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Abstract

Leprosy, also known as Hansen's disease, is a chronic infectious disease caused by Mycobacterium leprae. It primarily affects the skin, peripheral nerves, upper respiratory tract, and eyes. Leprosy is characterized by skin lesions, numbness, and muscle weakness, which can lead to severe nerve damage, deformities, and disabilities if left untreated. The disease has two main clinical forms: Paucibacillary and Multibacillary leprosy, with various subtypes. Early detection, treatment, and support are crucial to prevent long-term complications. This article provides an overview of leprosy, its types, symptoms, diagnosis, treatment, and precautions.

Keywords

Hansen's disease, Mycobacterium leprae, skin lesions, muscle weakness, Paucibacillary leprosy, Multibacillary leprosy.

Introduction

A survey done in Maharashtra, India, showed Rates of three to nine cases per10 000 population, and that 3% of these newly diagnosed cases were in children [1]. Leprosy is caused by Mycobacterium leprae a microorganism that has predilection for the skin and nerves. The disease progresses slowly, with symptoms appearing months or even years after exposure. Leprosy is characterized by skin lesions, numbness, and muscle weakness, which, if left untreated, can lead to severe nerve damage, deformities, and disabilities [4]Contrary to historical misconceptions, leprosy is only mildly contagious and spreads through prolonged, close contact with an infected person, usually via respiratory droplets. There are two main clinical forms of the disease [3] Paucibacillary leprosy: Fewer lesions, lower bacterial load, and a more limited immune response. Multibacillary leprosy: More widespread lesions, higher bacterial load, and a stronger immune system involvement . Leprosy is classified into several types based on the severity of symptoms, immune response, and bacterial load. The two primary forms are Paucibacillary and multibacillary leprosy, but more specific types are outlined in the Ridley-Joplin classification, which is commonly used to categorize the disease [2] The types of leprosy

1. Tuberculoid Leprosy (TT)

Immune response: Strong immune system response, which limits bacterial growth.

Symptoms: Fewer, well-defined skin lesions that are dry and numb due to nerve involvement. The disease progresses slowly and is less contagious [6]Bacterial load: Low or undetectable.

           
            Tuberculoid  Leprosy.png
       

 Fig: 1. Tuberculoid  Leprosy

2. Lepromatous Leprosy (LL)

Immune response: Poor immune response, allowing bacteria to multiply. Symptoms: Numerous lesions, thickened skin, nodules, and widespread nerve damage, leading to severe deformities if untreated. It affects many parts of the body, including the face, hands, and feet.

Bacterial load: High, making it more contagious.

       
            . Lepromatous Leprosy.png
       

Fig: 2. Lepromatous Leprosy

3. Borderline Tuberculoid Leprosy (BT)

Immune response: Intermediate between tuberculoid and lepromatous types.

Symptoms: More lesions than tuberculoid leprosy, but still relatively few, with some nerve damage.

Bacterial load


            Borderline Tuberculoid Leprosy.png
       

Fig: 3 . Borderline Tuberculoid Leprosy

4. - Multiple skin lesions (>5)

- Irregularly shaped lesions

- Numbness or reduced sensation

- Enlarged nerves

- Positive AFB in skin scrapings/biopsies

- LST & serological testable)

Immune response: Weaker immune response, closer to lepromatous leprosy.

Symptoms: More numerous lesions and more nerve involvement compared to borderline tuberculoid, but not as severe as lepromatous leprosy[8] .

Bacterial load: Higher than in borderline tuberculoid.

       
            Borderline lepromatous leprosy.png
       

Fig: 4. Borderline lepromatous leprosy

5. Mid-Borderline Leprosy (BB)

Immune response: Unstable, intermediate between tuberculoid and lepromatous types.Symptoms: Varying numbers of lesions with variable nerve involvement. This type can shift toward either the.  tuberculoid or lepromatous end of the spectrum over time[9] .

Bacterial load: Moderate to high

            
            Mid- Borderline Leprosy.png
       

Fig: 5. Mid- Borderline Leprosy

6. Indeterminate Leprosy

Immune response: The body's immune response has not fully developed, and the disease can progress in either direction (towards tuberculoid or lepromatous).

Symptoms: Few, mildly pigmented patches without significant nerve damage.

Bacterial load: Low, but the disease can progress if not treated [10] .


