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Dermatologic Manifestations of Leprosy Clinical Presentation

  • Author: Felisa S Lewis, MD; Chief Editor: Dirk M Elston, MD  more...
 
Updated: Apr 12, 2016
 

History

In general, leprosy affects the skin, peripheral nerves, and eyes. Systemic symptoms of leprosy are also possible. Specific symptoms vary with the severity of the disease.

Prodromal symptoms are generally so slight that leprosy is not recognized until a cutaneous eruption is present. However, 90% of patients have a history of numbness first, sometimes years before the skin lesions appear.

Temperature is the first sensation that is lost. Patients cannot sense extremes of hot or cold. The next sensation lost is light touch, then pain, and, finally, deep pressure. These losses are especially apparent in the hands and feet; therefore, the chief complaint may be a burn or ulcer in an anesthetic extremity.

Other parts of the body that might be affected by leprosy are the cool areas, which can include superficial peripheral nerves, the anterior chamber of the eyes, the testes, the chin, malar eminences, earlobes, and knees. From this stage of leprosy, most lesions evolve into the tuberculoid, borderline, or lepromatous types.

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Physical

Assess for physical signs of leprosy in 3 general areas: cutaneous lesions, neuropathies, and eyes.

For cutaneous lesions, assess the number and distribution of skin lesions. A hypopigmented macule with a raised border is often the first cutaneous lesion. Plaques are also common. Lesions may or may not be hypoesthetic. Lesions on the buttocks often indicate borderline disease.

Regarding neuropathies, assess for areas of hypoesthesia (light touch, pinprick, temperature and anhidrosis), especially peripheral nerve trunks and cutaneous nerves. The most common nerve affected is the posterior tibial nerve. Others commonly damaged are the ulnar, median, lateral popliteal, and facial nerves. Besides sensory loss, patients may have associated tenderness and motor loss. Nerve palpation, monofilament testing, and voluntary muscle testing are the most useful clinical tests for detecting nerve damage.[19]

Clinical grading of nerve thickness, tenderness, and pain should be recorded to track changes over time and with therapy.[20] Eye damage is most often seen with facial lesions. Lagophthalmos (inability to close the eye), a late finding in persons with lepromatous leprosy, results from involvement of the zygomatic and temporal branches of the facial nerve (cranial nerve [CN] VII). Involvement of the ophthalmic branch of the trigeminal nerve (CN V) can result in reduced corneal reflex, leaving dry eyes and reduced blinking.

Clinical tests

Certain tests can be performed in the clinic to aid in the diagnosis of leprosy.

Tissue smear testing/slit-skin smears

An incision is made in the skin, and the scalpel blade is used to obtain fluid from a lesion. The fluid is placed on a glass slide and stained by using the Ziehl-Neelsen acid-fast method or the Fite method to look for organisms. The bacterial index (BI) is then determined as the number of organisms at 100X with oil immersion. Skin smears have high specificity but low sensitivity because 70% of all patients with leprosy have negative smear results. However, this test is useful because it detects the most infectious patients.

Histamine testing

This test is used to diagnose postganglionic nerve injury. Histamine diphosphate is dropped on healthy skin and affected skin, and a pinprick is made through each site. The site forms a wheal on healthy skin, but not on skin where nerve damage is present.

Methacholine sweat testing

An intradermal injection of methacholine demonstrates the absence of sweating in leprous lesions. This test is useful in dark-skinned patients in whom the flare with the histamine test cannot be seen.

Diagnostic criteria for leprosy [21]

The diagnosis of leprosy is primarily a clinical one. In one Ethiopian study, the following criteria had a sensitivity of 97% with a positive predictive value of 98% in diagnosing leprosy. Diagnosis was based on 1 or more of the 3 following signs:

  • Hypopigmented or reddish patches with definite loss of sensation
  • Thickened peripheral nerves
  • Acid-fast bacilli on skin smears or biopsy material

Classification [22]

The Ridley-Jopling classification is used to differentiate types of cutaneous leprosy and helps in determining the prognosis. A general classification of disease is based on the number of skin lesions present and the number of bacilli found on tissue smears. Paucibacillary disease (indeterminate leprosy and tuberculoid leprosy) has fewer than 5 lesions and no bacilli on smear testing. Five or more lesions with or without bacilli (borderline leprosies and lepromatous leprosy) is considered multibacillary disease. Classification may be further refined by considering other criteria, such as the number of body areas affected and the size of the largest skin lesions.[23]

Indeterminate leprosy

This early form causes one to a few hypopigmented or, sometimes, erythematous macules. Sensory loss is unusual. Approximately 75% of affected persons have lesions that heal spontaneously. In some, the disease may persist in this indeterminate form. In those with weak immunity, the disease progresses to one of the other forms.

