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Infectious Disease > Week 1 > Flashcards

Week 1 Flashcards

1
Q

Minimum inhibitory concentration

A

concentration of drug bacteria stops growth

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2
Q

Minimum bactericidal concentration

A

concentration of bactericidal drug at which 99% of bacteria are killed

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3
Q

DQ CRIMES

A

important metabolism and/or hepatic elimination:

Clindamycin, Chloramphenicol
Rifampin
Isoniazid
Metronidazole
Erythromycins
Sulfonamides, Streptogramins
Doxycycline
Fluoroquinolones
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4
Q

Features of Gram Positive organisms

A

1) Lipoteichoic acid

2) Thick peptidoglycan cell wall (accessible outer PG wall)
- PG can be up to 90% of cell wall

→ blue/purple

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5
Q

Features of Gram Negative organisms

A

1) Porins inserted in LPS outer membrane (endotoxin)
2) Thin peptidoglycan cell wall

3) Periplasmic space between cytoplasmic membrane and thin PG layer (B-lactamase location)
→ pink

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6
Q

Pattern Recognition Receptors (PRRs)

A

on epithelium, T, B, NK cells, phagocytes, dendritic cells

1) Transmembrane (surface) = TLR
2) Cytosolic = NOD, TLR
3) Extracellular = CD14, LBP

PRRs recognize PAMPs and DAMPs

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7
Q

Gram + Cocci (2)

A

1) Staph

2) Strep

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8
Q

Gram + Rods (bacilli) (7)

A

1) Bacillus
2) Clostridium
3) Gardnerella (gram variable)
4) Lactobacillus
5) Listeria
6) Myobacterium (acid fast)
7) Propionibacterium

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9
Q

Gram + branching filamentous (2)

A

1) Actinomyces

2) Nocardia (weakly acid fast)

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10
Q

No cell wall (2)

A

1) Mycoplasma

2) Ureaplasma (contains sterols, which do not gram stain)

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11
Q

Gram - cocci (2)

A

1) Moraxella catarrhalis

2) Neisseria

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12
Q

Gram - bacilli enterics (13)

A

1) Bacteroides
2) Camplyobacter
3) E. Coli
4) Enterobacter
5) Helicobacter
6) Klebsiella
7) Proteus
8) Pseudomonas
9) Salmonella
10) serratia
11) Shigella
12) Vibrio
13) Yersinia

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13
Q

Gram - bacilli respiratory

A

1) Bordatella
2) Haemophilus (pleomorphic)
3) Legionella (silver stain)

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14
Q

Gram - bacilli zoonotic

A

1) Bartonella
2) Brucella
3) Francisella
4) Pasteurella

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15
Q

Gram - pleomorphic (2)

A

1) Chlamydia (giemsa)

2) Rickettsiae (giemsa)

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16
Q

Gram - spirochettes (3)

A

1) Borrelia (giemsa)
2) Leptospira
3) Treponema

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17
Q

Penicillin G and V

Mechanism

A

Cell wall synthesis inhibitors

-Bind penicillin-binding proteins (transpeptidases) and block transpeptidase crosslinking of peptidoglycan in cell wall

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18
Q

Penicillin G and V

Toxicity (3)

A

1) Type I anaphylaxis reaction
2) Type III rash
3) convulsions at very high doses

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19
Q

Penicillin G and V

Resistance

A

Penicillinase (B-lactamase) cleaves B-lactam ring

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20
Q

Penicillin G and V

Administration / metabolism

A

Pen G = IV and IM
Pen V = oral

renal excretion
bactericidal

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21
Q

Penicillin G and V

Clinical use (3)

A

1) Gram + cocci and rods (staph, strep, entero, actinomyces)
2) Gram - rods (Neisseria, M. catarrhalis)
3) Spirochete (T. pallidum)

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22
Q

Amoxicillin, Ampicillin

Mechanism

A

Cell wall synthesis inhibitors

-Bind penicillin-binding proteins (transpeptidases) and block transpeptidase crosslinking of peptidoglycan in cell wall