            Indeterminate Leprosy.png
       

Fig: 6. Indeterminate Leprosy

Notable signs and symptoms [4]

1. Skin Symptoms:

Discolored patches: Pale or reddish areas on the skin with loss of sensation.

Thick, dry skin: Some areas of the skin may become thick, stiff, or dry. Nodules or lumps: Raised growths or nodules may appear, especially on the face and earlobes.

Ulcers: Open sores, particularly on the soles of the feet.

2. Nerve Damage Symptoms:

Loss of sensation: Affected areas may become numb or lose the ability to feel temperature, touch, or pain. Weakness or paralysis: Muscle weakness, particularly in the hands and feet.

Enlarged peripheral nerves: Thickening or swelling of nerves, especially around the elbow or knee, or in the neck. Burns or injuries: People may injure themselves without realizing it due to the loss of sensation.

3. Eye Symptoms:

Eye problems: Loss of blinking reflex or chronic eye dryness, which can lead to vision problems or blindness.

4. Other Symptoms:

Nasal congestion: Stuffy nose or nosebleeds, which may occur when leprosy affects the lining of the nose.

Loss of eyebrows or eyelashes: In advanced cases, leprosy can cause hair loss on the  [7] .

Diagnosis

The diagnosis of leprosy typically involves a combination of clinical, bacteriological, and histopathological findings. A thorough medical history, physical examination, and sensory testing are performed to assess skin lesions, nerve damage, and other symptoms. Laboratory tests, such as bacteriological examination, serological tests, and PCR, may be conducted on skin scrapings, biopsies, or blood samples to detect the presence of Mycobacterium leprae. The other techniques for different types of leprosy are [8] .


Table 1:-  Types , Diagnosis and Treatment of leprosy

 

S.N

Types

Diagnosis

Treatment [28,33,38]

1

Tuberculoid leprosy

- Early diagnosis is crucial to prevent nerve damage and disability

- Clinical features: Single or few hypopigmented skin lesions

- Lesions may be numb or have reduced sensation

Enlarged nerves, especially in the arms and legs

- Muscle weakness or paralysis

- Laboratory tests: Skin scrapings or biopsies to detect acid-fast bacilli (AFB)

-Lepromin skin test (LST) to assess immune response

-Serological tests (e.g., ELISA) to detect antibodies against M. leprae

-Diagnostic criteria:

- Presence of AFB in skin lesions or nerves

-Positive LST or serological tests

-Consistent clinical features and medical history

- Differential diagnosis:

- Other skin conditions (e.g., vitiligo, eczema)

- Neurological disorders (e.g., neuropathy, nerve entrapment) Other infectious diseases (e.g., tuberculosis, syphilis) [11]

 

 

1. Antibiotics:

- Rifampicin (monthly)

- Clofazimine (monthly)

- Dapsone (daily)

2. Duration: 6-12 months

3. Monitoring:

- Regular check-ups

- Skin lesion assessments

- Nerve function tests

4. Additional treatments:

- Pain management (if needed)

- Wound care (if needed)

- Physical therapy (if needed)

 

 

2

Lepromatous leprosy

- Multiple skin lesions or nodules

- Lesions may be discolored, raised, or ulcerated

- Enlarged lymph nodes, especially in neck and groin

- Enlarged spleen or liver

- Eye problems (e.g., dryness, ulcers, vision loss)

- Testicular atrophy or infertility

- Nerve damage (e.g., numbness, tingling, weakness)

- Positive skin scrapings or biopsies for acid-fast bacilli (AFB)

- Positive Lepromin skin test (LST) or serological tests

- Consistent clinical features and medical history

 

1. Antibiotics:

- Rifampicin (monthly)

- Clofazimine (monthly)

- Dapsone (daily)

- Ofloxacin or minocycline (may be added in some cases)

2. Duration: 12-24 months (or longer in some cases)

3. Monitoring:

- Regular check-ups

- Skin lesion assessments

- Nerve function tests

- Eye exams (as lepromatous leprosy can cause eye problems)

4. Additional treatments:

- Thalidomide (in some cases, to reduce inflammation)

- Corticosteroids (to reduce inflammation and swelling)

- Pain management (if needed)

- Wound care (if needed)

- Physical therapy (if needed)

5. Rehabilitation:

- Physical rehabilitation (to improve mobility and function)

- Occupational therapy (to improve daily living skills)

- Eye rehabilitation

3

Borderline tuberculosis Leprosy

Multiple skin lesions (more than 5)

- Lesions may be irregularly shaped and edges are not well-defined

- Lesions may be slightly raised or flat

- Numbness or reduced sensation in lesions

- Enlarged nerves, especially in arms and legs

- Positive skin scrapings or biopsies for acid-fast bacilli (AFB)

- Lepromin skin test (LST)

- Serological tests  [12].

