|
|
SPECIAL REPORT |
|
Year : 2014 | Volume
: 1
| Issue : 1 | Page : 23-27 |
|
Containing leprosy: Current epidemiological status, detection and management strategies, and experiences at a tertiary level center
Sandeep Arora1, Sukriti Baveja1, Aradhana Sood1, Gulhima Arora2
1 Department of Dermatology, Army College of Medical Sciences and Base Hospital, Delhi Cantonment, New Delhi, India 2 Consultant Dermatologist, Primus Superspecialty Hospital, Chanakyapuri, New Delhi, India
Date of Web Publication | 3-May-2014 |
Correspondence Address: Sandeep Arora Department of Dermatology, Base Hospital, Delhi Cantonment, New Delhi - 110010 India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2349-0977.131858
Leprosy, an infectious disease, described since ancient times and endemic in India since then, has been eliminated (elimination defined as a prevalence of less than 1 case per 10,000 population) as a public health problem in December 2005. World Health Organization and National Leprosy Eradication Program (NLEP) have now focused on reducing the disease burden in the population. Data indicates that annual fresh case detection rate remains high with a high incidence of multibacillary cases. A review of present NLEP figures and those reported in a number of studies reflect a discordance and caution by dermatologists. A review of present policy, epidemiological status in the population, and our experience is presented. Data from Base Hospital, Delhi Cantonment, over the past 3 years, including patients treated as well as those on surveillance is presented. A higher incidence of paucibacillary cases was seen, with a high incidence of pure neuritic involvement (15%), reactions (24.7%), and deformities (28.37%). Tenosynovitis was observed with increasing frequency. Future challenges in containing the epidemic to reduce the disease burden in population will require regular assessment of treatment measures, especially the use of fixed drug therapy as well as rehabilitation of the affected. Dermatologists shall play a central role in any such endeavor in the management of this disease. Keywords: Deformities in leprosy, fixed drug therapy, leprosy elimination
How to cite this article: Arora S, Baveja S, Sood A, Arora G. Containing leprosy: Current epidemiological status, detection and management strategies, and experiences at a tertiary level center. Astrocyte 2014;1:23-7 |
How to cite this URL: Arora S, Baveja S, Sood A, Arora G. Containing leprosy: Current epidemiological status, detection and management strategies, and experiences at a tertiary level center. Astrocyte [serial online] 2014 [cited 2023 May 28];1:23-7. Available from: http://www.astrocyte.in/text.asp?2014/1/1/23/131858 |
Introduction | |  |
Leprosy is a chronic granulomatous infectious disease caused by Mycobacterium leprae affecting the skin and peripheral nerves. Described in the literature and in historical books it has been known to be endemic in India as is evidenced by its mention in Sushruta Samhita. [1] This disease was epidemic in different parts of the world; it appeared, peaked, and gradually subsided. [2],[3] Concerted efforts by various agencies across the world resulted in it being eliminated as a public health problem in the year 2000 and from India in 2005.
The foundation for leprosy elimination was probably laid with the introduction of antibacterial therapy in the form of Promin followed by Dapsone monotherapy [4] Dapsone resistance and discovery of additional dugs with fewer side effects led to the recommendation of multidrug therapy (MDT) by the World Health Organization (WHO) in 1981. [5] Since then despite a few shortfalls, it has near universal adoption. MDT since its introduction has not changed except for duration of treatment, which has been recommended in multibacillary (MB) cases for 1 year and continues to be recommended for 6 months in paucibacillary (PB) cases.
