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Final

MCRO 423 Final: Final Study Guide

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Department
Microbiology
Course Code
MCRO 423
Professor
Winstead

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Description
Pyogenic Cocci I: Staphylococcus & Micrococcus Staphylococcus: Gram (+), Catalase (+), skin/mucous membranes, endogenous infections. - Lab Diagnostic • MSA (Mannitol Salt Agar): high salt inhibits most but staph. Fermentation of Mannitol turns it pinkyellow • TG agar: Tellurite reduction forms shiny black colonies • Coagulase: Formation of clots • Agglutination Test (Staphytex): Antigens on latex beads clump if S. aureus is present. - Staph Species: S. aureus, S. epidermidis, S. saprophyticus, S. lugdunensis. S. haemolyticus Staphylococcus aureus • Toxins Cytotoxins: Destroys cells Surface Adhesin Virulence Factor Exfoliating Toxin (ETA & ETB): serine proteases, causes skin to slough off, staphylococcal scalded skin syndrome (SSSS). Enterotoxins: Food poisoning Toxic Shock Syndrome (Toxin-1) Staphylococcal Exoenzymesd • Staphylococcal Disease: Cutaneous infections: Impetigo (pus pockets on face), Folliculitis (Inflam. of hair follicle), Carbuncle (localized boil goes deeper into tissue) Systemic Infections: Pneumonia, meningitis, osteomyelitis, septic arthritis, acute endocarditis. Staphylococcus epidermidis: Frequent contaminant of blood cultures nd Staphylococcus saprophyticus: 2 leading cause of UTI’s. Distinguishing: Resistance to novobiocin Staphylococcus lugdunensis: Most common cause of valve endocarditis in native hearts - Clinical ID of Staph Coagulase Mannitol Trehalose PO4-ase Novobiocin S. aureus + A A + Sens S. epi - - - + Sens S. sap - A A - resist - Treatment of S. aureus: less than 10% are susceptible to penicillin. MecA gene: codes for PBP. Normal penicillin binding protein is targeted by antibiotics but this one has a much lower affinity. Pyogenic Cocci II: Streptococcus and Enterococcus Streptococcus: Gram (+), Catalase (-), Oxidase (-), non-motile, (-) for nitrate reduction, Microaerophiles and fac anaerobe - Rebecca Lancefield (1895-1981): antibodies vs. strep. A-W - Group A: Streptococcus Pyogenes Small clearish colonies, Beta-hemolytic. Sensitive to bacitracin. DISTINGUISHING: hemolysis, PYR (+), NO VACCINE • Immune Evasion: 1. Prevent Phagocytosis Capsule- hyaluronic acid looks like host HA. M-protein- Dimer that sticks out. Used for adherence/stopping phag/Ag- variability. All strains have it. Prevents C3b binding 2. Avoid Complement M-protein- stops C3b binding, preventing MAC attack 3. Ag-Variability M-protein: different for different strains. This is how you can get strep over and over. • Adherence/Invasion of S. Pyogenes 1. Adherence M-protein F-protein- Bind fibronectin (especially in respiratory epithelium) Capsule- sticking to cells 2. Invasion F-protein- get past epithelial barrier • Toxins Produced by S. pyogenes 1. Streptococcal pyogenic exotoxins Spe A, B, C, F All Super Ag- pathological amplification of normal T-cell responses Heat labile and cause Scarlet fever, rash, necro fasciitis, and TSSS in systemic 2. Streptolysin S Cause Beta-hemolytic lysis RBC & WBC. Kills phagocytes by causing them to release its toxins. We have no immune response to this guy 3. Streptolysin O We make Abs (antibodies) against this guy: ASO- anti-streptolysin O Distinguish longer term Strep glomerular nephritis, rheumatic fever 4. Streptokinase, hyaluronidase: Important for deeper invasion Helps w/ systemic spread, cleanse connective tissue. • Suppurative (pus-producing) Diseases caused by S. pyogenes Strep Throat Scarlet Fever-comes from strep throat. Rash comes from strains w/ Spe toxin Skin-infections: Folliculitis, Cellulitis, Impetigo, Necrotizing fasciitis/bacterial gangrene • Delayed Abs Mediated Diseases caused by S. pyogenes (nonsuppurative) 1. Rheumatic fever: M-protein strains, cross rxn abs w/ heart tissue, elevated ASO 2. Glomerulonephritis: throat and skin - Group B: Streptococcus agalactiae Beta-hemolytic, smaller and lightly colored. Bacteremia in newborn meningitis. DISTINGUISHING: Hippurate hydrolysis, resistant to bacitracin, CAMP (+) • Disease of Group B Strep Carried~ 10-30% + Urogenital tract (passed to newborn 60%) Newborn