Mycobacterium leprae Important Properties




Дата канвертавання24.04.2016
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Mycobacterium leprae

Important Properties

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. Humans are the natural hosts, although the armadillo appears to be a reservoir for human infection in the Mississippi delta region where these animals are common.

The optimal temperature for growth (30°C) is lower than body temperature; it therefore grows preferentially in the skin and superficial nerves. It grows very slowly, with a doubling time of 14 days. This makes it the slowest-growing human bacterial pathogen. One consequence of this is that antibiotic therapy must be continued for a long time, usually several years.

Disease:This organism causes leprosy (Hansen's disease).



Transmission

Infection is acquired by prolonged contact with patients with lepromatous leprosy, who discharge M. leprae in large numbers in nasal secretions and from skin lesions.



Pathogenesis

The organism replicates intracellularly, typically within skin histiocytes, endothelial cells, and the Schwann cells of nerves. The nerve damage in leprosy is the result of two processes: damage caused by direct contact with the bacterium and damage caused by CMI attack on the nerves.

There are two distinct forms of leprosy—tuberculoid and lepromatous—with several intermediate forms between the two extremes .


  1. In tuberculoid leprosy, the CMI (cell mediated immunity)response to the organism limits its growth, very few acid-fast bacilli are seen, and granulomas containing giant cells formThe lepromin skin test result is positive. The lepromin skin test is similar to the tuberculin test .

  2. In 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.

Clinical Findings

The incubation period averages several years, and the onset of the disease is gradual. In tuberculoid leprosy, hypopigmented macular or plaque-like skin lesions, thickened superficial nerves, and significant anesthesia of the skin lesions occur. In lepromatous leprosy, multiple nodular skin lesions occur, resulting in the typical leonine (lion-like) facies. After the onset of therapy, patients with lepromatous leprosy often develop erythema nodosum leprosum (ENL), which is interpreted as a sign that cell-mediated immunity is being restored. ENL is characterized by painful nodules, especially along the extensor surfaces of the tibia and ulna, neuritis, and uveitis.

The disfiguring appearance of the disease results from several factors: (1) the skin anesthesia results in burns and other traumas, which often become infected; (2) resorption of bone leads to loss of features such as the nose and fingertips; and (3) infiltration of the skin and nerves leads to thickening and folding of the skin.

Laboratory Diagnosis

In lepromatous leprosy, the bacilli are easily demonstrated by performing an acid-fast stain of skin lesions or nasal scrapings. Lipid-laden macrophages called "foam cells" containing many acid-fast bacilli are seen in the skin. In the tuberculoid form, very few organisms are seen and the appearance of typical granulomas is sufficient for diagnosis.



Treatment

The mainstay of therapy is dapsone (diaminodiphenylsulfone), but because sufficient 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. Thalidomide is the treatment of choice for severe ENL reactions.



Prevention

Isolation of all lepromatous patients, coupled with chemoprophylaxis with dapsone for exposed children, is required. There is no vaccine.


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