Transcription of interview with Warwick Britton – own and leprosy story - conducted in August 2004 by Jeanette Hyland
for the ILA Global Project on the History of Leprosy.
How did you come to be involved in leprosy?
As a 5th year medical student, I went to do an elective in December 1971 in Manoram, in Thailand. I arrived and I was somewhat unexpected as I was meant to be going to Shanta Bhawan Hospital in Kathmandu, but because of the war between India and Pakistan, during Bangladesh’s emergence, all the flights were stopped from Bangkok to Kathmandu. A week before I left, I had to re-organise and I knew people in Overseas Missionary Fellowship (the old CIM or China Inland Mission), so I went to the OMF hospital. They didn’t know what to do with me when I arrived and they were running a leprosy course, so I went to the leprosy course. There was a woman there I think called June Morgan, and she was the OMF doctor who ran the OMF leprosy work at Manoram.
So she was the teacher?
Yes, she was English and she was running the course. So I did that and did other work as a medical student. Quite enjoyed that, and also had contact with leprosy patients in the hospital. I remember there was a blind leprosy lady who had become a Christian. In fact the church in central Thailand was still quite weak then, there was no real Christian ministry there until after the Second World War. Before then most of the Christian ministry had been in the hills, so at McCain and at Chang Mai in central Thailand, there hadn’t been a lot because it is a highly malarias area. Manoram was sited there when OMF had to leave China and they were looking for other places to go. One of the reasons they went to central Thailand was that there was very little Christian work there for health reasons and lots of other reasons. In fac,t the church in that part of the world had really grown out of a number of leprosy patients who had become Christians and this particular lady was one of them.
So I did the elective and came back to Australia, trained in medicine. During that time, my wife and I were medical registrars at the Royal Prince Alfred Hospital in Sydney. And in actual fact we went to the Post Moresby General Hospital where there was quite some leprosy. Ken Cleasy was the Professor of Surgery there. Ken is an Australian surgeon who, among other things, is an excellent neurosurgeon and through that had become responsible for a lot of the leprosy work in PNG. We have met him at various leprosy conferences round the world. So we saw a bit of leprosy there, but infinitely more tuberculosis.
Then I went and did a Diploma in Tropical Medicine in Liverpool and then we went to Nepal in July 1978.
Was leprosy part of that course too?
Yes, there was a small component on leprosy I think we had a couple of lectures which if my memory serves me right I think Michael Waters did. No, that’s not true it wasn’t Michael then it was actually Stanley Browne. Stanley Browne came and did those lectures. That was the first time I met him.
We went to Nepal and then went to Tansen which is in west Nepal where there was extensive leprosy work, and in fact, my wife Annette (Britton) was actually responsible for the leprosy out-patients. I was responsible for the whole of the out-patients and also for the inpatient medicine. Annette used to do the leprosy clinic each day and I used to do that as well and so we both got involved with a lot of leprosy patients and I looked after a lot of leprosy patients whilst there.
Was Dr Pedley still around then?
No, this is 1978, so he had retired a few years before. My wife actually went to school with one of his sons in south India. We never actually met Dr Pedley. We met his daughter at a conference whilst we were in England and his son-in-law, and I knew other people in the leprosy field. The leprosy clinic which he ran for many years, all the patient notes were in his meticulous and careful handwriting, so we saw a lot of the work that he had done there.
What is your impression of the work Dr Pedley did?
I guess I know of it in a broader sense as well. I think there were two aspects to his work. First he was not actually attached to leprosy -only institutions. From his point of view, leprosy work was better done from a generalist base. He had of course worked in specialist leprosy institutions. He was, I think, the second doctor at Anandaban and the first that worked for any length of time at Anandaban Hospital, I think he went there in 1959 and on the board he is listed as the medical superintendent for a year or two. I think he went there from China, having worked in China and India, but I think he felt more at home with leprosy in a generalist environment, which I would say philosophically is the right way to go, that if it is possible. Even so, the leprosy clinic at Tansen certainly had considerable support from the Leprosy Mission (TLM) so there is a real place for specialist-focused organisations and they may work through a diversity of means.
