Leprosy Training Courses, Nilphamari, Bangladesh, 2016

Leprosy Mailing List – December 18,  2015

Ref.:    (LML) Leprosy Training Courses, Nilphamari, Bangladesh, 2016

From:  Ruth Butlin, Nilphamari, Bangladesh

---

Dear Dr. Schreuder,

As the WHO draft strategy mentions, there is an on-going need for preservation and dissemination of leprosy expertise. The Leprosy Mission Bangladesh regularly offers courses related to leprosy at its training centre in Nilphamari, where experienced facilitators and leprosy-affected people are available to ensure trainees fully understand the issues addressed.

-       Clinical leprosy – a basic course for doctors, 12 - 17 March, 2016

-       Leprosy orientation for administrators, 20 - 22 March 2016

I attach information on two upcoming courses. Could you please distribute them through the leprosy Mailing List?

Thank you.

Yours sincerely,

C Ruth Butlin

Medical advisor to DBLM hospital and rural health programmes of TLM Bangladesh

The diagnosis of leprosy is not always easy

Ref.:   The diagnosis of leprosy is not always easy

From: B Naafs, Munnekeburen, The Netherlands

---

Dear Salvatore,

I refer to last week messages about early diagnosis of lepromatous leprosy.  Kindly, find in attachment the paper of J A da Costa Nery et al. “Hansen’s disease in a general hospital: uncommon presentations and delay in diagnosis” J Eur Acad Dermatol Venereol 2009 Feb;23 (2):150-6. Epub 2008 Sep 10.  I would be very grateful if you forward it to the leprosy mailing list.

The diagnosis of leprosy is not always easy, as it is generally stated and thought. To be aware that a condition or complaint could be leprosy is a start.  As leprosy is suspected it has to be proven.  The cardinal signs of leprosy have to be investigated.  They are loss of sensation in a skin lesion, enlarged peripheral nerves and positive slit-skin smear examination (*).  When two of these three signs are positive, leprosy is diagnosed. 

Ninety nine per cent of all leprosy patients can be diagnosed in the above mentioned way.  Herewith I will say a few words about one exception (indeterminate leprosy) and, two particular conditions namely: early lepromatous leprosy and diffuse lepromatous leprosy (also called Lapati’s leprosy or “Lepra bonita”).

Indeterminate leprosy

The diagnosis of indeterminate leprosy depends on awareness. Loss of sensation is often hardly present or is absent, nerves are not enlarged and skin smear is negative.  Even biopsy may be hardly helpful.  It is “the time that makes the diagnosis” and thus careful follow-up of the patient is needed for a few months.

Early lepromatous (LL) leprosy

In an early state LL leprosy is often not diagnosed, though these patients can be extremely infective.  Awareness and skin smear may be of help.  When people do not think of leprosy it can be easily missed. 

Diffuse lepromatous leprosy (Lapati’s leprosy)

In early and late diffuse lepromatous leprosy mostly nothing is to be seen or found, only the patient may complain of some aches and pain or having the feeling of dropping things or of sleeping skin.  In late diffuse leprosy the patient looks younger and has a smooth skin due to infiltration [lepra bonita].  Skin smears in both groups of patients are positive.

Nery’s  paper addresses these problems.  Herewith I report part of the conclusions:-

<< Multibacillary (MB) leprosy, especially close to the lepromatous end of the spectrum, may mimic other diseases, and the patient cannot be diagnosed without a biopsy or a slit skin smear examination.  Leprosy should be considered in all patients with skin lesions not responding to treatment, especially when they have neurological deficits, and live or have lived in a leprosy endemic area. >>

Ben Naafs

(*)

The Diagnosis of Leprosy

S Noto, P A M Schreuder and B Naafs

Leprosy mailing list - October 2011

About early diagnosis of lepromatous leprosy

Ref.:   About early diagnosis of lepromatous leprosy
From: M Leide W. de Oliveira, Rio de Janeiro, Brazil

---

Dear Dr Noto,

I share the same point of view of my colleagues regarding the last discussion on the LML about early diagnosis of lepromatous (LL) leprosy.  Despite some advanced multibacillary (MB) cases still being diagnosed everywhere in Brazil, the great majority of them are early mid borderline (BB) or LL Hansen´s Disease.  I have also seen cases presenting single nodular lesion, located mainly in the buttocks or Achilles tendon, without any infiltration or nerve involvement.  Other patients only present episodes of a few erythema nodosum leprosum (ENL) reaction lesions.