MUST COMBINE with Clavulanic acid to protect against destruction by B-lactamase

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23
Q

Amoxicillin, Ampicillin

Clinical use (8)

A

Extended spectrum penicillin

“HHELPSS kill enterococci”

1) H. pylori
2) H. influenzae
3) E. coli
4) Listeria monocytogenes
5) proteus mirabilis
6) Salmonella
7) Shigella
8) Enterococci

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24
Q

Amoxicillin, Ampicillin

Toxicity (4)

A

1) Type I anaphylaxis reaction
2) Type III rash
3) convulsions at very high doses
4) Pseudomembranous colitis

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25
Q

Amoxicillin, Ampicillin

Mechanism of resistance

A

Penicillinase in bacteria (B-lactamse) cleaves B-lacta ring

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26
Q

Amoxicillin, Ampicillin

administration / metabolism

A

Oral

AmOxacillin is better oral

Renal excretion

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27
Q

Diclocacillin, Nafcillin, Oxacillin, Methicillin

Mechanism

A

PENICILLINASE-RESISTANT
–> bulky R group blocks B-lactamase from accessing B-lactam ring

Cell wall synthesis inhibitors

-Bind penicillin-binding proteins (transpeptidases) and block transpeptidase crosslinking of peptidoglycan in cell wall

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28
Q

Diclocacillin, Nafcillin, Oxacillin, Methicillin

Clinical use (1)

A

1) MSSA (not MRSA)

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29
Q

Diclocacillin, Nafcillin, Oxacillin, Methicillin

Toxicity (2)

A

1) Hypersensitivity reactions

2) Interstitial nephritis

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30
Q

Diclocacillin, Nafcillin, Oxacillin, Methicillin

Administration / excretion

A

Renal excretion

Oral (not methicillin or nafcillin)

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31
Q

Piperacillin, Ticarcillin

Mechanism

A

ANTI-PSEUDOMONAL

Cell wall synthesis inhibitors

-Bind penicillin-binding proteins (transpeptidases) and block transpeptidase crosslinking of peptidoglycan in cell wall

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32
Q

Piperacillin, Ticarcillin

administration / metabolism

A

IV ONLY

renal excretion

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33
Q

Piperacillin, Ticarcillin

Clinical use (2)

A

EXTENDED SPECTRUM

1) Pseudomonas
2) Bacteroides

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34
Q

Piperacillin, Ticarcillin

Toxicity

A

1) Hypersensitivity reactions (I and III)

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35
Q

Cephalosporins (generation 1-5)

mechanism of action

Toxicity?

A

B-lactam drug, inhibits cell wall synthesis but less susceptible to penicillinases

Bactericidal

Less severe allergy than penicillins (can give to patient with type III allergy, but not type I allergy to penicillins)

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36
Q

1st generation cephalosporins

2 names

A

cefazolin, cephalexin

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37
Q

cefazolin, cephalexin (1st gen)

uses (4)

A

PEcK

1) Proteus mirabilis
2) E. Coli
3) Klebsiella pneumoniae

4) **used before surgery to prevent S. aureus wound infections

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38
Q

2nd generation cephalosporins

3 names

A

cefoxitin, cefaclor, cefuroxime

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39
Q

cefoxitin, cefaclor, cefuroxime (2nd gen)

Use (7)

A

HEN PEcKS

1) Haemophilus influenzae
2) Enterobacter aerogenes
3) Neisseria
4) Proteus mirabilis
5) E. Coli
6) Klebsiella pneumoniae
7) Serratia

