In sexually transmitted infections, it is important to differentiate a painful ulcer from a painless one. This is because painless ulcers are seen in the chancre of primary syphilis while painful tender ones are seen in Herpes and though rare, in chancroid (H. ducreyi).
I can guess that it must be due to peripheral nerves, but how does this happen?
What: Try asking the subject!
Why: Pain is about perception by the brain... in extreme cases, it can be perceived even in the absence of the the region where it is perceived. Case in point, phantom limb pain in cases of amputees.
I suppose your question, stated in another way is : What promotes pain in one type of an STD such as chancroid vs. the painless chancre. I don't think the knowledge of that pathophysiologic mystery makes much of a difference in the clinical setting, but it is certainly a good question.
" I don't think the knowledge of that pathophysiologic mystery makes much of a difference in the clinical setting"
Strange thinking!
Course of clinical management of pain has a great deal to do with the reason (when it is known).
Maybe it meant that when a cure is readily available, digging too much into the pathophysiology won't help much, at least clinically....
But there must something fundamentally different between the two.
By the way, painless ulcers, apparently, can be found also in Leishmania major infection too
Dear
According to my analysis pathophysiologic mystery can not make critical difference in the clinical setting.
Thank
Marius
As a clinician, I think that if the PATIENT says that the ulcer is painful, the ulcer IS PAINFUL. So the physician has to treat pain.
Of course, the physician can collect data about patients and diseases, to analyze pathophysiological aspects. The comparison between ulcer painful and non-painful may give some useful information.
Best regards
Maurizia
Pain is a symptom, so the patient "decides" when the ulcer pains whatever it cause be.
Perhaps some pathogens would invade peripheral nerve fibers during the pathogenesis as their skin lesions developed. So we know the existence of neurosyphillis and postherpetic neuralgia.
Some pathogens might numb nerve fibers, others might fire them.
The pathogens also might release some chemical substance into the periphery in the early phase.
Possible mechanisms include cytokines, inflammatory mediators, inhibitory neurotransmitters or anything.
You just asked a great question. It is a fundamental issue.
You could take down some samples of peripheral nerve fibers closely near the skin lesions to do pathology (even electric microscopy). To see what happened?
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