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Indian Journal of Community Medicine

A Study of Leprosy Cases Among Contacts in West Bengal

Author(s): Anima Halder (Biswas), Malay Mundle*, Uchhal Kumar Bhadra*, Raghunath Mishra**, Banamali Sinha Mahapatra***

Vol. 26, No. 2 (2001-04 - 2001-06)

Deptt. of Community Medicine, Medical College, Calcutta *Deptt. of Community Medicine, PGIMER, Calcutta **Deptt. of Community Medicine, R.G. Medical College, Calcutta ***Deptt. of Community Medicine, Bankura Sanmilani Medical College, Calcutta

Abstract:

Research questions: What is the fate of household contacts of leprosy cases? What is the immunological status of these persons?

Hypothesis: Multiple case families have greater lepromin negativity than control families.

Objectives: To find out the infectivity of leprosy cases to their household contacts. To investigate the susceptibility or immunity of contacts towards leprosy.

Study design: Case control design with prospective follow-up of contacts for 3 years.

Setting: Calcutta urban slums where the leprosy cases were found.

Participants: All members of 100 families with leprosy cases and 100 families with no leprosy case, amounting to 540 and 460 members respectively, i.e., a total of 1000 persons. Intradermal lepromin test was done for all members of both the groups.

Statistical analysis: Z test for difference of proportions was applied.

Results: No lepromatous secondary case developed from lepromatous index case. Among the contacts of index cases, secondary cases were mostly tuberculoid (73.0%). Average lepromin negativity among cases was 35.3%, among non-affected contacts was 15.3% and among controls was 7.8%, clearly showing that immunity was highest among controls and least among cases. 74 lepromatous and 8 borderline cases were lepromin negative but the rest were lepromin positive.

Conclusions: Family contacts of cases were less immune to leprosy than the controls, hence there lies the importance of finding means to improve CMI for lepromin negative persons.

Keywords: Lepromin, Contacts, Susceptibility, Cell-mediated immunity

Introduction:

In 1995, estimated leprosy cases in the world amounted to 1.8 million, out of which 1.3 million were registered and 1 million were being treated with multi drug therapy (MDT). India accounted for 1/4th of the total estimated leprosy case-load in the world1.

Registered cases in India were 0.45 million and estimated cases were 0.55 million. The prevalence rate of leprosy was 5.8/10,000 in India in 1997 with West Bengal (12.3/10,000), Bihar (19.2/10,000) and Orissa (16.0/10,000) being the worst affected1.

Hence the need for finding out the infectivity of leprosy cases among their household contacts as well as the susceptibility of the contacts to leprosy. So, the present study was undertaken.

Material and Methods:

This prospective 3 year follow-up study was carried out in the department of Dermatology, STD and Leprology of the School of Tropical Medicine, Calcutta, from 1993 to 1996, using a case-control design. One hundred case families were selected by simple random sampling from the records of the leprosy clinic. Another 100 families having no leprosy case but living in adjacent area of selected case families were taken by simple random sampling, forming the control group. Clinical, bacteriological and immunological examinations were done for all the subjects. Information as regards socio-economic conditions, environmental factors and other relevant information was gathered by means of a pretested schedule, by house-to-house visit. All members of the families of both the groups were requested to attend the clinic for the lepromin test (Mitsuda). All study and comparison subjects were followed up at 6-monthly intervals for three consecutive years to ascertain their clinical and bacteriological status at each follow-up. Only household contacts of index cases were considered. These contacts were also classified in regard to living in the same house, in the same room or sharing the same bed.

A whole body chart was filed in at the first encounter and a subsequent 6 monthly review of charting was done. 0.1 ml suspension of 16x106 leprae was injected intradermally and the nodule formed at the site of injection was measured by slide callipers after 3-4 weeks. Doubtful reactions were excluded from the study. The test was interpreted as follows:

Less that 3 mm 3.5- negative
3.5-4.5 mm 1+
4.5 mm 5.0-7.5 mm 2+
7.5-10.0 mm or ulceration 3+

Results and Discussion:

Table I: Distribution of case and control family members according to age and sex.

Age group Case family members Control family members
(Years) Male Female Total Male Female Total
0-9 58 44 102 54 48 102
10-19 110 78 188 76 62 138
20-29 46 28 74 26 30 56
30-39 42 42 94 38 40 78
40-49 34 08 42 38 26 64
50 & above 24 16 40 16 06 22
Total 314 226 540 248 212 460

Table I shows that males were more than females in both the groups but age and sex distributions did not differ significantly between case and control groups. Moreover, religion, socio-economic status and type of family did not have much influence on the prevalence of leprosy.

Table II: Type of index case and total contacts with type of case developed among contacts.
Type of
index case
No. of
index case
No. of
contacts
No. of
affected
contacts
(%)
Lepromatous* 74 321 136 (42.4)
Borderline* 08 67 24 (35.8)
Tuberculoid** 16 34 14 (41.2)
Indeterminate** 02 18 4 (22.2)
Total 100 440 178 (40.5)

*Multibacillary; **Paucibacillary

Table II shows that, out of 100 index cases, 74 were lepromatous, 8 borderline, 16 tuberculoid and 2 indeterminate. 321 contacts of the 74 lepromatous cases produced 136 leprosy cases.