However, one of the great results of household contact examinations and continuous local campaigns in Brazil, is a large number of indeterminate leprosy, as well as borderline leprosy diagnosed before nerve damage, in a stage of evanescent skin patches.  In Rio de Janeiro state for instance, the regional Society of Dermatology (SBD-RJ) has been working with the state program manager to insert skilled professors of dermatology in local campaigns at the peripheral municipalities of the metropolitan region.  Also, at the most prevalent municipalities in the minor cities over the last 3 years.  This is justified by the weakness of the primary health care in these areas and it is not only useful to find new leprosy cases but also to train family health teams and medical residents on dermatology.

In fact this strategy started in 1998 in Rio de Janeiro city and in the beginning of the years 2000, expanded to municipality of Duque de Caxias next to Rio de Janeiro city, where I performed a project funded by the Netherlands Leprosy Relief (NLR) from 2003-2007.  The results can be observed in Graphic 1: the detection rate of Hansen´s Disease in the whole state of Rio de Janeiro shows a 46.8% reduction from 2001 to 2010 and, at the same period, the reduction achieved in Duque de Caxias municipality was 56.35%.  However, this peripheral municipality is presenting now the same detection rate of the whole state at the beginning of the decade.

The fluctuation observed in this municipality could be related to the sporadic but also continuous case finding activities, as the basic care network of Duque de Caxias covers only 30% of its population in addition to management weaknesses.  The decrease in the detection rate of course influenced the current prevalence rate of the state to be less than 1/10,000 inhabitants.  Nevertheless, local case finding activity to allow early diagnosis and interruption of the transmission of the source of infection in the peripheral area, is mandatory in order to sustain the decline.

The state detection rate decrease (Graphic 1) was gradual, without fluctuation in accordance with the epidemiological behaviour of this endemic disease.  So that I believe on its sustainability, if the peripheral and poorest areas continuing receiving efforts to Hansen´s Disease control advocacy.  No less important is the social and economic development of these municipalities.

Maria Leide W. de Oliveira

Medical School-Dermatology Sector/Federal University  of  Rio de Janeiro (UFRJ)

Graphic 1. 

No Hypopigmented Lesion, No Nerve Thickening, But Its Leprosy!

Ref.:   No Hypopigmented Lesion, No Nerve Thickening, But Its Leprosy!
From:

1.
H K Kar, New Delhi, India

2.

D Palande, Kurichikuppam, Pondicherry, India

---

1.

Dear Dr Noto,

I appreciate to note the comment from Dr Warren on article "No hypo-pigmented lesion, no nerve thickening, but leprosy" by A Singh et al (Indian J Dermatology, 2012.).  There is a great change in clinical presentation of lepromatous (LL) leprosy in India, must be the same in Brazil, the two most leprosy populated countries.  It requires a lot of data generation from the published and unpublished documents for the future leprologists, dermatologists and physician especially for early diagnosis of LL through suspecting clinically and confirming on slit skin smear (SSS) examination.  

For early LL, especially in the stage of early infiltration in the skin without any nerve involvement clinically, only a doctor with sharp clinical acumen can suspect this stage when he/she examines the patient in a natural light and confirm with SSS.  Recently, very unusual presentations of LL have been documented with single nodular lesion, single nerve lesion, and few evanescent ENL lesions.
Our teaching program on leprosy should focus on these aspects to our younger generation medical students in graduate and post graduate level.