The world health assembly in the year 1991 initially set the target for leprosy elimination at a global level by the year 2000. [6],[7] This target for "elimination" was defined as a prevalence of less than 1 case per 10,000 people. Follow-up studies indicated that there was a dramatic fall in the number of leprosy cases from an estimated prevalence (PR) of 21.1 per 10 000 population to less than 1 per 10,000 people in 2000 by effecting a cure in 14 million over the past 20 years with four million alone since the year 2000. Leprosy as a public health problem has been eliminated from 119 of the 122 countries affected. Global prevalence of leprosy at the end of 2012 was 189,018 cases and incidence was 232,857 with 220,810 (95%) of these cases reported from 16 countries and only 5% of new cases were from rest of the world. [8] Areas of high endemicity exist in a number of countries, including India. Indian incidence alone accounted for 58% of these new cases. [9]
Elimination in India was achieved at a national level on December 31,2005, although some individual states are yet to achieve it. Of the 642 districts, 543 had achieved a PR<1/10,000 by March 2012 and 27 districts in the states of Assam, Chhattisgarh, D&N Haveli, Delhi, Gujarat, Maharashtra, Orissa, West Bengal, and Uttar Pradesh persist with a PR>2/10,000. [10]
Studies report deformity numbers variously from a low of 1.4% to an alarming high of 13%-37%. [11],[12],[13],[14],[15] Those with disability at initial presentation and with pure neuritic disease carry the highest risk of persistent deformities even after treatment. [16],[17]
Classification of patients as PB and MB recommended by WHO and NLEP is based on the number of lesions, peripheral nerve thickening and slit skin smear positivity. Six or more skin lesions, more than one peripheral nerve involvement and or skin smear positivity are labeled as MB cases. [18] This classification hence necessitates appropriate MDT depending on the spectrum the patient belongs to. This spectrum of disease has shown an increasing trend toward MB cases with reports ranging from 75.5% to 95.5% [12],[19],[20] in contrast to the reported incidence of 49% vide NLEP. [10]
Recommendations on chemotherapy for leprosy in 1982 forwarded MDT with a view to counter chances of resistance to Dapsone monotherapy or to other drugs if used alone. [21] MDT effectively combined bactericidal Rifampicin with Dapsone and Clofazimine for an effective treatment. Indian recommendations for MB cases were initially in variance from WHO. These have been brought in line since 1986 and have now been uniformly adopted. [18],[22] NLEP in 1994 recommended a 24-month Fixed Drug (FD) MDT in 1994 and 12-month FD MDT in 1998. Single lesion PB is recommended to be treated by WHO with a single dose of Rifampicin (600 mg) Ofloxacin (400 mg), and Minocycline (100 mg), which according to NLEP is recommended to be treated as any other PB case. [18],[23]
WHO does not recommend post-treatment surveillance in contrast to US National Hansen's Disease Program (NHDP) treatment recommendation. WHO advises patients to report in case of any changes in skin, eyes, and nerve involvement, whereas US-NHDP recommends surveillance of 5 years in PB cases and 10 years in MB cases.
Experience at a Tertiary-Level Leprosy Center | |  |
Analysis of data at the Department of Dermatology of Base Hospital, Delhi Cantonment, was done. The center serves as a referral center for leprosy centers of the Armed Forces of North India. The dependent patient population is the serving population and their dependents. We conducted a retrospective analysis of 2 years and followed the patients prospectively for a period of 1 year in the year 2013 [Table 1].  | Table 1: Epidemiological Profile of Patients in the Last 3 Years at our Center
Click here to view |
Inclusion Criteria and Study Cohort
All patients diagnosed at Base Hospital, Delhi Cantonment, as well as those referred for management were included in the study. Patients placed on surveillance in the preceding 5 years were also observed. The basis of diagnosis was clinical findings, skin clippings, histopathological correlation, and nerve conduction studies in pure neuritic cases. A total of 356 patients of Hansen's disease were managed in the study period.
Assessment, Treatment, and Follow up
For the purpose of epidemiological correlation, these patients were classified as PB/MB as well as on the basis of Ridley-Jopling classification into Indeterminate, Tuberculoid, Borderline-tuberculoid, Borderline-Borderline, Borderline-Lepromatous, and Lepromatous. Those with only nerve thickening in the absence of skinlesions were classified as Pure Neuritic.
All patients received institutional management during which they were housed as inpatients for a minimum period of 6 months to a maximum of 1 year and were followed up on treatment on an outpatient (OPD) basis. The total duration of treatment was dictated by WHO recommendations and clinical response as assessed by the treating dermatologist on a day-to-day basis. Patients who were intolerant to standard WHO MDT or were Glucose-6-phosphate dehydrogenase deficient were placed on monthly Rifampicin, Ofloxacin, and Minocycline (ROM) therapy. All patients were placed on surveillance after completing treatment and underwent complete clinical assessment, including skin clippings and histopathological examination, at the end of the period of surveillance.
Observations
PB cases as defined in NLEP accounted for the majority (63.4%). These cases presented to the treatment center1-13 months after noticing their lesions. MB cases accounted for 36.6% of cases. The duration of illness from the point of initial symptom to final diagnosis was noticeably higher in MB ranging from 1 month to more than 10 years. Pure neuritic involvement accounted for 15.4% (55 cases) with 42 patients having two or more nerve involvement and 13 single nerve involvement. Among the late presenters, this group accounted for the majority. Cross-specialty referrals from other specialist OPDs, such as surgeons and rheumatologists, accounted for 14 cases.
