Tuesday, May 15, 2012

Introduction, transmission, pathogenesis and lab diagnosis of Leprosy (Hansen’s disease)



Also known as Hansen’s disease, leprosy is a chronic infectious disease caused by acid fast bacillus, Mycobacterium leprae. In 1873, Dr. Hansen discovered bacteria in leprosy lesions, which rule out that leprosy is a hereditary disease or a punishment from the gods.
 Leprosy
1.       Mainly affects: Skin, Peripheral nerves and mucosa of upper respiratory tract (because their optimal temperature for growth is 30OC).
2.       May affect: Any organs.
Some points to remember:
1.       Leprosy is not highly infectious /very contagious
Infection is acquired by prolonged contact with patients with lepromatous leprosy (heavy shedders) who discharge M. leprae in large numbers in nasal secretions and from skin lesions.


2.       Route of Transmission: Skin and inhalation
3.       M. leprae multiplies very slowly (with a doubling time of 14 days; slowest growing human bacterial pathogen)
Consequence: antibiotic therapy must be continued for a long time, usually several years.
4.       Incubation period of the disease is about five years. Symptoms can take as long as 20 years to appear.
5.       Leprosy is curable

Pathogenesis:
M. leprae replicates intracellularly, typically within skin histiocytes, endothelial cells, and the Schwann cells of nerves. The cell mediated immunity plays the major part in determining the response of the host to the infection.
There are two distinct forms of leprosy-tuberculoid and lepromatous with several intermediate forms between the two extremes.
1.       Tuberculoid leprosy: very few acid fast bacilli in skin smear (Paucibacillary disease) : Cell mediated immune (CMI) response  is adequate and lepromin test is positive.
2.       Lepromatous leprosy: large numbers of Mycobacterium leprae chiefly in masses within the lepra cells, often grouped together like bundles of cigars or arranged in a palisade (Multibacillary disease)  .The cell mediated immune  (CMI) response to organism is poor  and the lepromin test is negative.
Ridley and Jopling (1966) have introduced a scale for classifying the spectrum of leprosy into five groups-

1.       Tuberculoid (TT)
2.       Borderline tuberculoid (BT)
3.       Borderline (BB)
4.       Borderline Lepromatous (BL)
5.       Lepromatous (LL)
According to WHO, leprosy is divided into two groups, paucibacillary and multibacillary.
Comparison of tuberculoid and  lepromatous leprosy
Feature
Tuberculoid leprosy
Lepromatous leprosy
Type of lesion
One or few lesions with little tissue destruction
Many lesions with marked tissue destruction
Number of acid fast bacilli
Few
Many
Likelihood of transmission of leprosy
Low
 High
Cell Mediated response to M. Leprae
Present
Reduced or latent
Lepromin skin test
Positive
Negative

Lepromin Skin Test: The lepromin skin test is not used to diagnose leprosy but to determine what type of leprosy a person has. Lepromin skin test is similar to tuberculin test.  An extract of M.leprae is injected intradermally and induration is observed 48 hours later in those whom a cell-mediated immune response against organism exist.
Lepromin test is employed mostly for the following two purposes.
1.       To classify the lesions of leprosy patients.
2.       To assess the prognosis and response to treatment.

Lab diagnosis  of Leprosy
a.       Microscopy (Slit-skin smear stained with modified Ziehl Neelsen stain: 4 to 5% Sulphuric acid as decolourising agent)
·         Sample: Skin lesions or nasal scrapings or specimen from ear lobules.
·         Test to perform: Acid fast stain
i.                    For Lepromatous leprosy: lipid laden macrophages called ‘foam cells” containing many acid fast bacilli are seen in the skin.
ii.                   For Tuberculoid leprosy: Very few acid fast bacilli are seen and appearance of typical granulomas is sufficient for diagnosis 

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