Regards,

Dr (Prof.) H K Kar
Dean, PGIMER, Dr R M L Hospital
Consultant & HOD
Department of Dermatology, STD & Leprosy
P.G.I.M.E.R. and Dr Ram Manohar Lohia Hospital
Baba Kharag Singh Marg
New Delhi-110001

2.

Dear Dr Noto,

I very much appreciate and would like to repeat what Dr. Grace has written [LML May 28^th, 2012] especially the sentence:-

“This is a timely reminder and one wonders how many of these patients are treated for some other disease or just not treated till the leprosy is definite and that often means that deformity or disability will result.  Also the patients most likely to have this type of lesion are those at lepromatous end of spectrum and so most likely to transmit the disease to their contacts; even if they are not manifesting obvious lesions”.

Dinkar D. Palande

No Hypopigmented Lesion, No Nerve Thickening, But Its Leprosy!

Ref.:   No Hypopigmented Lesion, No Nerve Thickening, But Its Leprosy!
From: G Warren, Sydney, Australia

---

Dear Dr Noto.,

Thank you very much to Ms Nathalie Koumans for her message [LML may 22nd, 2012].  I was very pleased to open the new list posted from Infoleps of leprosy articles, available on line.  This article was of particular interest.
“No Hypopigmented Lesion, No Nerve Thickening, But Its Leprosy!”
Ashish Singh, S Ambujam, and N S Pradeep Kumar
Indian J Dermatol. 2012 Jan-Feb; 57(1): 73–74.
doi:  10.4103/0019-5154.92689

This is a very timely article based on the general acceptance of the W.H.O. definition that a patient with leprosy must have a skin patch with a definite loss of sensation.  The writers describe a very common problem in many countries where the pinkish ENL spot may become and go and may ulcerate and become infected and may even be uncomfortable but, the quickest way of checking the diagnosis of leprosy is often by a slit skin smear.  Yes, I am afraid that good reliable technicians able to do a good smear are becoming more rare, but It is important that general dermatologists and physicians need to remember that early Lepromatous leprosy may have very vague lesions or fluctuating ones (as ENL does) that have no loss of pain or obvious abnormality in touch.

Yes, “what we do not think about we will never diagnose” and in endemic countries we need to still be aware that  leprosy is present but, we will not diagnose it if we do not look for it.

Having worked in eastern Asia for many years I am very familiar with this early LL type of leprosy in which there are no obvious lesions for many years though if one palpates carefully one realises that there is some infiltration.  If the positive diagnosis is made at that early stage then there is often no real problems managing reaction and recovery does occur relatively rapidly without deformity or disability.  

I vividly remember one middle aged Chinese woman whose face was generally infiltrated but, she had no obvious edges and no definite lesion.   However on careful examination one could feel the infiltration and appreciate that the upper lip was not as infiltrated as the rest of the face.  The diagnosis was made because a nodule on her arm was biopsied!   In follow up we found slit skin smears with bacteriological index (BI) of 3+ and 4+ in every site where we examined even if there was no sign of a definite lesion.

This is a timely reminder and one wonders how many of these patients are treated for some other disease or just not treated till the leprosy is definite and that often means that deformity or disability will result.  Also the patients most likely to have this type of lesion are those at lepromatous end of spectrum and so most likely to transmit the disease to their contacts; even if they are not manifesting obvious lesions.

May we really look for these cases and early treatment will help to keep the numbers of new cases down.

Yours sincerely,

Grace Warren
Previously Med Superintendent of  Hong Kong leprosarium 1959-1975. 
Adviser in Leprosy  and Reconstructive Surgery for the Leprosy Mission Asia 1975-1995.