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40
Q

3rd generation cephalosporins

3 names

A

ceftriaxone, cefotaxime, ceftazidime

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41
Q

ceftriaxone, cefotaxime, ceftazidime (3rd gen)

uses

A

1) serious gram - infections resistant to other B-lactams

Ceftriaxone –> meningitis, gonorrhea, disseminated Lyme disease

Ceftazidime –> Pseudomonas

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42
Q

Ceftaroline

A

5th gen cephalosporin

action against MRSA

does not cover pseudomonas

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43
Q

Cephalosporins

mechanism of resistance

A

structural changes in penicillin binding proteins (transpeptidases) e.g. MRSA

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44
Q

Carbapenems

(imipenem, Ertapenem, meropenem, doripenem)

Mechanism

A

Broad spectrum B-lactamase-resistant cell wall synthesis inhibitor

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45
Q

Imipenem

A

Broad spectrum B-lactamase-resistant carbapenem

always coadministered with CILASTATIN (inhibits renal dehydropeptidase I) –> decreases inactivation of drug in renal tubules

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46
Q

Carbapenems

administration / metabolism

A

IV ONLY

renal excretion

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47
Q

Carbapenems

Toxicity (1)

A

GI distress

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48
Q

Carbapenems

Clinical use

A

1) Wide spectrum reserved for resistant organisms

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49
Q

Monobactams (Aztreonam)

Mechanism

A

Cell wall synthesis inhibitor

Less susceptible to B-lactamases

synergistic with aminoglycosides

**NO cross allergenicity with penicillins

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50
Q

Monobactams (Aztreonam)

Clinical use (1)

A

1) Gram negative rods only

* for penicillin-allergic patients or renal insufficiency who cannot tolerate aminoglycosides

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51
Q

Vancomycin

Mechanism

A

Inhibits cell wall peptidoglycan formation by binding D-ala D-ala portion of cell wall precursors

bactericidal

not susceptible to B-lactamases

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52
Q

Vancomycin

administration / metabolism

A

Poor oral absorption

given IV or oral

renal excretion

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53
Q

Vancomycin

Toxicity (5)

A

1) Nephrotoxicity
2) Ototoxicity
3) Thrombophlebitis
4) Chills, fever, rash
5) Red Man Syndrome (prevent with pre tx with anti-histamine, slow infusion rate)

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54
Q

Vancomycin

Clinical use

A

1) Narrow spectrum, Gram + (**MRSA, staph epidermidis, enterococcus, C. diff/oral)

for serious multi-drug resistant organisms

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55
Q

Vancomycin

Mechanism of resistance

A

modification of amino acids D-ala D-ala –> D-ala D-lac

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56
Q

Fluoroquinolones

drug names

A 
Ciprofloxacin
Norfloxacin
Levofloxacin
Ofloxacin
Moxifloxacin
Gemifloxacin
Enoxacin
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57
Q

Fluoroquinolones

Mechanism

A

Inhibit prokaryotic enzymes topoisomerase II (DNA gyrase) and topoisomerase IV

Bactericidal

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58
Q

Fluoroquinolones

Administration / metabolism

A

Good PO or IV

Renal/HEPATIC* excretion

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59
Q

Fluoroquinolones

Toxicity (5)

A

1) CANNOT take with antacids or theophylline
2) GI upset
3) Contraindicated in PREGNANT WOMEN, nursing mothers, and CHILDREN (< 18 yrs) –> Cartilage damage
4) Tendonitis/tendon rupture in people > 60 yrs or pt taking prednisone
5) May prolong QT

“FluroquinolONES hurt attachments to your BONES”

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60
Q

Fluoroquinolones

Clinical use (1)

A

1) Gram - rods in urinary and GI tracts (including Pseudomonas and Neisseria)

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61
Q

Fluoroquinolones

Mechanism of resistance (3)

A

Chromosome encoded mutations in DNA gyrase, plasmid-mediated resistance, efflux pumps

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62
Q

Aminoglycosides

drug names

A

Gentamycin
Neomycin
Tobramycin
Streptomycin

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63
Q

Aminoglycosides

administraiton / metabolism

A

Renal excretion

IV or IM

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64
Q

Aminoglycosides

toxicity (4)