Table III: Distribution of affected contacts according to type of leprosy.
Type of index case Type of affected contacts Total
Tuberculoid Borderline Indeterminate
Lepromatous (n=74) 96 8 32 136
Borderline (n=8) 18 - 06 24
Tuberculoid (n=16) 12 - 02 14
Indeterminate (n=2) 04 - - 04
Total 130(73.0%) 8(4.5%) 40(22.5%) 178

Table III reveals that, out of those 136 cases among 321 contacts of lepromatous cases, 96 were tuberculoid, 8 borderline and 32 indeterminate. 67 contacts of 8 borderline cases developed 24 leprosy cases, 18 of which were tuberculoid while the rest were indeterminate. 14 leprosy cases developed from 34 contacts of 16 tuberculoid cases, 12 of which were tuberculoid while 2 were indeterminate. Out of 18 contacts of 2 indeterminate cases, 4 leprosy cases developed, all being tuberculoid in type. It is noteworthy that no lepromatous secondary case developed, even among contacts of lepromatous index cases. By and large, tuberculoid cases were predominant, being 130 out of 178 cases among contacts, i.e., 73.0%. These findings corroborate those of Doull et al2,3, Guinto et al4, Md Ali and Prosad5 and S.K. Noordeen6,7.

Table IV: Distribution of leprosy cases developed among contacts showing age, sex and type of contact.
Age group Sex Type of contact Total Percentage
(years) Male Female Same room Same bed Household
5-9 26 10 08 22 6 36 64.3
10-14 08 06 08 06 0 14 25.3
15-19 04 05 04 0 2 06 10.7
Total 38 18 20 28 8 56 100.0
Percentage 67.8 32.2 35.7 50.0 14.3 100

Table IV shows that 50% of the household contacts shared the same bed, 35.7% shared the same room while 14.3% lived in the same house. During the three year follow-up period, it was observed that secondary cases were more among persons sharing the same bed than the same room, which was again more than persons living in the same house (3.5:2.5:1.0). Besides, most of the cases occurred among the 5-9 year age group. This supports the observation by Noordeen7 that infants and children are more susceptible to leprosy.

Lepromin negativity increased with age among cases. Among non-affected contacts, percentage of lepromin negativity ranged from 12.5 to 20. Among controls this range is even lower, being 3.6% to 12.5% only. This shows that susceptibility to leprosy was highest among cases with average lepromin negativity of 35.3%, somewhat less among contacts, with 15.3% negative lepromin and least among controls with only 7.8% negative lepromin.

Table V: Lepromin result among index and contact cases in relation to type of leprosy.
Type of leprosy No. of index cases with No. of affected contact with
+Lepromin -Lepromin +Lepromin -Lepromin
Lepromatous 0 74 0 0
Borderline 0 08 02 6
Tuberculoid 16 0 126 4
Indeterminate 02 0 34 6
Total 18 82(82.0%) 162 16(9.0%)

Table V shows that all 74 lepromatous and 8 borderline cases have negative lepromin i.e. lack of cell-mediated immunity (CMI), the 16 tuberculoid and 2 indeterminate cases have positive lepromin.

Among the affected contacts, 6 out of 8 borderline cases were lepromin negative (75%), 4 out of 130 tuberculoid cases were lepromin negative (3.1%) and the figure was 6 out of 34 for indeterminate type.

Hence it is seen that family contacts of cases were less immune to leprosy than members of the comparison group.

Conclusion:

The study determined the immune status of persons who live in contact with leprosy patients. Most of the contacts who developed leprosy tested lepromin negative, indicating a lack of CMI. This being an important predisposing factor for leprosy to occur, the development of a proper vaccine with adequate seroconversion is mandatory.

Acknowledgement:

We express our deep sense of gratitude to all the faculty and staff of the department of Dermatology, STD and Leprology at the School of Tropical Medicine, Calcutta and especially to the late Prof. S.K. Chowdhury, Head of department, for their guidance and co-operation.

References:

  1. World Health Organization. Leprosy Elimination Campaign. W.H.O., Geneva, 1996.
  2. Doull et al. The incidence of Leprosy in Cordova and Talisay, Cebu. Int J Lepr, 1942; 10: 107-31.
  3. Doull et al. An epidemiologist's view of Leprosy. Bulletin of World Health Organization, 1961; 34: 839.
  4. Guinto et al. The Trend of Leprosy in Cordova and Talisay, Cebu Province. Philippines Intl J Lepr, 1954; 22: 409.
  5. Mohammad Ali and Prosad. Contact Surveys in Leprosy. Lepr Rev, 1966; 37: 1973.
  6. Noordeen SK. Infectivity of Leprosy. In: Chatterjee BR, ed. A window on Leprosy, Gandhi Memorial Leprosy Foundation, New Delhi, 1978; 59-63.
  7. Noordeen SK. The Epidemiology of Leprosy. Leprosy, Hastings RC, Churchill Livingstone, Edinburgh, 1985; 20-26.
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