Randy Dotinga is a medical writer based in San Diego, Calif.
Could bacteria in the lower urinary tract play a role in urologic chronic pelvic pain syndrome (CPPS)? The jury is still out, but the authors of a new study say they weren’t able to find any evidence that germs are at fault.
San Diego-Could bacteria in the lower urinary tract play a role in urologic chronic pelvic pain syndrome (CPPS)? The jury is still out, but the authors of a new study say they weren’t able to find any evidence that germs are at fault.
“Our preliminary research hasn’t been able to confirm that microorganisms are the cause of the majority of urological pain syndromes,” said lead author J. Curtis Nickel, MD, professor of urology at Queen’s University in Kingston, Ontario. But, he said, the search continues.
Chronic pelvic pain is one of the most common conditions urologists treat, accounting for about 8% of male outpatient visits (including cases of prostatitis) and a bit less for females, Dr. Nickel said.
“Most urologists find this the most frustrating condition to deal with because there are no good surgical treatments and no good medications. And big pharma companies aren’t providing funding to do research.”
There are some clues that scientists may be missing an infectious component to chronic pelvic pain, he said.
“So we decided to use the most modern technology to see if we could find a microorganism or a spectrum of microorganisms that would cause this condition that we’ve just been missing. Maybe there’s an organism that we don’t usually culture,” added Dr. Nickel, who presented the findings at the AUA annual meeting in San Diego.
Dr. Nickel and colleagues collected urine samples from patients with urologic CPPS (161 female, 96 male) and age-matched controls (164 female, 97 male). They tested them with the Ibis T-5000 Universal Biosensor using BAC plate assay.
A total of 136 species (57 genera) were detected in the VB1 sample; VB2 contained 109 species (52 genera). Mean VB2 species count per person was 2.50 and 2.29 among female cases and controls, respectively, compared with 1.33 and 1.08 for males, respectively.
At the species level in VB1, Lactobacillus gasseri and Streptococcus pneumoniae were more prevalent among cases than controls, while Staphylococcus capitis/caprae was under-represented among cases (L. gasseri, OR=3.74, p=.007; S. capitis/caprae, OR=0.263, p=.011; S. pneumonia, OR=3.45, p=.007).
VB1 samples among cases were also more likely to have gram-negative organisms than controls (OR=1.88, p=.008). For VB2, the only statistical difference observed was at the genus level for Corynebacterium (lower prevalence among urologic CPPS patients compared to controls, OR=0.34, p=.011).
Essentially, there was little difference between cases and controls in terms of microorganisms. However, Dr. Nickel cautioned that he and his co-authors don’t understand the full picture.
“There may be microorganisms that we have overlooked, like a microorganism that we don’t usually culture or a cryptic organism we failed to detect,” he said. “This was an initial run.”
The next step, he said, is to study the urine of patients who experience flares of their symptoms to see if any microorganisms turn up.
“The flares could be related to a microbial presence,” he said.
Researchers will also compare inflammatory biomarkers in cases and controls to see if there are signs of infection. “If we find signs, we’ll look at phenotypes to see if a particular symptom goes with a particular microbial presence or pattern,” he said.UT
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