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Identification In 1882, Robert Koch isolated the causative agent of Tuberculosis, Mycobacterium tuberculosis. Globally, Tuberculosis claims the lives of an estimated 3 million lives. However, approximately 90% of those exposed to M. tuberculosis never become ill, due in part to vast variability in the bacterium. The most dangerous form of TB is caused by MDR TB (Multi-Drug Resistant Tuberculosis).
Pathogenesis There are two kinds of human tuberculosis infections, primary and post-primary. Primary occurs when dust particles containing viable bacteria are ingested and settle in the lungs. In healthy individuals, macrophages tend to keep populations in check. In individuals with compromised immune systems, the bacteria are not effectively controlled. Acute pulmonary infection ensues followed by massive destruction of lung tissue and migration to other parts of the body. A diagnostic test, known as
the tuberculin test, is used to measure hypersensitivity. Tuberculin,
a protein extracted from M. tuberculosis, is injected into an individual.
If the area elicits a localized immune reaction within 1-3 days, the results
are considered tuberculin-positive. Induration (hardening) and edema indicates
that the person has been exposed to the organism and developed antibodies,
but may not necessarily have the disease. For most individuals, immune
protection gained from previous exposure is lifelong. Manifestations Severe coughing fits, during which blood my be present, is the classic sign of the disease. Individuals also experience weight loss, lack of appetite, lethargy, and fever. It is important to note that a person infected with TB may feel healthy, but have a persistent cough. Treatment The disease may be spread by infected individuals simply by coughing or speaking. Chemotherapy of tuberculosis has been successful along with administration of streptomycin. Real success came with the discovery of isonicotinic acid hydrazide (INH), a nicotinamide derivative specifically targeted for mycobacteria. Though the mode of action is not completely understood, it is thought to inhibit the synthesis of mycolic acid, a complex lipid that interacts with the peptidoglycan of the mycobacterial cell wall. As little as 5 pmol results in complete inhibition of mycolic acid synthesis and thus, loss of outer integrity and cell death. Mycobacterial resistance to INH is increasing at a phenomenal rate, particularly among AIDS patients. Typically, treatment lasts 12 months and patients must take daily doses throughout this time. Failure to follow the regimen may result in re-infection and increased bacterial tolerance to INH. Due to the prevalence of MDR-TB in many rest homes and hospitals, a cocktail approach to treatment is used, by administering several antibiotics. Prevention Certain individuals are predisposed to infection based on overcrowding, hormonal imbalances, aging, and malnutrition. Currently, state and federal agencies in the United States are experimenting with programs designed to help people remember to take their medication while being treated for tuberculosis. MDR-TB arose primarily due to irresponsible actions by people on antibiotics. Patients did not follow antibiotic treatment guidelines, thus weaker cells were killed while the strongest survived. These surviving cells evolved resistance to many antibiotics making MDR-TD very dangerous and difficult to treat. |
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