Dermatologic Manifestations of Leprosy Workup

  • Author: Felisa S Lewis, MD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Aug 5, 2011
 

Laboratory Studies

  • Skin biopsy
    • The presence of an inflamed nerve in a skin biopsy specimen is considered the criterion standard for diagnosis.
    • The skin biopsy sample should be examined for morphologic features and for the presence of acid-fast bacilli. Biopsy is useful for determining the morphologic index, which is used in the evaluation and treatment of patients. The morphologic index is the number of viable bacilli per 100 bacilli in the leprous tissue. The bacterial index of granuloma (BIG) does not differentiate between viable and nonviable bacilli.[29]
    • See Histologic Findings below.
  • Lepromin testing
    • This test indicates host resistance to Mycobacterium leprae. Its results do not confirm the diagnosis, but they are useful in determining the type of leprosy.
    • A positive finding indicates cell-mediated immunity, which is observed in tuberculoid leprosy. A negative finding suggests a lack of resistance to disease and is observed in patients with lepromatous leprosy. A negative result also indicates a worsened prognosis.
    • To perform this test, bacillary suspension is injected into the forearm. An assessment of the reaction at 48 hours is called the Fernandez reaction, and a positive result indicates delayed hypersensitivity to antigens of M leprae or mycobacteria that cross-react with M leprae. When the reaction is read at 3-4 weeks, it is called the Mitsuda reaction, and a positive result indicates that the immune system is capable of mounting an efficient cell-mediated response.
  • Serology and polymerase chain reaction (PCR) testing: Although useful in detecting multibacillary disease, these are not widely performed because they fail to reliably detect early or mild forms of leprosy.
    • Serology can be used to detect antibodies to M leprae –specific phenolic glycolipid-I (PGL-I). This test is useful primarily in patients with untreated lepromatous leprosy, because 90% of patients have antibodies. However, antibodies are present in only 40-50% of patients with paucibacillary disease. PGL-I antibody levels decline significantly during MDT; therefore, these levels may be monitored for chemotherapy effectiveness.[30]
    • A dipstick assay test called the M leprae lateral flow test can detect PGL-I antibodies within 10 minutes with a sensitivity of 90-97.4% in multibacillary leprosy patients. It has the added advantages of using whole blood (versus serum), the technique is easily taught, the results are easily interpreted, and it requires no special equipment.[31]
    • The use of the anti–45-kd and modified anti-PGL-I antibody assays in combination may be more sensitive in detecting cases of paucibacillary leprosy than either assay individually.[32]
    • PCR analysis targeting 16s ribosomal RNA can be used to detect and identify M leprae. The technique is used most often when acid-fast bacilli are detected but clinical or histopathologic features are atypical. Specimens for PCR should be fixed in alcohol or should be rapidly processed because prolonged formalin fixation decreases the sensitivity.[33]
    • The development of a one-step reverse transcriptase PCR assay may be more sensitive in detecting bacilli in slit smears and skin biopsy specimens. This RNA-based assay is also effective for monitoring bacteria clearance during therapy.[34]
  • Other: Although laboratory studies help in making a definitive diagnosis of leprosy, such tests are usually unavailable in remote areas and in some developing countries.
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Imaging Studies

  • Radiographs
    • Plain radiographs may be useful to detect and monitor leprosy-induced bone changes.[35]
    • Resorption, fragmentation, and maligned fractures are common signs of leprosy-induced bone changes. Medullary sclerosis or wavy diaphyseal borders indicate diaphyseal whittling.
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Histologic Findings

In the indeterminate form, findings are nonspecific. Histiocytes and lymphocytes are scattered, with some concentration around dermal appendages and nerves. At times, an acid-fast bacillus can be observed in a nerve bundle. The number of dermal mast cells may be increased.

In the tuberculoid form of leprosy, well-developed epithelioid granulomas are observed in the papillary dermis, often around neurovascular structures. The granulomas are surrounded by lymphocytes, which extend into the epidermis. Langhans giant cells are common. Dermal nerves are destroyed or swollen because of the granulomas. Acid-fast bacilli are not observed. S-100 is useful in identifying nerve fragmentation and differentiating it from other granulomatous disease.[36]

In the borderline tuberculoid form, well-developed epithelioid cell granulomas are apparent and diffuse, but few or no Langhans giant cells are observed. Few lymphocytes are present in the epidermis in this form, compared with tuberculoid leprosy. Bacilli are absent or rare, but they can be found in dermal nerves and in the arrector pilorum. Nerves are moderately swollen.

In the borderline borderline form of leprosy, diffuse epithelioid granulomas that lack giant cells are observed in the dermis below the subepidermal zone of uninvolved papillary dermis (ie, grenz zone). Nerves are slightly swollen, and acid-fast bacilli are present in moderate numbers.

In the borderline lepromatous form, smaller granulomas with some foamy changes and numerous lymphocytes are observed. Nerves often have an onionskin appearance as a result of invasion of the perineurium. A few epithelioid cells may be observed.

In the lepromatous form of leprosy, a diffuse infiltrate of foamy macrophages is present in the dermis below a subepidermal grenz zone. An enormous number of acid-fast bacilli develop within the foamy macrophages, singly or in clumps, called globi. Lymphocytes are scant, and giant cells are typically absent. Numerous bacilli invade the nerves, but these are fairly well preserved with little infiltrate. Nodular, or dermatofibromalike lesions in lepromatous leprosy, referred to as histoid leprosy, result in a diffuse fascicular arrangement of spindled cells in the dermis admixed with foamy macrophages that contain numerous bacilli.

The histoid form has spindle-shaped clusters of histiocytes in a whorled or parallel pattern. In paucibacillary histoid leprosy, these clusters are in the papillary and mid dermis. Multibacillary histoid leprosy has a grenz zone with the histiocytes located in the mid and deep dermis.[37] Globus formation is usually absent. They also tend to grow in an expansive, rather than infiltrative, manner. Bacilli are notably longer than ordinary lepra bacilli.

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Contributor Information and Disclosures
Author

Felisa S Lewis, MD  Staff Physician, Department of Dermatology, Madigan Army Medical Center

Felisa S Lewis, MD, is a member of the following medical societies: American Academy of Dermatology, International Society of Dermatology, and Women's Dermatologic Society

Disclosure: Nothing to disclose.

Coauthor(s)

Theresa Dressler Conologue, DO, FAAD  Physician, Department of Dermatology, Geisinger Medical Center

Theresa Dressler Conologue, DO, FAAD is a member of the following medical societies: American Academy of Cosmetic Surgery, American Academy of Dermatology, and American Society for Laser Medicine and Surgery

Disclosure: Nothing to disclose.

Elyse Harrop, MD  Clinical Instructor, Department of Dermatology, Metrohealth Medical Center

Elyse Harrop, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology

Disclosure: Nothing to disclose.

Specialty Editor Board

Terry L Barrett, MD  Clinical Professor of Dermatology and Pathology, University of Texas Southwestern School of Medicine; Director, ProPath Dermatopathology, Dallas, Texas

Terry L Barrett, MD is a member of the following medical societies: American Academy of Dermatology, American Dermatological Association, American Medical Association, American Society of Dermatopathology, College of American Pathologists, and United States and Canadian Academy of Pathology

Disclosure: Nothing to disclose.

Michael J Wells, MD  Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association

Disclosure: Nothing to disclose.

Lester F Libow, MD  Dermatopathologist, South Texas Dermatopathology Laboratory

Lester F Libow, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Texas Medical Association

Disclosure: Nothing to disclose.

Catherine M Quirk, MD  Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania

Catherine M Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

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