Mycobacterium leprae by xiuliliaofz


									Vaccines: A vaccine against tuberculosis has been available since early in the twentieth
century. It is produced from bacilli Calmette-Guerin (BCG), an attenuated strain of M.bovis.
when injected intradermally, it can confer tuberculin hypersensitivity & an enhanced ability to
activate macrophages that kill pathogen.

                                       Mycobacterium leprae
Humans are the natural hosts, although the armadillo may also be a reservoir for human
infection. The optimal temperature for growth (30 ْC) is lower than body temperature; It
therefore grows preferentially in the skin & 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
Transmission: Infection is acquired by prolonged contact with patients with lepromatous
leprosy, who discharge M.leprae in large numbers in nasal secretions & from skin lesions. The
disease occurs world wide, with most cases in the tropical areas of Asia & Africa.

Pathogenesis: The organism replicates intracellularly, typically within skin histiocytes,
endothelial cells, & Schwann cells of nerve. There are two distinct forms of leprosy –
tuberculoid & lepromatous- with several intermediate forms between the two extremes (table-
      1) In tuberculoid leprosy, the cell-mediated immune response to the organism limits its
         growth, very few acid-fast bacilli are seen, granulomas containing gaint cells form, &
         the lepromin skin test result is positive. The lepromin skin test is similar to the tuberculin
         test. An extract of M.leprae is injected intradermally, & induration is observed 48hrs
         later in those in whom a cell-mediated immune response against the organism exists.
      2) In lepromatous leprosy, the cell mediated response to the organism is poor, the skin &
         mucous membrane lesions contain large numbers of organisms, foamy histocytes rather
         than granulomas are found, & the lepromin skin test result is negative.

      Clinical significance: In tuberculoid leprosy, the lesions occur as large maculae (spots) in
      coolar body tissues such as skin (especially the nose, outer ears, & testicles), & in
   superficial nerve endings. Neuritis leads to patches of anesthesia in the skin. The lesions are
   heavily infiltrated by lymphocytes & giant & epitheliod cells, but caseation does not occur.
   The patient mounts a strong cell mediated immune response & develops delayed
The course of lepromatous leprosy is slow but progressive. Large numbers of organisms are
present in the lesions & reticuloendothelial system, & immunity is severely depressed.

Table-1 Comparison of tuberculoid & lepromatous leprosy
feature                                                                   Lepromatous leprosy
                               Tubercloid leprosy

Type of lesion               Few lesion with little tissue destruction    Many lesions with tissue
No. of acid-fast bacilli     Few                                          Many
Likelihood                 of Low                                         High
transmitting leprosy

Cell mediated response Present                                            Reduced or absent
to M.leprae
Lepromin skin test           Positive                                     negative

Lab identification: M.leprae is an acid fast bacillus. It has not been successfully maintained in
artificial culture, but can be grown in the footpads of mice & in the armadillo, which may also
be a natural host although playing no role inhuman disease. Laboratory diagnosis of
lepromatous leprosy, where organisms are numerous, involves acid fast stains of specimens
from nasal mucosa or other infected area. In tuberculoid leprosy, organisms are extremely rare,
& dignosis depends on clinical findings & the histology of biopsy material.

Treatment: Several drugs are effective in the treatment of leprosy, including sulfones such as
dapsone, refampin, & clofazamine. Treatment is prolonged, & combined therapy is necessary
to ensure the suppression of resistant mutants. Treatment is given for at least 2 years or until
the lesions are free of organisms.

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