The second thing was that Pedley was very bright. He had made the observation, as others had at that time, that leprosy was more common in children of mothers with lepromatous leprosy, and so he began investigating how leprosy was transmitted. So he prepared a very focused study for a very small amount of money, bought some muslin cloth from the bazaar, autoclaved it, and got the patients to blow their nose into this to concentrate the mucous, and he demonstrated acid-fast bacilli.
These he assumed were leprosy; of course, he couldn’t prove that. He could have proved that the patients did not have tuberculosis. I don’t know if he did that. But there was no way to culture even TB at Tansen. He then actually treated the patients with dapsone for three months and the ‘nose blows’, as he used to call them, became negative.
So he demonstrated first, that organisms left the patient through the nose and second, that treatment reduced the organisms. It was also attached to the concept that leprosy could be transmitted through breast milk. So he used to exhaustively try to examine if leprosy was present in breast milk. We actually don’t think that’s the case now, it is far more likely knowing that a mother with lepromatous leprosy feeding her baby only had to sneeze once and the baby was exposed to 10s of millions of bacilli although he did actually show – in patients with lepromatous leprosy you can show leprosy bacilli anywhere, and I think he did actually show them in the skin round the nipple and so on. So that is still referenced. It does not actually prove that leprosy is taken up through the respiratory passages, but it is a pretty strong inference.
So has that become clear yet?
Well, it has never been – the difficulty is that you can’t actually show the site of uptake. It is assumed to be through the upper airways, through the nose or naso-pharynx and most people accept that. Some people say that has not been formally proven because it is not like a lung where you can actually show a focus. There have been some attempts by ENT examining the newly-diagnosed leprosy patients to actually show a focus- It is everywhere else as well - Yes - but of course, the infection occurred years and years, even decades before that, so what you have to show is that the contact of the leprosy patient has a lesion at the back of their nose and that is extremely difficult.
It certainly has been shown that material aerosol generated - not just droplets, particularly sneezing, coughing - that leprosy can survive about 7 days is dust, in the soil. And that aerosol from soil could spread and I think the respiratory passages are still the most likely.
So when you were in Tansen you were in general medicine?
Yes, we looked after a whole bunch of things and the leprosy patients were generally well looked after. It was quite a large leprosy clinic with about 250 new patients each year. Of course this was 1979, we were only there for two and half years. We had moved from using low dose intermittent dapsone – which is an appalling way microbiologically to use an antibiotic – and of course spread resistance, which you would expect it to. When we in New Guinea, we still saw patients who were on 25 mgs, three times a week or so. That had all been switched to 100 mgs daily in Tansen, but we were starting to see patients relapsing, and we saw patients with the characteristic pearly like lesions of secondary dapsone resistance. Whilst we were there, in fact, we started initiating high dose rifampacin, just giving a single dose of 600mg, with Dapsone, on the basis that we were recognising drug resistance. The literature was replete with episodes of secondary dapsone resistance and then primary dapsone resistance. It was in 1982 that the Committee on the Chemotherapy of Leprosy recommended multi-drug therapy. We were, I guess, starting that. Chlorphazamine was available for reactions, so we were initiating that.
So your own career has taken you more and more into leprosy?
No, well my major interest, I guess, was Tuberculosis. So after we had been there in Tansen for a couple of years, we looked around for what to do. I wrote to some folk in England within the MRCTB and actually met with the director of that unit because we happened to be in Delhi at the same time he was in Delhi. Subsequent to that I was actually offered a job with the MRCTB, but we had been away from Australia 4 years and wanted to come back, so I thought I’d do a PhD on respiratory epidemiology.
So I wrote to a senior colleague who organised for a scholarship and I started doing a PhD on the epidemiology of asthma using a method of measuring bronchial hyper-responsiveness to measure asthma in the community. So I started in January 1982 and within about three weeks realised this was not the job for me but through a variety of circumstances it became obvious that I actually had to complete the study, so over a six months period I enrolled 1200 kids, 600 in Belmont and 600 in Wagga, did this study, collected all the data with research assistants. Subsequently the Belmont part of that is the longest running cohort study of asthma in the world actually.
