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Leprosy Clinical Presentation

  • Author: Darvin Scott Smith, MD, MSc, DTM&H; Chief Editor: Michael Stuart Bronze, MD  more...
 
Updated: May 09, 2016
 

History

Symptoms

Symptoms are as follows:

  • Painless skin patch accompanied by loss of sensation but not itchiness (Loss of sensation is a feature of tuberculoid leprosy, unlike lepromatous leprosy, in which sensation is preserved.) Chronic insensate patch is seen in the image below.
  • Chronic insensate patch due to leprosy infection. Chronic insensate patch due to leprosy infection. Ho Chi Minh City, Vietnam. Courtesy of D. Scott Smith, MD.
  • Loss of sensation or paresthesias where the affected peripheral nerves are distributed
  • Wasting and muscle weakness
  • Foot drop or clawed hands (may result from neuritic pain and rapid peripheral nerve damage; as seen in the image below)
  • Characteristic clawed hand deformity caused by uln Characteristic clawed hand deformity caused by ulnar involvement in leprosy. Daloa, Ivory Coast. Courtesy of D. Scott Smith, MD.
  • Ulcerations on hands or feet (ulcer at the metatarsal head is seen in the image below)
  • Chronic nonhealing ulcer at the metatarsal head re Chronic nonhealing ulcer at the metatarsal head resulting from loss of sensation in the feet. Karigiri, Tamil Nadu, India. Courtesy of Tara Ramachandra.
  • Lagophthalmos, iridocyclitis, corneal ulceration, and/or secondary cataract due to nerve damage and direct bacillary skin or eye invasion [12]

Symptoms in reactions

Symptoms in reactions are as follows:

  • Type 1 (reversal) - Sudden onset of skin redness and new lesions
  • Type 2 (erythema nodosum leprosum [ENL]; as seen in the image below) - Many skin nodules, fever, redness of eyes, muscle pain, and joint pain
    Patient with erythema nodosum leprosum type 2 reac Patient with erythema nodosum leprosum type 2 reaction several weeks after initiation of drug therapy. This photograph was taken after tendon release. Redwood City, California. Courtesy of D. Scott Smith, MD.

Travel

Leprosy should be considered in anyone who has lived in the tropics or who has traveled for prolonged periods to endemic areas.

Exposure

The incubation period of leprosy is long, ranging from a few months to 20-50 years. The mean incubation time is estimated to be 10 years for lepromatous leprosy and 4 years for tuberculoid leprosy. The organism's slow dividing time (once every 2 wk) contributes to the challenge of epidemiologically linking exposures to the development of disease.

Because of immunologic reasons, only around 5-10% of the population is estimated to be susceptible to infection.

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Physical

The cardinal signs of leprosy include hypoesthesia, skin lesions, and peripheral neuropathy. The first physical signs of leprosy are usually cutaneous. The subtype of leprosy often determines the degree of skin involvement.

Physical examination

Physical examination should include the following:

  • Evaluation of skin lesions
  • Careful sensory and motor examination
  • Palpation of peripheral nerves for pain or enlargement, with particular attention paid to the following locations:
    • Elbows - Ulnar nerve
    • Wrist - Superficial radial cutaneous and median nerves
    • Popliteal fossa - Common peroneal nerve
    • Neck - Great auricular nerve

Physical findings in specific leprosy subtypes

Tuberculoid leprosy

The initial lesion is often a sharply demarcated hypopigmented macule that is ovoid, circular, or serpiginous. The lesions may be somewhat elevated with a dry scaly center and erythematous borders.

Common lesion sites include the buttocks, face, and extensor surfaces of limbs. The perineum, scalp, and axilla are not normally involved because of the temperature differential in these zones, as predilection is toward cooler zones.

As the disease progresses, lesions tend to destroy the normal skin organs such as sweat glands and hair follicles.

Superficial nerves that lead from the lesions tend to enlarge and are sometimes palpable. The patient may experience severe neuropathic pain. Nerve involvement can also lead to trauma and muscle atrophy.

Lepromatous leprosy

This form is characterized by extensive bilaterally symmetric cutaneous involvement, which can include macules, nodules, plaques, or papules. Multiple flat hypopigmented lesions are seen in the image below.

Multiple flat hypopigmented lesions on shoulder an Multiple flat hypopigmented lesions on shoulder and neck, suggestive of multibacillary leprosy. Note ulceration of hypothenar area of hand, indicative of ulnar neuropathy. Redwood City, California, United States. Courtesy of D. Scott Smith, MD.

Unlike lesions in tuberculoid leprosy, those in lepromatous leprosy have poorly defined borders and raised and indurated centers. As in all forms of leprosy, lepromatous lesions are worst on cooler parts of the body. Common areas of involvement include the face, ears, wrists, elbows, buttocks, and knees.

