No treatment required. It is standard practice for men with infertility and category IV prostatitis to be given a trial of antibiotics and/or anti-inflammatories, although evidence of efficacy are weak. Since signs of asymptomatic prostatic inflammation may sometimes be associated with prostate cancer, this can be addressed by tests that assess the ratio of free-to-total PSA. The results of these tests were significantly different in prostate cancer and category IV prostatitis in one study.

IgG4-related disease responds well, and often dramatically, to glucocorticoid therapy, provided that advanced fibrotic lesions have not resulted in irreversible damage, and this has included resolution of radiologic findings. Men given glucocorticoids to treat IgG4-related disease at other anatomical sites sometimes report relief of their lower urinary tract symptoms, suggesting that IgG4-related prostatitis may be underdiagnosed.

Cases are however likely to get misdiagnosed as benign prostatic hyperplasia and to get treated alternatively with medications such as alpha blockers. The efficacy of alpha blockers in IgG4-related prostatitis remains unclear.

Antibiotic therapy has to overcome the blood/prostate barrier that prevents many antibiotics from reaching levels that are higher than minimum inhibitory concentration. A blood-prostate barrier restricts cell and molecular movement across the rat ventral prostate epithelium. Treatment requires prolonged courses (4–8 weeks) of antibiotics that penetrate the prostate well. The fluoroquinolones, tetracyclines and macrolides have the best penetration. There have been contradictory findings regarding the penetrability of nitrofurantoin , quinolones (ciprofloxacin, levofloxacin), sulfas (Bactrim, Septra), doxycycline and macrolides (erythromycin, clarithromycin). This is particularly true for gram-positive infections.

In a review of multiple studies, Levofloxacin (Levaquin) was found to reach prostatic fluid concentrations 5.5 times higher than Ciprofloxacin, indicating a greater ability to penetrate the prostate.

Persistent infections may be helped in 80% of patients by the use of alpha blockers (tamsulosin (Flomax), alfuzosin), or long term low dose antibiotic therapy. Recurrent infections may be caused by inefficient urination (benign prostatic hypertrophy, neurogenic bladder), prostatic stones or a structural abnormality that acts as a reservoir for infection.

In theory, the ability of some strains of bacteria to form biofilms might be one factor amongst others to facilitate development of chronic bacterial prostatitis.

Escherichia coli extract and cranberry have a potentially preventive effect on the development of chronic bacterial prostatitis, while combining antibiotics with saw palmetto, lactobacillus sporogens and arbutin may lead to better treatment outcomes.

Bacteriophages hold promise as another potential treatment for chronic bacterial prostatatis.

The addition of prostate massage to courses of antibiotics was previously proposed as being beneficial and prostate massage may mechanically break up the biofilm and enhance the drainage of the prostate gland. However, in more recent trials, this was not shown to improve outcome compared to antibiotics alone.

Antibiotics are the first line of treatment in acute prostatitis. Antibiotics usually resolve acute prostatitis infections in a very short time, however a minimum of two to four weeks of therapy is recommended to eradicate the offending organism completely. Appropriate antibiotics should be used, based on the microbe causing the infection. Some antibiotics have very poor penetration of the prostatic capsule, others, such as ciprofloxacin, trimethoprim/sulfamethoxazole, and tetracyclines such as doxycycline penetrate prostatic tissue well. In acute prostatitis, penetration of the prostate is not as important as for category II because the intense inflammation disrupts the prostate-blood barrier. It is more important to choose a bactericidal antibiotic (kills bacteria, e.g., a fluoroquinolone antibiotic) rather than a bacteriostatic antibiotic (slows bacterial growth, e.g. tetracycline) for acute potentially life-threatening infections.

Severely ill patients may need hospitalization, while nontoxic patients can be treated at home with bed rest, analgesics, stool softeners, and hydration. Men with acute prostatitis complicated by urinary retention are best managed with a suprapubic catheter or intermittent catheterization. Lack of clinical response to antibiotics should raise the suspicion of an abscess and prompt an imaging study such as a transrectal ultrasound (TRUS).