From that initial study we ended up writing four papers and I could have done my PhD on that but then I switched to immunology. No one was interested in Tuberculosis in those days, but leprosy was an interesting model in immunology because of the spectrum of leprosy so later in the year I managed to persuade someone to let me work on leprosy and in three and half years I did a PhD characterising antigens with monoclonal antibodies and did a PhD on the immunology of leprosy instead. I had originally trained as a gastroenterologist but through that I actually became an immunologist. And in 1986, we went back to Nepal for four years and when we came back to Australia in 1990 I got a job at the university as a clinical immunologist.
What observations would you like to make about the understanding of leprosy, how it has grown over the past 20 years?
Well, over the last 30 years it has been enormous. I mean Shepherd grew M leprae in mouse footpads in the mid 60s. It takes nine months and is very, very slow. The rate of accumulation of knowledge was extremely slow and also programmes just focused on chemotherapy even though he had done studies trying to calculate vaccines.
It was really in the early 1980s that the tools of cellular immunology became available which measure cellular immune responses as opposed to antibody responses. People started doing this in leprosy and I guess there were two lines of research.
One line of research was trying to looking at the basis of lepromatous leprosy – leprosy had a spectrum – tuberculoid leprosy where there are very potent T-cell responses that restrain the growth of the organisms. They don’t actually prevent the growth because the person actually has leprosy so tuberculoid leprosy is not a model of sterilising immunity, but of contained infection. But it is the disease manifestation that is the characteristics of the lesion and the destruction of peripheral nerves which is largely due to the host’s cellular immune response. So what determines this spectrum response? That is a fundamental question which is applicable to other areas of immunology of leprosy and of another intracellular infection called Leishmania. These are two prototype examples of the variation in the immune response so the same pathogen can have very different appearances of clinical disease and that is largely because of immune response. So that is one avenue of research and that continues today with ever increasing sophistication now we use gene arrays and whole gene technology, very sophisticated technological tools, but still addressing the same fundamental question. Much of this research has actually described or defined the leprosy spectrum at a very precise molecular and cellular level, but it does not actually explain why the spectrum is established. There are very fundamental paradigms and very plausible explanations, but we don’t know which of those explanations are true and may be none of them or some of them. So that question of why does the host respond to the organism in such a diverse way to produce such a diverse manifestation of disease? That is the kind of fundamental question.
The second question is because the leprosy bacillus cannot be grown in tissue or microbiological culture. This always represents a great conundrum to study the organism when you can’t get at it, so immunology provided a way into that because Jerne, Kohler and Milstein, the 1984 Nobel Prize winners for their ‘theories concerning the development of control of the immune system and the discovery of the principal of production of monoclonal antibodies’, made this technology very widely available to get the cell lines. So this was being widely used by the late 1970s and in fact in the late 1970s people were recognising this was a very powerful tool because you could make antibodies and purify antibodies which recognised a single antigenic determinate, a single what we call epitome or part of a protein or carbohydrate molecule and these were highly specific. Normally when you immunise an animal the animal might make hundreds of different antibodies to the same pathogen. By using what is called monoclonal antibodies, you could come out with a single antibody which just recognised just one epitome.
My PhD was making monoclonal antibodies to M leprae and finding and characterising antigens because we could not grow the organism. So I got 10mg of M leprae protein from the World Health Organisation and characterised that in a four year PhD., made thirty six monoclonal antibodies and characterised six antigens, four proteins and two carbohydrate antigens. There were three other laboratories which did this round the world in a big way and from these we were able to identify the genes which encoded those proteins. This was a route into characterising the genetic material even though we could not grow the organism.
I did that for four years and went back to Nepal to be involved in the laboratory to try and apply some of this new knowledge. Then the research project in Sydney continued, a colleague did a PhD and then another colleague, and when I came back in 1990, I inherited that work and we continued working on leprosy mainly for about five years and then during the last decade we have worked mainly on Tuberculosis.
