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Leprosy in Seychelles: current situation and perspectives
 
 
Claude Yersin, MD (1), Laxmi Shah, MBBS, DDS (2)
  1. Senior Registrar, Communicable Diseases Control Unit, Ministry of Health, Seychelles;
2) Principal Medical Officer, Dermatology Unit, Ministry of Health, Seychelles
 
 
 

Abstract

To reduce the prevalence of leprosy to below one case per 10,000 population, the Word Health Organization recommends a strategy combining a simplified case definition (skin lesion with loss of sensation, nerve involvement and skin smear), a classification of cases into paucibacillar and multibacillar categories, and a multidrug therapy according to the classification. In Seychelles, where the disease is endemic, leprosy has been eliminated as a public health problem since 1994 (i.e. the incidence was less than one new case per 10,000 population per year). However, during these last five years, the proportion of new cases with positive skin smear was 57%, a value four times higher than expected Therefore, it is possible that some paucibacillar cases remain undetected. Surveillance and detection of leprosy cases, particularly those with a discrete paucibacillar presentation, has been therefore strenghtened with awareness campaigns targeting the population and health care providers. This campaign aims at eradicating the disease in Seychelles, i.e. a complete termination of transmission as a result of the total disappearance of the disease-causing organism. (SMDJ, 1999;6:21-23.)

 

Introduction

Mycobacterium leprae, a strongly acid-fast rod-shaped bacillus, is the etiological agent of leprosy, a chronic infectious disease known since immemorial time and that has left behind a terrifying image of mutilation and rejection from society in human history.

At the beginning of 1999, 719’332 leprosy cases were reported in the world by 76 countries and the registered global prevalence of leprosy is actually around 1.4 per 10’000 population (4). India, Brazil and Indonesia account
 
Table 1. Tuberculoid and lepromatous leprosy
 
Tuberculoid leprosy (Figure 1)
Lepromatous leprosy (Figure 2)
Immunity Strong cell-mediated immunity Weak to absent cell-mediated immunity
Slit skin test No or very few bacilli in lesions Large number of bacilli in lesions
Skin lesions Few (1-3), asymmetric macules or hypopigmented or erythematous plaques with well-defined margins 

Hypo- or anesthesia , dry, hairless

Numerous, bilateral, symmetric infiltrated plaques and nodules, 

Erythematous ill-defined margin 

Conserved sensation, no loss of hair

Nerves 1-2 nerves in same region may show early thickening Multiple nerves show late thickening with neurological deficit: "glove and stocking" anesthesia, paresis
Early symptoms Localized skin numbness Nasal stuffiness, crusts, blood stained discharge, edema of legs and ankles
Other organs None Later in the disease: inflammation of the eyes, bone destruction
Communicability Weak or nil Moderate
 

for around 90% of all cases in the world. In the Indian Ocean, Madagascar reported 12’989 registered cases at the start of 1999, a prevalence rate of 8.0 per 10’000 population (4).

The disease affects mainly the skin, the peripheral nerves and less frequently the eyes, the mucosa of the upper respiratory tract, the muscles, the bones and the testes. Leprosy is transmitted from one untreated person to another via the respiratory tract or the skin (possibly also the gastrointestinal route). Among the people infected, after an incubation period from several months to several decades (1), only 5% of the adults develop the disease, but 60% of the children who are more susceptible do so (2).

The type of helper T-cells population responding to the infection dictates the form of the disease that develops. Patients with predominantly TH1 response develop tuberculoid leprosy with strong cell-mediated response to M. leprae antigens, while patients with predominantly TH2 response have weak to absent cell-mediated immunity to M. leprae and develop lepromatous leprosy (3). The clinical presentation of these two polar forms of the disease is described in Table 1.

The initial discreet skin lesion in leprosy (before its differentiation in tuberculoid or lepromatous form) is called indeterminate and mycobacteriae are not seen by slit skin test in these lesions.

The clinical presentations that cannot be classified as tuberculoid or lepromatous are considered as the borderline portion of the leprosy spectrum (Figure 3) lying between the tuberculoid and lepromatous poles and are called borderline-tuberculoid, borderline-borderline and borderline-lepromatous in the classification of Ridley-Jopling.

