Saturday, January 31, 2015

(LML) How Efficacious is MDT

Leprosy Mailing List – January 31,  2015

Ref.:    (LML) How Efficacious is MDT

From:  HK Kar, New Delhi, India



Dear Dr Helen,


I would like to react to the letter by Dr. Helen Roberts, LML January 29, 2015. We appreciate her concern. Instances of relapse are not uncommon with standard fixed duration WHO MDT even after full course of treatment.


So many factors come to our mind regarding possible causes of relapse in that particular case. Is the classification wrong? Is the fixed duration MDT regimen  not adequate to kill all organisms, particularly when BI is 4+ or above. Is the culprit  presence of  persisters? Did the patient real take the full course of treatment at home even though  taken full courses from Medical centre? Is it a case of reinfection since the source of infection is still persisting in the community either in human being or environment? And so many other possible factors.


Each case has to be examined separately and retreated adequately. Fortunately Multi Drug resistance is only been  reported in leprosy in few case reports. But we have to be adequately prepared to face the future challenge with 2nd line regimen with existing available antileprosy drugs or newer regimens for the future. 


Thanks once again for bringing this challenging topic to limelight.




Dr Kar


Dr (Prof.) H K Kar

Professor in Dermatology
Director and Med. Superintendent
P.G.I.M.E.R. and Dr Ram Manohar Lohia Hospital
Baba Kharag Singh Marg
New Delhi-110001

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(LML) How Efficacious is MDT

Leprosy Mailing List – January 31,  2015

Ref.:   (LML) How Efficacious is MDT

From:  Dr. Grace Warren, Sidney, Australia


 Dear Pieter,



Thank you for publishing these letters regarding relapse after routine WHO MDT.  It is interesting to note that several people are stating similar things. One wonders how many more patients do not really have the bacteria eliminated by the now 12 months, originally 2 year recommendation, of WHO as treatment for MB Leprosy.


I started treating leprosy in 1959 and at our hospital we had an excellent lab tech who did slit skin smears from 6 sites every 2 months while they were in our institution.  We showed that true LL required a year to drop the BI by one point i.e. it took 5 years to go from 6 down to 1 and then after that it may take another year or two to negativity. That was with Dapsone alone. When other drugs came available, we added them and found that they really did not increase the rate of negativity by any significant degree, but certainly made a difference in patients in whom we suspected dapsone resistance.  When we did the drug trials with Clofazamine we found the BI did fall a bit quicker, but not much more so, but there was far less ENL


In those days we gave Dapsone for life. Even so we did occasionally see relapse of skin lesions, a return of positive skin smear, or more neuritic symptoms, quite a long time after the patient was smear negative. This was usually after discharge and one wonders if the patient was always regular with his medication. Of course he said he was, but we would usually treat as if he had dapsone resistance.


Interestingly, in the letter from Dr Shetty in Mumbai in which he quotes several who relapsed after DDS monotherapy (one only given for twelve years). It was always stated to be needed for life!!!!  One of them is florid lepromatous in the picture that sure would need far more than a terminated course of DDS only.


However, in the 1960s I had contact with a research institution who showed that the bacilli were able to resist even daily supervised Rifampicin and hide in nerves for several years while the patient was on daily Rifampicin supervised. Even after 5 years of the daily supervised Rifampicin live fully sensitive bacilli could be isolated in testicular nerves!!  So one wonders if this type of record has been considered. Is it that the bacilli do hide in nerves and can come out and restart the disease when the routine MDT is stopped?

There is no way that one can check on the regularity of the patient taking their drugs and there is no way we can check on the presence of viable bacilli in a patient. In the 1980s we did see some relapses in those in whom we stopped MDT after 2 years as recommended. So a number of us continued, others thought cessation of medication was acceptable.  Often I would continue with Clofazamine alone for a couple of years with a satisfaction in seeing a reduction in relapse and/or reaction in the many patients across Asia that I supervised.


One important point is that steroids are so often given for reaction. It has been shown that the number of bacilli do not fall significantly while on Steroids. On steroids the bacilli run for cover probably deep in the nerves where they cannot easily be got. So one should not include the length of time on steroids as part of the MDT duration. It is advised by many good leprologists that the duration of MDT after the steroids are stopped should be long enough to ensure that the patient has at least the recommended duration of MDT without steroids. I feel the use of Prednisolone has produced many problems that are often unrecognised at the time.


For all LL and BL patients I would give 24 months at least. Not only 12 months and as I have already stated. Often continue for a prolonged period as we do not want relapse. It is also important to arrange for follow up visits - I would say for all MB patients at least 5 years.


So for the query in the attached letter I do not think it is a re-infection. I think it is just that the disease was not eliminated initially and/or the patient does not have enough good natural resistance or else has other medical problems like poor nutrition or intercurrent disease.