Clinical case. Borderline leprosy in reaction in a boy

 Leprosy Mailing List – April 6th, 2012 

Ref.:   Clinical case. Borderline leprosy in reaction in a boy.From: Warren G., Melbourne, Australia

---

Dear Dr Noto,

I would like to congratulate Dr Barreto and Dr Cabral on the excellent case presentation (LML 24 March 2012) that opens the way to discussion of several important points.  There were some interesting picture of biopsies, but one wonders what type of lesions were biopsied.  One would expect those type of pictures from the BT end of spectrum but I wonder if any biopsy was taken from a vague lesion?

1. The lesions appeared at age 4 with no known contacts of leprosy, but we do not know the incidence of leprosy in the area or if the patient had lived elsewhere.  The state of Mato Grosso is well known for his leprosy endemicity.  Was any (extended) contact examination done?

2. The condition was diagnosed as eczema at several occasions, by different health staff and even by the local leprosy reference centre.  It does accent in endemic areas that any skin lesion not reacting to normal treatment needs to be followed up and the possibility of leprosy should be taken into account.  Even the local leprosy clinic did not think about this possibility.  This is an aftermath we are seeing in many place now that the statement that leprosy is eliminated has resulted in many early cases being missed.  WHAT WE DO NOT LOOK FOR WE WILL NEVER SEE!  One should be highly suspicious of eczema that continued for twelve months not reacting to treatment.

3. I am interested in the degree of affection of the nerves.  There is no mention of sensory changes (in the lesions, hands and feet).  Perhaps a little hard  to test, in a 5 year old. The history implies no motor nerve deficit, but the biopsy showed bacilli in nerves and some nerves were easily palpable and visible.  The use of steroids  is certainly indicated.  We see that the inflammation has settled clinically in 2 months so hopefully he should not develop further nerve involvement.  The steroids cannot reverse any real damage to the actual fibres that has occurred, but there is no point in continuing the steroids as their job is to reduce the inflammation.  However, it will not encourage regrowth of damaged fibres. 

4. Long experience with dozens of patient with this type of reaction has shown me that 10-12 weeks of steroids is all that most need and then the continued use of MDT, possibly with extra clofazimine to prevent and control further reaction.  I certainly did find that in lepra reaction in the BL/BBish type one often had both types of reaction at the same time (acute redness and even ulceration of the lesions that looked real BB/BT and ENL on the BL/LL ones).  In the pictures of the patient in question there is definitely a suggestion of BLish type lesions on wrists and also the ear lobe) and even around the knees.  Yes, he has downgraded, but lesions now are right across the spectrum and I would not be surprised if there was some early ENL in those arm and face (ear lobe) lesions or, that ENL comes once the steroid is discontinued.  Hence the suggestion that extra clofazimine may be of help. 

5. Steroids are often continued for a prolonged period and does a lot of harm to the patient’s own metabolism.  I have seen too many patients die because they had had long periods of steroids and for various reasons they were not restarted when medical complications arose (e.g. one teenage boy got a severe flue 6 months after 5 years of steroids stopped and he did not get adequate medical care and he died within a week). 

6. The other problem that is often forgotten is that steroids are effective  in preventing inflammation.  At the same time, the body’s own abilities to control the infection are slowed down by the steroids and this affects the ability of the body to reduce the degree of infection caused by M. leprae.  In fact in a well controlled drug trial severe LL patients were given Rifampycin daily under supervision for 5 years.  After that time the disease appeared controlled, but nerve biopsy and culture revealed M. leprae that were fully sensitive to the Rifampycin.  It is now accepted that the antibiotics while being able to kill the bacteria in the blood and other tissues, but cannot eliminate them from the nerves.  Once MDT is completed the bacteria come out, start multiplying again and the patient will relapse in years time. Hence, once definite durations for MDT were suggested by W.H.O., we  started counting the months recommended  as those not on steroids.  If a patient had 3 months steroids he had 24 plus 3 months of MDT for Multibacillary leprosy.  This certainly seemed to prevent many relapses.  In patients with less natural resistance ie the LL/BL type of disease that is well developed at diagnosis, I feel they need longer MDT than that recommended by W.H.O. to ensure no relapse. 