1. Antibiotics:

- Rifampicin (monthly)

- Clofazimine (monthly)

- Dapsone (daily)

2. Duration: 12-18 months

3. Monitoring:

- Regular check-ups

- Skin lesion assessments

- Nerve function tests

4. Additional treatments:

- Pain management (if needed)

- Wound care (if needed)

- Physical therapy (if needed)

4

Multiple skin lesions

- Irregular shapes and sizes

- Numbness or reduced sensation

- Symmetrical or asymmetrical distribution

- Enlarged lymph nodes and/or nerves

- Muscle weakness or paralysis (in advanced cases)

 

1. Topical creams or ointments:

- Corticosteroids to reduce          inflammation

- Antimicrobial creams for bacterial or fungal infections

- Topical antibiotics for bacterial infections

2. Oral medications:

- Antibiotics for bacterial infections

- Antifungals for fungal infections

- Antihistamines for allergic reactions

- Retinoids for psoriasis or other skin conditions

3. Light therapy:

- UVB phototherapy for    psoriasis, vitiligo, or other skin conditions

- PUVA (psoralen + UVA) therapy for severe psoriasis or other skin conditions

4. Systemic treatments:

- Corticosteroids for severe inflammation

- Immunomodulators for autoimmune-related skin conditions

- Biologics for psoriasis, hidradenitis suppurativa, or other skin conditions

5. Surgical treatments:

- Excision or removal of lesions (e.g., cysts, tumors)

- Mohs surgery for skin cancer

6. Lifestyle changes:

- Wound care and dressings for ulcerated lesions

- Sun protection and sunscreen use

- Stress management and relaxation techniques

5

Mid-borderline Leprosy

- Multiple skin lesions

- Lesions are irregularly shaped, slightly raised

- Numbness or reduced sensation in lesions

- Enlarged lymph nodes and nerves

- AFB (acid-fast bacilli) present in skin scrapings or biopsies

- Lepromin skin test (LST) may be positive or negative

- Borderline features between tuberculoid and lepromatous leprosy[14] .

 

 

1.Antibiotics:

- Rifampicin(600-1200 mg) once

a month

- Clofazimine(300-600 mg) once

a month

- Dapsone

2. Duration: 12-18 months

3. Monitoring:

- Regular check-ups every 2-3

month

- Skin lesion assessments

- Nerve function tests (NFTs) every 6-12 months

4. Additional treatments:

- Pain management (e.g., analgesics) if needed

- Wound care (e.g., dressings, debridement) if needed

- Physical therapy if needed

5. Reversal Reaction (RR) management:

- Prednisolone (40-60 mg) daily for 2-4 weeks if RR occurs

6. Erythema Nodosum Leprosum (ENL) management:

- Thalidomide (100-300 mg) daily for 2-4 weeks if ENL occurs

7. Follow-up:

- Regular follow-up appointments for 5 years after treatment completion

 

 

6

Indeterminate Leprosy

- Single or few hypopigmented skin lesions

- Lesions may be slightly raised or flat

- Numbness or reduced sensation may be absent

- Enlarged lymph nodes and nerves usually absent

- AFB (acid-fast bacilli) not typically found in skin scrapings or biopsies

- Lepromin skin test (LST) may be negative or weakly positive

- Clinical features and laboratory tests inconclusive

- Requires close monitoring for progression to other forms of leprosy [15] .

