Leprosy Mailing List – February 8, 2020
Ref.: (LML) All is different than you think: to re-interpret with the present findings what was seen by clinicians in the past
From: Ben Naafs, Munnekeburen, the Netherlands
Dear Pieter,
Thanks Laila for her complements. Her question is very valid (LML, February 6, 2020). It is nice when one writes something, that is a not a generally accepted explanation, to get well-meaning critical response and questions about it.
I wrote that 80% of the infected people, independently of their Cell Mediated Immunity towards M. leprae antigenic determinants, will not be able to develop the bacterial infective disease leprosy. This is due to their genetic composition. The other 20% can. Luckily not all develop the disease, because of their adaptive Immunity (mostly CMI) prevents it. Depending on their genetic determined adaptive immunity, modulated by the route of infection (upper respiratory system versus skin), the size and frequency of inoculum and the encounter with other bacteria, viruses and toxins, (from environment or vaccinations).
How did I come to that? Just observation and questioning. The first observation was in Ethiopia in the early seventies. When most people were treated livelong. Only a few tuberculoid and indeterminate were released from treatment (RFT). There were in that time villages with a prevalence of 5 % of leprosy or even slightly more. I looked it up; there was only an island in the pacific who had 40% of the inhabitants in a lifetime diagnosed with leprosy (in-breading?). When we started to RFT clinically inactive borderline patients after 5 year of dapsone monotherapy, many relapses were seen within two years. The one's who relapsed were those with a positive BI at the start of their anti-leprosy treatment. Observed was that when they relapsed, they were mostly more tuberculoid and later on downgraded. The same as we saw in dapsone resistant patients.
When AIDS became rampant the number of leprosy patients did not go-up. Among those who were HIV positive there were not more leprosy patients than among those HIV negative. Observing patients who had leprosy with HIV\ AIDs, in the time that there was no treatment, we observed disappearance of lesions even when they were not treated for leprosy. The biopsies and the smears in the short time they lived showed some increase in BI.
We thought downgrading could be responsible. Earlier in Zimbabwe when we were not aware of AIDS in our patients, we biopsied some of these rapid downgrading patients and saw a persistence of Langhans' giant cells in rapidly downgrading leprosy lesions ( Lyons NF at al. Int J Lepr Other Mycobact Dis. 1985 Mar;53(1):1145). Later on we biopsied some known leprosy/AIDS patients who downgraded like the ones we described in the paper and saw that the original described patients could have been AIDS/leprosy as well.
Then came HAART and as Opromolla and I forecasted leprosy became visible. The CMI restored and leprosy became visible as IRIS. If you look into data of areas endemic in HIV and leprosy, one may notice that with HAART treated (leprosy infected patients), the (leprosy) prevalence may go up to 10-15% (15% is a safe guess - I have not seen more then 5-7%). We noticed with MariAngela (Sao Paulo) that in organ transplant patients when the immunosuppressive therapy diminished also leprosy developed as an IRIS. That is what you saw in your patients who were treated with biologicals which suppressed their immunity. During the suppression M. leprae could multiply. Stopping you get an IRIS.
Regards,
Ben
Note Editor:
Immune reconstitution inflammatory syndrome (IRIS) is a condition seen in some cases of AIDS or immunosuppression, in which the immune system begins to recover, but then responds to a previously acquired opportunistic infection with an overwhelming inflammatory response that paradoxically makes the symptoms of infection worse (Wikipedea).
LML - S Deepak, B Naafs, S Noto and P Schreuder
LML blog link: http://leprosymailinglist.blogspot.it/
Contact: Dr Pieter Schreuder << editorlml@gmail.com
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