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Mycobacteria

Mycobacteria. Ziad Elnasser, MD, Ph.D. Mycobacteria. Structurally is gram positive rod, characteristic of acid fastness. M. tuberculosis is the leading cause of infectious disease deaths in the world. M. leprae and leprosy. Atypical mycobacteria and immunecompromised conditions.

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Mycobacteria

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  1. Mycobacteria Ziad Elnasser, MD, Ph.D

  2. Mycobacteria • Structurally is gram positive rod, characteristic of acid fastness. • M. tuberculosis is the leading cause of infectious disease deaths in the world. • M. leprae and leprosy. • Atypical mycobacteria and immunecompromised conditions. • 0.2-0.4 x 2-10 μ, nonmotile, obligate aerobes, nonspore former, N-glycolyl muramic acid instead of N-acetyl muramic acid.

  3. Structure • Polysaccharides, proteins and lipids in the cell wall. • Mycolic acids are long chain fatty acids >60% of the cell wall. • Mycosides, sulfolipids, Lipoarabinomannan (LAM) analogous to LPS of g- bacteria. • Porins and others.

  4. Structure • Hydrophobic cell wall → no regular stains. • Acid fastness. • Enhanced growth with 10% CO2, PH 6.5 to 6.8). • Classification is based on phenotypic, nutritional, growth rate, pigmentation of colonies in light or dark, biochemical tests, fatty acids, rRNA and DNA sequences → Probes.

  5. Diseases • Many pathogenic species, M. tuberculosis in humans only, others in special cases. • Chronic course, granulomas no disease to follow. • No exotoxins, or endotoxins. • DTH response leads to destruction of macrophages having the organisms, CMI activates macrophages.

  6. M. tuberculosis • AFB, irregular beads, 37C, Complexed media, CO2 ehancement, 12-24 hours generation time. • Lowenstein-Jensen media, Dry rough, buff-colored colonies in 3-6 weeks. • Cording, Niacin production, hydrophobic so it is resistant. • PPD.

  7. Tuberculosis • Systemic, immune response, chronic pneumonia with fever, cough, bloody sputum and wt loss. • Chronic wasting then death (consumption) • 200-700/100,000 deaths, white plague. • Poverty, ignorance and low socioeconomic status, developed countries. • Aerosol, milk, 10 bacilli is enough, the closer the area the more infectivity. • Very low in developed countries, old age, AIDS→ reactivation. • 30 millions globally, 8 mil new cases 2-3 mil die.

  8. Pathogenesis • Primary is the initial infection. • Bacilli in alveoli, then macrophages. • Hilar LNs drainage, systemic any where. • Tubercle → multinucleated giant cells, epitheliod cells, lymphocytes, caseous necrosis in the center. • Fibrosis healing, sub apical area of lungs, organism die. • Kidneys. • Reactivation. • Virulence related to structure.

  9. Immunity • Lubeck disaster, genetic effect. • DTH and CMI in 2-6 weeks. • DTH destroys nonactivated macrophages. • CMI destroys activated macrophages. • Both T helper and T cytotoxic participates. • If CMI is impaired lots of bacilli seen with less epitheloid cells accumulation.

  10. Clinical Aspects • Primary could be asymptomatic or fever, malaise, large LNs, infiltrates in the lung, fibrosis, calcify (ghon focus), could dissaminate (milliary). • Reactivation TB: 10% recover from primary, old age, immunesuppression, malnutrition, alcoholism, DM, loss of spouse, pregnancy, AIDS. • Bloody cough, fever, malaise, fatigue, wt loss, granulomas, 2-5 years death.

  11. Diagnosis • Tuberculin: PPD, measures DTH, standardized, 5 TU. • Intradermal injection. • Interpretation. • Laboratory Dx: ZN staining, sputum, urine, • N-acetyl-cystein role and NaOH. • Media. • Automated systems. • DNA probes.

  12. Treatment • Isoniazid. Para-aminosalicylic acid • Ethambutol. Ethionamide. • Rifampin. Cycloserine. • Pyrazinamide. Fluoroquinolones. • Strepotomycin. Kanamycin, etc. • Multiple drug combination! • Multi drug resistance. • Failure of therapy?

  13. Prevention • Prophylactic antibiotics. • BCG vaccine, only in PPD negative individulas. • Contraindications to the vaccine.

  14. Mycobacteria other than Tuberculosis (MOTT) • M.kansasi, M.avium-intracellulare complex M. scrofulaceum. In lungs. • In tissue: M. fortuitum, M. marinum, M. ucerans. • No case to case transmission. • Grow more rapidly, colored colonies, dark, or light. • More resistant to antimicrobial agents.

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