Wednesday, November 9, 2011

“PB-ish” leprosy in the paler skins


Leprosy Mailing List – November 2nd, 2011 
Ref.:   “PB-ish” leprosy in the paler skins
From:  G  Warren, Sydney, Australia

Dear Dr Noto.,
Thank you very much for circulating the TEXT and SLIDES of “The Diagnosis of Leprosy”.  Of course, last year, when the original version was produces I was carefully following and participating the discussions together with you, Drs Schreuder and Naafs.  With pleasure, I also offered some contributions, to help the newer workers to learn the tricks we have learnt, by often bitter experience, over many years. -
There seemed to be a number of letters in the week ending 16th October and some excellent pictures on dark skin.  However, last weekend I wrote to you a letter that some how seems to have slipped through  the cracks, that I think would help especially those workers faced with the PB-ish [paucibacillary] leprosy in the paler skins but, I have seen no evidence of it so, I send again (after this note) in the hope that you will be able to circulate it.  I feel it makes some important points about the diagnosis and management of PB-ish leprosy
Sunday 16th October.
Dear Dr Noto,
Thank you for publishing Dr Barreto’s letter [LML Oct. 15th, 2011 “What is paucibacillary (PB) leprosy?”].  I have seen many patients who were initially treated as paucibacillary leprosy according to the WHO guidelines who have returned 3-10 years later with obviously mid borderline/borderline lepromatous (BB/BL) type lesions.  On careful history taking one can realise that initially the patients was never properly classified.  According to WHO the PB leprosy is less than 5 lesions, but in their guide book there is no other specific requirement.  PB implies few bacilli and in true tuberculoid (TT) leprosy the lesions are usually well defined and on one area of the body implying that the bacilli are not wide spread.  However bacilli can well be in nerves in other parts of the body and they do not produce skin lesions.  As Dr Barreto implies patients may well be multibacillary (MB) with marked neural leprosy but very few skin lesions.
In Teaching in Asia I used to stipulate that to be treated as PB the patients’ lesions must be all in one area of the body; this unfortunately, is not  according to WHO classification.  We often had no possibility of doing a slit-skin smear examination and so deemed it preferable to give the MB treatment and prevent “relapses”.  In the last 10 years I have treated a number of immigrants to Australia who have previously been treated in an endemic country for PB leprosy and have represented 3-7 years later, in Australia, with definite BB-ish leprosy!  One almost pure lepromatous (LL) type of disease and the lesions were hardly visible even on the relapse.  Yes I call it relapse not reinfection.
As Dr Barreto states the bacilli live in the nerves, and may be in very high concentration in the nerves while there are few in the skin, and it has been shown that the bacilli can survive, for many years, in the nerves  in spite of heavy doses of rifampicin, and can emerge later, still fully sensitive to rifampicin, to  continue the Infection.  So, I would plead with clinicians if there is any possibility of having less that excellent natural resistance, that the patient be given MB treatment rather than PB.  
Also treat intercurrent medical conditions that could reduce the patient ability to deal with the leprosy infection.  Also do not just brush aside the possibility of relapse.  It turns up more frequently than appears in the statistics because there is now no continuous registrar and as Dr Rao states (in LML 15th Oct)  it is difficult to convince the authorities that a patient has a relapse when he represents with new lesions.  He was previously stated to be cured when he finished the WHO stated duration of medication.  WHO official statement of relapse is very low so makes the present policy (of PB and MB drug routines) seem effective.  I know that most of the real LL, and BL patients I treat have much more anti-leprosy medication that the stated 12 months.  We do not want relapses in our clinics.
Hence I agree - - What is paucibacillary leprosy?- - by definition it is those with few bacilli - - therefore those in whom the bacilli have not yet been able to multiply frequently because of the short duration of infection eg. as in Indeterminate (I) leprosy- or those who have enough natural resistance to have been able to produce effective T lymphocytes to control the infection so the numbers cannot become great.  In both of these situations I feel we need to follow up the patient at least for several years to make sure that they really are cured, if we give the 6 months double drug therapy.
Let’s really control the infection by ensuring that those we do diagnose are fully treated to eliminate their infection.  Let’s over-treat not under-treat.
Yours sincerely,
Grace  Warren
Sydney, Australia
Previously Adviser for The Leprosy Mission In Asia (1975-95)

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