Fungal and Viral Prostatitis
Still No Supporting Studies Published
Fungal Infection
With the exception of studies which state that
fungal
invasion of the prostate is rare there are no published studies
supporting the theory that a yeast or fungus is the cause of chronic
prostatitis/chronic pelvic pain syndrome (CP/CPPS).
Some men are convinced they have been helped by an antifungal (anti-candida) diet. This may be for 2 reasons:
1) Anti-candida diets restrict many foods which may be causing food
intolerance reactions, such as wheat
and milk.
2) Sugar and sugary foods, forbidden on anti-candida diets, can
cause a sudden flare in symptoms, thus misleading men into believing
the sugar is "feeding" their "fungal infections".
But this effect is most probably due to subtle
biochemical processes having nothing to do with fungus.
Viral Infection
The latest study (2002) searching for viruses
in CP/CPPS prostates concluded that the major suspected viruses
are not to blame:
VIRAL GENOMES CANNOT BE DEMONSTRATED IN PROSTATES OF PATIENTS
WITH SYMPTOMATIC CHRONIC PELVIC PAIN SYNDROME (CPPS) AND LOCALIZED
PROSTATE CANCER
Markku J Leskinen*, Seinäjoki, Finland; Raija Vainionpää,
Stina Syrjänen, Turku, Finland; Timo Kylmälä, Tampere,
Finland; Mikael Leppilahti, Timo Marttila, Seinäjoki, Finland;
Teuvo L Tammela, Tampere, Finland
Introduction and Objectives:
The etiology of chronic pelvic pain syndrome (CPPS) remains mostly
unknown. Bacterial etiology has been suggested by PCR findings.
Reports of viral etiology in CPPS are few and systematic studies
of viral involvement in CPPS using the PCR techniques have not been
published. The aim of the present study was to investigate possible
viral etiology of CPPS using the PCR techniques.
Methods:
The PCR was used to detect genomes of cytomegalovirus (CMV), herpes
simplex viruses type 1 (HSV-1) and type 2 (HSV-2) and human papilloma
viruses (HPV) from radical prostatectomy specimens of patients with
symptomatic CPPS and non-symptomatic controls. Consecutive patients
with localized prostate cancer (T0-T2) in whom radical prostatectomy
was considered were evaluated for symptoms of CPPS using the NIH-CPSI
–questionnaire. Ten patients with moderate to severe prostatitis
symptoms (NIH-CPSI –score >16, pain domain score >9)
and ten patients with no symptoms of prostatitis (NIH-CPSI –score
<3) as controls were included in the study. A tissue sample was
harvested and frozen to –70 C immediately after the surgical
removal of the prostate. HSV-1 and HSV-2, and CMV genomes were analyzed
by PCR and by hybridization with the lanthanide labeled probes.
For PCR, nucleic acids were extracted by the High Pure Viral Nucleic
Acid Kit (Roche Molecular Biochemicals). HSV-1 and HSV-2 DNA was
amplified by PCR using the biotinylated primers and europium-labeled
(for HSV-1) and samarium-labeled (for HSV-2) probes, which were
from the glycoprotein D genes. The detection was done by time-resolved
fluorometry and the results were obtained as counts per second.
For CMV, the primers (nucleotides 731-755, 1165-1141) and the europium-labeled
probe (nucleotides 1140-1121) were from a conserved region of CMV.
For HPV, MY09/MY11 primers targeting the L1 open reading frame of
the genome were used. After PCR, the samples were hybridized with
high-risk (types 16, 18, 31, 33, 35, 39, 45, 51, 52, 54, 56 and
58) HPV oligoprobe mixtures. The probes were labeled with digoxigenin
(DIG Oligonucleotide 3'-End Labeling Kit, Boehringer Mannheim).
The detection was done using anti-digoxigenin conjugated to alkaline
phosphatase and visualized with the chemiluminescence substrate
CSPD (DIG Luminescent Detection Kit, Boehringer Mannheim).
Results:
All 20 samples studied were negative for genomes of tested viruses.
Conclusions:
The study could not demonstrate etiological relationship between
HSV, HPV, CMV and CPPS.