A

accumulates in kidneys and ear –>

1) nephrotoxicity
2) Ototoxicity (especially with loop diuretics)
3) Neuromuscular blockade
4) Teratogen

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65
Q

Aminoglycosides

Mechanism

A

Bactericidal

IRREVERSIBLE inhibition of initiation complex through binding of 30S subunit

can cause misreading of mRNA and block translocation

Require O2 for uptake –> ineffective against anaerobes

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66
Q

Aminoglycosides

Clinical use

A

1) Severe gram - rod infections
- synergistic with B-lactam abx

2) Neomycin for BOWEL SURGERY

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67
Q

Aminoglycosides

Mechanism of resistance (1)

A

Bacterial transferase enzymes inactivate drug by acetylation, phosphorylation, or adenylation

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68
Q

Tetracyclines

drug names

A

Tetracycline, doxycycline, minocycline

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69
Q

Tetracyclines

Mechanism

A

BacterioSTATIC

Bind 30S and prevent attachment of aminoacyl-tRNA

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70
Q

Tetracyclines

administration / metabolism

A

good PO

Doxy eliminated fecally –> can use in pts with renal failure

others renally excreted

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71
Q

Tetracyclines

Toxicity (5)

A

1) do not take with MILK or ANTACIDS, or IRON-containing preparations (divalent cations bind drug in gut and inhibit absorption)
2) GI distress
3) Discoloration of teeth and inhibition of bone growth in children < 8yrs
4) Photosensitivity
5) Fungal superinfections

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72
Q

Tetracyclines

Clinical use (4)

A

1) Borrelia Burgdorferi
2) M. Pneumoniae
3) Rickettsia
4) Chlamydia

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73
Q

Tetracyclines

Mechanism of resistance (1)

A

Decrease uptake or increased efflux out of bacterial cells by plasmid-encoded transport pumps

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74
Q

Chloramphenicol

mechanism

A

blocks peptidyl transferase at 50S ribosomal subunit

BacterioSTATIC

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75
Q

Chloramphenicol

Clinical use

A

1) Meningitis (H. influenzae, N. Meningitis, Strep. Pneumoniae)
2) Rocky Mountain Spotted Fever (Rickettsia, rickettsii)

**Limited use due to severe toxicity (but cheap so used in developing countries)

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76
Q

Chloramphenicol

Toxicity (3)

A

1) Anemia (dose dependent)
2) Aplastic anemia (dose independent)
3) Gray baby syndrome (in premature infants - lack liver UDP-glucuronyl transferase)

High toxicity

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77
Q

Chloramphenicol

Metabolism / administration

A

Glucuronidation (hepatic)

PO or IV

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78
Q

Chloramphenicol

Mechanism of resistance (1)

A

plasmid encoded acetyltransferase inactivates the drug

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79
Q

Clindamycin (Licosamide)

Mechanism

A

Blocks peptide transfer (translocation) at 50S ribosomal subunit

BacterioSTATIC

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80
Q

Clindamycin

Clinical use (3)

A

1) Anaerobic infections (bacteroides, C. perfringens) in aspiration pneumonia, lung abscesses, and oral infections
2) Invasive group A strep infections
3) **treats anaerobic infections ABOVE the diaphragm

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81
Q

Clindamycin

Toxicity (2)

A

1) Pseudomembranous colitis

2) fever, diarrhea

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82
Q

Clindamycin

administration / metabolism

A

PO or IV

penetrates BONE

Hepatic metabolism

83
Q

Oxazolidinones (Linezolid)

Mechanism

A

inhibit protein synthesis by binding 50S subunit and preventing formation of the initiation complex

84
Q

Oxazolidinones (Linezolid)

Metabolism / administration

A

Good PO and IV

Hepatic metabolism

85
Q

Oxazolidinones (Linezolid)

Clinical use (1)

A

1) Gram + including MRSA and VRE (severe infections)

86
Q

Oxazolidinones (Linezolid)

Toxicity (5)