meningitis: Through vaginal birth. Early onset-in utero/birth. Late onset- 3 week old infant. Defining virulence  capsule. Symptoms-sometimes fever, constant fussiness. Treatment-penicillin, vancomycin etc. WBC or bacteria in cerebrospinal fluid are signs of infection (Gram + cocci). Can only stain anthrax from blood - Viridans Streptococi Urogenital tract. Don’t have any Lancefield serotypes. Cause cavities & endocarditiss. Go from oral cavity to heart to cause endocarditis. There IS a vaccine - Streptococcus pneumoniae “pneumococcus” No Lancefield. Capsule: very big required to be virulent because they have sensitive walls • Diseases 1. Pneumonia 2. Sinus infections. Otitis media 3. Meningitis (non-infant): Kids (pre-vaccine/unvaccinated)/ Many different serotypesAbs bind to capsule polysaccharide. Pneumococcal vaccine: original was 7 valent, recently 13 valent for kids, 23 valent for adults. • Lab Diagnosis of Streptococcus pneumoniae Gram (+), sensitive to optochin, slimy green colonies, S. pneumoniae lysed by bile. Quelling Reaction: capsule swelling w/ addition of abx. Hemolysin, pneumonia associated w/ aspiration. Enterococcus - Enterococcus (old group D): Enterococcus faecalis, faecium Nosocomial infections abx resistant. Gamma w/ some alpha. Super bugs: VRE-Vancomycin resistant enterococcus. - Group D: Streptococcus bovis Prescence associated w/ colon cancer. Optochin resistant, non-bile soluable, PYR (+), grow in 6.5% NaCl, broad temp range (10-45 C) Pyogenic Cocci III: Neisseria & Others Neisseria Only true Gram (-) cocci, pussiest of bacteria, super inflammatory, rely on asymptomatic carriers. Catalase/motility/nitrate (-), oxidase (+). Oxidizes glucose and maltose • Species: Neisseria gonorrhoeae (STD), meningitides (strict human pathogens), sica, & mucosa (commensals) - Neisseria meningitides • Invasion: crosses endothelium. Blood  blood brain barrier  meningitis • Virulence factors 1. Polysaccharide capsule: 13 defined serotypes based on capsule. B most common Group B: low immunogicity; hard to make antibodies/immune response (Abs). Potential cross-protection in vaccine for B 2. Bind human Transferrin & Lactoferrin: protein that bind human transferrin and lactoferrin which helps bacteria compete w/ host for Iron. HIGHLY HOST SPECIFIC strictly host pathogen. 3. IgA protease: Cleave human IgA (abs in mucosal sites). Helps with carrage of organism 4. Rmp protein: outer membrane protein complexes with lipid A endotoxin. Abx made are not effective, and bing harmlessly to bacteria. Lets them avoid effective abs binding. 5. Lipoligosaccharide (LOS): Low immunity, blebs out and causes big inflammation. 6. Pili protein: span bacterial membrane. Important for attachment to nasopharynx. Anti-phagocytic and undergo antigenic variation. 7. Opa  suppress T-helper Opc  cross endothelium • Clinical Diseases of G. meningitides 1. Meningitis – Child (5=> and in daycare. 6-24 months very susceptible) & young adults. Close to 100% mortality when not treated. Neurologic sequel sometimes. Droplet spread 2. Meningococcemmia – disseminated septicemia, characterized by petechial skin lesions, Waterhouse Friderchsoon syndrome (septic shock). 3. Meningococcal pneumonia- usually complication of prior respiratory infection • Lab Diagnostics: Gram stain of cerebral spinal fluid. O sugar test for differentiate from gonocci. Ferment glucose & mannitol. • Treatment: Susceptible to penicillin and cephalosporin. VACCINE: available for strains (polysaccharide capsule) A, C, Y, W and one coming for B - Neisseria gonorrhoeae • Virulence attachment/invasion 1. Opa proteins 2. Pili- attachment 3. Por B (porin protein)-very w/ strains. Reduce degranulation of neutrophils (phagocytes), inhibits complement. Inhibits neutrophils 4. IgA protease 5. Invades/Multiplies w/in cells 6. Pili C- Ag variation • Pathogenesis of N. gonorrhoeae: Induce (TNFalpha-proinflamm cytokine can go to TSSS if it goes systemic. Cause of most of the symptoms) Invade intracellular phagocyte (inhibits killing in granules) • Clinical Diseases 1. Gonorrhea: Disease in young adults. Females (20-50%) with complications of (10-20 %). 2. Conjunctivitis- Newborns. Othalmia neonatorum conjunctivitis. 3. Gonococcemia- disseminated septicemia, skin, and joint infection, leading cause of purulent arthritis. 