7. Hence I hope that the boy affected will have at least twelve months full MDT after the steroids are stopped.  He is obviously borderline in type and so should have some ability to  eliminate and control the infection. 

8. I am interested to see if he was given tricyclics.  Yes, I use them a lot on adults and think they are excellent in helping to minimise tension and fear of the disease.  However, I must confess  I rarely give tricyclics to small children though have frequently use Phenobarb with good results.  They  can help reduce the duration that one needs to give the steroids.

I do hope your presentation will encourage others to look more carefully for diagnosisand use steroids wisely.

Yours sincerely,

Grace Warren

Previously  Superintendent Hong Kong Leprosarium ( 1960-75)
Advisor in leprosy and   Reconstructive surgery in Asia  ( 1975-95)

Clinical case. Borderline leprosy in reaction in a boy

  Leprosy Mailing List – March 28th, 2012 

Ref.:   Clinical case. Borderline leprosy in reaction in a boyFrom: P. Vijayakumaran, Chennai, India

---

Dear Salvatore,

I refer to the clinical case circulated by via the Leprosy Mailing List – March 24th, 2012.  Thank you very much to Dr Barreto and Dr Cabral for sharing the interesting case history (not so interesting for the person affected).  I congratulate the team for providing all details for better understanding of the situation and also appropriate management of the condition. I am not a pathologist.  Here are my impressions:

·         The presentation was atypical so that it could not be related to leprosy.

·         Health staff are not aware of presentations of leprosy.

·         Leprosy referral hospital may have un-trained staff who cannot identify leprosy.

·         Multiple nerve involvement is characteristic of borderline leprosy.  That too with in a period of one year goes more in favour.

·         Bacteriological Index of 2+ at all sites (probably all selective sites – that means active lesions) may indicate that the disease has progressed beyond borderline tuberculoid leprosy (towards lepromatous leprosy).

·         Biopsy - 3+ positive and presence of globi are indicative of lepromatous side of leprosy spectrum.

·         Biopsy – Globi and macrophages are characteristics of lepromatous side of the spectrum.

Fig.1 & 2               : Any trained eye will suspect leprosy.

Fig.3 & 4               : Misleading presentation because of scaling and central healing.

Fig.5, 6 & 7          : Trained eyes should be able to suspect leprosy.

Fig.8                    : Explains importance of examination of peripheral nerves. Again trained eyes and hands comes to my mind.

Fig.15 & 16          : Clearly clinical presentation of BB leprosy. 

This child is fortunate to have intact nerve function. This also warrants close observation for possibility of fresh episodes of reactions and especially neuritis. 

I once again thank the authors and the LML for sharing their experience. 

With best wishes,

Dr.P.Vijayakumaran,

Regional Medical Coordinator South,

German Leprosy and TB Relief Association India,

#4, Gajapathi street, Shenoy Nagar,

Chennai – 600030, India

Clinical case. Borderline leprosy in reaction in a boy

 Leprosy Mailing List – March 24th, 2012 

Ref.:   Clinical case. Borderline leprosy in reaction in a boy.From: Barreto, J., S. Paulo, Brazil

---

Dear Salvatore and Pieter,

Thank you very much for inviting me to circulate a clinical case on the leprosy mailing list.  I believe it is a good and useful initiative.  Herewith we (myself and José Cabral Lopez) present the case of a 5 years old boy from Brazil with borderline leprosy in reaction.  We will really appreciate any comment about the case.

Best regards,

Jaison

LL patients may have no obvious skin lesions and no changes in sensation for years

Leprosy Mailing List – January 24^th, 2012 

Ref.:    LL patients may have no obvious skin lesions and no changes in sensation for years
From:  G. Warren, Sidney, Australia

---

Dear Dr Noto,

It was good to see Dr Lockwood’s letter (LML Jan. 20^th, 2012) regarding the “Elimination” in Brazil, and her acknowledgement that recognition of leprosy cases will continue for many decades.