Over time, the relapse rate is high, exceeding 50%. However, recent research indicates that combination therapies offer a better prognosis than antibiotics alone.

A 2007 study showed that repeated combination pharmacological therapy with antibacterial agents (ciprofloxacin/azithromycin), alpha-blockers (alfuzosin) and Serenoa repens extracts may eradicate infection in 83.9% of patients with clinical remission extending throughout a follow-up period of 30 months for 94% of these patients.

A 2014 study of 210 patients randomized into two treatment groups found that recurrence occurred within 2 months in 27.6% of the group using antibiotics alone (prulifloxacin 600 mg), but in only 7.8% of the group taking prulifloxacin in combination with Serenoa repens extract, Lactobacillus Sporogens and Arbutin.

Prostatitis is inflammation of the prostate gland. Prostatitis is classified into acute, chronic, asymptomatic inflammatory prostatitis, and chronic pelvic pain syndrome.

In the United States, prostatitis is diagnosed in 8 percent of all urologist visits and 1 percent of all primary care physician visits.

Asymptomatic inflammatory prostatitis is a painless inflammation of the prostate gland where there is no evidence of infection. It should be distinguished from the other categories of prostatitis characterised by either pelvic pain or evidence of infection, such as chronic bacterial prostatitis, acute bacterial prostatitis and chronic pelvic pain syndrome (CPPS). It is a common finding in men with benign prostatic hyperplasia.

Granulomatous prostatitis is an uncommon disease of the prostate, an exocrine gland of the male reproductive system. It is a form of prostatitis, i.e. inflammation of the prostate, resulting from infection (bacterial, viral, or fungal), the BCG therapy, malacoplakia or systemic granulomatous diseases which involve the prostate.

In recent years the prognosis for CP/CPPS has improved with the advent of multimodal treatment, phytotherapy, protocols aimed at quieting the pelvic nerves through myofascial trigger point release and anxiety control, and chronic pain therapy.

In a small minority of cases of urethral syndrome, treatment with antibiotics is effective, which indicates that in some cases it may be caused by bacterial infection which does not show up in either urinalysis or urine culture. For chronic urethral syndrome, a long term, low-dose antibiotic treatment is given on a continuous basis or after intercourse each time if intercourse appears to trigger symptoms.

As low oestrogen may also be considered a source for urethral syndrome, hormone replacement therapy, and oral contraceptive pill (birth-control pills) containing oestrogen are also used to treat the symptoms of this condition in women.

In a preliminary 2005 open label study of 16 treatment-recalcitrant CPPS patients, controversial entities known as nanobacteria were proposed as a cause of prostatic calcification and symptoms found in CPPS. Patients were treated with EDTA (to dissolve the calcifications) and 3 months of tetracycline (a calcium-leaching antibiotic with anti-inflammatory effects, used here to kill the "pathogens"), and half had significant improvement in symptoms. Scientists have expressed strong doubts about whether nanobacteria are living organisms. Research in 2008 showed that "nanobacteria" are merely tiny lumps of abiotic limestone.

Phytotherapeutics such as quercetin and flower pollen extract have been studied in small clinical trials; the evidence is insufficient to judge safety or efficacy.

The evidence supporting a viral cause of prostatitis and chronic pelvic pain syndrome is weak. Single case reports have implicated herpes simplex virus (HSV) and cytomegalovirus (CMV) but a study using PCR failed to demonstrate the presence of viral DNA in patients with chronic pelvic pain syndrome undergoing radical prostatectomy for localized prostate cancer. The reports implicating CMV must be interpreted with caution because in "all" cases the patients were immunocompromised. For HSV the evidence is weaker still and there is only one reported case and the causative role of the virus was not proven, and there are no reports of successful treatments using antiviral drugs such as aciclovir.