1-3% of infection in Females. • Lab Diagnosis of N. gonorrhoeae: Chocolate and MTM media • Treatment: Resistant to penicillin, ciprolfaxin. Ceftriaxone. No Vaccine. Chemoprophylaxin for newborn eye infections only. Others Gram (-) cocci - Moraxella catarrhalis: Respiratory tract infections, otitis media, sinusitis, pneumonia, inert on sugars, DNAse (+) - Eikenella corrodens: opportunistic pathogens, hard to grow, endocarditis - Kingella kingae: arthritis in kids Corynebacterium, Listeria & Erysipelothrix Listeria Gram (+) bacilli. Weakly Beta-hemolytic. CAMP (+), motility • Infection Cycle of Listeria: (a) Internalin protein-binds to cadherin. (b) Vesicle has decreased pH which activates Listeriolysin O. (c) Listeriolysin O will lyse vesicle and move to cytosol (d) Listeria replicates in cytosol and makes Act-A which polymerizes actin in a polar direction, pushing bacteria to the membrane. Spread through basal membrane helps it possibly get into a macrophage. • Clinical Diseases 1. Listeriosis-food poisoning (fecal-oral). Neonatal can be early or late onset. Early in utuero can lead to still birth, abortion, defects. Late passed through birth canal, and can lead to meningitis in 2-3 weeks. 2. Meningitis (Adults) - In immune compromised adults. 3. Bacteremia- Replicates in blood • Listeria Immune Response: Cellular Immunity (T & mhcrophages) • Lab Diagnosis of L. monocytogenes: OCLA, CAMP (+), parasol motility, Esculin hydrolysis Erysipelothrix rhusiopathiae: Long chains, found in veterinarians/zookeepers/farmers - Erysipeloid: Skin infection, hint: zoonosis Corynebacterium - Corynebacterium diptheriae First toxoid pediatric vaccine. Would disproportionally affect poor in tightly packed housing. Found on skin, UT. • Clinical Disease 1. Diptheria- membrane forms in throat and chokes host to death 2. Cutaneous diphtheria- shankers • Immune Response to C. diphtheria Humoral Immunity: Abs vs toxin Antitoxin: purified horse Abs. Passive immunity, would not work 2 time because we make Abs against horse Abs. DTaP vaccine • Pathogenesis of C. diphtheria Diphtheria toxin inhibits protein synthesis AB toxin. (a) B part bind to EGF (b) A gets into cell (c) inactivates elongation factor-2, prevents protein synthesis. • Clinical Diagnosis: Tinsdale Medium, Pyrazinamidase (-), catalase (+), nonmotile, granules, Elek test for toxigenic C. diph • Treatment of Diphtheria: Maintain open airway. Treat with penicillin/erythromycin. - Corynebacterium jeikeium: Hospital found - Corynebacterium urealyticum: Urogenital opportunist, kidney stones, very urease (+) Enterobacteriacae Gram (-), non-sporeforming, catalase (+), oxidase (-), Facultative anaerobes. 30% bacteremia, 70% o UTI’s, lots of gastroenteritis. Pathogenic Enterobacteriacae: Salmonella, Shigella, Yersinia, E. coli (depends on strain) Opportunists Enterobacteriacae: E. coli, Klebsiella, Proteus, Citrobacter, Serratia. Opportunistic in either in a new location, or in immune compromised. • Serological Classification 1. Flagella H. antigen, spreading through host 2. LPS Lipopolysaccharide or endotoxin [O polysaccharide, polysacch, core & exotoxin] Changes among species 3. Capsule  K antigen, heat labile 4. Pili conjugation & adherence • Gastroenteritis caused by Enterobacteriacae 1. Non-Invasive- Due to toxin produced & not the bacteria invading & destroying epithelial barrier (Vibrio cholera, ETEC) 2. Invasive- Invade epithelial barrier (Shigella, Salmonella) 3. Systemic – (Salmonella typhi, Campylobacter jeikeium) • Common Virulence Factors 1. Endotoxin-lipid A 2. Capsule- Immune evasive 3. Antigenic Variation- K & H Ag 4. Type III Secretion System- Protein syringe spans membrane 20 proteins form pseudo syringe. Allows, delivery of contents into host. Only found in Gram (-). Salmonella - Salmonella enterica, serovar Typhi: Facultative intracellular pathogens, cause membrane ruffling to internalize the bacteria. • Virulence of S. Typhi TTSS 1: injects Sip A (Stabilize host actin, induces ruffling, cause endocytosis). TTSS 2: injects SspH (activated in vacuoles prevent phagolysosome fusion w/ endosome. Allows survival in cell). • Clinical Disease of Salmonella 1. Gastroenteritis- Get it from chicken, eggs, dairy. S. Typhermurium: High infection dose, person to person spread. S. Typhi: Low infectious dose, aslo person to person. Diarrhea, not bloody, but induces vomiting. 