 

Principles for diagnosis and treatment of leprosy

In 1991, the World Health Assembly resolved to eliminate leprosy as a public health problem by the year 2’000, meaning reducing the prevalence of leprosy to below one case per 10’000 population (5). To reach this goal, the central part of the strategy was to make the WHO- recommended multidrug therapy (MDT) accessible to all patients. Since 1981, MDT has proved to be highly effective in curing the disease, reduces the period of treatment, prevents development of drug resistance and reduces risk of relapse (6).

 

Identification of the patients has been made easy by a simple and clear case definition (7). A case of leprosy is indeed defined for a person having one or more of the following features: 1) hypo-pigmented or reddish skin lesion(s) with definite loss of sensation; 2) involvement of the peripheral nerves, as demonstrated by definite thickening with loss of sensation in the skin and/or weakness of muscles supplied by the affected nerve (nerve thickening by itself, without neurological deficit is often not a reliable sign of leprosy); 3) skin smear or skin biopsy (Figure 4) positive for acid-fast bacilli.

Diagnosed patients are classified into three groups because of different therapeutic regimen (7,8) (Table 2).

 

Table 2. WHO classification and treatment of leprosy
 
WHO classification Treatment
Paucibacillary single skin lesion (one skin lesion) Single dose of rifampicine, ofloxacine and minocycline
Paucibacillary (PB) leprosy 

(2-5 skin lesions)

Rifampicine and dapsone during six months
Multibacillary (MB) leprosy 

(more than 5 skin lesions)

Rifampicine, dapsone and clofazimine during 12 months
 

PB leprosy refers to patients showing negative smears at all sites and matches with the indeterminate, the tuberculoid and some of the borderline-tuberculoid forms of leprosy. MB leprosy refers to patients showing positive smears at any site and includes all forms from the borderline tuberculoid to the polar lepromatous. Among newly detected cases, skin-smear positive patients generally represent only 10 to 20% of the total number (7).

 

Situation in Seychelles

The Seychelles islands are known to be an endemic area for leprosy since the beginning of the 19th century. Grainger reported 7the history of leprosy in Seychelles (9,10). Since implementation of MDT in 1982, 74 leprosy cases have been treated and cured up to now. No case treated with MDT has relapsed so far. Table 3 shows the distribution and selected characteristics of all leprosy cases registered from January 1994 to August 1999 in Seychelles.

In the series displayed in Table 3, MDT was used in all eight patients. Four patients completed the treatment and are considered as cured and four are still on treatment. One patient experienced an erythema nodosum leprosum (type 2 reaction) in the course of treatment (11) and was controlled successfully with steroid.

The penultimate case of this short series (Case 2) was a women aged 31, complaining of progressive sensory loss on the right leg for six months. She showed a single 5 by 7
 
Table 3. Distribution and characteristics of leprosy cases in Seychelles (Jan. 1994 – Aug. 1999)
Year
New cases
Defaulter*
Prevalence per 10.000
Age (y)
Sex
Slit skin smear
Skin biopsy
WHO
classification
1994
1
0
0.14
16
m
pos
-
MB
1995
0
1
0.13
41
m
pos
-
MB
1996
1
0
0.13
5
m
pos
-
MB
1997
1
0
0.13
35
m
pos
-
MB
1998
1
0
0.13
23
m
neg
pos
MB
1999
(8 months)
3
0
0.57
33 (Case 1)
31 (Case 2)
46 (Case 3)
f
f
m
neg
neg
Pos
pos
neg
-
MB
PB
MB
 
cm hypo-pigmented, well defined macule on the anterior side of the upper part of the right leg with loss of sensation (Figure 1). There was also a loss of sensation on the medial side of the right big toe. No thickening of the peripheral nerves was noticed. The slit skin smears (skin lesion, ears, nose) were negative for acid-fast bacilli as was a skin biopsy of the skin lesion margin. She was diagnosed as paucibacillar leprosy of the tuberculoid type. No source case could be identified.

The last case (Case 3) was a man, chronic alcoholic, aged 46, whose mother had been diagnosed with leprosy many years ago. Apart from several alcohol-related admissions to hospital, he had no remarkable medical history. Since 4-6 weeks, he presented a rapidly progressive generalized rush with subcutaneous 0.5 to 2 cm nodules and innumerable reddish papules (Figure 2). Examination revealed weakness of the adduction of the right little finger with a loss of sensation of the same finger and bilateral painless thickening of the ulnar and lateral popliteal nerves. The slit skin smear of a papule showed numerous acid-fast bacilli (Figure 4). Diagnosis was multibacillar leprosy of the lepromatous type.

