in ABP. Though more research is needed on this topic, it does appear that risk factor modification may help prevent progression of ABP to CBP.

Enhancing Healthcare Team Outcomes

Acute bacterial prostatitis is associated with an enormous burden on healthcare costs. While physicians manage the acute infection, the key is to prevent the condition in the first place. Nurses should be aware that unnecessary urethral catheterization should be avoided. In addition, the pharmacist should remind physicians that administering prophylactic antibiotics prior to a transrectal biopsy can lower the risk of a urinary tract infection and bacteriuria. The nurse should also educate the patient on adequate hydration and use of antipyretics. If the patient develops urinary retention, he should seek immediate medical assistance.[13][14] (Level V) 

Outcomes

Patients who do respond to antibiotics do have a good outcome. However, those who do not seek treatment or do not respond to antibiotics may have lower rates of fertility. Other studies have reported that patients with heavy bacterial inoculation also tend to have impaired sperm motility and viability. Abscess formation is a rare complication of acute bacterial prostatitis and is known to occur in diabetics, patients who are immunocompromised and those who have undergone urethral instrumentation or have prolonged indwelling urinary catheters. Rare reports exist of pyelonephritis, chronic prostatitis, and sepsis. At least 10% of patients with acute bacterial prostatitis will develop chronic pelvic pain syndrome.[5][15] (Level V)


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Bacterial Acute Prostatitis - Questions

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Which is true of acute prostatitis?



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Which of the following is not true of acute prostatitis?



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A male presents with pain in the perineum, penile tip, testicle, and scrotum, which has been going on for the past 3 months. He had lower back pain a week ago, but the pain has since subsided. A clear milky discharge from the penis and nocturia are also noted. On physical examination, his prostate is boggy and tender to palpation. What is the most common cause of this chronic form of prostatitis?



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In a patient with suspected prostatitis, how many urine samples are collected?



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Which statement about acute bacterial prostatitis is FALSE?



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A male patient presents with gradual onset of low back pain. The patient also has generalized muscle pain and dysuria. Select the most likely diagnosis.



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Which of the following statements is true concerning an adult male with fever, low back pain, and perineal discomfort?



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A 52 year old male complains of low back pain, dysuria, fever, and chills. The prostate is exquisitely tender and boggy. Prostatic fluid has many neutrophils. Select the most probable infectious organism.



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How can the diagnostic yield of a urine specimen from a patient with prostatitis be increased?



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A 38-year-old male with no significant past medical history presents to the emergency department with sudden onset fever, dysuria, and malaise. Upon presentation, his vitals are T 101.5, HR 85, RR 14, BP 129/73, SaO2 98%. He has a soft and non-tender abdomen with no costovertebral tenderness. Prostate exam demonstrates a tender and enlarged prostate. His post-void residual is 10 cc. He is sexually active with one long-term partner and has no history of sexually transmitted infections. He denies urethral discharge, and none is noted on exam. Midstream urinalysis is nitrite positive with large leukocyte esterase, 3+ bacteria, 30 WBCs, and 3 RBCs. The patient's serum WBC is 8, and his lactic acid is 0.4. Laboratory evaluation is otherwise unremarkable. Urine gram stain shows gram-negative rods. Urine culture is pending. What are the most appropriate treatment and disposition for this patient?



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A 29-year-old male presents to a urologist as a referral from his primary provider with a six-month history dysuria, urinary hesitancy, and vague pelvic discomfort. The patient has just finished a 6 week course of ciprofloxacin with no improvement in his symptoms. Urine culture results obtained 6 weeks ago shows no growth. He has a history of HTN but is otherwise healthy. He is sexually active and has had two partners over the past year. He denies urethral discharge. Vitals in the office are temperature 98.3F, heart rate 72 bpm, blood pressure 153/87 mmHg, respiratory rate 14/minute, and SaO2 99% on room air. His prostate is slightly enlarged but non-tender on exam. His exam is otherwise unremarkable. What is the next appropriate step in management?