Hoarseness, loss of eyebrows and eyelashes, and nasal collapse secondary to septa perforation may occur in advanced cases of disease. Involvement of the eye may include keratitis, glaucoma, or iridocyclitis as seen in the image below.

Man with advanced deformities caused by unmanaged Man with advanced deformities caused by unmanaged leprosy. Keratitis, loss of eyebrow, thickened skin, and typical hand impairments. Ho Chi Minh City, Vietnam. Courtesy of D. Scott Smith, MD.

The leonine facies associated with leprosy develop as the disease progresses, and the facial skin becomes thickened and corrugated.

Axillary and inguinal adenopathy may develop, in addition to scarring of the testes and subsequent gynecomastia and sterility.

Nerve involvement in lepromatous leprosy is not as severe as in tuberculoid leprosy, since nerves, although visibly thickened and highly infected, still function reasonably well in early stages of the disease.

Borderline tuberculoid leprosy

The lesions are few or moderate and asymmetric with almost complete anesthesia. Peripheral nerves are often involved and thickened asymmetrically, and cutaneous nerves are sometimes enlarged.

Midborderline leprosy

The number of skin lesions is moderate, and they are asymmetrical and somewhat anesthetic. Peripheral nerves may be somewhat symmetrically enlarged, but cutaneous nerves are not.

Borderline lepromatous leprosy

Moderate to numerous slightly asymmetrical skin lesions appear with minor or no anesthesia. Peripheral nerves are often enlarged symmetrically, but cutaneous nerves are not.

Indeterminate leprosy

Skin lesions are typically either hypopigmented or hyperpigmented macules or plaques. Patients may note that these lesions are anesthetic or paresthetic.

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Causes

M leprae is the causative agent associated with leprosy, which has been recognized as an infectious disease for the last 2 millennia. M leprae was discovered as the causative agent in 1873. The acid fast, gram-positive bacillus is an obligate intracellular organism with a predilection for Schwann cells and macrophages. M leprae has not been successfully grown using artificial media.

The route of transmission has not been definitively established, although human-to-human aerosol spread of nasal secretions is thought to be the most likely mode of transmission in most cases. Leprosy is not spread by touch, since the mycobacteria are incapable of crossing intact skin. Living near people with leprosy is associated with increased transmission. Among household contacts, the relative risk for leprosy is increased 8- to 10-fold in multibacillary and 2- to 4-fold in paucibacillary forms. Animal reservoirs do exist (armadillos, certain nonhuman primates), and cases of suspected zoonotic transmission have been reported.

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Contributor Information and Disclosures
Author

Darvin Scott Smith, MD, MSc, DTM&H Adjunct Associate Clinical Professor, Department of Microbiology and Immunology, Stanford University School of Medicine; Chief of Infectious Diseases and Geographic Medicine, Department of Internal Medicine, Kaiser Redwood City Hospital

Darvin Scott Smith, MD, MSc, DTM&H is a member of the following medical societies: American Medical Association, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, International Society of Travel Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Emily Anderson Kelly Stanford University

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Charles V Sanders, MD Edgar Hull Professor and Chairman, Department of Internal Medicine, Professor of Microbiology, Immunology and Parasitology, Louisiana State University School of Medicine at New Orleans; Medical Director, Medicine Hospital Center, Charity Hospital and Medical Center of Louisiana at New Orleans; Consulting Staff, Ochsner Medical Center

Charles V Sanders, MD is a member of the following medical societies: American College of Physicians, Alliance for the Prudent Use of Antibiotics, The Foundation for AIDS Research, Southern Society for Clinical Investigation, Southwestern Association of Clinical Microbiology, Association of Professors of Medicine, Association for Professionals in Infection Control and Epidemiology, American Clinical and Climatological Association, Infectious Disease Society for Obstetrics and Gynecology, Orleans Parish Medical Society, Southeastern Clinical Club, American Association for the Advancement of Science, Alpha Omega Alpha, American Association of University Professors, American Association for Physician Leadership, American Federation for Medical Research, American Geriatrics Society, American Lung Association, American Medical Association, American Society for Microbiology, American Thoracic Society, American Venereal Disease Association, Association of American Medical Colleges, Association of American Physicians, Infectious Diseases Society of America, Louisiana State Medical Society, Royal Society of Medicine, Sigma Xi, Society of General Internal Medicine, Southern Medical Association

Disclosure: Received royalty from Baxter International for other.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Additional Contributors

Fred A Lopez, MD Associate Professor and Vice Chair, Department of Medicine, Assistant Dean for Student Affairs, Louisiana State University School of Medicine

Fred A Lopez, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, Infectious Diseases Society of America, Louisiana State Medical Society

Disclosure: Nothing to disclose.

