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Medical Microbiology Tutorial: Bacterial Infections. Tuberculosis and Staphylococcus aureus

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|dw:1570325777851:dw| note: I'm only grouping these two together because they're both bacterial infections, and I don't have enough content to make them both separate tutorials

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\({\bf{Tuberculosis:}}\) |dw:1570326369924:dw| caused by: Mycobacterium tuberculosis transmission: airborne Brief History: - 1869: Jean Antonie Villemin demonstrates that TB is an infectious disease, showed that injecting TB-infected tissue from animals could cause TB in humans - late 1880's: Robert Koch isolates the bacteria that causes TB and develops tuberculin from TB extract (not successful at preventing TB) - 1908-1921: development of BCG vaccine by Albert Calmette and Camille Guérin. typically not used in the United States since TB is pretty rare here Latent vs Active: There are two stages, the latent and active stages. The latent stage is asymptomatic and non-contagious. Can be diagnosed w/ TB skin test and blood tests but x-ray scans appear normal. If detected, is recommended to be treated. The active stage does show symptoms and is contagious. TB skin tests, blood tests, phlegm tests are positive, plus x-ray scans appear abnormal. Symptoms: As stated before, these typically only show up in active stage. - weight loss - loss of appetite - fever - chills/night sweats Treatment: - medications such as Isoniazid, Rifampicin, Pyrazinamide, Ethambutol - open-air treatment - untreated latent TB goes on to become full-blown TB in about ~10% of cases

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\({\bf{Staphylococcus~aureus:}}\) - most common drug-resistant pathogen - MRSA: methicilin-resistant S. aureus is the most commonly known one, and of great concern to researchers and medical professionals > MRSA are resistant to beta-lactams like penicillin. MRSAs contain beta-lactamase which cleaves rings in beta-lactams, making them ineffective - causes a wide variety of diseases/ailments ranging from skin conditions like boils or impetigo, to more serious conditions like toxic shock, pneumonia, meningitis, and sepsis treatments: antibiotics such as clindamycin, minocycline, doxycycline Features: these are mostly designed to get around the host immune system and proliferate - adhesins: bind to host surface cell receptors + complement factors, can inhibit complement activation cascade, interferes w/ immune responses - leukocidins: toxins that kill host cells - immunoglobin binding proteins: bind to host immunoglobins - autolysins: break down old peptidoglycan so new peptidoglycan can be formed and bacterial growth can occur - proteases: target and cleave host immunoglobins - superantigens: activate T cells and cytokine release

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