The Mycobacteria CLS 261 PDF

The Mycobacteria CLS 261 General characteristics Bacilli – branched or filamentous Non-motile Non-spore-forming High lipid content in CW (mycolic acid) General characteristics Aerobic Very slow growing (2-3 d to 2-6 wks), 20-40C Require complex media, increased CO2 Saprophytes an...

The Mycobacteria CLS 261 General characteristics Bacilli – branched or filamentous Non-motile Non-spore-forming High lipid content in CW (mycolic acid) General characteristics Aerobic Very slow growing (2-3 d to 2-6 wks), 20-40C Require complex media, increased CO2 Saprophytes and parasites Mycobacterium tuberculosis Characteristics Obligate aerobe Short rods to filaments – appearance depends on growth medium Slow-growing – 3-6 weeks Buff-colored, rough, raised, wrinkled colonies Mycobacterium tuberculosis Virulence factors Cord factor = surface toxic glycolipid Responsible for serpentine growth Toxic - inhibitory to phagocytic cells Antigenic Clinical Infection - Tuberculosis Oldest communicable disease Identified by Dr. Robert Koch  Koch’s postulates Estimated one-third of world population infected (~ 2 billion!!) Clinical Infection - Tuberculosis Major global public health problem ~8 million new cases each year 1.13 million deaths Second leading cause of death due to a M/O (COVID #1) in 2022 Multi-drug resistance, AIDS, social factors, IV drug abuse, immigration Clinical Infection - Tuberculosis Transmitted by droplet infection Infection depends on: Cellular immunity Amount of exposure Virulence of organism Clinical Infection - Tuberculosis Viable in sputum droplets for up to 6 weeks Inhaled droplets enter respiratory tract  alveoli Clinical Infection - Tuberculosis In most infections: Alveolar macrophages phagocytize M/O 4-6 weeks for cellular immunity (T cells) to peak Regression and healing of lesions (granuloma/tubercles) A granuloma is an area of tightly clustered immune cells, or inflammation, in your body. They form around an infection or foreign object in your body. They can form almost anywhere, but they’re most often found in your lungs. Some tissue damage if antigen load is high Clinical Infection - Tuberculosis In immunocompromised patients: Immune system may not be able to overcome Liquefaction and cavity formation Bronchial irritation  coughing  spread of M/Os Clinical Infection - Tuberculosis May become bloodborne  disseminate to other organs Possible to have active and healing lesions at same time Potential for reactivation of disease Fever, SOB, night sweats, chills, fatigue, anorexia, weight loss, productive sputum, hemoptysis, lung cavities Tuberculosis Clinical Infection - Tuberculosis Diagnosis Observation of acid-fast bacilli recovered from sputum cultures Culture on egg-based medium Positive PPD test Injection of attenuated tubercle bacilli Look for redness and induration within 48h Does not distinguish between active case and previous exposure Mantoux test Injection of purified protein derivative (PPD) from M. tuberculosis cultures Lesion ≥10mm within 48-72 hours of injection indicates current or prior infection Two Step TST BCG vaccine Vaccination prepared with live, attenuated bovine Mycobacterium strain (bacillus Calmette-Guérin) Must be PPD-negative The vaccine is 70 to 80% effective against the most severe forms of TB, such as TB meningitis in children. It's less effective in preventing respiratory disease, which is the more common form of TB in adults. Most sources average 60% protective.  Clinical Infection - Tuberculosis Treatment Isoniazid Kills intracellular and extracellular M/Os Low toxicity, low cost, oral administration Rifampin Second line drugs – kanamycin, amikacin, etc M/O resistance and patient non-compliance implicated in failed treatment TB Treatment The preferred regimen for treating adults with TB remains a regimen consisting of an intensive phase of 2 months of isoniazid (INH), rifampin (RIF), pyrazinamide (PZA), and ethambutol (EMB) followed by a continuation phase of 4 months of INH and RIF. Antibiotic resistant organisms much more difficult to treat Mycobacterium leprae Clinical infection – leprosy Affects skin, mucous membranes, peripheral nerves Humans are the only known hosts Rare in U.S. and other western countries Reported cases usually from areas with warm climate Mycobacterium leprae Photomicrograph of M. leprae taken from a skin lesion Clinical Infection - Leprosy Two forms: Tuberculoid (skin and nerve)  Few M/O in tissue  High CM immune response  Anesthesia and parathesia  Extremity damage Leprosy Lepromatous (skin and nerve) Many M/O in lesions and blood Depressed or absent CM immune response Mucosal areas most commonly affected Disfigurement Leprosy Most patients exhibit manifestations of both categories Death due to secondary bacterial infections or amyloidosis Clinical Infection - Leprosy Diagnosis Look for acid-fast bacilli in skin lesions (indistinguishable from M. Tuberculosis) M. leprae cannot be cultured Treatment Dapsone Immunotherapy  MOTT (mycobacteria other than tuberculosis) Environmental bacteria and opportunists M. avium, M. intracellulare, M. kansasii, M. marinum, M. fortuitum Clinical infection Usually seen in older patients with underlying respiratory conditions Don’t react to PPD Close contacts are PPD-negative Most common systemic opportunistic bacterial infection in immunocompromised MOTT Diagnosis M/O demonstrated in blood, tissue, lymph nodes, bone marrow, liver Treatment Multi-drug therapy required