Due to the concomitant presence of bladder disorders, gastrointestinal disorders, and mood disorders, research has been conducted to understand whether CP/CPPS might be caused by problems with the hypothetical bladder-gut-brain axis.

Research has been conducted to understand how chronic bladder pain affects the brain, using techniques like MRI and functional MRI; as of 2016 it appeared that people with CP/CPPS have increased grey matter in the primary somatosensory cortex, the Insular cortex, the insular cortex, and the anterior cingulate cortex, and in the central nucleus of the amygdala; studies in rodents have shown that blocking the metabotropic glutamate receptor 5 which is expressed in the central nucleus of the amygdala, can block bladder pain.

Prostatic secretions escape into the stroma and elicit an inflammatory response.

In people who do not require hospitalization and live in an area where there is a low prevalence of antibiotic-resistant bacteria, an fluoroquinolone by mouth such as ciprofloxacin or levofloxacin is an appropriate initial choice for therapy. In areas where there is a higher prevalence of fluoroquinolone resistance, it is useful to initiate treatment with a single intravenous dose of a long-acting antibiotic such as ceftriaxone or an aminoglycoside, and then continuing treatment with a fluoroquinolone. Oral trimethoprim/sulfamethoxazole is an appropriate choice for therapy if the bacteria is known to be susceptible. If trimethoprim/sulfamethoxazole is used when the susceptibility is not known, it is useful to initiate treatment with a single intravenous dose of a long-acting antibiotic such as ceftriaxone or an aminoglycoside. Oral beta-lactam antibiotics are less effective than other available agents for treatment of pyelonephritis. Improvement is expected in 48 to 72 hours.

IgG4-related prostatitis is the term used to describe prostate involvement in men with IgG4-related disease (IgG4-RD), which is an emerging fibroinflammatory disease entity which is characterised (i) by a tendency to mass forming lesions in multiple sites of the body and (ii) by usually a prompt response to steroid therapy.

Men with IgG4-related prostatitis may also present with manifestations of IgG4-RD at other sites anywhere in the body; involvement of different areas of the body can occur either at the same time (synchronously) or at different periods of time (metachronously).

The evidence that preventive antibiotics decrease urinary tract infections in children is poor. However recurrent UTIs are a rare cause of further kidney problems if there are no underlying abnormalities of the kidneys, resulting in less than a third of a percent (0.33%) of chronic kidney disease in adults. Whether routine circumcisions prevents UTIs has not been well studied as of 2011.

In people suspected of having pyelonephritis, a urine culture and antibiotic sensitivity test is performed, so therapy can eventually be tailored on the basis of the infecting organism. As most cases of pyelonephritis are due to bacterial infections, antibiotics are the mainstay of treatment. The choice of antibiotic depends on the species and antibiotic sensitivity profile of the infecting organism, and may include fluoroquinolones, cephalosporins, aminoglycosides, or trimethoprim/sulfamethoxazole, either alone or in combination.

Acute prostatitis is a serious bacterial infection of the prostate gland. This infection is a medical emergency. It should be distinguished from other forms of prostatitis such as chronic bacterial prostatitis and chronic pelvic pain syndrome (CPPS).

Some research suggests that cranberry (juice or capsules) may decrease the number of UTIs in those with frequent infections. A Cochrane review concluded that the benefit, if it exists, is small. Long-term tolerance is also an issue with gastrointestinal upset occurring in more than 30%. Cranberry juice is thus not currently recommended for this indication. As of 2015, probiotics require further study to determine if they are beneficial.

The term "prostatitis" refers, in its strictest sense, to histological (microscopic) inflammation of the tissue of the prostate gland. Like all forms of inflammation, it can be associated with an appropriate response of the body to an infection, but it also occurs in the absence of infection.

In 1999, the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) devised a new classification system. For more specifics about each type of prostatitis, including information on symptoms, treatment, and prognosis, follow the links to the relevant full articles.

