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
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.
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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