It would be true to say that many of the people who in the early 1990s, certainly to the mid 1990s, who worked in Tuberculosis, most of them have actually worked on leprosy. Tuberculosis was a bit passé as a biological problem, people thought you could just use antibiotics and that would be fine where leprosy presented many more challenges because a) what causes the leprosy spectrum and b) how do you study leprosy organisms. Now over the last decade, tuberculosis has become huge and many more people have started working on it. The group of people who really got in initially in the 1990s were mainly ex-leprosy people.
So these two questions continued driving research in the 1990s and the capacity developed for the organism to be characterised on the basis of their whole genomes, rather than just on the basis of their antigens and then the genetic code for the organism was sequenced. That was a long and laborious task for reasons I will not go into. It was probably one of the first organisms targeted, but along the way as processes improved, many more organisms were included. In fact, a number of common pathogens, Haemophilis, Streptococcus and others had their genes sequenced, and then, in fact, the tuberculosis genome which was started for some years, three or four years after the leprosy genome was completed in 1998 and the leprae genome was only completed in 2001. So it took 10 years and these days it could all be done in 6 months.
So where has that led?
Well, both the TB and leprosy genomes were sequenced in the Pasteur Institute in Stuart Coles’s Lab. Another strain of Tb was sequenced in the States, but no-one else has shown a commitment to leprosy genetics the way that Stuart Coles’s group has. That has provided a lot of information just of itself. By sequencing the genome, it became very apparent that there are very large differences between leprosy and tuberculosis, and secondly, it provides information which can be used from a research point of view.
In some ways – well – in simple terms, the genome of M tuberculosis consists of about 3,900 genes and each gene encodes protein and there is some redundancy, that is there is sometimes more that one gene that encodes similar proteins. OK. The genome of M leprae, which is a little bit smaller, the whole genome only encodes 1600 proteins so it contains less than half the number of genetic information even though it is of a similar size. The reason is that in tuberculosis, all of the genes are very close together, the genome is very dense, some overlapping, very, very close together. In leprosy there are whole areas that look like cemeteries for genes where genes which are present in tuberculosis are absent, mutated, deficient, so it is as if the organism has restricted itself to the minimum set of genes which allow it to be a viable mycobacterium, but, in fact, it can only replicate in a very narrow biological niche which is humans and possibly an animal, probably armadillos in the wild, but it is a very limited host range; whereas, other organisms are much more able to replicate outside the host. Paradoxically that is more helpful for studying tuberculosis than for study of leprosy because it allows you to define what are the minimum set of genes which allow it be to a Mycobacterium and therefore which genes you might target for new drugs. A number of groups are actually persuing that using comparative genomics.
So this whole enormous amount of new knowledge led to understanding what happens in the body and how to respond to things like reactions and things like that?
At one level you can say it doesn’t, at one level just understanding how the host and the pathogen co-exist with one another, understanding that is very important. 95% of people infected with Mycobacterium leprae never get the disease, after massive exposure they don’t get the disease while 5% do. Understanding that really requires an understanding of the organism and the host. In the case of tuberculosis, which is a much, much more important human pathogen, still TB is the 7 th major cause of mortality and morbidity in the world from all possible causes of death. Many other infections are coming under control: tuberculosis isn’t and tuberculosis kills 3,000,000 people a year, leprosy kills not many. TB is such an important pathogen that we actually need to understand everything about TB, and we cannot necessarily predict which parts of that understanding will need to be the most effective intervention. So that’s at one level, the fundamental knowledge of these extremely important human pathogens will lead to benefit.
The second aspect though is that while we are in the process of study, you learn lots of other things which may be applicable. We now know which proteins – there are some proteins which are only in TB and some which are only in Leprosy and my group was involved in cloning, that is isolating the gene for a protein which is not in TB but is in Leprosy and some other related environmental mycobacteria. We don’t know why that is, it is almost the most potent protein antigen in M leprae, we actually don’t know why and it is a very good diagnostic reagent. You can use it to measure antibodies very specific to leprosy and there are a number of others like that so in fact quite a range of diagnostic tools and also assays which allow you to measure what is happening during reaction.
