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 Emerging Infectious Diseases * Volume 3 * Number 1 * January-March 1997
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Letters
Prostatitis and Benign Prostatic Hyperplasia: Emerging Infectious Diseases?
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To the Editor: In their excellent article, Molecular Approaches to the
Identification of Unculturable Infectious Agents, Gao and Moore (1) point
out that molecular approaches should be unleashed on diseases such as
sarcoidosis, Kawasaki disease, and type I diabetes mellitus, which are
thought but not proven to be infectious. The authors, however, are
overlooking the more common and most likely infectious disease of unknown
etiology today--prostatitis.
According to the pathologist McNeal, the prostate gland is the most
commonly diseased internal organ of the human body (2). Prostatitis is the
most common prostate disease, resulting in more physician visits than
either benign prostatic hyperplasia or prostate cancer, according to the
National Institutes of Health (3). Despite its frequency, prostatitis as a
disease and as a histologic lesion is understudied (4).
By the Meares and Stamey culture localization procedure, in which the first
voided urine, a midstream urine, the expressed prostatic secretions, and a
final voided urine are compared, more than 90% of cases in patients with
chronic pelvic symptoms are labeled as "nonbacterial" prostatitis or
prostatodynia, both of which are thought to be incurable diseases (5).
The University of Washington has documented white blood cell counts as high
as 38,000 per mm3, in "nonbacterial" prostatitis patients (6). According to
urologist Thomas Stamey, up to 50% of all men experience symptoms of
prostatitis during their lifetimes (7). The prostatitis lesion was found in
40 (44%) of 91 men at random autopsy (8). In another study of 100
consecutive autopsies on men who died suddenly in automobile accidents and
from other causes, the prevalence of histologic signs of prostatitis
increased with age and was highest when benign prostatic hyperplasia was
also present. Prostatitis was present in 22% of men under 40 years of age
and in 60% of those over 40 years of age (9).
In fact, the line between benign prostatic hyperplasia and prostatitis is
blurred. Prostatitis as a histologic lesion has been found in 98% of
patients with benign prostatic hypertrophy (10). Microbial tests on benign
prostatic hyperplasia tissue have found significant rates of infectivity.
In another study, more than 70% of transurethral resection of the prostate
specimens showed clinical or laboratory signs of infection (11). Benign
prostatic hyperplasia and prostatitis cannot be distinguished by symptoms,
and some believe that they may be the same disease.
In these days of prostate specific antigen testing, more than 50% of men
who undergo biopsies for prostate cancer have a prostatitis lesion whether
they have cancer or not (Gottesman et al., unpublished data; McNeal,
personal communication, 1995). Prostatitis occurs at an early age, and
prostate cancer decades later, in the same part of the prostate gland, the
peripheral zone.
Why aren't DNA techniques being unleashed on what is apparently the most
common and most purulent unknown inflammatory disease in menan
inflammatory lesion that is associated with benign prostatic hyperplasia
and prostate cancer? Surely, DNA microbial testing has important
implications for all three major prostate diseasesprostatitis, benign
prostatic hyperplasia, and prostate cancer.
Brad Hennenfent
Director, The Prostatitis Foundation
Chicago, Illinois, USA
References
  1. Gao S-J, Moore PS. Molecular approaches to the identification of
     unculturable infectious agents DNA vaccines for emerging infectious
     diseases: what if? Emerg Infect Dis 1996;2:159-67.
  2. McNeal JE. The prostate gland: morphology and pathobiology. Monographs
     in Urology 1988;9:3.
  3. National Institutes of Health. The National Kidney and Urologic
     Diseases Advisory Board 1990 long-range plan. Bethesda (MD): U.S.
     Department of Health and Human Services, Public Health Service,
     National Institutes of Health, 1990.
  4. Hennenfent BR. The economics of urological care in the 21st century
     [letter]. Urology 1996;47:285-6.
  5. Weidner W, Schiefer HG, Krauss H, Jantos CH, Freidrich HJ,
     Altmannsberger M. "Chronic prostatitis" a thorough search for
     etilogically involved microorganisms in 1,461 patients. Infection
     1991;19:S119-25.
  6. Krieger JN, Egan KJ, Ross SO, Jacobs R, Berger RE. Chronic pelvic
     pains represent the most prominent urogenital symptoms of "chronic
     prostatitis." Urology 1996;48:715-22.
  7. Stamey TA. Pathogenesis and treatment of urinary tract infections.
     Baltimore: Williams and Wilkins, 1980.
  8. McNeal J. Regional morphology and pathology of the prostate. Am J Clin
     Pathol 1968;49:347-57.
  9. Bostrom K. Chronic inflammation of the male accessory sex glands and
     its affect on the morphology of the spermatozoa. Scand J Urol Nephrol
     1971;5:133.
 10. Kohnen PW, Drach GW. Patterns of inflammation in prostatic
     hyperplasia: a histologic and bacteriologic study. J Urol
     1979;121:755-60.
 11. Riedash G, Morhing K, Brkovic D. Concentration of ofloxacin in
     prostatic tissue during TURP. Drugs 1993;45 (Suppl. Preprint).
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     Emerging Infectious Diseases
     National Center for Infectious Diseases
     Centers for Disease Control and Prevention
     Atlanta, GA