Practice Essentials
Leprosy was described almost 3000 years ago and is still associated with stigma. The causative pathogen, Mycobacterium leprae, was first described in 1873, when Gerhard Armauer Henrik Hansen discovered it while examining lymph nodes and other tissues obtained from patients with leprosy. Significant progress was made during the 20th century in the treatment and eradication of this disease, and the World Health Organization (WHO) estimates that the worldwide prevalence has decreased from more than 5 million cases in the 1980s to less than 140,000 cases in 2021. [1]
Signs and symptoms
Neuromuscular symptoms associated with this disease are occasionally the first to be observed. Patients may also present with a history of chronic nasal discharge, which is frequently observed in individuals with lepromatous leprosy who have upper airway compromise. The hallmark clinical findings in leprosy are hypopigmented skin lesions with loss of sensation. These lesions are observed more frequently in the cooler areas of the body, such as the nose and earlobes. (See Presentation for more detail.)
Management
Prolonged therapeutic regimens have traditionally been recommended in the treatment of leprosy; however, more recent recommendations focus on regimens with shorter duration. The drugs that are more frequently used in the treatment of leprosy include rifampin, dapsone, clofazimine, ofloxacin, minocycline, and clarithromycin. Reconstructive surgery may be indicated in patients with soft tissue defects, particularly for plantar ulcerations in patients with leprosy. (See Treatment for more detail.)
Go to Leprosy for more information.
Pathophysiology and Etiology
Leprosy is a chronic granulomatous disease caused by infection with M leprae. The exact mechanism of M leprae transmission remains unknown; however, direct human-to-human contact, contact with respiratory secretions from infected individuals, and vertical transmission have been considered the most likely routes of transmission.
In North America and South America, the nine-banded armadillo is a zoonotic reservoir for M leprae. In the United Kingdom, Mycobacterium lepromatosis has been detected in red squirrels. [2]
Most pathophysiologic changes observed in leprosy are caused by the ability of M leprae to survive in macrophage cells. Although the incubation period of M leprae can be several decades, it generally averages 5-7 years. [3]
Epidemiology
United States statistics
Most observed infections are acquired abroad. In California, cases of leprosy have been reported in persons who have emigrated from Mexico and Southeast Asia. Leprosy is also occasionally reported in Texas and Louisiana. In 2002, 133 cases of leprosy were reported in the United States. In 2006, approximately 6,500 persons with leprosy were living in the United States. [4]
International statistics
The WHO has estimated the global prevalence of leprosy to be 10-12 million cases, with most reported in Africa and Asia, particularly in the Indian subcontinent. The worldwide incidence rate is 2 cases per 10,000 population. In some areas, as many as 10% of cases develop in children younger than 15 years, among whom paucibacillary (PB) forms are more frequent. [5]
Age-, sex-, and race-related demographics
Although leprosy is rarely reported in infancy, it can affect all ages. In areas of high prevalence, leprosy among children represents 7-10% of new cases. [5, 6, 7, 8, 9] The male-to-female ratio is 2:1 to 3:1. Leprosy has no known racial predilection. Rather than race, lower socioeconomic status has traditionally been considered a risk factor for leprosy in endemic areas.
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Infiltration of ear lobes in patient with lepromatous leprosy.
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Man with advanced deformities caused by unmanaged leprosy: keratitis, loss of eyebrow, thickened skin, and typical hand impairments. Ho Chi Minh City, Vietnam. Image courtesy of D. Scott Smith, MD.