Tuberculoid leprosy

Skin lesions are few. One erythematous large plaque is usually present, with well-defined borders that are elevated and that slope down into an atrophic center. The lesions can become arciform or annular. They can be found on the face, limbs, or elsewhere, but they spare intertriginous areas and the scalp. Lesions can be dry and scaly, hypohidrotic, and hairless. Another presentation involves a large, asymmetric hypopigmented macule. Both types of lesions are anesthetic and involve alopecia.

Spontaneous resolution can occur in a few years, leaving pigmentary disturbances or scars. Progression can also occur, leading to borderline-type leprosy. In rare instances in which a patient is untreated for many years, the lepromatous type can develop.

Neural involvement is common in persons with tuberculoid leprosy; it leads to tender, thickened nerves with subsequent loss of function. The great auricular, common peroneal, ulnar, and radial cutaneous and posterior tibial nerves are often prominent. Nerve damage can happen early, resulting in wrist drop or foot drop.

Borderline tuberculoid leprosy

Lesions in this form are similar to those in the tuberculoid form, but they are smaller and more numerous. The nerves are less enlarged and alopecia is less in borderline tuberculoid leprosy than in other forms. Disease can remain in this stage, it can convert back to the tuberculoid form, or it can progress to lepromatous leprosy.

Borderline borderline leprosy

Cutaneous lesions consist of numerous, red, irregularly shaped plaques that are less well defined than those in the tuberculoid type. Their distribution may mimic those of the lepromatous type, but they are relatively asymmetric. Anesthesia is only moderate. Regional adenopathy may be present. Disease may remain in this stage, it may improve, or it may worsen.

Borderline lepromatous leprosy

Lesions are numerous and consist of macules, papules, plaques, and nodules. Annular punched-out–appearing lesions that look like inverted saucers are common. Anesthesia is often absent. As with the other forms of borderline leprosy, the disease may remain in this stage, it may improve, or it may regress.

Lepromatous leprosy

Early cutaneous lesions consist mainly of pale macules. Late infiltrations are present with numerous bacilli. Macular lesions are small, diffuse, and symmetric. The skin may be smooth and shiny, but skin changes do not occur in lepromatous leprosy until late in the course. Therefore, early lepromatous leprosy lesions have little or no loss of sensation, nerves are not thickened, and sweating is normal. Nerve loss is slow and progressive.

Hypoesthesia occurs first over extensor surfaces of the distal extremities, followed by weakness in the same areas.

Alopecia affects the lateral aspects of the eyebrows (madarosis), spreading to the eyelashes and then the trunk. Scalp hair remains intact.

Lepromatous infiltrations can be diffuse, can occur as nodules (called lepromas), or can be plaques. The diffuse type results in the thickened skin appearance of a leonine facies. Neuritic lesions are symmetric and slow to develop.

Eye involvement occurs, causing pain, photophobia, decreased visual acuity, glaucoma, and blindness.

Nasal infiltration can cause a saddle-nose deformity and impaired olfaction. Hoarseness ("leprous huskiness") and stridor are a result of laryngeal involvement.[24]

Oral lepromas, usually located on the hard and soft palate, uvula, tongue ("cobblestoning"), lips, and gums, can progress to necrosis and ulceration. Tissue destruction may result.[25]

Infiltration of the helix or megalobule (elongation and wrinkling of the earlobe) may occur.

Lymphadenopathy and hepatomegaly can result from organ infiltration.

Aseptic necrosis and osteomyelitis can occur with repeated trauma after joint invasion.

Brawny edema of the lower extremities is a late finding.

Unlike the other types of leprosy, lepromatous leprosy cannot convert back to the less severe borderline or tuberculoid types of disease.

Histoid leprosy

This is a recognized clinical variant of lepromatous leprosy.[26] It can occur as a result of M leprae resistance to monotherapy of MDT. Reports of de novo histoid leprosy suggest that it may also possibly evolve from borderline or indeterminate leprosy. Paucibacillary and multibacillary forms also exist. They may present as firm plaques or nodules. The lesions may occur on the thighs/buttocks, back, face, and extremities, especially bony areas like the elbows and knees. Eyebrows and nasal cartilage are usually spared.