Shwetha Ravindranath Katta, MD JJM Medical College, Davangere, India

Disclosure: Nothing to disclose.

Acknowledgements

Tara Ramachandra, MD Stanford University School of Medicine

Disclosure: Nothing to disclose.

References
  1. Reibel F, Cambau E, Aubry A. Update on the epidemiology, diagnosis, and treatment of leprosy. Médecine et Maladies Infectieuses. 2015 Sept 02. Volume 45, Issue 9:383–393.

  2. Scollard DM, Adams LB, Gillis TP, Krahenbuhl JL, Truman RW, Williams DL. The continuing challenges of leprosy. Clin Microbiol Rev. 2006 Apr. 19(2):338-81. [Medline]. [Full Text].

  3. Schreuder PAM, Noto S, Richardus JH. Epidemiologic trends of leprosy for the 21st century. Clinics in Dermatology. 2015 Nov 04. Volume 34, Issue 1:24-31.

  4. The World Health Organization. Diagnosis of Leprosy. Leprosy Elimination. Available at http://www.who.int/lep/diagnosis/en/. Accessed: April 15, 2016.

  5. U.S. Department of Health and Human Services. National Hansen's Disease (Leprosy) Program. Health Resources and Services Administration. Available at http://www.hrsa.gov/hansensdisease/. Accessed: March 23, 2016.

  6. Fred F. Ferri. Leprosy. Ferri's Clinical Advisor 2015: 5 books in 1. Philadelphia, PA: Elsevier/Mosby; 2015. 687.e4-687.e5.

  7. Truman RW, Singh P, Sharma R, et al. Probable zoonotic leprosy in the southern United States. N Engl J Med. 2011 Apr 28. 364(17):1626-33. [Medline].

  8. Joyce MP, Scollard DM. Leprosy (Hansen's Disease). Conn's Current Therapy. 2004. 100-105.

  9. Ustianowski AP, Lockwood DN. Leprosy: current diagnostic and treatment approaches. Curr Opin Infect Dis. 2003 Oct. 16(5):421-7. [Medline].

  10. Anderson GA. The surgical management of deformities of the hand in leprosy. J Bone Joint Surg Br. 2006 Mar. 88(3):290-4. [Medline].

  11. The World Health Organization. Transmission of Leprosy. Leprosy Elimination. Available at http://www.who.int/lep/transmission/en/. Accessed: April 15, 2016.

  12. Walker SL, Lockwood DN. Leprosy. Clin Dermatol. 2007 Mar-Apr. 25(2):165-72. [Medline].

  13. Anderson H, Stryjewska B, Boyanton BL, et al. Hansen disease in the United States in the 21st century: a review of the literature. Arch Pathol Lab Med. 2007 Jun. 131(6):982-6. [Medline].

  14. Martinez AN, Talhari C, Moraes MO, Talhari S. PCR-based techniques for leprosy diagnosis: from the laboratory to the clinic. PLoS Negl Trop Dis. 2014 Apr. 8 (4):e2655. [Medline].

  15. Health and Human Resources Administration. Hansens Disease. National Hansen's Disease (Leprosy) Clinical Center. Available at http://www.hrsa.gov/hansensdisease/clinicalcenter.html. Accessed: April 15, 2016.

  16. Van Veen NH, Nicholls PG, Smith WC, Richardus JH. Corticosteroids for treating nerve damage in leprosy. Cochrane Database Syst Rev. 2007 Apr 18. CD005491. [Medline].

  17. Kai M, Nguyen Phuc NH, et al. Analysis of Drug-Resistant Strains of Mycobacterium leprae in an Endemic Area of Vietnam. Clin Infect Dis. Mar 2011;52(5):e127-32.

  18. Singh P, Busso P, Paniz-Mondolfi A, et al. Molecular Drug Susceptibility Testing and Genotyping of Mycobacterium leprae Strains from South America. Antimicrob Agents Chemother. 2011 Jun. 55(6):2971-3. [Medline]. [Full Text].

  19. Bakker MI, Hatta M, Kwenang A, et al. Risk factors for developing leprosy--a population-based cohort study in Indonesia. Lepr Rev. 2006 Mar. 77(1):48-61. [Medline].

  20. Britton WJ, Lockwood DN. Leprosy. Lancet. 2004 Apr 10. 363(9416):1209-19. [Medline].

  21. Deps PD, Guedes BV, Bucker Filho J, Andreatta MK, Marcari RS, Rodrigues LC. Characteristics of known leprosy contact in a high endemic area in Brazil. Lepr Rev. 2006 Mar. 77(1):34-40. [Medline].

