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Micro TA Review 1

Micro TA Review 1. April 4, 2013. Tips & hints Memorization … this is the time! Flashcards, stories, whatever it takes. You really do need to know this. Pathogen  clinical presentatio n & vice versa Questions: know all the answers It goes fast – try to keep up as best you can!

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Micro TA Review 1

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  1. Micro TA Review 1 April 4, 2013

  2. Tips & hints • Memorization… this is the time! • Flashcards, stories, whatever it takes. • You really do need to know this. • Pathogen  clinical presentation & vice versa • Questions: know all the answers • It goes fast – try to keep up as best you can! • Resources • Clinical Micro Made Ridiculously Simple • Lippincott Micro Cards • TA PPTs • Firecracker

  3. Bacterial Cell Walls

  4. Bacterial Genetics TRANSFORMATION: Ability to take up naked DNA of RELATED bacteria from environment (especiallyS. pneumo, H. influenzae, and Neisseria -- SHiN) TRANSPOSITION: Segments of DNA that can “jump” from one chromosomal location to another via excision and reincorporation. Can also jump from chromosome to plasmid and vice versa. TRANSDUCTION: Bacteriophage (virus that infects bacteria)transfers bacterial DNA from one bacteria to another. Can be generalized (lyticphage) or specialized (lysogenicphage).

  5. Bacterial Genetics CONJUGATION: “Bacterial Sex”– may involve UNRELATED bacteria, requires direct contact and transfer is UNIDIRECTIONAL. Two options: • F+ x F-: Fplasmid contains genes for conjugation and it is transferred via pilus (no transfer of chromosomal genes). • Hfr x F-: Fplasmid can become incorporated into DNA-- now called an Hfr cell and now may transfer plasmid + some flanking chromosomal genes.

  6. Normal Bacterial Flora •Skin: –Normal: Staphylococcus epidermidis –Transient: S. aureus •Upper Respiratory tract –Normal: Anaerobic cocci, Viridans Streptococci –Transient: Neisseria spp., Streptococcus pneumoniae, Haemophilus influenzae •Gastrointestinal Tract –Anaerobic GNR (Bacteroides), Enterobacteriaceae (E. coli), Enterococci •Genitourinary tract – Normal: Lactobacillus – Transient: GBS

  7. Virulence Factors • •Ability to block arms of immune system (phagocytosis, antibodies, complement)(Staph aureus- Protein A; Strep pyogenes- M protein) • •Slime and biofilms(Staph epi, Strep viridans) • •Toxins (endotoxin vs. exotoxin)(Endotoxin: gram negatives; Exotoxin: Staph aureus, Strep pyogenes) • •Adhesion(Staph sapro) • •Flagella • •Ability to survive phagocytosis(Strep pyogenes, hyaluronic acid capsule) • •Ability to survive in hostile environments

  8. Exotoxin v. Endotoxin

  9. Superantigens • Definition: • Superantigen toxins allow the non-specific binding of MHC II with T cell receptors, resulting in polyclonal T cell activation (versus other toxins, which are just monoclonal activation so not as intense). • Polyclonal T-cell population  cytokine storm  multisystem disease and shock. • Examples: • S. aureus: TSST-1 • S. pyogenes: Exotoxin A

  10. Antibiotic Targets

  11. Antibiotic Classes Cell Wall Synthesis Inhibitors: Peptidoglycan Cross-Linking Penicillins, Cephalosporins, Carbapenems (Beta-Lactams) • Mechanism: bind to transpeptidases (aka PBP)→inhibit cross-linking of peptidoglycan no cell wall  death by osmolysis • Resistance via beta lactamases, altered penicillin binding protein, altered porins. Cell Wall Synthesis Inhibitors: Peptidoglycan Synthesis Vancomycin • Mechanism: binds D-alaD-ala portion of cell wall precursors  inhibits peptidoglycan synthesis. • Resistance via amino acid change from D-ala D-ala to D-ala D-lac; gram-negatives are intrinsically resistant because vanco can’t cross outer membrane. Protein Synthesis Inhibitors Macrolides, Tetracyclines, Aminoglycosides Inhibitors of DNA Polymerase Activity Fluoroquinolones, Metronidazole Folic Acid Synthesis Inhibitors Sulfonamides and Trimethoprim(TMP/SMX)

  12. OVERVIEW!Do not be overwhelmed. this week’s focus: gram+ cocci

  13. Gram Positive Cocci Also see the table in your lab manual!

  14. Types of Hemolysis Also: Strep viridans Also: Staph aureus, GBS Enterococci have variable hemolysis

  15. IN THE LAB • Gram + cocci in clusters • Coagulase +, catalase + • Beta-hemolytic • EPIDEMIOLOGY • Nosocomial and community, all ages • CLINICAL • Pyogenic skin infxn (impetigo, cellulitis, abscesses) • Acute endocarditis (v. S. viridanssubacute) • Osteomyelitis • Septic arthritis • Toxin-related syndromes (see below) • VIRULENCE FACTORS • Protein A, biofilm, capsule, coagulase, catalase, hemolysins, penicillinase • Toxins:TSST-1 (superantigen, causes Toxic Shock Syndrome); enterotoxin (preformed superantigen, causes gastroenteritis); exfoliative toxin (causes scalded skin syndrome) • TREATMENT • Most strains secrete penicillinase MSSA, treat with nafcillin • Some strains alter the PBP  MRSA, treat with vancomycin cluster of grapes Staphylococcus aureus scalded skin impetigo

