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“Miliary Tuberculosis”. They may affect any part of the body – bones, joints, lymph nodes, etc. The lesions that are formed can be either exudative (soft tubercle) or

 


6. Since HIV-1 and HIV-2 viruses are similar in genomic

structure and morphology, antibodies to them may

cross react. Reactive test bands for both HIV-1 and

HIV-2 do not necessarily imply mixed infection.

However, to reduce cross-reactivity and better

discrimination, Retroscreen-HIV uses a synthetic

peptide gp36 with highly conserved epitopes for

HIV-2 detection instead of recombinant gp36

antigen.

7. As with all diagnostic tests, a definitive clinical

diagnosis should not be based on the result of a single

test, but should only be made by the physician after all

clinical and laboratory findings have been evaluated.

8. Retroscreen-HIV should only be used as a screening

test and its results should be confirmed by other

supplemental methods before taking clinical

decisions.

TUBERCULOSIS

Mycobacterium Tuberculosis

Tuberculosis is the leading cause of death in the world from

a single infectious disease. The World Health Organization

(WHO) has declared it a global emergency. The resurgence

of the disease with Multi Drug Resistant TB (MDRTB) is a

major concern.

Microbiology

Mycobacterium is straight or curved rod shaped, nonmotile bacteria. They are obligate aerobes, growing well

in well aerated regions (lungs is the primary organ) and

intracellular in nature.

It exhibits “acid fastness” – due to the impermeability

of their cell walls to certain dyes and stains. Despite this

once stained, acid-fast bacteria will retain dyes when

heated and treated with acidified organic compounds.

One such method is the “Ziehl-Neelson stain”. Acid-fast

bacilli appear pink in a contrasting background.

They can be cultured in solid and liquid media.

Solid media: Lowenstein-Jenson, Middle Brook medium.

Liquid medium: Dubos’ medium.

674 Concise Book of Medical Laboratory Technology: Methods and Interpretations Classification

Mycobacteria can be classified as:

Tubercle bacilli – causing tuberculosis

Human – M. tuberculosis

Bovine – M. bovis

Murine – M. microti

Avian – M. avium

Cold blooded – M. marinum.

Lepra bacilli – causing leprosy

Human–M. leprae

Murine–M. leprae murium.

Mycobacteria causing skin ulcers

M. ulcerans

M. bathei.

Atypical mycobacteria

Photochromogens

Scotochromogens

Rapid growers

Saprophytic mycobacteria

M. butyricum, M. phlei, M. stercosis.

Pathogenesis

The source of infection is usually an open case of

pulmonary tuberculosis. The disease progression can be

divided into 5 stages:

Stage 1: Inhalation of droplet nuclei containing the

bacteria that are non-specifically taken up by alveolar

macrophages. They are not activated.

Stage 2: After 7–21 days of infection. The bacilli multiply in

the macrophages until it bursts.

Stag 3: Lymphocyte infiltration and macrophage activation

at the site of infection occurs. Activated lymphocytes

releases cytokines and gamma interferon. At this stage the

tuberculin skin becomes positive, indicating that the host

is developing an immune response. But this response is

also responsible for much of the immune pathology.

In this stage, the “tubercle” formation begins—They

are vascular granuloma composed of central zone of giant

cells with or without caseation and peripheral zone of

lymphocytes and fibroblasts.

Serology/Immunology 675

Stage 4: In this stage, the growing tubercle invades the

bronchus and also invades an artery or other blood

supply line. The hematogenous spread of the bacilli may

result in extrapulmonary tuberculosis, also known as

“Miliary Tuberculosis”. They may affect any part of the

body – bones, joints, lymph nodes, etc. The lesions that

are formed can be either exudative (soft tubercle) or

productive lesions (hard tubercle).

Stage 5: The tubercle liquefies, the liquid is very

conducive to the growth of bacilli and the bacteria begin

to multiply rapidly extracellularly. The large antigen

load causes the wall of bronchi to become necrotic and

rupture resulting in cavity formation. When these lesion

heals, it becomes fibrous and calcifies forming “Ghon

complex”.

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