Leprosy Clinical Presentation

Updated: Aug 24, 2018
  • Author: Darvin Scott Smith, MD, MSc, DTM&H; Chief Editor: Michael Stuart Bronze, MD  more...
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Presentation

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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