Pure neural leprosy

This occurs in the absence of skin lesions, presenting with mononeuritis (isolated peripheral nerve involvement, including cranial nerves), mononeuritis multiplex, and polyneuritis.[27] Nerve abscesses have been reported.[28] Slit-skin smears are negative. However, cutaneous lesions may follow, which would require reclassification into one of the traditional categories listed above.[29]

Other findings

Other findings may include lepra reactions, which are complications that occur in 20-50% of patients after the start of therapy or occasionally before therapy (see Complications).

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Causes

Leprosy is caused by M leprae, an obligate intracellular, acid-fast, gram-positive bacillus.

Most persons are immune to leprosy. Subclinical disease is common in endemic areas, and the infection progresses to clinical disease in only a select few.

Biopsies of nasal and oral mucosa of individuals who remain untreated for years have demonstrated M leprae positivity,[30, 31] suggesting respiratory secretions are the main cause of infection. However, transmission is not completely understood.

Exposure to insect vectors and infected soil has also been suspected as a possible mode of transmission.

In endemic countries, household contacts of patients are at increased risk for contracting leprosy. The relative risk is 8-10 times for lepromatous leprosy and 2-4 times for tuberculoid leprosy. In nonendemic countries, household contacts rarely acquire the disease.

HIV infection is not a risk factor for acquiring leprosy, nor does it increase the clinical symptoms or virulence of leprosy. However, latent cases of leprosy infections may emerge as part of the immune reconstitution inflammatory syndrome after starting highly active antiretroviral therapy.[32, 33]

One report describes 2 cases of leprosy developing after treatment with infliximab.[34] Both patients developed type I reversal reactions after stopping the TNF-alpha inhibitor. Another patient developed a type I reversal reaction after stopping adalimumab therapy, despite no prior diagnosis of leprosy.[35]

Several cases of tattoo inoculation leprosy have been reported, most in India.[36]

Leprosy has been reported in conjunction with visceral leishmaniasis (kala-azar).

Several reports have described leprosy developing in solid organ transplant recipients (especially kidney) and after bone marrow transplantation. It is not clear about the susceptibility of patients due to general immunosuppressive conditions (as with HIV infection); however, most affected transplant recipients developed multibacillary disease.[37, 38]

The following genes have been associated with leprosy; hence, susceptibility or resistance to leprosy may be at least partially inheritable[12] :

With the first genome-wide association study (GWAS), the following loci have markers with the strongest associations:

  • HLA-DR-DQ: HLA-DR2 and HLA-DR3 (tuberculoid disease), as well as HLA-DQ1 (lepromatous leprosy); HLA-DRB1*04 is associated with resistance, and HLA-DRB1*10 is associated with susceptibility to leprosy in Brazilian and Vietnamese patients. [39] RIPK2, TNFSFIS
  • LACC1, CCDC122, and NOD2
  • Additionally, there are numerous studies looking into the role of other HLA, KIR, MICA and cytokine genes in contracting leprosy. [40]
  • Genetic variants have been found in the shared promoter region of the PARK2 (parkin) and PACRG genes expressed on monocytes.
  • Lymphotoxin-alpha (LTA) + 80 expressed on dendritic cells appears to be a risk factor for early-onset leprosy, independent of PARK2/PARCG and HLA class I and HLA-DRB1 genes. [41, 42]
  • Polymorphisms in the gene promoter regions of TNF (multibacillary leprosy) and IL-10 (-819T allele) are noted in leprosy susceptibility.
  • Mutations in TLR1 and TLR2 may be involved in susceptibility and/or resistance to other infectious diseases.
  • Polymorphisms in the NRAMP1 gene appear on macrophages in multibacillary disease in African patients.
  • TaqI polymorphism (tt genotype) at exon 9 of the vitamin D receptor gene is noted. [43]
  • IFGR1 gene promoter polymorphisms found in one family demonstrated an autosomal recessive susceptibility to leprosy. [44]
  • Genetic markers that may identify those more susceptible to T1R and T2R include polymorphisms in vitamin D receptor, IL-6, complement component C4b, TLR1 and TLR2, and natural resistance-associated macrophage protein 1 (NRAMP1). [45]
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Contributor Information and Disclosures
Author

Felisa S Lewis, MD Chief, Dermatology, Fort Belvoir Community Hospital

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

Disclosure: Nothing to disclose.

Coauthor(s)

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, American Academy of Dermatology

Disclosure: Nothing to disclose.

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, American Society for Laser Medicine and Surgery

Disclosure: Nothing to disclose.

Specialty Editor Board

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

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

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

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

Disclosure: Nothing to disclose.

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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)
 
 
 
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