Leprosy Mailing List – August 20, 2026
Ref.: (LML) Long-lasting adverse impact of chemoprophylaxis & what actually works
From: Joel Almeida, Mumbai, India
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Dear Pieter and colleagues,
Thanks to Dr. Ben Naafs for his comments (LML 18 Aug 2026).
Re: zero of 208 unprotected BL cases showing BI 5+ or 6+ in nasal smears: the data is in the very same Davey and Rees article (1974 Lepr Rev 45(2):121-34 ).
Should fear and prejudice be created against subclinically infected persons who shed few if any bacilli, and who have >95% chance of self-limiting or eliminating the bacilli without developing signs or sequelae or onward transmission? Just protecting their natural macrophage defences is likely to be the most effective approach. Zhijian Chen group's discoveries of cGAS and STING (Science 2013), together with de Toledo Pinto et al demonstration of M. leprae DNA triggering cGAS-STING and the upregulation of OASL with suppression of autophagy and vit D-induced cathelicidin (J Inf Dis 2016 214;311-320) underline the importance of avoiding short-term chemoprophylaxis in order to protect macrophage defences. It does not matter how strong the anti-microbial or how many doses: if anti-microbials are used at all then the duration must outlast the bacillary debris in autophagy-suppressed macrophages, and also the availability of concentrated viable bacilli from the surroundings (typically from unprotected LL high-shedders). Otherwise bacilli will replicate in the macrophages sabotaged by short-term chemoprophylaxis, boosting the risk of "silent" non-inflammatory nerve damage via PGL1 (macrophage iNOS and excess NO, Madigan et al Cell 2017). Then visible deformity can be the very first detectable sign of HD (leprosy). It is no comfort to a person who suffers visible deformity after accepting short-term chemoprophylaxis that M. leprae invariably involves nerves from the very earliest stages of infection, even just within the nose. Subclinical infection with invariable nerve involvement, yet frequent self-limiting or elimination of bacilli, is not the same as visible deformity.
What about a biologically targeted approach that conserves macrophage defences? mLAMP ( for DNA or RNA as desired ) is 100% specific. Financial costs for mLAMP using indigenous kits/methods and large volumes are likely to be much lower than the suggested estimates. As already suggested, it is worth it in any case. The most relevant costs of disease can be measured in lost eyes, hands and feet. A cheap intervention that is ineffective is simply a waste of money. That is even more so if the cheap intervention is both ineffective and harmful. By contrast, a highly effective intervention is affordable in every sense: saving eyes, hands, feet and saving money in an era of severe financial constraints. Ending a disease is one of humanity's biggest dreams and aspirations. A highly effective intervention is affordable in every sense. Even the stream of future financial savings approaches infinity if the only people remaining at risk of HD are reckless or poorly informed gardeners in armadillo states. Besides, the Find Treat End (FTE) strategy by encouraging persons with lived experience to serve as trained aides to health workers (nasal swab collection, muscle weakness testing, encouraging uninterrupted treatment, comforting distressed persons, assisting with social and rehab entitlements etc) helps to replace prejudice and fear with respect. People with lived experience can lead grassroots activities to create the victory. They will also be the most appropriate persons to lead the victory parade in cluster after cluster.
The elephant in the room, identified by Davey & Rees in 1974 yet under-emphasized, has been cryptic asymptomatic LL high-shedders. Without protection for them, it is impossible to stop HD (leprosy). With protection for them, it is difficult to maintain frequent transmission. The environment allows bacilli to survive, but it does not provide a culture medium for replication. Tens of millions of bacilli per sample or per day are not available from a single environmental sample of soil or water, unless it has been recently replenished by an unprotected high-shedder. This means that transmission can be interrupted very rapidly by a synchronous sweep to identify every cryptic asymptomatic LL high shedder in a cluster or a migratory corridor. Prompt full treatment including regular check-ups will not only protect them but also switch off transmission, confirmed and maintained by mop-up rounds. It is like turning off nearly all the taps. It becomes very difficult for the metaphorical ground to remain wet with disease. Transmission is likely to collapse within weeks per cluster.
The process can be visualised. Go into a cluster on Monday, do a sweep for nasal swabs & semi-quantitative mLAMP by Tuesday, start full treatment on Wednesday of every cryptic asymptomatic LL high-shedder. Take nasal swabs in periodic follow-up sweeps. Do this in parallel or in sequence to spread the success.
We are not in the dark if we rely on science. It weighs evidence and inference only. Votes are irrelevant to biology. What was a distant dream during the past decade is now an achievable success. Is it wrong to reach for success?
With all sincerity,
Joel Almeida
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LML - S Deepak, B Naafs, S Noto and P Schreuder
LML blog link: http://leprosymailinglist.blogspot.it/
Contact: Dr Pieter Schreuder << edit...@gmail.com
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