Page 176 - Concise Pathology for Exam Preparation ( PDFDrive )

7 Infections 161

made based on colony pigmentation and morphology; however, biochemical tests are
a must for species recognition.
3. Molecular typing: M. tuberculosis is isolated and species identification is done by
molecular methods or high-pressure liquid chromatography of mycolic acids (reducing
the time required for confirmation to 2–3 weeks).
4. Tuberculin sensitivity test (TST): It is based on the principle that M. tuberculosis in a
concentrated liquid culture medium (purified protein extract or PPD) can elicit a skin
reaction when injected subcutaneously into patients with tuberculosis. A person is
given the tuberculin and asked to return within 48–72 h to have a trained health care
worker look for a reaction on the arm (swelling, induration and erythema) and measure
its size. Redness by itself is not considered part of the reaction. The lack of mycobacte-
rial species specificity, subjectivity of interpretation and batch-to-batch variations limits
the usefulness of PPD.
5. In vitro assays that measure T cell release of IFN-g in response to stimulation
with the highly tuberculosis-specific antigens ESAT-6 and CFP-10: These are com-
mercially available assays (Interferon g release assay or IGRA). IGRAs are more specific
than the TST as a result of less cross-reactivity due to BCG vaccination and sensitization
by non-tuberculous mycobacteria. IGRAs also appear to be at least as sensitive as the
TST for active tuberculosis.

Leprosy

• Also called Hansen disease, leprosy is a chronic infectious disease caused by Mycobac-
terium leprae, a weakly acid fast intracellular bacillus.
• Transmission occurs by close and prolonged contact with an infected individual or
through nasal droplets.
• The incubation period of leprosy can vary from 2 to 10 years.
• It can be experimentally introduced in animals like armadillo and chimpanzee.
• It is possible to grow the bacterium in the laboratory by injection into footpads of mice,
however, it does not grow on artificial media or in cell culture.

Pathogenesis
• Genetic factors are thought to play a role in the pathogenesis of leprosy (based on the
observation of clustering of leprosy in certain families).
• Malnutrition and prolonged close contact with the infected person facilitates the devel-
opment of the disease.
Classification
• Ridley and Jopling classified leprosy into six categories: indeterminate leprosy, tuber-
culoid leprosy, borderline tuberculoid leprosy, mid-borderline leprosy, borderline lepro-
matous leprosy and lepromatous leprosy.
• World Health Organization (WHO) has replaced the older, more complicated classifica-
tion system with a simpler system that identifies two main types of leprosy—paucibacillary
and multibacillary. Paucibacillary leprosy is defined as five or fewer skin lesions with the
absence of bacilli in skin smears, and multibacillary leprosy is defined as six or more skin
lesions and positive skin smears (Table 7.3).
• Paucibacillary leprosy (Fig. 7.3) includes indeterminate, tuberculoid and borderline tuber-
culoid leprosy. It typically presents with one or more hypopigmented skin macules, which
show sensory loss (due to peripheral nerve damage caused by the host immune cells).
• Multibacillary leprosy (Fig. 7.4) includes mid-borderline, borderline lepromatous and
lepromatous leprosy. It presents with symmetric skin lesions, nodules, plaques and
frequent involvement of nasal mucosa. However, detectable nerve damage is a late
occurrence.
• Borderline leprosy is a lesion of intermediate severity between pauci and multibacillary
leprosy, and is the most common form. Skin lesions resemble tuberculoid leprosy, but
are larger, more numerous and irregular; peripheral nerve involvement with loss of
sensation is common. This type is unstable and may convert into lepromatous leprosy
or may undergo a reversal reaction.

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