Mycobacterium leprae causes the disease leprosy. It grows preferentially in cooler areas of the body like the skin and nerves. Leprosy occurs worldwide in tropical areas and is transmitted through prolonged contact with infected individuals. There are two main forms of leprosy - tuberculoid leprosy where the immune system can control the infection and lepromatous leprosy where the immune response is very poor. Treatment involves multidrug therapy with dapsone, rifampin and clofazimine for several years. Prevention requires isolation of patients and chemoprophylaxis for exposed individuals as there is currently no vaccine.
Mycobacterium leprae causes the disease leprosy. It grows preferentially in cooler areas of the body like the skin and nerves. Leprosy occurs worldwide in tropical areas and is transmitted through prolonged contact with infected individuals. There are two main forms of leprosy - tuberculoid leprosy where the immune system can control the infection and lepromatous leprosy where the immune response is very poor. Treatment involves multidrug therapy with dapsone, rifampin and clofazimine for several years. Prevention requires isolation of patients and chemoprophylaxis for exposed individuals as there is currently no vaccine.
Mycobacterium leprae causes the disease leprosy. It grows preferentially in cooler areas of the body like the skin and nerves. Leprosy occurs worldwide in tropical areas and is transmitted through prolonged contact with infected individuals. There are two main forms of leprosy - tuberculoid leprosy where the immune system can control the infection and lepromatous leprosy where the immune response is very poor. Treatment involves multidrug therapy with dapsone, rifampin and clofazimine for several years. Prevention requires isolation of patients and chemoprophylaxis for exposed individuals as there is currently no vaccine.
Mycobacterium leprae causes the disease leprosy. It grows preferentially in cooler areas of the body like the skin and nerves. Leprosy occurs worldwide in tropical areas and is transmitted through prolonged contact with infected individuals. There are two main forms of leprosy - tuberculoid leprosy where the immune system can control the infection and lepromatous leprosy where the immune response is very poor. Treatment involves multidrug therapy with dapsone, rifampin and clofazimine for several years. Prevention requires isolation of patients and chemoprophylaxis for exposed individuals as there is currently no vaccine.
Download as PPTX, PDF, TXT or read online from Scribd
Download as pptx, pdf, or txt
You are on page 1of 26
Leprosy
Mycobacterium leprae is the organism
causes leprosy. M. leprae has not been grown in the laboratory, either on artificial media or in cell culture. It can be grown in the mouse footpad or in the armadillo. Armadillo Humans are the natural hosts, although the armadillo may also be a reservoir for human infection. The optimal temperature for growth is 30°C lower than body temperature; it is therefore grows preferentially in the skin and superficial nerves. It is the slowest-growing human bacterial pathogen. Transmission: Infection is acquired by prolonged contact with patients with leprosy, who discharge M. leprae in large numbers in nasal secretions and from skin lesions. The disease occurs worldwide, with most cases in the tropical areas of Asia and Africa. Pathogenesis:
The organism replicates intracellularly,
typically within skin histiocytes, endothelial cells, and the Schwann cells of nerves. There are two distinct forms: 1.tuberculoid leprosy 2.lepromatous leprosy There is several intermediate forms between the two extremes. Tuberculoid leprosy: The cell-mediated immune (CMI) response to the organism limits its growth, very few acid- fast bacilli are seen, and granulomas containing giant cells form. The CMI response consists primarily of CD4- positive cells and a Th-1 profile of cytokines, namely, -interferon, interleukin-2, and interleukin-12. It is the CMI response that causes the nerve damage seen in tuberculoid leprosy. The lepromin skin test result is positive. An extract of M. leprae is injected intradermally, and induration is observed 48 hours later in those in whom a cell-mediated immune response against the organism exists. Lepromatous leprosy: The cell-mediated response to the organism is poor, the skin and mucous membrane lesions contain large numbers of organisms, foamy histiocytes rather than granulomas are found, and the lepromin skin test result is negative. Note that in lepromatous leprosy, only the cell-mediated response to M. leprae is defective. The cell-mediated response to other organisms is unaffected, and the humoral response to M. leprae is intact. However, these antibodies are not protective. Clinical Findings: 1.The incubation period averages several years, and the onset of the disease is gradual. 2.In tuberculoid leprosy: Hypopigmented macular or plaque-like skin lesions, thickened superficial nerves, and significant anesthesia of the skin lesions occur. 3.In lepromatous leprosy: Multiple nodular skin lesions occur, resulting in the typical leonine (lionlike) facies. Leonine facies After the onset of therapy, patients with lepromatous leprosy often develop erythema nodosum leprosum (ENL). ENL is characterized by painful nodules, especially along the extensor surfaces of the tibia and ulna. Erythema nodosum leprosum The disfiguring appearance of the disease results from several factors: (1) The skin anesthesia results in traumas, which often become infected. (2) Resorption of bone leads to loss of features such as the nose and fingertips. (3) Infiltration of the skin and nerves leads to thickening and folding of the skin. Patients with forms of the disease intermediate between tuberculoid and lepromatous can progress to either extreme. Laboratory Diagnosis:
1.In lepromatous leprosy:
The bacilli are easily demonstrated by performing an acid-fast stain of skin lesions or nasal scrapings. 2.In the tuberculoid form: Very few organisms are seen and the appearance of typical granulomas is sufficient for diagnosis. 3.Cultures are negative because the organism does not grow on artificial media. 4.No serologic tests are useful. Treatment: The therapy used is dapsone (diaminodiphenylsulfone).
Because resistance to the drug has emerged,
combination therapy is now recommended, e.g., dapsone, rifampin, and clofazimine for lepromatous leprosy and dapsone and rifampin for the tuberculoid form. Treatment is given for at least 2 years or until the lesions are free of organisms. Prevention:
Isolation of all lepromatous patients, coupled
with chemoprophylaxis with dapsone for exposed children, is required. There is no vaccine.