  22. Jacobson RR, Krahenbuhl JL, Yoder L. Overview of Leprosy. UpToDate. 2006.

  23. Leprosy. World Health Organization. Available at www.who.org.

  24. Moschella SL. An update on the diagnosis and treatment of leprosy. J Am Acad Dermatol. 2004 Sep. 51(3):417-26. [Medline].

  25. National Hansen's Disease (Leprosy) Program. U.S. Department of Health and Human Services. Available at http://www.hrsa.gov/hansensdisease/index.html. Accessed: July 21, 2014.

  26. Rao PS, Sugamaran DS, Richard J, et al. Multi-centre, double blind, randomized trial of three steroid regimens in the treatment of type-1 reactions in leprosy. Lepr Rev. 2006 Mar. 77(1):25-33. [Medline].

  27. Sridharan R, Lorenzo N, Narasimhan L. Leprosy. Medscape Reference. 2005.

  28. van Beers SM, Hatta M, Klatser PR. Patient contact is the major determinant in incident leprosy: implications for future control. Int J Lepr Other Mycobact Dis. 1999 Jun. 67(2):119-28. [Medline].

 
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Hands with Z-thumbs, clawing, contractures, and shortening of fingers due to repetitive injury and healing. Ho Chi Minh City, Vietnam. Courtesy of D. Scott Smith, MD.
Patient with facial nerve palsy and contractures of the hand. Daloa, Ivory Coast. Courtesy of D. Scott Smith, MD.
Chronic insensate patch due to leprosy infection. Ho Chi Minh City, Vietnam. Courtesy of D. Scott Smith, MD.
Characteristic clawed hand deformity caused by ulnar involvement in leprosy. Daloa, Ivory Coast. Courtesy of D. Scott Smith, MD.
Chronic nonhealing ulcer at the metatarsal head resulting from loss of sensation in the feet. Karigiri, Tamil Nadu, India. Courtesy of Tara Ramachandra.
Multiple flat hypopigmented lesions on shoulder and neck, suggestive of multibacillary leprosy. Note ulceration of hypothenar area of hand, indicative of ulnar neuropathy. Redwood City, California, United States. Courtesy of D. Scott Smith, MD.
Man with advanced deformities caused by unmanaged leprosy. Keratitis, loss of eyebrow, thickened skin, and typical hand impairments. Ho Chi Minh City, Vietnam. Courtesy of D. Scott Smith, MD.
Histopathology of leprosy: Large numbers of acid-fast bacilli (in clusters) in histiocytes and within nerves. Fite-Faraco stain 500 X. Courtesy of Tara Ramachandra and D. Scott Smith, MD.
Patient with multibacillary leprosy showing subsequent erythema nodosum leprosum reaction. Santa Clara, California. Courtesy of D. Scott Smith, MD.
Patient with erythema nodosum leprosum type 2 reaction several weeks after initiation of drug therapy. This photograph was taken after tendon release. Redwood City, California. Courtesy of D. Scott Smith, MD.
Increased pigmentation on the face due to clofazimine therapy. Courtesy of D. Scott Smith, MD.
WHO Multidrug Therapy Regimens. Courtesy of WHO, Leprosy Elimination, http://www.who.int/lep/mdt/en/, accessed April 15, 2016.
Leprosy prevalence rates, 2014. Courtesy of WHO, Leprosy: Global situation, http://www.who.int/lep/situation/en/, accessed April 28, 2016.
Table 1. Multidrug Therapy Plan Recommended by the WHO
Type of Leprosy Daily, Self-Administered Monthly Supervised Months of Treatment
Paucibacillary Dapsone 100 mg Rifampicin 600 mg 6
Single-lesion paucibacillary Rifampicin 600 mg,



Ofloxacin 400 mg,



Minocycline 100 mg



N/A Single dose
Multibacillary Dapsone 100 mg,



Clofazimine 50 mg



Rifampicin 600 mg,



Clofazimine 300 mg 



12
Pediatric Dapsone 2 mg/kg,



Clofazimine 1 mg/kg



Rifampicin 10 mg/kg,



Clofazimine 6 mg/kg



Same as in adults
Table 2. US Recommendations for Multidrug Therapy [15]
Type of Leprosy Daily, Self-Administered Monthly Supervised Months of Treatment
Paucibacillary Dapsone 100 mg,



Rifampicin 600 mg



N/A 12
Single-lesion paucibacillary Dapsone 100 mg,



Rifampicin 600 mg



N/A 12
Multibacillary Dapsone 100 mg,



Rifampicin 600 mg,



Clofazimine 50 mg



N/A 24
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