That is at a basic scientific level. That doesn’t actually describe the progress in the management of leprosy which I think has been very substantial. Although the mantra of “the elimination of leprosy as a public health problem” can be misunderstood, the actual goal of treating as many leprosy patients as effectively as possible has been a fantastic initiative. When it became obvious, by the late 1980s, that multi-drug therapy - we should remember that MDT which was introduced in 1982 was introduced without any clinical trial and this is because of the nature of leprosy as such a slow and progressive disease that it takes you a decade to do a clinical trail properly - because of the wide distribution of the primary and secondary dapsone resistant strains that MDT was introduced. It took about 7-8 years for people to see that in the countries which were using MDT it was effective. It had a little bit of a leg up because the places where it was implemented tended to be the places which had good leprosy control programmes and dapsone control programmes so when MDT was implemented on the background of effective leprosy control programmes that had been going for a decade or so, - and properly applied dapsone monotherapy was an effective leprosy control measure - so MDT added to properly applied dapsone control programmes, it was successful so that it really tipped the balance in south India, Thailand, China and a number of other countries where the prevalence was starting to fall anyway.
In the regions such as north India, some of the African countries, it has been slower to have an impact. Since the leprosy elimination programme was widely promulgated in 1990, 11,000,000 people have been treated for leprosy. I think it is clear that in many places complication rates have fallen and people have been treated earlier. It is also true that the leprosy incidence rate, that is case detection of new cases, has not declined in the same way that leprosy prevalence has. But the problem was not the goal; the problem was the time scale for the goal was shorter than realistic, so over a 20 year period, I think MDT will have a major effect - you would need about 30 years to control leprosy in a community. So the number of people receiving drugs has dramatically fallen from five millions down to 600,000 or so round the world, but the new case detection rate, and it has been well measured round the world, has remained high and went up partly because of more active case finding in eradication campaigns and things such as that.
It has certainly given leprosy – in leprosy endemic countries now leprosy has the connotation of a treatable disease. That is actually an enormous change, even though some leprosy patients are hard to manage and some, a small proportion of leprosy patients get worse when you treat them but most don’t.
In what world now is it regarded as treatable, in the medical world, in the general public world?
I would think in leprosy endemic countries which have had good health education programmes so you can travel on trains in India and talk to people they say leprosy is not what it was in the past, you can treat leprosy now, not that they would be happy if their children married someone with leprosy. Nevertheless, it is a vast difference from 30 years ago when leprosy was not seen as a treatable condition.
Leprosy is going to be around for decades and there is a problem that once you get to a certain level, it is not worth the – leprosy no longer rates highly in the order of health problems in that country. So in most countries of the world, HIV and Tuberculosis are far greater health problems – that’s the truth. So as it falls down the order of health priorities, it is possible for the quality of the leprosy programmes to decline, and there may even be a bit of a rebound, in fact the rebound will not be as severe as in tuberculosis or malaria because of the length of time it takes to get the disease. It also means that even once you get to a level of low prevalence, it will probably take a generation for the disease to actually die out in a community.
The countries which have not reached that stage are getting fewer. In fact 65% of leprosy patients are in India and that means predominately in north India, and if you add Nepal and Bangladesh that represents three quarters of the world’s leprosy patients – up to 80%. You add Brazil and you get up to 85%. The numbers in Africa are smaller, they are more widely distributed which actually means the actual eradication there will be just as difficult because once it gets to a prevalence rate that does not justify specialist control programmes, then the quality of treatment and the rate of decline of the problem will fall.
However in the context of things, if the treatment of leprosy through MDT, which is very effective, if made accessible, I think it will eventually decline. It depends too on the context, on the degree of chaos in the country – one is not suddenly going to be able to control leprosy in Sudan for instance.
In the context of stable government and infrastructure …
Yes. That is one of the problems with leprosy, that it is probably one of the first things to fall off the agenda, so in countries where, in a country like Indonesia where there is still quite a lot of leprosy overall as a health problem, it is of less importance than TB.