1.Antibiotics:

Rifampicin(600-1200 mg) once a month

Clofazimine(300-600 mg) once a month

Dapsone

2.Duration: 12-24 months

3. Monitoring:

Regular check-ups every 2-3 months

Skin lesion assessments

Nerve function tests (NFTs) every 6-12 months

4. Additional treatments:

Pain management (e.g., analgesics) if needed

Wound care (e.g., dressings, debridement) if needed

Physical therapy if needed

5.Reversal Reaction (RR) management:

Prednisolone (40-60 mg) daily for 2-4 weeks if RR occurs

- Erythema Nodosum Leprosum (ENL) management:

- Thalidomide (100-300 mg) daily for 2-4 weeks if ENL occurs


Precautions [17]

1. Avoid close contact with infected individuals.

2. Wear protective clothing and gloves when handling potentially contaminated materials.

3. Wash hands frequently, especially after contact with potentially contaminated materials.

4. Avoid touching or shaking hands with individuals with leprosy.

5. Avoid sharing personal items like towels, bedding, or clothing.

6. Keep skin lesions or wounds clean and covered.

7. Avoid walking barefoot in areas where leprosy is common [33] .

8. Use insect repellents to prevent mosquito bites (mosquitoes can transmit leprosy).

9. Get vaccinated (BCG vaccine is available in some countries).

10. Early detection and treatment can prevent long-term nerve damage and disability [20].

CONCLUSION

In conclusion, leprosy is a complex chronic disease requiring comprehensive management, research, and awareness efforts. Early detection, treatment, and support are crucial to prevent long-term complications and improve the quality of life for those affected. Further research will help elucidate the etiopathogeny and clinical manifestations of leprosy, ultimately informing strategies for diagnosis, treatment, and prevention. By addressing the multifaceted aspects of leprosy, we can work towards reducing its impact and improving outcomes for individuals and communities affected by this chronic condition.