  16. Staphylococcus epidermidis IN THE LAB • Gram + cocci in clusters • Coagulase - (vs S. aureus), catalase +, novobiocin sensitive (vs S. sapro) • Gamma-hemolytic EPIDEMIOLOGY • Nl. flora of the skin; nosocomial & iatrogenic CLINICAL • Foreign body or device infxns (think prosthetics, IV lines, Foley catheters) • Common contaminant in blood cultures VIRULENCE FACTORS • Biofilm: extracellular scaffold that mediates attachment to foreign devices TREATMENT • Vancomycin & remove the infectious source (i.e., remove the device)

  17. Staphylococcus saprophyticus IN THE LAB • Gram + cocci in clusters • Coagulase - (vs S. aureus), catalase +, novobiocin resistant (vs S. epi) • Gamma-hemolytic EPIDEMIOLOGY • Sexually active women  2nd most common cause of UTI (1st is E. coli) CLINICAL • UTI (burning, urgency, frequency) VIRULENCE FACTORS • Specialized mucosal receptors TREATMENT • Folic acid synthesis inhibitors (TMP/SMX)

  18. Streptococcus pyogenes (GAS) IN THE LAB Gram + cocci in chains Catalase – (vs Staphs), bacitracin sensitive (vs GBS) Beta-hemolytic EPIDEMIOLOGY All ages CLINICAL Suppurative (bc of host neutrophil response): pharyngitis (“strep throat”), cellulitis (inc. erysipelas), impetigo, necrotizing fasciitis Non-suppurative(toxigenic): scarlet fever, Streptococcal Toxic Shock Syndrome Delayed (immunologic): rheumatic fever, poststreptococcal glomerulonephritis VIRULENCE FACTORS M protein, superantigen, streptolysin S & O, streptokinase, SpeA, B, C, anti-C5a peptidase, hyaluronidase (in capsule), T antigen, DNAase Diagnose recent infxn with ASO titers (antistreptolysin O) TREATMENT Penicillin strep throat w/oropharyngealpetechiae

  19. Streptococcus agalactiae (GBS) Streptococcus agalactiae IN THE LAB Gram + cocci in chains Catalase – (vs Staphs), bacitracin resistant (vs S. pyogenes) Beta-hemolytic EPIDEMIOLOGY Neonates, peripartum women, diabetics CLINICAL Neonatal sepsis, pneumonia, meningitis Maternal sepsis Less commonly: UTI, endocarditis VIRULENCE FACTORS Not important TREATMENT/PROPHYLAXIS Beta-lactams (penicillin) Group B is Bad for Babies!

  20. Enterococcus(E. faecalis, E. faecium) Enterococcus IN THE LAB Gram + cocci in pairs or chains Catalase – (vs Staphs) Variable hemolysis (alpha or gamma) Subdivided into Lancefield Group D and non-Lancefield Group D depending on carbs in cell wall EPIDEMIOLOGY Nl GI flora; nosocomial infxn (esp VRE) CLINICAL UTI, subacute endocarditis, biliary tract infxn Peritonitis Nosociomalsuperinfxn bacteremia VIRULENCE FACTORS Dextran (glycocalyx) helps bind to heart valves TREATMENT Inherent antibiotic resistance to cephalosporins Now have vancomycin resistance as well (VRE)  treat with daptomycin or ampicillin + aminoglycoside

  21. Strep viridans (S. mutans, S. sanguis) IN THE LAB Gram + cocci in chains Catalase – (vs Staphs), optochin resistant (versus S. pneumo) Alpha-hemolytic EPIDEMIOLOGY Nl oropharynx flora CLINICAL S. mutans dental caries (cavities) S. sanguis  subacute bacterial endocarditis (heart valve damage) VIRULENCE FACTORS Dextran (glycocalyx) helps bind to heart valves TREATMENT Penicillin (usually sensitive to lotsa antibiotics) foliage growing on mitral valve from oral cavity

  22. Streptococcus pneumoniae IN THE LAB Gram + lancet-shaped cocci in pairs (“diplococci”) Catalase – (vs Staphs), optochin sensitive (versus S. viridans) Alpha-hemolytic EPIDEMIOLOGY See later lectures CLINICAL Most common cause of MOPS: bacterial Meningitis in kids & elderly, Otitis media in kids, community-acquired Pneumonia, Sinusitis. Also, sepsis. VIRULENCE FACTORS Polysaccharide capsule prevents phagocytosis. Diagnose with Quellung reaction (capsular “swellung”) TREATMENT Penicillin Some resistance  high dose penicillin & cephalosporins Lotsa resistance  vancomycin

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