One report states that in at least one country there is an incidence of 50% of graded 2 disability in new cases at diagnosis.  This surely means that the clinicians just do not know early leprosy. Unfortunately as, I have often said before, I believe that this is largely due to the WHO statement that to be diagnosed as leprosy the patient needs an anaesthetic skin patch!  I have worked in many countries (27) and find so many variants in early presentation, partly racial but, in some groups the highly infectious LL patients may have no obvious skin lesions and may have no changes in sensation for twenty years and, even then many of them do not have any anaesthesia; though they may have altered sensory perception.  In the same way as Most diabetics do not have anaesthetic feet; they feel each step as it hits the ground but they may not feel a cut or even a broken bone causes no pain.  Yes, I have seen WHO consultants refuse to register patients with positive skin smears because they had no anaesthesia.  Also I have seen many “Primary persistent neuritic” leprosy patients not registered because they have no skin patch.

Surely we need to somehow get these recognised so that we do get  more accurate figures.  The present statements that leprosy Elimination is progressing is causing reduction in available funds.  The present figures really do not give any idea of how much leprosy is spreading.  In India there are hundreds of children being diagnosed now.  Is it really changing or just that people are now looking and revising their strategies, for which I am very thankful.

Can these new Statistics from India inspire others to try and do something similar?  What can be done to modify that Definition of leprosy as published in the WHO guide to Elimination.  That definition is certainly not the one in most reliable Text books on Leprosy which state the patient needs at least one of three clinical signs, which are patches, nerve involvement or positive skin smears.  While that definition stands many early patients will not be diagnosed at a time when it is possible and easy to eliminate the disease before serious deformity has been caused.

Keep it up Brazil and may others follow your lead and may we proceed to a more practical approach to the control of this disease.  The use of that word elimination makes Governments try and forget that it is still a problem and can easily flare up again to a major problem unless constantly looked for.  I teach my students “What you do not look for you will never see”.  Let’s try and get everyone looking for leprosy again.

Grace Warren,

Previously advisor for the Leprosy Mission in Asia. (1975-1995)

What is in paucibacillary (PB) leprosy?

Leprosy Mailing List – November 9th, 2011 

Ref.:   What is in paucibacillary (PB) leprosy?

From: B Naafs and P A M Schreuder, The Netherlands

---

Dear Salvatore,

We thank Dr. Jaison for his message “What is paucibacillary (PB) leprosy?” (LML Oct. 15^th, 2011).  We just want to make a few observations to add to the discussion.

1. Dr. Leiker recognised that there existed a classification between tuberculoid (TT) and borderline tuberculoid (BT) leprosy.  He called that LRT = Low Resistant Tuberculoid.  It presents one or a few lesions (not symmetrically distributed) with a few satellites.  Skin smears are mostly negative.  It was a group of patients who hardly had problems or went into reaction.  It is a pity this was never taken up by the international leprosy community.

2. In the old times BT with a max. smear bacteriological index (BI) of 1+ were indeed treated as PB.  It later on turned out that especially BT with multiple lesions relapsed.  In those cases were nerve biopsies were taken, many of those had a positive RC nerve biopsy (Dr. Ben Naafs).  To reduce the PB relapse rate to a lower level a new clinical classification system was put in place: those patients with less than 6 lesions or with not more than 1 nerve involved were called PB.  That indeed had the intended result.

3. Indeed, when smears would be taken in PB patients, 2 - 4% will be positive (ref. 1).  Sometimes even a single lesion turns out to be positive.  In case of  nerve biopsies in PB patients even more will be  positive.  Nevertheless, we do not find a relapse rate of 2 - 4% in PB patients, much less so.  Even in the old times, not all BT smear positives or with many lesions relapsed.

4. The first result of the Uniform MDT schedule shows  that the PB relapse rate has become even lower than the MB relapse rate.  Which could have been expected.