When I was studying leprosy immunology if you like, that was quite a long time ago now, they used to say that when there was an epidemic of leprosy it waxed and waned over one hundred years - do we know whether we are in that kind of phenomenon in the leprosy world of India and Nepal?
That’s a little bit hard to measure because it is occurring in an environment of active case finding and treatment. I think – probably a better way to look at it – because of the nature of the infection and the inability to grow the organism, we still probably don’t understand the actual natural history of leprosy.
Leprosy may be slow to decline for a variety of reasons. One reason is just because of the long incubation period. New patients will come out of the woodwork and you just have to keep at the task for 30 or 40 years.
The second reason might be in fact that it is only a small number of leprosy patients that are transmitters – you can have an effective programme but if you are missing the high transmitters they will disseminate. We know that in tuberculosis not all patients with tuberculosis are as efficient at transmitting so you may have a patient who transmits to 20 patients a year and another to three and we actually say that there is an actual median of ten cases per year from any new patient with tuberculosis, but the spectrum may be very wide. This is particularly true in lepromatous leprosy so not only is there a long incubation period, it may be that if your programme is not identifying the small number of high transmitters [through whom] the infection is maintained in the community. That can be the case and because leprosy is a disease of poverty for a variety of reasons, probably because of malnutrition and other factors which actually enhance progression of the disease, because of high transmission rates, because of overcrowding, because of poor medical care, all these things contribute to high incidence in poor people. These are the people who have the least effective public health programmes and so in the large urban conglomerations or in difficult to reach areas, hilly areas, or for more socially distinct populations which don’t interact with the health service – for a whole variety of reasons, high transmitters may not come into contact with the health service. So behind that is this whole leprosy eradication campaign and that has had a certain success in India but we still don’t know whether that is going to be an effective programme for actually blocking transmission if that is the case.
The third possibility is that we may have the natural history wrong and it may be that after infection people may have an actual focus of leprosy in the nose or back of the pharynx which replicates to a certain level if it is a cellular immune response which actually controls the infection, and during a period of time which might be weeks – it may be that someone who has been infected, who is going to actually control the infection and never manifest disease, may have a period of sub-clinical infection which is infectious. Right? That is a completely different scenario because that actually means that treating patients alone is not completely adequate for controlling the infection. If that’s the case, then one needs to be considering more effective vaccine or chemo-prophylactic programmes to treat contacts. There is a large study of 25,000 people going on in Bangladesh to examine this. There’s another prophylactic study which has gone on in Indonesia, and there is actually renewed interest because BCG is more effective against leprosy than tuberculosis.
Although we have actually made a vaccine which is effective against leprosy alone, I don’t think a leprosy-alone vaccine will even be marketed. But it is quite conceivable new tuberculosis vaccines will be marketed. One of the things we need to ensure is that any new tuberculosis vaccine also has the leprosy component and some of the candidates actually don’t. From a public health point of view one needs to ensure that any new vaccine is effective against leprosy as well as TB.
Has the study of AIDS and immunology shed any light on the pathology in leprosy?
No … in the case of tuberculosis - yes. In the case of leprosy it has been surprising that in fact out of 16 or 17 studies only two have shown any increased incidence of leprosy in HIV infected subjects. Almost all studies have shown the opposite. One of the ones was a study in Ethiopia where one of two individuals kind of explained the difference completely and one in Tanzania was also relatively small. The general teaching is that HIV per say does not affect, either the kind of leprosy you get or whether in fact you get clinical leprosy. End of first interview.
Transcription of interview - Warwick Britton, continued, conducted in August 2004 by Jeanette Hyland for the ILA Global Project on the History of Leprosy.
The simple explanation for leprosy not being affected by HIV is that the rate of development of the disease is so slow that people die of their HIV before the leprosy is a problem; whereas, tuberculosis develops much more rapidly. The other reason is, may be, it is likely that you have to become profoundly immunodeficient to lose the responsiveness to leprosy; whereas, TB is a more virulent pathogen and as the immune system starts to wane, the pathogen takes over more quickly, and certainly once you are severely immune-compromised, there are many other infections in leprosy endemic countries which will get you before leprosy does. Simple pneumonia for instance, people with HIV are susceptible to pneumonias.