Lepra reactions were observed in 88 cases (24.7%). Type I reaction was observed in 74 and Type II in 13 cases. One case of lucio phenomenon was observed. A higher incidence of reactions has been reported in literature consistent with our findings. [12] Persistent Type I reactions were frequently observed (30% of Type I reaction cases) and long-term steroid use was needed. All Type II reactions were managed with thalidomide with a good response. Three of these cases needed repeated courses of thalidomide for persistent Erythema Nodosum Leprosum (ENL) reaction. Late reversal reactions were seen in seven cases. All these cases were presented during the surveillance period after having completed their MDT.
Deformities were observed in 101 cases (28.37%) [Table 2]. Higher prevalence of deformities has been reported in a number of studies. [12],[15],[24] Claw hand was seen in 59cases, foot drop in 28,trophic ulcers in 17, and lagophthalmos in 3 cases. A higher incidence of claw hand was seen in PB cases (79.6%)and a higher incidence of foot drop in MB cases (75%). This was possibly on account of earlier diagnosis in PB cases and consequently earlier detection of deformities in them. Trophic ulcers were observed in 18 cases, 7 of which did not have any other deformity. Nerve abscesses were observed in 11 patients. These were managed with oral prednisolone. All resolved over a period of 3 to 6months.
Atypical presentations in our study included tenosynovitis, Histoid Hansen's, a case of lucio phenomenon, late presentations with palatal perforation [Figure 1] and another with laryngeal involvement. Tenosynovitis was observed in 10 cases [Figure 2]. All patients with tenosynovitis presented without reaction. Eight cases were not given any specific treatment and resolved upon continuation of MDT. Two needed surgical intervention. No acid-fast bacilli or evidence of inflammatory cells was seen either on Fine Needle Aspiration Cytology or synovial biopsy. | Figure 1: Hard palate perforation in longstanding untreated lepromatous leprosy.
Click here to view |
 | Figure 2: Tenosynovitis with bilateral bursitis in Paucibacillary patient (Left) and tendoachilles involvement in a lepromatous patient (Right).
Click here to view |
Arthritis was not seen in our patient base. Five cases of Histoid Hansen's were seen. All these cases presented with tumid papules and plaques with widespread involvement particularly the face, ear lobules, and trunk. MB MDT was instituted and clinical and microbiological resolution was noticed within 2-3 years of treatment.
Alternative regimen of ROM was instituted in 11 cases. All these patients were MB cases. They did not exhibit a course different from those on standard MDT. Three of these exhibited an upgrading reaction.
All our patients in the follow-up period showed no evidence of relapse.
Discussion | |  |
The spectrum of patients in our study was a majority of PB cases. This is in variance with other studies [12] but similar to the NLEP progress report. [10] This was possibly because our patient population represented a diverse geographical area giving a more Pan India picture such as the NLEP figures.
The incidence of reactions was as has been reported. [6],[12] It was similar in those on standard WHO MDT or ROM MDT. The high incidence of deformities reflects active disease and the need to continue containing leprosy in this post-elimination period.
Manifestations such as tenosynovitis, a feature reported rarely in the literature earlier are now recognized along with other rheumatologic manifestations. [25],[26],[27] We observed 10 cases all in MB spectrum. Their importance lies in diagnosing cases presenting with tenosynovitis in the dermatology OPD along with features suggestive of leprosy and it's reactions. [28],[29],[30]
Detecting patients after a prolonged undiagnosed illness with deformities was not uncommon before institution of NLEP. The two cases in this study diagnosed after more than 10 years (14 and 23 years) highlight the importance of our continuous efforts despite success in elimination. Patients such as these serve as reservoirs of leprosy in the population.
Conclusions | |  |
The future management of leprosy elimination is based on early detection of the infected, their deformities, and the management within the confines of fixed drug therapy and follow up. With the national goal of leprosy elimination being achieved by the end of 2005, the thrust has now shifted to the detection of leprosy in the community based on the WHO-Enhanced Global Strategy to further reduce leprosy disease burden (2011-2015) in the community. [8],[18]
The convenience of shorter fixed drug therapy [31],[32] has only made it easier for the international as well as national health policy. The dermatologists, however, are not convinced by the shorter duration of therapy and prefer to treat patients based on the findings and clinical evidence of infection. [22] This serious disconnect between public health experts and health planners versus the clinician who irrespective of the public health policy leads to management of these patients with longer duration of therapy. The entry and exit points of the enrolled patient despite being dictated and limited to 1 year shall hence not reflect the true picture. Herein lies the danger wherein a population of infected is not accounted for.