REFERENCES

  1. Araújo M. Hanseníase no Brasil. Rev Soc Bras Med Trop. 2013; 36(3):373-382.
  2. Prevedello FC, Mira MT. Hanseníase: uma doença Genética? An Bras Dermatol. 2007; 82(5):451-9.
  3. Gracie R, Peixoto J, Soares F, Hacker M. Análise da Distribuição geográfica dos casos de hanseníase. Rio de Janeiro, 2001 a 2012. Ciênc. Saúde coletiva. 2017; 22(5):1695-1704.
  4. Foss NT. Hanseníase: aspectos clínicos, imunológicos Terapêuticos. An Bras de Imunol. 1999, 74(2).
  5. Andrade P, Ferreira P, Machado A, Messias S, Sales A, Nery J, et al. Histoid leprosy: a rare exuberant case. An Bras Dermatol. 2015; 90(5):756-757.
  6. Leal D, Cazarin G, Bezerra L, Albuquerque A, Felisberto E. Programa de Controle da Hanseníase: uma Avaliação da implantação no nível distrital. Saúde Debate. 2017; 41(1):209-228.
  7. El Darouti MA, Hussein S, SR Al Tahlang, et al. Clinical study of nail changes in leprosy and comparison with nail changes in diabetic patients. Eur Acad Dermatol Venerol. 2011;25(3):290–295. https://doi.org/10.1111/j.14683083.2010.03783
  8. Belachew WA, Naafs B. Position statement: Leprosy: Diagnosis, treatment and follow-up. Europe Acad Dermatol Venerol. 2019;33(7):1205–1213. https://doi.org/10.1111/jdv.15569
  9. James W, Berger T, Elston D. Andrews’ diseases of the skin. 11th ed. Philadelphia: Elsevier Saunders; 2011, Chapter 17, p. 334. ISBN 978 1 4377 0314 6.
  10. BuÈhrer-SeÂkula S, Cunha MGS, NT Foss, et al. Dipstick assay to identify leprosy patients who have an increased risk of relapse. Trop Med Int Health. 2001;6(4):317–323.
  11. Richardus JH, Habbema JD. The impact of leprosy control on the Transmission of M. leprae: is elimination being attained? Lepr Rev2007; 78: 330–37.
  12. Sekar B. Recent advances in immunodiagnostics of leprosy. Indian J Lepr 2007; 79: 85–106.61 Moet FJ, Pahan D, Oskam L, Richardus JH. Effectiveness of single Dose rifampicin in preventing leprosy in close contacts of patients With newly diagnosed leprosy: cluster randomised controlled trial. BMJ 2008; 336: 761–64.
  13. Schuring RP, Richardus JH, Pahan D, Oskam L. Protective effect of The combination BCG vaccination and rifampicin prophylaxis in Leprosy prevention. Vaccine 2009; 27: 7125–28.
  14. Duppre NC, Camacho LA, da Cunha SS, et al. Effectiveness of BCG Vaccination among leprosy contacts: a cohort study. Trans R Soc Trop Med Hyg 2008; 102: 631–38.
  15. Gillis T. Is there a role for a vaccine in leprosy control? Lepr Rev2007; 78: 338–42.65 Raman VS, O’Donnell J, Bailor HR, et al. Vaccination with the ML0276 antigen reduces local inflammation but not bacterial Burden during experimental Mycobacterium leprae infection. Infect Immune 2009; 77: 5623–30.
  16. Moet FJ, Pahan D, Oskam L, Richardus JH. Effectiveness of single Dose rifampicin in preventing leprosy in close contacts of patients With newly diagnosed leprosy: cluster randomised controlled trial. BMJ 2008; 336: 761–64
  17. Schuring RP, Richardus JH, Pahan D, Oskam L. Protective  effect of The combination BCG vaccination and rifampicin prophylaxis in Leprosy prevention. Vaccine 2009; 27: 7125–28.
  18. Duppre NC, Camacho LA, da Cunha SS, et al. Effectiveness of BCG Vaccination among leprosy contacts: a cohort study. Trans R Soc Trop Med Hyg 2008; 102: 631–38.
  19. Gillis T. Is there a role for a vaccine in leprosy control? Lepr Rev2007; 78: 338–42.
  20. Raman VS, O’Donnell J, Bailor HR, et al. Vaccination with the ML0276 antigen reduces local inflammation but not bacterial Burden during experimental Mycobacterium leprae infection. Infect Immune 2009; 77: 5623–30.
  21. United Nations Enable. The Millennium Development Goals (MDGs) and Disability. 2009 http://www.un.org/disabilities/Default.asp?id=1470 (accessed Jan 25, 2010).
  22. Merle CS, Cunha SS, Rodrigues LC. BCG vaccination and leprosy Protection: review of current evidence and status of BCG in leprosy Control. Expert Rev Vaccines 2010; 9: 209
  23. WHO. Enhanced global strategy for further reducing the disease Burden due to leprosy (plan period: 2011–2015). New Delhi: World Health Organization Regional Office for South-East Asia, 2008.
  24. Hatta M, van Beers SM, Madjid B, Djumadi A, de Wit MY, Klatser PR. Distribution and persistence of Mycobacterium leprae Nasal carriage among a population in which leprosy is endemic in Indonesia. Trans R Soc Trop Med Hyg 1995; 89: 381–85.
  25. Senior K. Stigma, chemoprophylaxis, and leprosy control. Lancet Infect Dis 2009; 9: 10.6 WHO Technical Advisory Group on Leprosy Control. Report of the Tenth Meeting of the WHO Technical Advisory Group on Leprosy Control. New Delhi: World Health Organization Regional office for South-East Asia, 2009.
  26. Arungiri S, et al. Detection of mutations in folp1, rpoB and gyrA genes Of M. leprae by PCR- direct sequencing—a rapid tool for screening Drug resistance in leprosy. Lepr Rev (in press).
  27. Moet FJ, Meima A, Oskam L, Richardus JH. Risk factors for the Development of clinical leprosy among contacts, and their relevance For targeted interventions. Lepr Rev 2004; 75: 310–26.
  28. Monot M, Honore N, Garnier T, et al. Comparative genomic and Phylogeographic analysis of Mycobacterium leprae. Nat Genet 2009; 41: 1282–89.
  29. Zhang FR, Huang W, Chen SM, et al. Genomewide association  of leprosy. N Engl J Med 2009; 361: 2609–18.
  30. Gillis T, Vissa V, Matsuoka M, et al. Characterisation of short Tandem repeats for genotyping Mycobacterium leprae. Lepr Rev 2009; 80: 250–60.
  31. Scollard DM, Adams LB, Gillis TP, Krahenbuhl JL, Truman RW, Williams DL. The continuing challenges of leprosy. Clin Microbiol Rev 2006; 19: 338–81.
  32. Feasey N, Wansbrough-Jones M, Mabey DC, Solomon AW. Neglected tropical diseases. Br Med Bull 2010; 93: 179–200.
  33. World Health Assembly. World Health Assembly resolution 1991. (accessed Jan 25, 2010).
  34. Burki T. Old problems still mar fight against ancient disease. Lancet2009; 373: 287–88.
  35. UN. We can end poverty 2015: Millennium Development Goals. (accessed Jan 25, 2010)

