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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

Micro TA Review 1

April 4, 2013

slide2

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
slide4

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).

slide5

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.
slide6

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

slide7

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
superantigens
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
antibiotic classes
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)

overview do not be overwhelmed
OVERVIEW!Do not be overwhelmed.

this week’s focus: gram+ cocci

gram positive cocci
Gram Positive Cocci

Also see the table in your lab manual!

slide14

Types of Hemolysis

Also: Strep viridans

Also: Staph aureus, GBS

Enterococci have variable hemolysis

staphylococcus aureus

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

staphylococcus epidermidis
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)
staphylococcus saprophyticus
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)
slide18

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

slide19

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!

slide20

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

slide21

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

slide22

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