What is in paucibacillary (PB) leprosy?

Leprosy Mailing List – November 12th, 2011

Ref.:   What is in paucibacillary (PB) leprosy? From: J Barreto, Bauru, S. Paulo, Brazil

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Dear Dr Noto,

Thank you very much to my friend Dr Ben Naafs, and also to Dr Pieter Schreuder for their comments (please see LML 9^th Sept., 2011).

1. Yes, there is a spectrum in leprosy classification, and low resistant tuberculoid is a fact, even though I have seen only less than 10 cases in more than 10 years, and in more than 15.000 slides of leprosy cases which I saw during 8 years as dermatopathologist at the Instituto Lauro de Souza Lima (ILSL).

2. According to 1971 Ridley’s Classification (Five from seven groups), there is a group called TI (Indefinite Tuberculoid), who develops type 1 reaction, but this group is not the same of tuberculoid reactional described by Wade and Lauro de Souza Lima in the beginning of the 20 century.  The name reactional tuberculoid leprosy, grouped later with BT patients in R&J Classification 1962/1966, should be deserved to patients with usually a lesion clinically and histopathologically indeterminate (early), whose developed, in most cases, a reaction in the first or second month of therapy, usually with few or no nerve symptoms, and the normal evolution was to cure.  These patients had a Mitsuda reaction of 2+, i.e., 6 to 10mm diameter, different from TT patients (>10mm or ulcerated).  Ridley, in his paper "Skin biopsy on Leprosy", 1987, second edition, pointed that TI is not the same as TR, though both undergone reactions.  At the ILSL we recognize 2 groups of low resistant tuberculoids: "T in reaction", which in turn are really BT patients, i.e., annular tuberculoid lesions with satellite lesions and erythema after the beginning of treatment, and "reactional tuberculoid", described above.

3. It is also important to know that is very difficult to distinguish, even histopathologically, true TT from BT cases.  Dr Fleury published a paper about this, in Hansenologia Internationalis.  Ridley (1974) pointed some clues, as the lower destruction of epidermis and dermal nerve branches, as well as the presence of more Langhans giant cells in granuloma, but the main clue is the bacilloscopy (slit-skin smear examination), and sometimes only the evolution over long term follow up.

4. About bacilloscopy, as many as 90% of smears are made with bad quality in Brazil, and I believe that few technicians in the world, as well, are able to perform it correctly.  I performed a study in 2010, in the state of Mato Grosso do Sul, Brazil, that I am going to present on the next International Leprosy Congress in Brazil.  Why I made a study in this state? Because the quality of smears, on indirect evaluation, was said more than 99% good, and for this reason, it was the model for the country.  Nevertheless, when we went to the field, and on direct evaluation, less than 10% of the smears were made in good conditions, i.e. good collection, fixation, staining and reading.  This is the likely reason which explains why patients with less than 5 lesions are said PB: the smear collection from the lesions needs a good technics, and usually it is not possible to make it with tools other than the fingers, and for this reason almost all technicians DO NOT COLLECT from lesions.  This is a fact.  Once in cases of initial borderline leprosy the bacilli are found only in lesions, of course, index points will show no bacilli, and patients will be considered wrongly PB.

5. How long must we wait to say the patient is healed?  5yrs?  10yrs?  How many long term follow up of PB patients, with good methodology, are described on literature?  On my recent review of literature for my PhD thesis, ALL of them had less than 10yrs, and ALL the relapsed cases in these studies were diagnosed only by spontaneous demand.  If we wonder that M. leprae can stay dormant in Schwann cells as many as 10yrs, and duplication time is almost 2 weeks, how many time must we wait to find and show viable bacilli on skin biopsies, or even on smears (which have lower accuracy), in order to distinguish between reversal reaction and relapse, after a short course of treatment in a borderline patient?

6. Finally, if, in a normal distribution of cases in the spectrum, only 10% have Mitsuda reaction positive (Ridley, 1974), and only these patients are able to destroy dormant bacilli inside nerve fibers, once metabolic inactive M. leprae will not be destroyed by MDT, what will be the real percentage of good prognosis MDT PB treated patients?

These are only some questions, which I still do not have answers.

Regards,

Jaison