Reference

  1. Araújo M. Hanseníase no Brasil. Rev Soc Bras Med Trop. 2013; 36(3):373-382.
  2. Prevedello FC, Mira MT. Hanseníase: uma doença Genética? An Bras Dermatol. 2007; 82(5):451-9.
  3. Gracie R, Peixoto J, Soares F, Hacker M. Análise da Distribuição geográfica dos casos de hanseníase. Rio de Janeiro, 2001 a 2012. Ciênc. Saúde coletiva. 2017; 22(5):1695-1704.
  4. Foss NT. Hanseníase: aspectos clínicos, imunológicos Terapêuticos. An Bras de Imunol. 1999, 74(2).
  5. Andrade P, Ferreira P, Machado A, Messias S, Sales A, Nery J, et al. Histoid leprosy: a rare exuberant case. An Bras Dermatol. 2015; 90(5):756-757.
  6. Leal D, Cazarin G, Bezerra L, Albuquerque A, Felisberto E. Programa de Controle da Hanseníase: uma Avaliação da implantação no nível distrital. Saúde Debate. 2017; 41(1):209-228.
  7. El Darouti MA, Hussein S, SR Al Tahlang, et al. Clinical study of nail changes in leprosy and comparison with nail changes in diabetic patients. Eur Acad Dermatol Venerol. 2011;25(3):290–295. https://doi.org/10.1111/j.14683083.2010.03783
  8. Belachew WA, Naafs B. Position statement: Leprosy: Diagnosis, treatment and follow-up. Europe Acad Dermatol Venerol. 2019;33(7):1205–1213. https://doi.org/10.1111/jdv.15569
  9. James W, Berger T, Elston D. Andrews’ diseases of the skin. 11th ed. Philadelphia: Elsevier Saunders; 2011, Chapter 17, p. 334. ISBN 978 1 4377 0314 6.
  10. BuÈhrer-SeÂkula S, Cunha MGS, NT Foss, et al. Dipstick assay to identify leprosy patients who have an increased risk of relapse. Trop Med Int Health. 2001;6(4):317–323.
  11. Richardus JH, Habbema JD. The impact of leprosy control on the Transmission of M. leprae: is elimination being attained? Lepr Rev2007; 78: 330–37.
  12. Sekar B. Recent advances in immunodiagnostics of leprosy. Indian J Lepr 2007; 79: 85–106.61 Moet FJ, Pahan D, Oskam L, Richardus JH. Effectiveness of single Dose rifampicin in preventing leprosy in close contacts of patients With newly diagnosed leprosy: cluster randomised controlled trial. BMJ 2008; 336: 761–64.
  13. Schuring RP, Richardus JH, Pahan D, Oskam L. Protective effect of The combination BCG vaccination and rifampicin prophylaxis in Leprosy prevention. Vaccine 2009; 27: 7125–28.
  14. Duppre NC, Camacho LA, da Cunha SS, et al. Effectiveness of BCG Vaccination among leprosy contacts: a cohort study. Trans R Soc Trop Med Hyg 2008; 102: 631–38.
  15. Gillis T. Is there a role for a vaccine in leprosy control? Lepr Rev2007; 78: 338–42.65 Raman VS, O’Donnell J, Bailor HR, et al. Vaccination with the ML0276 antigen reduces local inflammation but not bacterial Burden during experimental Mycobacterium leprae infection. Infect Immune 2009; 77: 5623–30.
  16. Moet FJ, Pahan D, Oskam L, Richardus JH. Effectiveness of single Dose rifampicin in preventing leprosy in close contacts of patients With newly diagnosed leprosy: cluster randomised controlled trial. BMJ 2008; 336: 761–64
  17. Schuring RP, Richardus JH, Pahan D, Oskam L. Protective  effect of The combination BCG vaccination and rifampicin prophylaxis in Leprosy prevention. Vaccine 2009; 27: 7125–28.
  18. Duppre NC, Camacho LA, da Cunha SS, et al. Effectiveness of BCG Vaccination among leprosy contacts: a cohort study. Trans R Soc Trop Med Hyg 2008; 102: 631–38.
  19. Gillis T. Is there a role for a vaccine in leprosy control? Lepr Rev2007; 78: 338–42.
  20. Raman VS, O’Donnell J, Bailor HR, et al. Vaccination with the ML0276 antigen reduces local inflammation but not bacterial Burden during experimental Mycobacterium leprae infection. Infect Immune 2009; 77: 5623–30.