2. Septicemia- S. Typhi, S. Paratyphi, S. Cholerasuis 3. Typhoid Fever: S. Typhi. Gest engulfed by macrophage under epithelial barrier. Replicates in macrophage & goes to liver, spleen, and bone marrow. Fever and then more gastroenteritis. Can lead to septic shock and organ failure. 1-5% chronic colonization of gallbladder (untreated). Typhoid Mary was the 1 associated carrier Shigella Big virulence plasmid with TTSS. Uses actin polymerization to move. Similar to Listeria. Humans are the only reservoir. • Species: dysenteriae, flexneri, boydii, sonnei. Can only use serological kits and sequencing to distinguish. • Pathogenesis of Shigella: (a) Adhesioninvasion via M-cell. (b) Phagocytosis by macrophage and inhibition of phagolysosome. Make proinflammitory cytokines and macrophage apoptosis occurs. (c) IL-1 induces transcytosis (movement across a barrier). (d) spread to other epithelial cells (intracellular). (e) Transmission NOTE: Shigella is solely in humans because only we express the appropriate receptor. This receptor is also up regulated in the kidneys which is how HUS can occur. • Shiga Toxin (Stx) of S. dysenteriae- AB exotoxin. B-pentamer binds host cell glycolipids. A-binds host 60s and inhibits protein synthesis. Leads to severe gastroenteritis with blood painful diarrhea. Can cause hemolytic uremic syndrome (HUS) in kidneys. Escherichia coli - Enterotoxigenic E. coli (ETEC) - Traveler’s Diarrhea (noninvasive, secretory similar to V. cholera). High infectious dose and usually spread through contaminated food/water LT-1: AB toxin that binds to host and upregulates adenylate cyclase, increases [ATP], which causes efflux of ions and water. - Enteropathogenic E. coli (EPEC) – Infant secretory diarrhea. Low infections dose BFP (bundle forming protein) attaches, TTSS injects Tir. Tir causes actin polymerization, cell death and destruction of vili. - Enteroaggregative E. coli (EAEC) – Infant & Travelers Diarrhea. Can cause chronic childhood diarrhea. AAF (aggregative adherence factor): fimbriae allow biofilm formation Cytotoxin & Enterotoxin  Enteroaggregative shiga toxin (EAST like LT-1), PE-T - Enterohemorrhagic E. coli (EHEC) - Causes hemorrhagic colitis like intestine instead of small. Most common transmitted and symptoms shown in 3-4 days. Usually in contaminated meats. HUS can occur as a complication. EHEC came from EPEC that acquired shiga-toxin - Other opportunistic E. coli diseases- UTI, neonatal meningitis, septicemia Yersinia pestis • Clinical Disease 1. Enterocolitis: Y. enterocolitica and Y. pseudotuburculosis. Swollen lymph nodes & colitis which mimics appendicidis. 2. Bacteremia: from blood transfusion, can replicate at low temp 3. Plague: zoonosis with rats/fleas/humans. Bubonic swollen lymph nodes, 75% mortality. Pneumonic goes septic and can die before showing symptoms 90% Klebsiella - Klebsiella pneumoniae: slimy capsule mucoid. Pneumonia and UTI’s - Klebsiella granulomatis: granulomas Other - Proteus mirabilis: Urease (+) - Enterobacter, Citrobacter, Morganella, Serratia Non-fermenting Gram (-) Bacilli Everywhere in enve. Carriers common in hospital, immune compromised, Abx resistance Pseudomonas - Pseudomonas aeruginosa: Gram (-) rods, OXIDASE (+), obligate aerobes, motile. Makes water soluble pigment. Don’t decolorize as well, so look a little gram +. • Quorum Sensing Biofilm: HSL=Homoserine lactone (las gene), inducible. Binds to transcription factors involved in biofilm production and causes the secretion of alginate. High density of bacteria have HSL auto-induced which binds to transcriptional receptor (PA 1, 2). • Virulence Factors 1. Adhesins- pili and biofilms. 2. Exotoxin A (ETA)- Acts like Diptheria toxin, causes tissue damage in wounds/burns, and corneal infections. 3. TTSS- epithelial barrier damage 4. Cytotoxins injected by TTSS: phospholipase C (exo U), Exoenzyme S/T promotes invasion by rearranges the cytoskeleton causes apoptosis. Causes bacteremia and septicemia 5. Exotoxin T- decreases wound healing 6. Exotoxin S/U- decrease IL-1, 18 (cytokines) 7. Las A/B Regulated by HSL. Degrade elastin, degrade complement proteins (immune evasive) 8.
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