MCRO 423 Final: Final Study Guide

23 Pages
Unlock Document

MCRO 423

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.
More Less

Related notes for MCRO 423

Log In


Join OneClass

Access over 10 million pages of study
documents for 1.3 million courses.

Sign up

Join to view


By registering, I agree to the Terms and Privacy Policies
Already have an account?
Just a few more details

So we can recommend you notes for your school.

Reset Password

Please enter below the email address you registered with and we will send you a link to reset your password.

Add your courses

Get notes from the top students in your class.