Prostatitis refers to inflammation of the prostate gland. Infection occurs when bacteria from the urethra or bladder enter the prostate. It has been reported that there are approximately 2 million outpatient visits yearly for prostatitis in the United States, accounting for 8 % of all urology office visits and 1 % of all primary care visits [23, 24].

The National Institutes of Health (NIH) established a classification of prostatitis into four categories: acute bacterial prostatitis, chronic bacterial prostatitis, chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS), and asymptomatic inflammatory prostatitis. Acute bacterial prostatitis presents with dysuria, frequency, and other symptoms of a urinary tract infection. E. coli is the most common causative pathogen. Signs of systemic infection are related to infection of the prostate and include fever, malaise, and general aches. Treatment for acute bacterial prostatitis is directed at gram-negative enteric bacteria. Trimethoprim-sulfamethoxazole, fluoroquinolones, and ampicillin with gentamicin are all reasonable options while awaiting urine culture sensitivities and should continue for a total of 1 month duration. Additionally, alpha-adrenergic blockers can be used to help reduce obstruction and urinary reflux. Rarely, prostatitis requires surgery and this is generally seen in the setting of a prostatic abscess. Chronic bacterial prostatitis is seen in patients with repeated urinary tract infections, most commonly E. coli. Patients will present with dysuria and pelvic or low back pain. Positive urinary cultures can be seen in between periods of symptomatic bacteriuria. Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) represents the most common type. Numerous medical therapies have been tried, but a definitive treatment still remains unknown. Patients in this subtype complain of LUTS and pelvic pain. Treatments to consider consist of anti-inflammatories, alpha-adrenergic blockers, and hormonal therapies. A recent study by Kong et al. evaluated the use of phosphodiesterase inhibitors, specifically mirodenafil, in combination with levofloxacin. The group receiving mirodenafil noted an improvement in LUTS; however, pain was unchanged [25]. CP/CPPS is further broken down into inflammatory and noninflammatory. Noninflammatory chronic pelvic pain syndrome is characterized by the absence of WBCs in prostatic fluid and no prostatic bacterial infection. Inflammatory CP/CPPS also called nonbacterial prostatitis is defined as WBCs in prostatic fluid, but no active prostate infection. The etiology may be related to reflux of urine into the prostate causing an irritant prostatitis. Asymptomatic inflammatory prostatitis is seen during the workup for other genitourinary pathologies such as following a prostate biopsy. A common finding is a large concentration of leukocytes in semen [26]. Granulomatous prostatitis, which is not included in the NIH classification, is seen following bacillus Calmette-Guérin (BCG) intravesical therapy for bladder cancer and tuberculosis.

A prostatic abscess, though uncommon, should be suspected when a patient being treated for bacterial prostatitis fails to improve with antibiotic therapy. E. coli is the most common causative organism and is typically caused by the reflux of infected urine into the prostate gland. Additionally, hematogenous spread usually secondary to Staphylococcus aureus and direct inoculation following a prostatic procedure can lead to formation of a prostatic abscess. Patients may present with LUTS, perineal pain, fever, chills, low back pain, or even sepsis [33]. A fluctuation in areas of the prostate can be noted on digital rectal examination, but will not always be apparent. Immunosuppression and uncontrolled diabetes place a patient at an increased risk. Management is antibiotic therapy with abscess drainage. Surgical intervention includes transurethral unroofing and resection, perineal incision and drainage, and percutaneous drainage. Recurrence of a prostatic abscess can occur following initial treatment, so repeat imaging to confirm resolution of the abscess is recommended. This is commonly done with TRUS; however, CT and MRI are feasible options [33].

A variety of cysts can exist in the prostate and can be asymptomatic or symptomatic depending on their origin and size. The overall prevalence of prostatic cysts is not known, but studies have shown medial cysts in up to 8 % of asymptomatic patients. Another small study found prostatic utricle (PU) cysts in 11 % of 150 infertile men, while no cysts were found in 30 fertile men. Prostatic cysts can be broken down into intraprostatic and periprostatic. Treatment is generally reserved for those cysts that may be associated with urinary obstruction, infertility, infection, or discomfort. The classification of prostatic cysts is based on their anatomic location which includes midline cysts, paramedian cysts, lateral cysts, and periprostatic cysts [37].

Galosi et al. proposed a new classification of prostatic cysts based on clinical and pathological features. They further described the appearance of the cystic lesions based upon imaging. Previous classifications have based cysts on clinical settings which included LUTS, oncology, infertility, and infectious disease [37]. They divided the cysts into six categories identified as type 1 through 6 in order: isolated medial cysts, ejaculatory duct cysts, parenchymal cysts, complicated cysts (hemorrhagic or infectious), cystic tumors, and parasitic cysts [37].

Midline cysts consist of PU cysts and Müllerian cysts. Müllerian cysts originate from remnants of the Müllerian duct, while PU cysts come from dilation of the prostatic utricle. These terms are sometimes used interchangeably; however, most literature classifies them as different entities. Midline cysts are located superior to the verumontanum in between the seminal vesicles. Müllerian cysts and PU cysts may be indistinguishable from one another on imaging, but there are differences on imaging to tell them apart. Müllerian duct cysts can originate lateral to midline given the anatomic location of the Müllerian ducts during embryology and anywhere along the Müllerian duct path. PU cysts should be precisely midline given the anatomic location the prostatic utricle. Aside from anatomic location, PU cysts communicate with the posterior urethra. This feature is not seen in Müllerian duct cysts. Müllerian duct cysts tend to be larger and occur later in life, while PU cysts occur in the first two decades of life. Lastly PU cysts have been associated with genitourinary abnormalities, while Müllerian duct cysts are isolated entities. Galosi also identified an enlarged PU in children, which is not a true cyst and is associated with an absent verumontanum and wide opening into the urethra. The enlarged PU is a tubular structure with squamous epithelium. A study involving 65 patients with Müllerian duct cysts evaluated the workup and management. Of the 65 patients, 27 underwent an invasive procedure which included transperineal or transrectal puncture in 9, endoscopic resection of the utricle meatus in 12, and large marsupialization in 6 patients. They noted improvement or cure in 82 % of the patients at roughly 4 years follow-up [38]. Halpern and Hirsch discuss a case report of a 35-year-old male with infertility found to have a Müllerian duct cyst. TRUS was used to guide transurethral laser incision of the cystic obstruction. Following incision, TRUS confirmed cystic decompression [39].

Ejaculatory duct cysts are paramedian cysts which can be congenital or acquired due to an ejaculatory duct obstruction. Evidence for an acquired ejaculatory duct cyst can be seen when there is a prostatic calculus or PU cysts. These cysts when aspirated contain spermatozoa or fructose [40].

Prostatic retention cysts are acquired and increase in frequency with advancing age in patients with BPH in the fifth and sixth decades of life. They result from the obstruction of prostate gland ductules resulting in upstream cystic dilation of the gland acini. On aspiration, spermatozoa are absent. BPH with cystic degeneration is the most common cystic lesion of the prostate and located in the transitional zone of the prostate gland [40]. They can be seen within the hyperplastic nodules and contain calculi and white or hemorrhagic fluid. The white fluid is corpora amylacea and hemorrhage is due to necrosis or infarction of prostatic nodules [40].