Acute prostatitis is relatively easy to diagnose due to its symptoms that suggest infection. Common bacteria are "E. Coli, Klebsiella, Proteus, Pseudomonas, Enterobacter, Enterococcus, Serratia," and "Staphylococcus aureus." This can be a medical emergency in some patients and hospitalization with intravenous antibiotics may be required. A full blood count reveals increased white blood cells. Sepsis from prostatitis is very rare, but may occur in immunocompromised patients; high fever and malaise generally prompt blood cultures, which are often positive in sepsis.
Antibiotics are the first line of treatment in acute prostatitis (Cat. I). Antibiotics usually resolve acute prostatitis infections in a very short period of time. 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, Co-trimoxazole and tetracyclines penetrate well. Severely ill patients may need hospitalization, while nontoxic patients can be treated at home with bed rest, analgesics, stool softeners, and hydration.
Full recovery without sequelae is usual.
Chronic bacterial prostatitis is a relatively rare condition (<5% of patients with prostate-related non-BPH LUTS) that usually presents with an intermittent UTI-type picture and that is defined as recurrent urinary tract infections in men originating from a chronic infection in the prostate. Dr. Weidner, Professor of Medicine, Department of Urology, University of Giessen, has stated: "In studies of 656 men, we seldom found chronic bacterial prostatitis. It is truly a rare disease. Most of those were E-coli." Symptoms may be completely absent until there is also bladder infection, and the most troublesome problem is usually recurrent cystitis.
In chronic bacterial prostatitis there are bacteria in the prostate but usually no symptoms. The prostate infection is diagnosed by culturing urine as well as prostate fluid (expressed prostatic secretions or EPS) which are obtained by the doctor doing a rectal exam and putting pressure on the prostate. If no fluid is recovered after this prostatic massage, a post massage urine should also contain any prostatic bacteria. Prostate specific antigen levels may be elevated, although there is no malignancy.
Treatment requires prolonged courses (4–8 weeks) of antibiotics that penetrate the prostate well (β-lactams and nitrofurantoin are ineffective). These include quinolones (ciprofloxacin, levofloxacin), sulfas (Bactrim, Septra) and macrolides (erythromycin, clarithromycin). 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.
The addition of prostate massage to courses of antibiotics was previously proposed as being beneficial.
It is though not without some risk, and has not been shown in more recent trials to improve outcome compared to antibiotics alone.
Over time, the relapse rate is high, exceeding 50%.
In chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) there is pelvic pain of unknown cause, lasting longer than 6 months, as the key symptom. Symptoms may wax and wane. Pain can range from mild discomfort to debilitating. Pain may radiate to back and rectum, making sitting difficult. Dysuria, arthralgia, myalgia, unexplained fatigue, abdominal pain, constant burning pain in the penis, and frequency may all be present. Frequent urination and increased urgency may suggest interstitial cystitis (inflammation centred in bladder rather than prostate). Ejaculation may be painful, as the prostate contracts during emission of semen, although nerve- and muscle-mediated post-ejaculatory pain is more common, and a classic sign of CP/CPPS. Some patients report low libido, sexual dysfunction and erectile difficulties. Pain after ejaculation is a very specific complaint that distinguishes CP/CPPS from men with BPH or normal men.
Theories behind the disease include autoimmunity, for which there is scant evidence, neurogenic inflammation and myofascial pain syndrome. In the latter two categories, dysregulation of the local nervous system due to past traumatic experiences or an anxious disposition and chronic albeit unconscious pelvic tensing lead to inflammation that is mediated by substances released by nerve cells (such as substance P). The prostate (and other areas of the genitourinary tract: bladder, urethra, testicles) can become inflamed by the action of the chronically activated pelvic nerves on the mast cells at the end of the nerve pathways. Similar stress-induced genitourinary inflammation has been shown experimentally in other mammals.
Prostatitis researcher Dr Anthony Schaeffer commented in a 2003 editorial of The Journal of Urology that: "It is well recognized that even if pathogenic bacteria are present in the prostate, as in men with established chronic bacterial prostatitis, they do not cause chronic pelvic pain unless acute urinary tract infection develops. Taken together, these data suggest that bacteria do not have a significant role in the development of the chronic pelvic pain syndrome. The clinical observation that antimicrobial therapy reduces symptomatology in men with chronic pelvic pain syndrome is being tested in a double-blinded NIH controlled study. Since antimicrobials may have anti-inflammatory activity, it is possible that these drugs may benefit the patient by reducing inflammation rather than eradicating bacteria."
A year after making that statement, Dr Schaeffer and his colleagues published studies showing that antibiotics are essentially useless for CP/CPPS.
The bacterial infection theory that for so long had held sway in this field was again shown to be unimportant in another 2003 study from the University of Washington team led by Dr Lee and Professor Richard Berger. The study found that one third of both normal men and patients had equal counts of similar bacteria colonizing their prostates.
Since the publication of these studies, the focus has shifted from infection to neuromuscular and psychological etiologies for chronic prostatitis (CP/CPPS).
There are no definitive diagnostic tests for CP/CPPS. This is a poorly understood disorder, even though it accounts for 90%-95% of prostatitis diagnoses. It is found in men of any age, with the peak onset in the early 30s. CP/CPPS may be inflammatory (category IIIa) or non-inflammatory (category IIIb). In the inflammatory form, urine, semen, and other fluids from the prostate contain pus cells (dead white blood cells or WBCs), whereas in the non-inflammatory form no pus cells are present. Recent studies have questioned the distinction between categories IIIa and IIIb, since both categories show evidence of inflammation if pus cells are ignored and other more subtle signs of inflammation, like cytokines, are measured. In 2006, Chinese researchers found that men with categories IIIa and IIIb both had significantly and similarly raised levels of anti-inflammatory cytokine TGFß1 and pro-inflammatory cytokine IFN-γ in their expressed prostatic secretions when compared with controls; therefore measurement of these cytokines could be used to diagnose category III prostatitis.
Normal men have slightly more bacteria in their semen than men with chronic prostatitis/pelvic myoneuropathy. The traditional Stamey 4-glass test is invalid for diagnosis of this disorder, and inflammation cannot be localized to any particular area of the lower GU tract.
Men with CP/CPPS are more likely than the general population to suffer from Chronic Fatigue Syndrome (CFS), and Irritable Bowel Syndrome (IBS). Prostate specific antigen levels may be elevated, although there is no malignancy.