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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.