  21. United Nations Enable. The Millennium Development Goals (MDGs) and Disability. 2009 http://www.un.org/disabilities/Default.asp?id=1470 (accessed Jan 25, 2010).
  22. Merle CS, Cunha SS, Rodrigues LC. BCG vaccination and leprosy Protection: review of current evidence and status of BCG in leprosy Control. Expert Rev Vaccines 2010; 9: 209
  23. WHO. Enhanced global strategy for further reducing the disease Burden due to leprosy (plan period: 2011–2015). New Delhi: World Health Organization Regional Office for South-East Asia, 2008.
  24. Hatta M, van Beers SM, Madjid B, Djumadi A, de Wit MY, Klatser PR. Distribution and persistence of Mycobacterium leprae Nasal carriage among a population in which leprosy is endemic in Indonesia. Trans R Soc Trop Med Hyg 1995; 89: 381–85.
  25. Senior K. Stigma, chemoprophylaxis, and leprosy control. Lancet Infect Dis 2009; 9: 10.6 WHO Technical Advisory Group on Leprosy Control. Report of the Tenth Meeting of the WHO Technical Advisory Group on Leprosy Control. New Delhi: World Health Organization Regional office for South-East Asia, 2009.
  26. Arungiri S, et al. Detection of mutations in folp1, rpoB and gyrA genes Of M. leprae by PCR- direct sequencing—a rapid tool for screening Drug resistance in leprosy. Lepr Rev (in press).
  27. Moet FJ, Meima A, Oskam L, Richardus JH. Risk factors for the Development of clinical leprosy among contacts, and their relevance For targeted interventions. Lepr Rev 2004; 75: 310–26.
  28. Monot M, Honore N, Garnier T, et al. Comparative genomic and Phylogeographic analysis of Mycobacterium leprae. Nat Genet 2009; 41: 1282–89.
  29. Zhang FR, Huang W, Chen SM, et al. Genomewide association  of leprosy. N Engl J Med 2009; 361: 2609–18.
  30. Gillis T, Vissa V, Matsuoka M, et al. Characterisation of short Tandem repeats for genotyping Mycobacterium leprae. Lepr Rev 2009; 80: 250–60.
  31. Scollard DM, Adams LB, Gillis TP, Krahenbuhl JL, Truman RW, Williams DL. The continuing challenges of leprosy. Clin Microbiol Rev 2006; 19: 338–81.
  32. Feasey N, Wansbrough-Jones M, Mabey DC, Solomon AW. Neglected tropical diseases. Br Med Bull 2010; 93: 179–200.
  33. World Health Assembly. World Health Assembly resolution 1991. (accessed Jan 25, 2010).
  34. Burki T. Old problems still mar fight against ancient disease. Lancet2009; 373: 287–88.
  35. UN. We can end poverty 2015: Millennium Development Goals. (accessed Jan 25, 2010)

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Bishesar Sahu
Corresponding author

Rungta Institute of Pharmaceutical Sciences & Research, Kohka Kurud road, Bhilai, Chhattisgarh

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Munmun Bhattacharya
Co-author

Rungta Institute of Pharmaceutical Sciences & Research, Kohka Kurud road, Bhilai, Chhattisgarh

Photo
Prerna Dhiwar
Co-author

Rungta Institute of Pharmaceutical Sciences & Research, Kohka Kurud road, Bhilai, Chhattisgarh

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Sangeeta Manjhi
Co-author

Rungta Institute of Pharmaceutical Sciences & Research, Kohka Kurud road, Bhilai, Chhattisgarh

Bishesar Sahu*, Munmun Bhattacharya, Prerna Dhiwar, Sangeeta Manjhi, Review Of Leprosy Types, Diagnostic Innovations and Evolving Treatment Modalities, Int. J. of Pharm. Sci., 2024, Vol 2, Issue 12, 276-285. https://doi.org/10.5281/zenodo.14266505

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