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A 38-year-old male presents with one week of worsening fever, dysuria, perineal pain, myalgias, and malaise. He has been on cephalexin for the past week after being diagnosed with a urinary tract infection at a walk-in clinic one week ago. He has a history of diabetes mellitus type 1 DM with a recent hemoglobin A1c of 11. Upon further questioning, he also admits to occasionally using intravenous heroin. Vital signs upon presentation to are temperature 103.7F, heart rate 123 bpm, blood pressure 110/58 mmHg, respiratory rate 18/min, and SaO2 98% on room air. His physical exam demonstrates suprapubic tenderness and fullness and an enlarged and tender prostate. He has no heart murmur or skin lesions. Post-void residual is 35 cc. Laboratory evaluation demonstrates WBC 23k and lactic acid of 3.1. Urinalysis demonstrates 3+ bacteria, positive nitrites, large leukocyte esterase. Urine gram stain demonstrates gram-negative rods. What are the next best steps in management?



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Bacterial Acute Prostatitis - References

References

Wolfe T,Smith C,Jacob R, Acute bacterial prostatitis in an adolescent patient following blunt trauma. Proceedings (Baylor University. Medical Center). 2018 Jan     [PubMed]
Kang CI,Kim J,Park DW,Kim BN,Ha US,Lee SJ,Yeo JK,Min SK,Lee H,Wie SH, Clinical Practice Guidelines for the Antibiotic Treatment of Community-Acquired Urinary Tract Infections. Infection     [PubMed]
Khan FU,Ihsan AU,Khan HU,Jana R,Wazir J,Khongorzul P,Waqar M,Zhou X, Comprehensive overview of prostatitis. Biomedicine     [PubMed]
Carroll DE,Marr I,Huang GKL,Holt DC,Tong SYC,Boutlis CS, Staphylococcus aureus Prostatic abscess: a clinical case report and a review of the literature. BMC infectious diseases. 2017 Jul 21     [PubMed]
Lee DS,Choe HS,Kim HY,Kim SW,Bae SR,Yoon BI,Lee SJ, Acute bacterial prostatitis and abscess formation. BMC urology. 2016 Jul 7     [PubMed]
Campeggi A,Ouzaid I,Xylinas E,Lesprit P,Hoznek A,Vordos D,Abbou CC,Salomon L,de la Taille A, Acute bacterial prostatitis after transrectal ultrasound-guided prostate biopsy: epidemiological, bacteria and treatment patterns from a 4-year prospective study. International journal of urology : official journal of the Japanese Urological Association. 2014 Feb     [PubMed]
Dévora Ruano O,de Diego García A,Hernando Real S, [Acute bacterial prostatitis by Ralstonia pickettii: clinical and epidemiological considerations of excepcional observation]. Medicina clinica. 2009 Jul 18     [PubMed]
Mouraviev V,McDonald M, An implementation of next generation sequencing for prevention and diagnosis of urinary tract infection in urology. The Canadian journal of urology. 2018 Jun     [PubMed]
Lee Y,Lee DG,Lee SH,Yoo KH, Risk Factor Analysis of Ciprofloxacin-Resistant and Extended Spectrum Beta-Lactamases Pathogen-Induced Acute Bacterial Prostatitis in Korea. Journal of Korean medical science. 2016 Nov     [PubMed]
Mirone V, [From cystitis to bacterial prostatitis: experience with levofloxacin]. Le infezioni in medicina : rivista periodica di eziologia, epidemiologia, diagnostica, clinica e terapia delle patologie infettive. 2009 Dec     [PubMed]
Walker NA,Challacombe B, Managing epididymo-orchitis in general practice. The Practitioner. 2013 Apr     [PubMed]
Liu L,Yang J, Physician's practice patterns for chronic prostatitis. Andrologia. 2009 Oct     [PubMed]
Gill BC,Shoskes DA, Bacterial prostatitis. Current opinion in infectious diseases. 2016 Feb     [PubMed]
Yoon BI,Kim S,Han DS,Ha US,Lee SJ,Kim HW,Han CH,Cho YH, Acute bacterial prostatitis: how to prevent and manage chronic infection? Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy. 2012 Aug     [PubMed]
Krieger JN,Thumbikat P, Bacterial Prostatitis: Bacterial Virulence, Clinical Outcomes, and New Directions. Microbiology spectrum. 2016 Feb     [PubMed]

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