A prevalence of less than one case per 10’000 population since 1994 (range 0.13-0.57 per 10’000) attests that leprosy is not a major public health problem in Seychelles. However, the proportion of new cases with positive skin smear was 57% (4/7), while this proportion is generally expected to range between 10 and 20% (7). Therefore, it is theoretically possible that as many as 15 to 35 cases of paucibacillar leprosy (tuberculoid pole) have remained undetected during these last 5 years. As these hypothetical yet undetected cases are likely to be little or not contagious, they would play a negligible role in disseminating the disease. However, prevalence of leprosy in Seychelles is currently not so low and detection in Seychelles of only a few more cases could result in prevalence higher than 1 per 10’000 in prevalence, which would be above the target set by WHO.

Eradication (i.e. complete stopping of transmission as a result of the total disappearance of the disease-causing organism) of leprosy in Seychelles within the next decade is not an utopia. Noticeably, medical care is equally and easily accessible to all inhabitants as it is delivered free of charge through health centres and hospitals evenly spread throughout the country. Uninterrupted supply of MDT drugs (rifampicin, dapsone and clofazimine) and proper distribution through the peripheral health centres has been done properly up to now. Ofloxacine and minocycline will be hopefully soon available locally. The Communicable Diseases Control Unit at Victoria Hospital is the unit where all patients with clinical presentation suggestive of leprosy are referred, where diagnostic procedures (slit skin smear, skin biopsy), treatment, and follow-up are organised. A system to identify and trace defaulters is implemented.

All health structures necessary to eradicate leprosy in Seychelles are in place. A campaign of active surveillance and detection of leprosy cases, particularly the discrete tuberculoid presentation of the disease, will help to reach this goal. Improvement in case detection will include sensitisation of the local population and health care providers.

In an endemic country, a person showing a hypo-pigmented or reddish skin lesion with definite loss of sensation is a case of leprosy

 

Acknowledgements

We are indebted to Drs. P. Thanikachalam and R. Krishnan for the microscopic preparations and to Dr. P. Bovet for pertinent advice.

 

References

  1. Isselbacher KJ, Braunwald E, Wilson JD, Martin JB, Fauci AS, Kasper DL. Harrison's Principles of Internal Medicine. 13th ed : McGraw-Hill, 1994.
  2. Bryceson A, Pfaltzgraff RE, eds. Leprosy. Medicine in the Tropics Series. 3rd Ed; Edimburgh: Churchill Livingstone, 1990.
  3. Britton WJ. Immunology of leprosy. Trans R Soc Trop Med Hyg 1993;87(5):508-14.
  4. World Health Organisation. Current global situation of leprosy, July 1999. Action Programme for the Elimination of Leprosy (LEP), http://www.who.int/lep/latest.htm.
  5. World Health Organization G. Leprosy Resolution WHA 44.9. Forty-fourth World Health Assembly, 13 May 1991.
  6. World Health Organization G. Chemotherapy of Leprosy. Report of a WHO Study Group, TRS 675, 1982.
  7. World Health Organization G. Report of the 7th WHO Expert Committee on leprosy June 1997. http://www.who.int/ lep/exp/ exp.htm.
  8. World Health Organization G. Multidrug Therapy. Questions and Answers. WHO/LEP/97.
  9. Grainger CR. Leprosy and Curieuse Island. Lepr Rev 1981;52:151-4.
  10. Grainger CR. Leprosy in the Seychelles. Lepr Rev 1980;5:43-9.

  11. Goodless DR, Ramos-Caro FA, Flowers FP. Reactional states in Hansen's disease: practical aspects of emergency management. South Med J 1991;84:237-41.
     
     
     
Figure 1. Case 2, 1999. Single hypo-pigmented anesthesic macula of the leg with scar of skin biopsy: tuberculoid paucibacillar leprosy.
 
 
Figure 2. Case 3, 1999. Generalized maculo-nodular rash without loss of sensation: lepromatous multibacillar leprosy.
 
Figure 3. Case 1,1999. Multiple hyperchromic maculo-papular lesions with healing center, without loss of sensation: borderline multibacillar leprosy.
 
Figure 4. Case 1, 1999. Skin biopsy with acid-fast bacilli (carbol-fuchsin, x 400)


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