LUNGS - Tuberculosis
Tuberculosis is a chronic communicable disease, caused by Mycobacterium tuberculosis (M. tuberculosis) .
It causes a necrotizing (caseating) granulomatous tissue reaction.
Mycobacterium tuberculosis infects about one-third of the world’s population and kills about three million patients each year.
Tuberculosis has been increasing in USA, Europe and especially in Africa.
Debilitating or immunosuppressive condition (Example: diabetes, alcoholism, malnutrition, chronic lung disease, acquired immune deficiency syndrome) may predispose to infection.
Two species of this organism causing tuberculosis are Mycobacterium tuberculosis and Mycobacterium bovis.
These are transmitted by inhalation of infective droplets produced by coughing, sneezing, and talking by a patient with “open” (cavitary) tuberculosis.
Pulmonary Tuberculosis is classically divided into two:
1.Primary tuberculosis (previously uninfected person).
2. Secondary or reinfection.
Primary pulmonary tuberculosis:
Primary pulmonary tuberculosis is an infection of persons who have not previous contact with tubercle bacillus.
Inhaled bacilli are commonly deposited in alveoli immediately beneath the pleura, usually on the lower part of the upper lobes or the upper part of the lower lobes.
It produces a single, small (about 1 cm), granuloma known as a Ghone focus.
The spread to draining ipsilateral bronchial or hilar lymph nodes results.
This combination of lung and lymph node lesions is called the Ghon complex.
In over 90% of adults, the infection is self-limited, because the cellular immune response is sufficient to control the multiplication of the bacilli and results in local fibrous scarring and calcification.
Most of the organisms die but a few remain viable for years.
Later, if immune mechanisms wane or fail, the resting bacilli may break out and cause serious tuberculous infection.
Progressive primary tuberculosis is rare, in which immune response fails to control multiplication of the tubercle bacilli.
Progressive primary tuberculosis is common in children under 5 years of age, but less common in normal adults (10%).
The primary Ghon’s focus in the lung and the caseous hilar lymph nodes enlarge rapidly, erodes the bronchial tree, and discharge bacilli producing primary tuberculous pneumonia.
Clinically, these cases show abrupt high fever, pleurisy with effusion and lymphadenitis.
If the tubercle bacilli gain access to the blood stream, disseminated military tuberculosis may occur.
Secondary pulmonary tuberculosis:
This is an infection in a person who has previous contact with tubercle bacillus. This person has already developed hypersensitivity and immunity against infection.
The development of cell-mediated, or type IV, hypersensitivity to the tubercle bacillus explains the organism’s destructiveness in tissues and also the emergence of resistance of the person to the organisms.
Delayed hypersensitivity (type IV) to the tubercle bacillus develops in 2 to 3 weeks after primary infection.
A sensitized individual shows increased induration (more than 5 mm) at the site of intradermal injection of purified protein derivative of Mycobacterium tuberculosis (PPD test).
A positive test result indicates sensitivity, but not active disease.
Once sensitization appears during infection, the tissue response becomes granulomatous (abundant epithelioid and histiocytes, occasional giant cells, and peripheral mononuclear cells).
There is often central, caseous necrosis of the granulomas.
The person also develops increased resistance to tuberculosis (ability to inhibit intracellular replication of bacilli).
Most of the secondary infections are due to reactivation of dormant bacilli in the primary lesions.
Occasionally, it is caused by re-infection with exogenous tubercle bacilli.
Secondary tuberculosis is generally found in the apices of the lungs, where oxygen tension is high and M. tuberculosis grows in high oxygen.
These lesions may progress to:
1. Cavitary fibrocaseous tuberculosis,
2. Tuberculous bronchopneumonia, or
3. Miliary tuberculosis.
Cavitary fibrocaseous tuberculosis:
Tuberculous cavity is formed in the lung due to the drainage of the caseous material through the bronchial tree.
Cavities are mostly localized in the apex and lined by yellowish-gray caseous material.
Blood vessels traversing the cavity show endarteritis with thrombosis.
The cavity is surrounded by fibrous tissue.
Pleura overlying the cavity show fibrinous pleurisy, often with serous effusion.
This type of tuberculous infection is seen in a hypersensitive individual.
The bacteria may spread rapidly throughout a large area of lung parenchyma producing diffuse bronchopneumonia.
Pulmonary exudates contain numerous bacilli.
Miliary tuberculosis :
This is the disseminated form of tuberculosis due to the spread of bacilli through lymphatics and blood vessels to produce minute, yellow-white lesions resembling millet seeds (hence “miliary”).
Common sites of miliary lesions are the lung, lymph nodes, kidneys, adrenals, bone marrow, spleen, liver, meninges, brain, eye-grounds, and genitalia.
Miliary tubercles are rarely seen in the pancreas, thyroid, striated muscles or heart.
All miliary lesions have the similar features and follow the same progression, namely focal collections of histiocytes, followed by epithelioid cells, Langhans giant cells, central caseation and eventual fibrosis and calcification.
Primary tuberculosis is usually asymptomatic.
The secondary form more often causes low-grade fever, night sweats, weight loss, productive cough with blood-streaked sputum, or hemoptysis.
Pleural involvement leads to pain chest and pleural effusion.
Diagnosis relies on culture of the organism or demonstration of acid-fast bacilli in sputum or biopsy tissue.
Prognosis depends on the extent of disease, the underlying health of the individual, and other variables.
Chemotherapy is effective, except neglected cases and those caused by highly drug-resistant tubercle bacilli.
Hematogenous spread of tubercle bacilli may produce:
1. Miliary tuberculosis with numerous minute foci of infection in many organs, particularly liver, bone marrow, spleen, and kidneys.
2. Isolated organ tuberculosis when disseminated organisms become established in only one or two organs, most often adrenals, kidneys, bone (tuberculous osteomyelitis), or female genital tract (salpingitis, endometritis).
Pulmonary tuberculosis due to atypical mycobacteria:
These atypical mycobacteria are acid-fast and morphologically resemble M. tuberculosis.
The best known are M. kansasii and M. intracellulare.
They differ from M. tuberculosis as follows:
1. Their growth rates and growth requirement is different.
2. They are not obligatory intracellular parasites and exist in the environment.
3. Primary infection is usually not recognized.
4. The reinfection is more indolent.
5. The organism is less sensitive to antituberculosis drugs.
6. The organisms are not transmitted from person to person.
7. Infection occurs due to impairment of host defense mechanisms.
8. They are less pathogenic than M. tuberculosis.