People who develop disease when they are infected with M leprae, do they have specific immuno-deficiency?
With leprosy it is only to the leprosy bacillus.
Is it genetic or acquired?
It is probably acquired but there are some genetic influences and again this is an area of modern research where we know there are a couple of genetic influences which are significant, but environmental factors are important. In the case of HIV, we now know that when you treat HIV that the immune system becomes stronger – with modern treatment of HIV – and paradoxically, when you treat HIV in someone who has latent leprosy infection, the immune system getting stronger can actually cause a reaction. So leprosy reaction during treatment for HIV may be the first manifestation of leprosy. I guess that just highlights the complexity of the interaction.
Leprosy is interesting because on one level, it is a very simple condition – if you have more than five skin patches you take treatment for 12 months, if you have less than five skin patches, you take treatment for six months – that’s it. That probably coped with 80% of leprosy. Though, at the other extreme, patients with leprosy reaction can present the most difficult clinical problem that you can be confronted with in a highly sophisticated environment. I occasionally get rung by colleagues, infectious disease physicians who are extremely good physicians who are looking after leprosy patients – and it is paradoxical – they do everything they think should be done and the patients get worse. So there is this small subset of leprosy patients with severe ENL or severe leprosy reaction who are extremely difficult to treat. So when you think that a poor medical officer or a health post aid may be left with managing this problem without any resources you can understand why some patients end up blind or with severe nerve reactions and damage - and all the aspects of leprosy we hoped we could control.
This is one of the reasons why leprosy is such an interesting medical problem, it is interesting scientifically, it is interesting in terms of clinical care, it is interesting sociologically, and it is interesting from a community perspective.
At one level optimizing a simple therapy that helps most is a good way to go and one should support that but also for the programme to have long-term credibility, it must also be seen to be able to treat and cope with difficult cases. That does not mean that everyone in the health service needs to know about that but a small sub-set of people do. That is quite hard for a health service with limited resources because you are saying we can treat this just like we treat hook worm, malaria and things like that with a simple recipe but somewhere in the system someone needs to be able to treat, to cope with the reactions, to cope with leprosy surgery, which is extremely beneficial but is highly specialised. I would have thought that 85% of leprosy patients who need leprosy surgery will never be able to benefit from it.
So that is the broad spectrum. The spectrum of care and facilities needed for leprosy is as broad as the spectrum of responses to the leprosy bacillus. That is a challenge for a health service with very limited resources with large HIV problems and so on.
Can we move now to another question entirely in relation to you own experience and stigma: because at least one of your hats has been specialising in leprosy have you found that affecting how people look at what you do and who you are?
In a leprosy endemic country - not particularly. I used to teach medical students at the Maharajgang campus is Kathmandu and I used to teach them all about leprosy as a means of teaching them immunology. That was just thought to be a bit odd. We would take the students out to the hospital and show them leprosy patients and so on. In a western environment, people would joke when I started to do my PhD, it was thought to be quite bizarre, because infectious disease was thought to on the decline. Of course, 1981 was the first reported case of HIV and in five or six years, it became obvious that we were not as good at managing infectious disease as we thought we were. I think it would be seen as a slightly odd thing to do. Only last week there was a memorial symposium for a senior staff member, a professor who had worked in Papua New Guinea for many years and had to retire because of serious illness so I was asked to give a talk on leprosy. So I gave a modern overview of leprosy to these assembled people from the university and Papua New Guinea. In one sense they thought it a good thing that people worked on a heath problem. But it is thought to be a bit odd. It wouldn’t work unless you were good at what you did. You have to do acceptable research – you can’t just say this is a problem and I will work on it. If you don’t do good research, you won’t get recognition. As a social problem, it is a paradigm for the kinds of social and personal aspects of health. It is no good feeling sorry for leprosy patients if you are not good at treating them. On the other hand it is no good if you are good at treating them, but are no good at relating to and responding to them. You need competency as well as kindness.
I think on that note we will wind up- thank you Warwick.