Dermatology Online Journal

Letter: Conjugal leprosy: A rarity
Vandana Mehta MD DNB, Vani Vasanth MD, C Balachandran MD
Dermatology Online Journal 16 (5): 15

Department of Skin & STD, Kasturba Medical College, Manipal, Karnataka, India. vandanamht@yahoo.com

---

Abstract

Leprosy is a chronic infectious disease but conjugal leprosy in India is a rarity. Various hypotheses have been postulated to explain this rare phenomenon. Here we describe a family in South India, three members of which have been confirmed to be suffering from leprosy.

---

Introduction

Leprosy is a chronic infectious disease caused by the bacillus, Mycobacterium leprae. The rate at which leprosy spreads depends on the susceptibility and the opportunities for contact with M. leprae. Leprosy acquired from a marriage partner is termed conjugal leprosy. Conjugal leprosy is a rarity [1]. The rate of conjugal leprosy varies from 0.33 percent to 7.8 percent [2] in various studies. Various hypotheses have been postulated to explain this rare phenomenon. Herein we describe a family in South India, three members of which have been confirmed to be suffering from leprosy.

Case report

Figure 1

A 36-year-old goldsmith (patient 1), presented to us with an asymptomatic, erythematous, mildly scaly plaque on the forehead above the left eyebrow that had been present for 6 months (Figure 1). There were no other hypoanaesthetic patches on the body nor significant nerve thickening. Considering a differential diagnosis of lupus vulgaris, sarcoidosis, and tuberculoid Hansen disease, a skin biopsy was performed that showed epithelioid granulomas in a peri-appendageal distribution. Slit skin smear for AFB was negative.

Figure 2	Figure 3

The patient presented 3 weeks later with his father (patient 2) – a 68-year-old, retired businessman with multiple asymptomatic nodules on the upper limbs and trunk, which had been present for the past nine months. There was no history of sensory loss, hypopigmentation, hypoanaesthetic patches, motor weakness, or features suggestive of ENL lesions. A complete physical examination revealed multiple infiltrated papules and plaques over bilateral ear lobes, upper limbs, abdomen, and lower limbs (Figures 2 and 3). Sensation over the lesions and extremities was normal. There was no nerve thickening or evidence of motor weakness. Slit skin smear for AFB showed a bacillary index (BI) of 4+ and MI of 6 percent. Biopsy from a nodule was suggestive of lepromatous leprosy with an atrophic epidermis, a well-formed Grenz zone, and a diffuse lymphocytic infiltrate in the dermis.

Figure 4

The mother (patient 3) was called for examination. She also complained of a mildly scaly, erythematous plaque on the right forearm (Figure 4) associated with impaired sensation over the lesion and a history of tingling and numbness over the bilateral feet for a duration of 3 months. Examination revealed decreased sensation to prick and altered temperature sensation over the forearm lesion. A feeding nerve twig could be palpated at one edge of the plaque. Slit skin smear for AFB was negative and histopathological examination of the plaque showed features suggestive of BT Hansen disease.

The father (patient 2) was diagnosed with lepromatous leprosy and was the index case. He was commenced on multibacillary MDT regimen for 1 year and is on regular treatment with no new lesions or lepra reactions to date. Patients 1 and 3 could be considered as secondary cases and were commenced on paucibacillary MDT for 6 months in view of the presence of a single lesion and no nerve thickening. The lesions regressed with hyperpigmentation in both patients by the end of six months.

Discussion

Leprosy is a chronic infectious disease caused by the bacillus, Mycobacterium leprae. Although the causal agent was identified over a century ago, the route of transmission and the determinants of susceptibility to infection remain unknown. Contact with infectious cases does not always result in transmission of the disease and individuals exposed to the same infectious case often develop different clinically distinct forms of the disease.

Melendez et al. [3] studied the characteristics of leprosy among couples in the Colombian Caribbean Coast. Conjugal leprosy accounted for 5.4 percent of leprosy cases detected during the study period. Of the index cases, 84.6 percent were multibacillary, lepromatous cases; two had indeterminate leprosy and two were suffering from tuberculoid leprosy. Of the secondary cases, 61 percent were paucibacillary patients, 42 percent of them being tuberculoid. The time between leprosy being detected in index cases and the disease being detected in secondary patients varied from 5 to 40 years. Lepromatous leprosy in index cases was more frequently associated with leprosy in the couple. When the primary case was paucibacillary, no multibacillary leprosy occurred in the secondary case.

Similarly in our cases, the index case was the father with a nodular form of lepromatous leprosy, whereas the secondary cases developed the tuberculoid spectrum of the disease with the average duration between the onset of symptoms in the two being 3 months.

Recently, the genetic hypothesis for the determination of susceptibility to infection is being accepted widely. The observations supporting this are: (a) The number of siblings who develop lepromatous leprosy is higher when at least one parent has the disease than when neither is afflicted. (b) The incidence of lepromatous leprosy in individuals exposed to relatives with the disease is directly correlated with their degree of kinship. (c) Monozygotic twins exhibit higher concordance rates than dizygotic twins. Further, conjugal transmission is quite rare despite long term sharing of these characteristics by the spouses [4].

There are no specific tests to detect which of the exposed people will develop the disease. Chanteau et al. [5] conducted a sero-epidemiological surveillance of the contact population in 1984 in French Polynesia. ELISA was used to measure IgM anti-ND-O-BSA in the sera. In a population of 724 household contacts, 12.8 percent were seropositive, with 8 (1.1%) showing activity equivalent to multibacillary patients (1 of these 8 individuals developed a lepromatous form of leprosy); 87 percent were seronegative and 3 developed a paucibacillary form of the disease (2 BT, 1 I) without any antibody increase. Among those four contacts who developed leprosy, three were related to a multibacillary index case. These data suggest that this test may be useful for the prediction of multibacillary leprosy.

To conclude, in spite of ongoing, prolonged contact, conjugal leprosy is not frequent and requires several years to develop in the second person. We report this case here for its rarity and the uncommon transmission of leprosy to both the spouse and the offspring. This further stresses the feasibility of the genetic hypothesis in the transmission of conjugal leprosy.

References

1. Kaur P, Singh G, Srivastava J P. Conjugal leprosy. Ind J Dermatol Venereol Leprol 1975; 41: 74-76.

2. Noorden SK. The epidemiology of leprosy. In: Hastings, RC. Leprosy Ed. London: Churchill Livingstone. Chap 2, 1985. p. 15-30

3. Meléndez E, Fuentes J, Rodríguez G. Conjugal leprosy. Rev Salud Publica (Bogota). 2006 ;8 ( 1):24-32. [PubMed]

4. Smith DG. The genetic hypothesis for susceptibility to lepromatous leprosy. Hum. Genet 1979;50:163-177. [PubMed]

5. Chanteau S, Cartel J L, Guidi C, et al. Seroepidemiological study on 724 household contacts of leprosy patients in French Polynesia using disaccharide-octyl-BSA as antigen. Int J Lepr Other Myco dis 1988; 55(4):626-32. [PubMed]

© 2010 Dermatology Online Journal