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Higher risk of recurrent chronic prostatitis with antibiotics

Date:2012-10-06 click:

They are meant to protect us. But what if the immune system response to bacterial infection and antibiotics paradoxically leave us at risk for recurrent  and chronic infection and pain?

 

Using mice as the experimental model, investigators at the Washington University  have discovered that:

 

The vigor of immune response to bacterial infiltration of the bladder correlated with risk for recurrent infection.
Repeat UTI (urinary tract infection) and cystitis were less likely in mice with deficient immune systems.
Mice treated with antibiotics had immune infiltration of the bladder and were more likely to have recurrent infection.
So what does this have to do with prostatitis?

 

In humans, urinary tract infection is largely an illness of women. Many such infections can resolve spontaenously, although clearly many are treated with antibiotics. Understanding the pathology that underlies recurrence becomes important because recurrence is indidivually debilitating and because at the public health level infections are increasingly hard to treat because resistance to antibiotics is rising. The better we understand the mechanisms underlying recurrent urinary infection the better we can help the patient in distress and the more we may be able to reduce our dependence on antibiotics (and the less we potentially accelerate the development of antibiotic resistance).

 

The prostate is colonized with bacteria, but these are largely asymptomatic. However, in acute bacterial prostatitis the bacteria have found a way to overcome the man's defenses and can cause a clinical situation characterized by pain, bleeding, burning, weak urinary stream, fever, shakes, and chills. Patients in certain circumstances, e.g. spinal cord injury, are at particularly high risk of acute bacterial infection of the bladder and the prostate. In its severe bacterial forms, acute prostatitis is a potentially fatal illness that must be quickly treated with antibiotics.

 

The degree to which acute bacterial prostatitis recurs is not known partly because of difficulties in diagnosing acute prostatitis in the first place. Moreover, in surveying the medical literature the blurred lines between "recurrent bacterial acute prostatitis" and "chronic prostatitis" make it difficult to even begin to quantify the recurrence of acute bacterial prostatitis. Still, it seems clear that bacteria and prostatitis coexist, even as at one end of the clinical spectrum prostatitis may either de novo happen or secondarily become a non-bacterial illness (certainly an antibiotic resistant illness).

 

One of the pressing questions regarding the development of chronic clinical prostatitis is the role of bacteria. This is not just a research question. At the bedside, it matters because all patients with chronic prostatitis are treated with antibiotics, as if their illness is bacterial in origin; these are commonly completely ineffective, but that's another story.

 

Getting back to the mice, the findings beg a number of related questions for which we do not yet have an anwer:

 

Does the vigor of the immune response to the initial insult of acute bacterial prostatitis modify the risk of recurrence?
Does the use of antibiotics in itself modify the risk of recurrence and/or predispose to chronic prostatitis?

 

Today, patients with acute bacterial prostatitis, especially anybody with a febrile, septic presentation, have little choice but to rely on antibiotics for quick resolution and hope that the initial insult will not transform into a recurrent and/or chronic condition. The task of the researcher is to now seize upon the fascinating observations reported by the study to see if they can illuminate the evolution not only of bacterial and chronic cystitis but also bacterial and chronic prostatitis. Today, patients have better options such as Diuretic and Anti-inflammatory Pillthan often ineffective treatments and hope.

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