Leprosy is far from eliminated.  I have been fascinated with the number of patients that we have diagnosed who do not present with classical signs. As Leprosy does not receive any preference in Medical teaching schools, many clinicians are never really taught to look for leprosy.  In my work in Asia in the 1980s/90s I was surprised - I could  say horrified - to find that when I was invited to go to a Medical school to lecture on Leprosy I was often  informed it was first time that that school had had such a lecture  for many years, some for ever -  and that in endemic countries.


One of my favourite statements is along this line "What one does not look for one never sees and what one does not think about, one will never recognise!”  If people do not look for it they will never find it and if they do not take it seriously then the disease will often return! We need to ensure we find the disease early and treat it adequately.


May you really treat it fully- never try and hurry up the course of treatment, overtreat is better than undertreat.  I love Clofazamine. It is effective, resistance has not yet been seen to develop in a patient and it has virtually no undesirable side effects except perhaps the pigmentation that does go when the drug is stopped. If I  could only have  one drug for leprosy treatment  please let me have Clofazamine.,


Best wishes,


Grace  Warren,


Previously Advisor in Leprosy and Reconstructive Surgery for The Leprosy Mission International  in Asia ( 1975-1995)-   She  did leprosy work  in 26 countries for over 50 years.

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Thursday, January 29, 2015

(LML) How Efficacious is MDT


Leprosy Mailing List – January 29,  2015

Ref.:   (LML)  How Efficacious is MDT

From:  Helen Roberts, Kolkata, Bengal, India


Dear Pieter,

Thank Dr.V.P.Shetty for bringing up the issue of Relapse (LML January 29, 2015).

I would like to know what was presentation at the first diagnosis? Are the symptoms similar in nature?

At TLM Kolkata, we have also come across patients relapsing after completing full course of MDT/MB. Their clinical presentation was very similar to the first presentation including the smear status. They are sensitive to both Rifampicin and Dapsone.

The question we need to ask is this: if they responded to treatment successfully, why have they presented with similar clinical features - Has it something to do with the environment that they live in? - Is it reinfection from the soil bacteria?

Helen Roberts, Medical Superintendent
Premananda Memorial Leprosy Hospital,259, A, APC Road,Kolkata- 700 006. West Bengal
Mobile: 9831557368 ,Phone: 23506072,Skype : jainy.helen, Website:

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(LML) How Efficacious is MDT


Leprosy Mailing List – January 29,  2015

Ref.:    (LML)  How Efficacious is MDT

From:  V.P. Shetty, Mumbai, India


Dear Dr. Pieter,



We would like to share with LML readers some of our findings in the field where we work i.e in District Raigad, state of Maharashtra, India. We notice that relapse following MDT is not uncommon as it is projected out to be. Following are only few examples. The serious question that we would like to ask is how efficacious is MDT.



No. 1:


In Oct. 2009, A 28 years old male was seen with complains of, tingling and numbness over extremities. On examination, there were crops of nodular lesions on the back (see fig.1).  BI was 5+. We checked for drug sensitivity using molecular method, was sensitive to both DDS and RFP. 


History: Detected with MB leprosy in 1994, taken MB-MDT x 24 months, RFT in Nov. 1996.


Fig 1




Crop of nodular lesion on the back.



No. 2:


In March 2013, a 62 year old male was seen with multiple plaques & nodules (see fig below) and multiple thick nerves, BI=5+, using molecular technique mutation in fol-p gene (DDS resistance) was detected.

History: 1971- Numerous HPPs -Rx DDS mono x 12 years (RFT in~ 1983)

1st Relapse- In 1998 - Reappearance of HPPs -Rx MB MDT x 12mnths    (RFT 1999)

                       2011     - c/o multiple new NFI- No Rx~ Sept 2012 -  c/o few nodular lesions

 2nd Relapse- March 2013- Multiple plaques & nodules, multiple nerves thick, and BI=5+


Fig 2







No. 3 :


In April 2014, 70 year old male was seen with numerous nodular lesions all over body (see fig below). BI =6+, using molecular testing no mutation were seen


History: Detected with leprosy in 1972, was treated with DDS monotherapy for 12 years and released in 1984.


1st Relapse- Around 2007- reappearance of nodular lesion, treated with MBMDT for 24    months. RFT in 2010. 

2nd Relapse- April 2014 - detected with multiple nodular infiltration. BI=6+.


Fig: 3





No. 4:




Contacts and relapse around 2 child cases



Fig: 4


                      Family                                                                                          Neighbours























Left hand side-     Familial Contacts

Right hand side – Non Familial Contacts.