Classification into MB and PB has undergone a systematic and progressive simplification over a period of time. Differentiation of PB and MB cases for a health worker and administration of MDT by them has been addressed. However, a number of cases need a dermatologist's intervention in the absence of clear findings. These cases are likely to be missed or be undertreated. Skin smear testing is not routinely carried out in the field; hence many a deserving MB case is also missed. [33]
All our patients were administered supervised MDT as inpatients for at least 6 months as part of institutional management. The observations gained from our experience stress that defining the end point, as a numerical is not feasible in PB and MBcases. Skin smear negativity as in MB does not exist in PB case. [22] Hence these patients must be managed on a case-to-case basis, especially as there is no surveillance thereafter.
MB cases may continue to harbor viable bacilli lying dormant, resulting hence in relapses. [34] Those with a higher initial bacterial load at presentation have been demonstrated to be at the highest risk, necessitate longer treatment, and carry a higher chance of relapse.
Pure neuritic leprosy differentiation into PB and MB purely on a numerical of one or more than one nerve as a simplified subjective approach is not tenable as the end point of treatment is not defined. This subgroup is quite large as was also seen in our observations, and will definitely account for a majority of deformities if left undertreated. [35]
The issue of subclinical leprosy is assuming importance once the reservoir of infection increases with partially treated MB cases. This problem saddles the reduced focus on leprosy post the elimination target. [36],[37]
The spectrum of leprosy infection is diverse. Recognition and management of these cases must be simple to enable the Government programs to function at the grass root level. However, the various formes frustes of the disease make it imperative that the dermatologists be involved at every stage, including policy making and management of these patients. Longer duration as recommended by Marchoux chemotherapy study group for MB cases, [38] and the addition of immunotherapy in leprosy management [39] or addition of alternative MDT regimens as summarized by Malathi and Thapa [22] need to be explored to prevent the risks of under treatment and subsequent relapse. [40] Proponents of alternatives, such as universal MDT and alternative regimens, offer it as a solution to overcome the shortfalls of FD MDT. Adoption of these should be based on inputs from the treating physicians, the dermatologists in this case, lest leprosy goes the malaria way, with resurgence around the corner.
References | |  |
1. | Robbins G, Tripathy VM, Misra VN, Mohanty RK, Shinde VS, Gray KM, et al. Ancient Skeletal Evidence for Leprosy in India (2000 B.C.). PLoS One 2009;4:e5669. |
2. | Irgens LM, Bjerkedal T. Epidemiology of leprosy in Norway. The history of The National Leprosy Registry of Norway from 1856 until today. Int J Epidemiol 1973;2:81-9.  [ PUBMED] |
3. | Lockwood DN, Suneetha S. Leprosy: Too complex a disease for a simple elimination paradigm. Bull World Health Organ 2005;83:230-5. |
4. | Dogra S, Narang T, Kumar B. Leprosy - evolution of the path to eradication. Indian J Med Res 2013;137:15-35.  [ PUBMED] |
5. | WHO Tech Rep Ser No.675. WHO. Chemotherapy of leprosy for control programmes. Geneva: WHO; 1982. p. 1-33. |
6. | WHO. World Health Assembly, Elimination of leprosy: Resolution of the 44th World Health Assembly. Geneva: World Health Organization; 1991, Resolution No. WHA 44. |
7. | Anonymous Leprosy: Global situation. Wkly Epidemiol Rec 2007;82:225-31. |
8. | |
9. | WHO. Global leprosy situation. Wkly Epidemiol Rec 2012;87:317-28. |
10. | |
11. | Chaitra P, Bhat RM. Postelimination Status of Childhood Leprosy: Report from a Tertiary-Care Hospital in South India. Biomed Res Int 2013;2013:328673. |
12. | Singal A, Sonthalia S. Leprosy in post-elimination era in India: Difficult journey ahead. Indian J Dermatol 2013;58:443-6.  [ PUBMED] |
13. | Singal A, Sonthalia S, Pandhi D. Childhood leprosy in a tertiary-care hospital in Delhi, India: A reappraisal in the post-elimination era. Lepr Rev 2011;82:259-69. |
