What is paucibacillary (PB) leprosy?

Leprosy Mailing List – October 15^th, 2011 

Ref.:   What is paucibacillary (PB) leprosy?

From: Barreto J., Bauru, SP, Brazil

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Dear Dr Noto

I have seen many cases of "relapsed" borderline tuberculoid patients, 6 to 7 years after discharge by cure, and usually when they were treated as PB leprosy.  I am sending a note to the LML in order to listen to others colleagues opinion.

Regards,

Jaison

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WHAT IS PAUCIBACILLARY (PB) LEPROSY? CONSIDERATIONS ABOUT TRUE RELAPSES AND INSUFFICIENT TREATMENT

I don't understand why most borderline tuberculoid (BT) leprosy patients are still located in the same operational classification like polar tuberculoid (TT) patients, i.e., as "PB" leprosy, based only on skin smears.

What is PB leprosy? Since 1962, when Ridley & Jopling defined the spectrum, and in 1971, when Ridley revised and published the "5 of 7 groups Classification" (Ridley, 1972), it became clear that most BT leprosy patients tend to downgrade to BL, and this is the reason why most BL patients arise from downgrading of BT (Ridley, 1987).

Why? Because BT patients are usually Mitsuda negative (less than 5mm of diameter, or 0 to 1+ in Madrid classification); therefore, they clearly differ from Mitsuda positive patients (higher than 5mm of diameter).  This means that they do not develop well defined tuberculoid reaction, that is to say, full epitelioid transformation of macrophages with elimination of antigens (Michalany&Michalany, 1983).

This lack (or gap) of immunity, which differs from TT patients, is the likely reason which explains why the BT patients usually show many bacilli inside dermal nerve branches on Faraco-Fite stain, as well as more false "relapses" (due to insufficient treatment) and, recurrent reactions with neuritis when treated as PB (Nilsen, 1989; Revankar, 1989).

It is also important to say that slit-skin smears are positive only if there are, at least, 10 000 bacilli per gram of tissue (Bang, 2009).  In a 70kg adult, 14 kg (20% of the body weight) are represented by skin. So, in an attempt to find a positive smear, at least bacteriological index (BI) 1+, the patient should have a total load of 140 million of bacilli inside his skin.  This does not seem “few”, i.e., “PB”, in my opinion. 

BT patients may have BI of 1+ to 3+ in biopsy skin slides, this would represent a total skin load ranging from 140 million to 14 billion of bacilli.  It is assumed that at least 1 bacillus, in a million of M. leprae, will be naturally resistant to any single drug of the multi-drug therapy protocol (Hastings, 1998).  So, a total of 140 to 14 000 bacilli should be destroyed every month by the supervised rifampicin, but this drug destroys only metabolically active bacteria.  Once the duplication time of M. leprae is almost 14 days, every month, these dapsone resistant bacilli would have time to duplicate twice, at least.  Therefore, recurrent reactions and neuritis are foreseeable, probably due to continuing replication of bacilli not killed by dapsone during the lag phase (Opromolla, 2000).  There are evidences for this in a few cases.  I personally believe more in the role of autoimmunity. 

Finally, leprosy is a primarily neural disease and, as Schwann cells are bad antigen presenting cells, it is understandable that these patients could have as many as 4+ of bacilli inside nerve trunks which have undergone biopsy, even if the skin smears and biopsy indexes are negative (Barreto, 2007).

Jaison A. Barreto

Dermatologist and Leprologist

Instituto Lauro de Souza Lima

Bauru, SP, Brazil