Dr. V. P. Shetty

Senior Scientist

The Foundation for Medical Research
84-A, R. G. Thadani Marg, Worli,
Mumbai - 400 018. INDIA
Tel: 91 22 24934989 / 24938601
Fax: 91 22 24932876


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Monday, January 26, 2015

(LML) Infoleps Choice of new (e) publications on leprosy - 20150119

Leprosy Mailing List – January 26,  2015

Ref.:   (LML)   Infoleps Choice of new (e) publications on leprosy - 20150119

From:  Grace Warren, Sidney, Australia


Dear Pieter,



Thank you for updating us.  I have appreciated being able to look through the lists of papers and reading some.  I was very interested in the one from India about the prevalence at present.  I have heard that there is a high incidence of patients, in some countries at least,  who do actually have the disease caused by M.leprae but do not fulfil the official  WHO description for diagnosis ie a  skin lesion that is anaesethetic!!    I can certainly agree with that as in East Asia I have seen many patients with well-developed leprosy but who have no definite skin patches and no definite anaesthesia.


Then of course there are the  pure primary neuritic leprosy which I first met in Burma but later saw in many countries in which there is no skin lesion  but definite large nerves and neural deficits in many cases.  I was asked to see a teenager with one of these hand problems and there was no doubt it was due to leprosy but the  visiting  WHO consultant who had seen him a week before said Oh No he has no skin lesion!!!! 


Has anyone done an evaluation of how many of these are present as I suspect that the total of them would certainly increase the world wide statistics, if the ones we are given are for those who do comply with the WHO definition in the  WHO  book on diagnosis. Interesting thoughts -  one wonders how many are missed by well-intentioned workers.


Best wishes to your readers as they try and reduce the deformities and problems of these patients.


Grace  Warren


Previously consultant in Leprosy and reconstructive surgery in Asia for the Leprosy Mission International   (1975-1995)

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(LML) BT Hansen's Disease and nerve abscesses - surgical intervention or MDT alone?

Leprosy Mailing List – January 26, 2015

Ref.:   (LML) BT Hansen's Disease and nerve abscesses - surgical intervention or MDT alone? 

From:  Robert Jerskey, Carlsbad, California, USA


Dear Dr. Pieter,



I enjoyed reading Dr. Sunil D. Ghate’s fascinating case presentation and query early this month, and then most recently, his follow-up report which included the nerve ultrasonography [N.U.] (LML January 22, 2015).



I have also found the posted responses very informative, including of the risks of surgical intervention and possible permanent nerve damage, the importance of monitoring for early nerve function deficit, and the value of crafting a medical regimen in order to best prevent the patient going in to a “full reaction”.  



Speaking of Reaction, I am reminded of a retrospective study published over two decades ago re: facial patches, type 1 reaction, and facial nerve damage, by Hogewig, Kiran, and Suneetha.  [see below **]  Though this case does not fit the criteria at this time, I reference the study because of the new information that has come to the fore:  a small facial lesion just lateral to the right eye.  Whether the patient is determined to be with PB or MB leprosy, or in Reaction or not, [and as alluded to by Dr. Warren, there are risks for potential Reaction during the course of tx] the fact that there is a facial patch proximal to the eye, though small, and multiple nerve enlargement in the L UE (Left Upper Extrimity), I would aim to carefully monitor the facial and trigeminal nerve function as well.   



And, again, with multiple UE nerve involvement there may also be LE nerve enlargement, if only incipient.  Incidentally, judging by the N.U. findings, there might be some enlargement in the right radial cutaneous nerve, comparing its diameter vis a vis the median nerve value on the same limb?



Good to read that there is thus far no sensory or motor impairment.   However, I am wondering which tool[s] are being used to identify early sensory impairment.  I read that the patient is being followed with TST and VMT.   Would Dr. Ghate clarify what is “TST”?  Likely to be Tactile Sensory Test.  [or Temperature?]  The tactile test covers quite a repertoire; might be with a pen, cotton, monofilaments, paper clip, etc.  I want to re-visit what Dr. Palande emphasized in his recent posting re: this same patient:  “…using graded nylons. Unless graded nylons are used one would not know if there is early nerve function deficit.”   If these, otherwise known as monofilaments [MF], have not been used, is there access to them in the clinic/hospital. so as to establish a fresh baseline?  Any insidious sensory deficits that might have been missed thus far can very likely be identified and measured with the graded MF. 



In summary, besides my request for clarification of the sensory testing tool[s], it would be helpful to monitor for any “red flags” at other key structures at risk of morbidity as the focus continues, understandably, on the L UE: to also carefully monitor nerve function in the other extremities and the eyes as well.


Thank you, Dr. Ghate, I look forward to reading of any further developments; your patient is clearly under well-orchestrated care.  

Friendly greetings to all LML readers,



Robert Jerskey, LOTR, P.O.D. consultant, based in Carlsbad, California, USA


** See comment in PubMed Commons belowLepr Rev. 1991 Jun;62(2):143-9.  The significance of facial patches and type I reaction for the development of facial nerve damage in leprosy. A retrospective study among 1226 paucibacillary leprosy patients.

Hogeweg M1, Kiran KU, Suneetha S.


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