14. | Nardi SM, PaschoalVdel A, Chiaravalloti-Neto F, Zanetta DM. Leprosy-related disabilities after release from multidrug treatment: Prevalence and spatial distribution. Rev Saude Publica 2012;46:969-77. |
15. | Kar BR, Job CK. Visible deformity in childhood leprosy--a 10-year study. Int J Lepr Other Mycobact Dis 2005;73:243-8. |
16. | Sales AM, Campos DP, Hacker MA, da Costa Nery JA, Düppre NC, Rangel E, et al. Progression of leprosy disability after discharge: Is multidrug therapy enough? Trop Med Int Health 2013;18:1145-53. |
17. | Mendiratta V, Khan A, Jain A. Primary neuritic leprosy: A reappraisal at a tertiary care hospital. Indian J Lepr 2006;78:261-7 . |
18. | |
19. | Mukherjee PK, Das P, Rao PS. Time trends in MB-PB ratio among untreated leprosy patients attending a referral hospital in UP, India during 2001 to 2010. Indian J Lepr 2013;85:59-64. |
20. | Ramos JM, Reyes F, Lemma D, Tesfamariam A, Belinchón I, Górgolas M. The burden of leprosy in children and adolescents in rural southern Ethiopia. Paediatr Int Child Health 2014;34:24-8. |
21. | WHO Study Group. WHO Technical Report Series no. 847. Geneva: World Health Organization; 1994. Chemotherapy of leprosy. |
22. | Malathi M, Thappa DM. Fixed-duration therapy in leprosy: Limitations and opportunities. Indian J Dermatol 2013;58:93-100.  [ PUBMED] |
23. | Meima A, Richardus JH, Habbema JD. Trends in leprosy case detection worldwide since 1985. Lepr Rev 2004;75:19-33. |
24. | |
25. | Agarwal V, Wakhlu A, Aggarwal A, Misra R. Tenosynovitis as the presenting manifestation of leprosy. J Indian Rheumatol Assoc 2002;10:69-70. |
26. | Prasad S, Misra R, Aggarwal A, Lawrence A, Haroon N, Wakhlu A, et al. Leprosy revealed in a rheumatology clinic: A case series. Int J Rheum Dis 2013;16:129-33. |
27. | Mandal SK, Sarkar RN, Sarkar P, Datta S, Bandyopadhyay R, Bandyopadhyay D, et al. Rheumatological manifestations of leprosy. J Indian Med Assoc 2008;106:165-6. |
28. | Kahawita IP, Walker SL, Lockwood DN. Leprosy type 1 reactions and erythema nodosumleprosum. An Bras Dermatol 2008;83:75-82. |
29. | Walker SL, Lockwood DN. Leprosy Type 1 (reversal) reactions and their management. Lepr Rev 2008;79:372-86. |
30. | Pandhi D, Chhabra N. New insights in the pathogenesis of type 1 and type 2 lepra reaction. Indian J Dermatol Venereol Leprol 2013;79:739-49.  [ PUBMED] |
31. | Kumar A, Girdhar A, Girdhar BK. Twelve months fixed duration WHO multidrug therapy for multibacillary leprosy: Incidence of relapses in Agra field based cohort study. Indian J Med Res 2013;138:536-40.  [ PUBMED] |
32. | Ji B. Why multidrug therapy for multibacillary leprosy can be shortened to 12 months. Lepr Rev 1998;69:106-9.  [ PUBMED] |
33. | Shetty VP, Pandya SS. One year follow up of a cohort of suspected leprosy cases: Findings from a leprosy ′Selective Special Drive′ in Gadchiroli district, Maharashtra, India. Lepr Rev 2012;83:64-70. |
34. | Sharma A, Sharma VK, Rajwanshi A, Das A, Kaur I, Kumar B. Presence of M. leprae in tissues in slit skin smear negative multibacillary (MB) patients after WHO-MBR. Lepr Rev 1999;70:281-6. |
35. | Nardi SM, PaschoalVdel A, Chiaravalloti-Neto F, Zanetta DM. Leprosy-related disabilities after release from multidrug treatment: Prevalence and spatial distribution. Rev Saude Publica 2012;46:969-77. |
36. | Barreto JG, Guimarães Lde S, Frade MA, Rosa PS, Salgado CG. High rates of undiagnosed leprosy and subclinical infection amongst school children in the Amazon Region. Mem Inst Oswaldo Cruz 2012;107 Suppl 1:60-7. |
37. | Nsagha DS, Bamgboye EA, Assob JC, Njunda AL, Kamga HL, Zoung-Kanyi Bissek AC, et al. Elimination of leprosy as a public health problem by 2000 AD: An epidemiological perspective. Pan Afr Med J 2011;9:4. |
38. | Jamet P, Ji B. Relapse after long-term follow up of multibacillary patients treated by WHO multidrug regimen. Marchoux Chemotherapy Study Group. Int J Lepr Other Mycobact Dis 1995;63:195-201. |
39. | Sehgal VN, Sardana K. Immunoprophylaxis of leprosy: Current status and future prospects. Indian J Dermatol Venereol Leprol 2007;73:71-2.  [ PUBMED] |
40. | Arora PN. Leprosy: An update. Neurosci Today 1999;1:46-50. |
[Figure 1], [Figure 2]
[Table 1], [Table 2]
|