Page 174 - Textbook of Pathology, 6th Edition

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SECTION I

Figure 6.30 Miliary tubercles in lung having minute central caseation necrosis.

The slit smear technique gives a reasonable quantitative Myanmar (Burma), Madagascar and Nigeria, together
measure of M. leprae when stained with Ziehl-Neelsen constitute about 80% of leprosy cases, of which India
method and examined under 100x oil objective for accounts for one-third of all registered leprosy cases globally.
determining the density of bacteria in the lesion (bacterial In India, the disease is seen more commonly in regions like
index, BI). B.I. is scored from 1+ to 6+ (range from 1 to 10 Tamil Nadu, Bihar, Pondicherry, Andhra Pradesh, Orissa,
bacilli per 100 fields to > 1000 per field) as multibacillary West Bengal and Assam. Very few cases are now seen in
leprosy while B.I. of 0+ is termed paucibacillary. Europe and the United States.
Although lepra bacilli were the first bacteria identified
for causing human disease, M. leprae remains one of the few Mode of Transmission
bacterial species which is yet to be cultured on artificial Leprosy is a slow communicable disease and the incubation
General Pathology and Basic Techniques
medium. Nine-banded armadillo, a rodent, acts as an experi- period between first exposure and appearance of signs of
mental animal model as it develops leprosy which is disease varies from 2 to 20 years (average about 3 years).
histopathologically and immunologically similar to human The infectivity may be from the following sources:
leprosy. 1. Direct contact with untreated leprosy patients who shed
numerous bacilli from damaged skin, nasal secretions,
Incidence
mucous membrane of mouth and hair follicles.
The disease is endemic in areas with hot and moist climates 2. Materno-foetal transmission across the placenta.
and in poor tropical countries. According to the WHO, 3. Transmission from milk of leprosy patient to infant.
8 countries—India, China, Nepal, Brazil, Indonesia,
Immunology of Leprosy
Like in tuberculosis, the immune response in leprosy is also
T cell-mediated delayed hypersensitivity (type IV reaction)
but the two diseases are quite dissimilar as regards immune
reactions and lesions. M. leprae do not produce any toxins
but instead the damage to tissues is immune-mediated. This
is due to following peculiar aspects in immunology of
leprosy:
1. Antigens of leprosy bacilli. Lepra bacilli have several
antigens. The bacterial cell wall contains large amount of M.
leprae-specific phenolic glycolipid (PGL-1) and another
surface antigen, lipo-arabinomannan (LAMN). These
antigens of the bacilli determine the immune reaction of host
lymphocytes and macrophages. Another unique feature of
leprosy bacilli is invasion in peripheral nerves which is due
to binding of trisaccharide of M. leprae to basal lamina of
Schwann cells.

Figure 6.31 Lepra bacilli in LL seen in Fite-Faraco stain as globi 2. Genotype of the host. Genetic composition of the host as
and cigarettes-in-a-pack appearance inside the foam macrophages. known by MHC class (or HLA type) determines which