5. We are aware of Opromolla’s hypothesis, but which is not shared by many.  In Thailand we saw and treated (with steroids) successfully many patients with a late reaction.  The big majority of these patients improved and never relapsed (Dr. Pieter Schreuder).

May we also refer to the article by Maria Angela Bianconcini Trindade et al (reference 2): The histopathological changes in 167 biopsies from 66 leprosy patients were studied.  The patients were selected when their sequential biopsies demonstrated either different patterns or maintained the same pattern of granulomatous reaction over more than two years during or after the treatment of leprosy.  In 57 of the patients studied, a reactivation was seen which coincided with a decrease in the BI, suggesting that this reactivation (reversal reaction or type 1 leprosy reaction) coincides with an effective capacity for bacteriological clearance.  In nine patients, an increase of the BI or persistence of solid bacilli occurred during the reactivation, indicating proliferative activity, suggestive of a relapse.  The histopathological aspects of the granulomas were similar in both groups.  CONCLUSION: bacteriology (slit-skin smear examination) provided the only means to differentiate a reversal reaction from a relapse in patients with granulomatous reactivation.  The type 1 leprosy reaction may be considered as a partly effective immune reconstitution (reversal, upgrading reaction) or as a mere hypersensitivity reaction (downgrading reaction) in a relapse.

Abraços,

Ben Naafs

Pieter AM Schreuder

References
1.Rao PS, Ekambaram V, Reddy BN, Krishnamoorthy P, Kumar SK, Dutta A.Is bacteriological examination by skin smear necessary in all paucibacillary leprosy patients in mass control programmes? Lepr Rev. 1991;62:303-309
2.Trinade MA, Benard G, Ura S, Ghidella CC, AVelleira JC, Vianna FR, Marques AB, Naafs B, Fleury RN. “Granulomatous reactivation during the course of a leprosy infection: reaction or relapse. PLoS Negl Trop Dis. 2010 Dec 21;4(12):e921

Acute abdomen in lepromatous (LL) leprosy

Leprosy Mailing List – November 3^rd, 2011

Ref.:   Acute abdomen in lepromatous (LL) leprosy.
From: Barreto J, Bauru, S. Paulo, Brazil

---

Dear Salvatore, 

The questions that must be made about this case:

1. Is this patient with active (non treated) lepromatous leprosy?  If the answer is yes, Lucio's fenomenon must be ruled out; once it is not uncommom deep vascular trombosis in this type of leprosy.

2. Is this patient in erythema nodosum leprosum (ENL or type 2) reaction?  As well as in Lucio's fenomenon, deep trombosis also can occur during this reaction.  Dr Opromolla and Dr Raul Fleury published cases of deep vascular trombosis during type 2 reaction, in the past, in Hansenologia Internationalis (www.ilsl.br).  Some cases developed even myocardial infarction.

If the answer to both questions is no, other causes must be involved.

Regards,

Jaison 

Unnecessary laparotomy for abdominal pain and fever due to clofazimine

Leprosy Mailing List – November 3^rd, 2011 

Ref.:   Unnecessary laparotomy for abdominal pain and fever due to clofazimine

From: Bryceson A, London, UK

---

Dear Salvatore

I wonder if the patient was taking clofazimine.  If so, the red coloration might be due to clofazimine.  Clofazimine can cause abdominal pain, sometimes mimicking an acute abdomen.  The pain is thought to be due to an inflammatory reaction to crystals of the drug deposited in the small bowel mucosa and mesenteric lymph nodes.  For this reason the high starting dose (300 mg) of clofazimine that is used to control ENL (Type 2) reactions, should be reduced after 2 or 3 weeks.  References go back a long way, but here are some recent ones.

Jadhav MV, Sathe AG, Deore SS, et al. Tissue concentration, systemic distribution and toxicity of clofazimine--an autopsy study. Indian J Pathol Microbiol. 2004;47:281-283.

