USMLE STEP 1Test Bank For Microbiology NEW UPDATE WITH QUESTIONS AND CORRECT ANSWERS With Rationales |GRADED A

USMLE STEP 1Test Bank For Microbiology NEW UPDATE WITH QUESTIONS AND CORRECT ANSWERS With Rationales |GRADED A What is a special cellular component of fungal membrane targeted in anti-fungal medication? - ANSWER- Ergosterol A major sterol What is the special component of bacterial cell wall? - ANSWER- Peptidoglycan Where are the normal flora found? Contributions to health? Causes of infection? - ANSWER- Location: - found on body surfaces contiguous with outside environment (GI, etc.) - Semipermanent (dependent on life-changes) Contributions to health: - Protective functions by maintaining a certain pH other microorganisms cannot proliferate - Nutritional: synthesizing vitamin K + B Causes of infection: - "Getting lost" (E. coli to urethra causing UTI) - Overgrowth due to immunocompromised state Are there normal flora in the blood or organs? - ANSWER- No Sterile environment What is a medically important normal flora found in the nose? - ANSWER- Staphylococcus aureus What are the pathogenicity mechanisms? (8) - ANSWER- 1. Colonization (adherence) 2. Avoiding immediate destruction by host defense sys. 3. "Hunting + Gathering" needed nutrients 4. Antigenic variation 5. Ability to survive intracellularly 6. Type III secretion systems 7. Inflammation of Immune-mediated damage 8. Physical damage What are the types of colonization? - ANSWER- 1. Adherence to cell surface - *Pili*/fimbriae: primary mechanism in most G- bacteria (E. coli) - Teichoic acids: G+ bacteria (acts as an antigenic determinant) - Adhesins - IgA proteases 2. Partial adherence - biofilms (S. epidermidis, S. mutans) (Biofilms are densely packed microorganisms forming a protective 'film' by doing so; "cops standing outside of general admission; cannot get to people within general admission area doing illegal things") What are the types of mechanism used in avoiding immediate destruction by host defense system? - ANSWER- 1. Anti-phagocytic surface components (inhibit phagocytosis): - *Capsules*/slim layers: "bar of soap slippery" kj: "Some Killers Have Pretty Nice Capsules Bro" S: Streptococcus pneumoniae K: Klebsiella penumoniae H: Haemophilus influenzae type B P: Pseudomonas aeruginosa N: Neisseria meningitidis C: Cryptococcus neoformans B: Bordetella pertussis - Streptococcus pyogenes: M protein - Neisseria gonorrhoeae: Pili - Staphylococcus aureus: A protein (binds IgG-Fc portion) "MAP" 2. IgA proteases 3. Siderophores: steal (chelate) iron What are antigenic variation mechanisms and microorganisms? - ANSWER- - Changing surface antigens to avoid immune destruction - N. gonorrhoeae: pili + outer membrane proteins - Trypanosoma brucei rhodesiense + T. b. gambiense: phase variation - Enterobacteria: capsular and flagellar antigens may or may not be expressed What are bacteria with abilities to survive intracellularly (obligate/facultative)? - ANSWER- kj: "Listen Sally Yer Friend Bruce Must Leave" (Facultative Intracellular bugs) List: Listeria Sal: Salmonella Yer: Yersinia Fr: Francisella Bruce: Brucella M: Mycobacterium tuberculosis Le: Legionella Obligate intracellular: "stay inside cells when its Really Chilly and Cold" (Can't make own ATP) R: Rickettsia C: Chlamydia C:Coxiella 1. Evading intracellular killing by professional phagocytic cells: allows intracellular growth - M. tuberculosis: inhibiting phagosome-lysosome fusion (slime layer) - Listeria: escapes phagosome into the cytoplasm before phagosome-lysosome fusion (rocket-shooting cell to cell) 2. Invasins: ability to invade non-phagocytic cells - Yersinia pseudotuberculosis (causing diarrhea) What happens when intracellular organisms escape macrophage phagocytosis? - ANSWER- Macrophages "block" in the microorganism forming *granulomas* What is the type III secretion system? - ANSWER- Ability found in many pathogens Capable of secreting toxins into host cell (macrophages) without entering it; tunnel between bacteria to host cell What are immune-mediated damage mechanisms? - ANSWER- - Cross-reaction of bacteria-induced antibodies with tissue antigens (Rheumatic fever; type II hypersensitivity) - Delayed hypersensitivity and the granulomatous response (type IV hypersensitivity) - Immune complexes (type III; poststrep acute glomerulonephritis) - Peptidoglycan-*teichoic acid of G+ cells* (chemotactic neutrophils; structural toxin released at cell death) Infection: Physical damage mechanisms? - ANSWER- Swelling from infection Large size of organism may cause blockage Ulcerations What is LPS? G- or G+? - ANSWER- Lipopolysaccharide = Endotoxin - *Gram NEGATIVE* (part of outer membrane) - Toxic portion is *lipid A* (generally released at cell death; *exception*: N. meningitidis; over produces outer membrane fragments) - LPS is heat stable; cannot be converted to toxoid What is the endotoxin mechanism? - ANSWER- - LPS activates macrophages (release TNF-