Fw: (LML) Lepromatous leprosy needs longer treatment regimens

 

Leprosy Mailing List – September 13,  2020

 

Ref.:  (LML) Lepromatous leprosy needs longer treatment regimens

 

From:  Ben Naafs, Munnekeburen, the Netherlands

 

Dear Pieter

 

As usual the contribution of Joël Almeida is worthwhile reading and well documented (LML, August 28, 2020). He also makes that you want to respond. Since no one does I may go through his contribution with my own bias. I hope others respond too.

 

I agree with Joël that recurrences, relapses or reinfections of lepromatous disease are a major problem in leprosy control. Nearly all high bacteriological index (BI)positive patients have persisters. After developing the disease again, they contribute again to the infective pool. A shame is that with the present WHO-advised regimen(s), non-detected recurrences will most likely occur. One more shame is that the Ridley and Jopling classification (or any scientific classification) and the slit-skin smear examination are not implemented. Without these tools high bacterial load forms of leprosy, i.e. borderline lepromatous (BL), lepromatous (LL) and its variants: subpolar (LLs), polar (LLp ) and histoid leprosy, are more difficult to identify.

 

A relapsed LL patient has less symptoms because her/his adaptive immune system has collapsed. May be with exception of most of the LLp patients who have no adaptive immunity to M. leprae antigens at all. Their innate immunity and other mechanisms are responsible for the symptoms together with the load of bacteria, but even more difficult to detect clinically.

 

Joël proposes longer treatment regimens for lepromatous disease, I fully agree with him. The result will be less deformities. But I am not so sure whether this will also lead to less cases in the community if there are other than human sources as well. I think he should also consider the possible survival of M. leprae in the environment and in other hosts than the human being. These hosts (animals) will contribute to the infective pool too. It is important to notice/understand whether and how the environment may contribute to survival of the bacillus.

 

Relapses have a role in maintaining infection in developed cities and towns, where M. leprae cannot survive in the environment due to the dry cement and wooden floors without cracks, not so much in shanty towns and rural areas where M. leprae can survive for some time in the environment. It may well be that in China and Congo in the area's he mentioned no other host than the human is available, and the surrounding areas are not allowing survival of the bacillus. The surrounding is hot and dry or cold and not moist, with houses without mud floors (because there bacilli can survive).

 

Shandong is characterized by a continental climate with cold winters and hot, dry summers. An area where M. leprae is not likely to survive in the environment. The area around Wamba (Uele) DR Congo consists of a rainforest-derived mosaic of dry, swamp, and secondary forest, with cultivated fields. I would think M. leprae could survive here. For some time. May be I am wrong. So, my argument against his arguments may fit for Shandung but not for Uele.

I am glad he acknowledged the genomes in a LLp patient that make survival of M. leprae possible, but I think that all lepromatous patients have these genes, necessary for M.leprae to survive. If their adaptive immune system is still on the alert (in borderline patients), this may lead to early symptoms and the downgrading borderline leprosy can be diagnosed early. In LLp there is no downgrading and there are hardly any symptoms. Thus, the argument of Joël to treat longer is even stronger.

In Borderline lepromatous patients the immune system to M. Leprae antigens slowly collapses during the downgrading. After a relapse the detection of the increase in bacilli takes a long time and the symptoms are not to severe so that the patient seeks no help. It is difficult to diagnose these patients early, biopsy and smears are often not enough.

In Zimbabwe in the mid 1980th we used the PGL-1 titre and diagnosed by an increase in serology some patients before other methods diagnosed the relapse. The same we have done in the Netherlands and diagnosed some relapses more or less early. We followed patients as long as they wanted. But we used only 2 years treatment. In the Netherlands exogenous infection does not occur.

When good serological (PGL-1,Lid1 or another antigen) and PCR follow-up is not possible, I fully agree with Joël treat to smear negativity or lifelong.

 

Ben

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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