Mathew BS, Pulimood AB, Prasanna CG, et al. Clofazimine induced enteropathy--a case highlighting the importance of drug induced disease in differential diagnosis. Trop Gastroenterol. 2006;27:87-88.

Sukpanichnant S, Hargrove NS, Kachintorn U, et al. Clofazimine-induced crystal-storing histiocytosis producing chronic abdominal pain in a leprosy patient. Am J Surg Pathol. 2000;24:129-135.

I made the same mistake in 1979

Bryceson A. Unnecessary laparotomy for abdominal pain and fever due to clofazimine.  Lepr Rev. 1979 Sep;50(3):258-9.

Best wishes,

Anthony Bryceson

Abdominal complication of clofazimine

Leprosy Mailing List – November 3^rd, 2011 

Ref.:   Abdominal complication of clofazimine

From: W S C Smith, Aberdeen, UK

---

Dear Dr Peton,

Thank you for circulating this photograph.  Had the patient been taking clofazimine – if so at what dose and for how long?

There are a few case reports in the literature of acute abdomen/abdominal pain associated with crystal formation due to clofazimine – I have attached reports from India, Thailand and Singapore – there are probably a few more.

Cairns Smith

http://informahealthcare.com/doi/abs/10.3109/00313029309068897

“PB-ish” leprosy in the paler skins

Leprosy Mailing List – November 2^nd, 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 16^th 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 16^th 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 15^th 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)

Histoid leprosy. Clinical case

Leprosy Mailing List – October 30^th, 2011 

Ref.:   Histoid leprosy. Clinical case

From: A G Barminus, Garkida, Adamawa State, Nigeria

---

Dear Dr Noto,

I wish to thank Dr Salafia (and also Drs Verduga and Barreto) for sharing with us their clinical experience in the field of leprosy.  I think that Dr Salafia’s case No 10 is histoid leprosy.  I would like contributing to this discussion by sending some clinical pictures of histoid leprosy for readers to see and advise (optimal length of treatment?).  They are hereby attached.  The pictures are mine and with the consent of the patient.

The patient is a new case of leprosy.  He never had any form of treatment for leprosy.  There was no nerve tenderness and the disability grade at diagnosis was zero.  No evidence of type 2 reaction.  Bacteriological index (BI) was 5+; the morphological index (MI) was 20 %.  Histology was not done as there is no facility for this in the area.  As for treatment, the patient was placed on normal multi-drug therapy (MDT) and he is still on it.  He is presently on the 6th month of MDT and there is just some improvement in the clinical picture.  How long will it take for these lesions to disappear?  Any experience?

Thank you very much in advance for your comments. 

Dr Augustine Barminus 

Chief Medical Officer

State dermatology hospital

Garkida

Adamawa state

Nigeria

The diagnosis of leprosy – SLIDES Part III. “Diagnosis and the clinical spectrum”

Leprosy Mailing List – October 28^th, 2011 

Ref.:   The diagnosis of leprosy – SLIDES Part III. “Diagnosis and the clinical spectrum”

From: S. Noto, Genoa, Italy

---

Dear Dr Dayanghirang,

Kindly, find in attachment the last section of the SLIDES of “The Diagnosis of Leprosy”.  Herewith are the slides relevant to Part III.  “Diagnosis and the clinical spectrum of leprosy”.

Best regards,

S. Noto

The diagnosis of leprosy – SLIDES Part II. The second cardinal sign

Leprosy Mailing List – October 24^th, 2011 

Ref.:   The diagnosis of leprosy – SLIDES Part II. The second cardinal sign

From: S. Noto, Genoa, Italy

---

Dear Dr Dayanghirang,

Kindly, find in attachment the SLIDES of “The Diagnosis of Leprosy”.  Herewith are those relevant to “The second cardinal sign of leprosy”.  The other slides will follow.

Best regards,

S. Noto