THE NEW ZEALAND

MEDICAL JOURNAL
Journal of the New Zealand Medical Association

The leprosy problem in the South Pacific

I am a New Zealander living in London. From 1966 to 1968, I was a medical officer,
specialising in leprosy, in the northern region of Nigeria. Patients were treated here in
villages by auxiliaries, using weekly doses of dapsone. In 1967, I carried out a
population survey and found that the prevalence of leprosy had declined from 67 per
1000 to 2 per 1000 after 15 years of dapsone monotherapy.1 This information,
together with other evidence, indicating that the disease can be eradicated, has
recently been published.2
Despite this optimism, leprosy remains a serious problem in the South Pacific. Recent
data from the World Health Organization (WHO) shows that there have been 94 new
cases in Kiribati, including 21 children.3 The incidence of childhood leprosy is very
significant, as an indicator of ongoing transmission. The percentage of 22%, next to
Micronesia and the Marshall Islands, is the highest in the world.
In contrast, in Vietnam, in a population of some 80 million and after a horrific civil
war there were only 10 new children with the disease. It appears that the Pacific
Leprosy Foundation continues to focus on managing patients after they have become
crippled rather than providing early treatment with multidrug therapy, which would
prevent the spread of the disease.
I produced maps of the area in Kaduna Province (Nigeria) where domiciliary
treatment could be obtained.1 No such maps appear to be available in Kiribati, or
where the focus of infection remains. Mobile clinics could be introduced through
nautical means of transport. The successful decline in Nigeria proves that field
workers should be only employed to treat leprosy and not integrated with other
diseases. This would stop workers being diverted to treat tuberculosis.
It appears that some workers have not been trained to recognise leprosy, although the
diagnosis and treatment is easy (WHO). It does not need highly qualified people to
work in leprosy. Any school leaver can be trained. In fact, the best leprosy auxiliary I
worked with in Nigeria could barely read or write, but he was always on time for the
weekly administration of dapsone and knew all the patients. There should be a good
response to treatment provided that the patients are not segregated.
Other countries listed in the Foundations website are Tonga, Fiji, Western Samoa and
Vanuatu. In The Weekly Epidemiological Record (a WHO publication),3 there were
three new cases in Fiji with no children; Samoa had eight with one child, but there
were no returns for Vanuatu and Tonga . Surely it is the Foundations responsibility to
ensure that all new cases are recorded, especially in children. In Tonga, there are
apparently no new infections, but this has to be confirmed by examining the contacts
of new child and multibacillary cases.
As there is now a Centre of International Health in Dunedin, I would suggest a
collaboration with the Pacific Leprosy Foundation, especially as professionals are
conducting surveys for tuberculosis.

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A recent publication entitled A strategy to halt leprosy transmission,4 reinforces these

points. For example, Few countries now have a surveillance-response system that
could provide the epidemiological data to map high-risk areas for leprosy, to monitor
the changing epidemiological pattern of the disease and to implement the required
interventions and School surveys, too, might provide clues: the finding of schoolage children with leprosy is a strong indicator of ongoing transmission.
This approach should also be adopted in Micronesia and the Marshall Islands where
the Pacific Foundation has recently taken over responsibility for leprosy. The high
prevalence of leprosy has been recognised since 1971, but little appears to have been
done here to prevent the spread of the disease. The Pacific Leprosy Foundation has
been given an award which could be put to good use and I am sure that the New
Zealand public would donate generously.
It has been claimed that the incubation period for leprosy is very long; at least 46
years and sometimes longer, but there is no evidence for this. Instead the decline in
the Karamui study suggests that it is quite short. The authors of the Lancet publication
write A serious obstacle, however, to gaining the full potential of contact tracing is
the absence of a diagnostic test for early-stage or sub-clinical infection in contacts.4
As you can see from the details in the chapter,2 we have shown that it is possible to
reproduce the features of tuberculoid leprosy as a result of an autoimmune response to
an antigen in peripheral nerve rather than a direct response to Mycobacterium leprae.
A specific positive skin test will produce an epithelioid cell granuloma, thus
reproducing the pathology of this form of the disease. This will define the incubation
period and determine whether there is a subclinical infection. It will also determine
whether transmission has ceased in a previously endemic area.
Money for research projects is available from the leprosy charities at
info@leprosyresearch.org I would strongly encourage New Zealand neuroscientists
to apply for a grant to isolate the non-myelin antigen involved. Details of the
procedure are available.5,6
Nerve damage is the main reason why leprosy is a serious disease. I have emphasised
that patients with non-lepromatous leprosy may develop acute sensory loss in all four
limbs.
On the basis of this clinical finding, rabbits were injected with a homogenate of
human sensory peripheral nerve plus adjuvant and electrophysiological recordings
were taken from the hind limb by Jim Pascoe at University College London. There
was a specific diminution of C fibre action potentials with preservation of A delta
fibres.7
This is also a good model to study pain mechanisms and diabetic neuropathy as well
as leprosy, so physiologists should also consider applying for a grant to continue this
work.
For any further information please contact me at clcraw66@outlook.com
Colin Crawford
London, UK

NZMJ 23 May 2014, Vol 127 No 1394; ISSN 1175 8716

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References:
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2.

3.
4.
5.
6.
7.

Crawford CL. The effect of outpatient dapsone in an area of endemic leprosy. Lepr Rev.
1969;40:15963.
Crawford CL. Towards the eradication of leprosy. In: Berhardt ed. Adv Med Biol. New York.
Nova Sci Publ. 2012;56:117127 (this is an open access publication and can be seen via
Google by typing in Colin Crawford eradication of leprosy).
World Health Organization. Global leprosy: update on 2012 situation. Wkly Epidemiol Rec.
2013;88:36580.
Smith CS, Nordeen SK, Richardus JH. et al. A strategy to halt leprosy transmission. Lancet
Inf Dis. 2014;14:9698.
Crawford CL, Hardwicke PMD. Ultrastructural features of epithelioid cell granuloma induced
by intradermal injection of xenogeneic nerve tissue. J Pathol. 1978;125:10713.
Hardwicke PMD, Crawford CL. Nature of the antigen of human sensory nerve that induces
granulomatous hypersensitivity. J. Neurochem. 1978;30:160911.
Crawford CL, Hobbs MJ. Neurotrophic factors in diabetic neuropathy Trends Neurosci.
1995;18:1516.

NZMJ 23 May 2014, Vol 127 No 1394; ISSN 1175 8716

URL: http://journal.nzma.org.nz/journal/127-1394/6133/

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