In 1968, Meares and Stamey determined a classification technique based upon the culturing of bacteria. This classification is no longer used.

The conditions are distinguished by the different presentation of pain, white blood cells (WBCs) in the urine, duration of symptoms and bacteria cultured from the urine. To help express prostatic secretions that may contain WBCs and bacteria, prostate massage is sometimes used.

Treatment protocol is not well established. Some sources report that approximately half of the patients will fully recover after lengthy (mean time 14.5 months, range 2–24 months) expectant management.

Treatment with steroids is lengthy and usually requires about 6 months. While some source report very good success with steroids most report a considerable risk of recurrence after a treatment with steroids alone. Steroids are known to cause elevation of prolactin levels and increase risk of several conditions such as diabetes, and other endocrinopathies which in turn increase the risk of IGM. Treatment with topical steroids to limit side effects was also reported in one case. For surgical treatment recurrence rates of 5-50% have been reported.

A 1997 literature review article recommended complete resection or corticosteroid therapy, stating also that long-term follow-up was indicated due to a high rate of recurrence.

Treatment with a combination of glucocorticoids and prolactin lowering medications such as bromocriptine or cabergoline was used with good success in Germany. Prolactin lowering medication has also been reported to reduce the risk of recurrence. In cases of drug-induced hyperprolactinemia (such as antipsychotics) prolactin-sparing medication can be tried.

Methotrexate alone or in combination with steroids has been used with good success. Its principal mechanism of action is immunomodulating activity, with a side effect profile that is more favorable for treating IGM.

Colchicine, azathioprine and NSAIDs have also been used.

Treatment is often with NSAIDs and antibiotics however, this is not always effective.

Urinary catheters should be inserted using aseptic technique and sterile equipment (including sterile gloves, drape, sponges, antiseptic and sterile solution), particularly in an acute care setting. Hands should be washed before and after catheter insertion. Overall, catheter use should be minimized in all patients, particularly those at higher risk of CAUTI and mortality (e.g. the elderly or those with impaired immunity).

Signs indicative of urethral syndrome include a history of chronic recurrent urinary tract infections (UTI) in the absence of both conventional bacterial growth and pyuria (more than 5 white blood cells per High Power Field). Episodes are often related to sexual intercourse.

Some physicians believe that urethral syndrome may be due to a low grade infection of the Skene's glands on the sides and bottom of the urethra. The Skene's glands are embryologically related to the prostate gland in the male, thus urethral syndrome may share a comparable cause with chronic prostatitis.

Possible non-infective causes include hormonal imbalance, trauma, allergies, anatomical features such as diverticula, and post-surgical scarring and adhesions.

The main infectious agents are Enterobacteriaceae (such as Escherichia coli and Klebsiella), Neisseria gonorrhoeae and Chlamydia trachomatis.

One study has shown that men with MAGI who have lower serum levels of total testosterone tend to have a more complicated form of MAGI, such as involving more than one site, than those with normal levels.

In 2011, the American Urological Association released consensus-based guideline for the diagnosis and treatment of IC.

They include treatments ranging from conservative to more invasive:

1. First-line treatments — patient education, self care (diet modification), stress management

2. Second-line treatments — physical therapy, oral medications (amitriptyline, cimetidine or hydroxyzine, pentosan polysulfate), bladder instillations (DMSO, heparin, or lidocaine)

3. Third-line treatments — treatment of Hunner's ulcers (laser, fulguration or triamcinolone injection), hydrodistention (low pressure, short duration)

4. Fourth-line treatments — neuromodulation (sacral or pudendal nerve)

5. Fifth-line treatments — cyclosporine A, botulinum toxin (BTX-A)

6. Sixth-line treatments — surgical intervention (urinary diversion, augmentation, cystectomy)

The AUA guidelines also listed several discontinued treatments, including long-term oral antibiotics, intravesical bacillus Calmette Guerin, intravesical resiniferatoxin), high-pressure and long-duration hydrodistention, and systemic glucocorticoids.