A

1) headaches
2) GI - diarrhea, nausea
3) Inhibits MAO –> serotonin syndrome
4) Bone marrow suppression (especially thrombocytopenia)
5) Peripheral neuropathy

87
Q

Oxazolidinones (Linezolid)

Mechanism of resistance (1)

A

point mutation of ribosomal RNA

88
Q

Macrolides

drug names

A

Erythromycin
Azithromycin
Clarithromycin

89
Q

Macrolides

Mechanism

A

Inhibit protein synthesis by blocking translocation

bind 23S rRNA of 50S ribosomal subunit

BacterioSTATIC

90
Q

Macrolides

administration / metabolism

A

Good PO and IV

Concentrations in lungs

HEPATIC metabolism to ACTIVE metabolite + BILIARY elimination

91
Q

Macrolides

Clinical use (4)

A

1) Atypical pneumonias (Mycoplasma, Chlamydia, Legionella)
2) STIs (Chlamydia)
3) Gram + cocci (strep infections in penicillin allergic patients)
4) Bordatella Pertussis

92
Q

Macrolides

Toxicity (7)

A

“MACRO”

1) gastrointestinal Motility issues
2) Arrhythmia caused by prolonged QT interval
3) acute Cholestatic hepatitis
4) Rash
5) eOsinophilia
6) Inhibits CYP450 (erythromycin, clarithromycin)
7) Increase serum concentration of theophyllines, oral anticogulants

93
Q

Macrolides

mechanism of resistance

A

Methylation of 23S rRNA binding site prevents binding of drug

94
Q

Trimethoprim

Mechanism

A

Inhibits bacterial dihydrofolate reductase

BacterioSTATIC

95
Q

Sulfonamides

Mechanism

A

Inhibits folate synthesis

Para-aminobenzoic acid (PABA) antimetabolites inhibit dihydropteroate synthase

BacterioSTATIC

**BACTERICIDAL when combined with trimethoprim`

96
Q

TMP/SMX

Clinical use (6)

A

1) UTIs
2) Shigella
3) Salmonella
4) Penumocystis jirovecii pneumonia treatment and prophylaxis
5) Toxoplasmosis prophylaxis
6) Chalmydia

97
Q

TMP/SMX

toxicity (5)

A

1) Kernicterus in neonates
2) Hypersensitivity reactions
3) Photsensitivity
4) Can displace other drugs from albumin
5) TMP (“TREAT MARROW POORLY”) can cause megaloblastic anemia, leukopenia, granulocytopenia (alleviate with folinic acid supplementation)

98
Q

Sulfonamides

Mechanism of resistance (3)

A

1) Altered enzyme (bacterial dihydropteroate synthase)
2) decrease uptake
3) Increased PABA synthesis

99
Q

Daptomycin

Mechansim

A

Lipopeptide that disrupts cell membrane of gram + cocci

100
Q

Daptomycin

Clinical use

A

1) S. aureus skin infections (Especially MRSA)
2) Bacteremia
3) Endocarditis
4) VRE

**Not used for pneumonia - avidly binds/inactivated by surfactant

101
Q

Daptomycin

Toxicity (1)

A

1) Myopathy, rhabdomyolysis

102
Q

Metronidazole

Mechanism

A

Forms toxic free radical metabolites in bacterial cell that damages DNA

Bactericidal, antiprotazoal

103
Q

Metronidazole

Clinical use (7)

A

GET GAP on the Metro

1) Giardia
2) Entamoeba
3) Trichomonas
4) Gardnerella vaginalis
5) Anaerobes (bacteroides, C. diff)
6) Used with PPI and clarithromycin for triple therapy against H. Pylori

**Treats anaerobic infection BELOW the diaphragm

104
Q

Metronidazole

Toxicity

A

1) Disulfuram-like reaction (severe flushing, tachycardia, hypotension) with alcohol
2) Metallic taste
3) Headache

105
Q

Nitromidazoles (Nitrofurantoin)

Mechanism

A

DNA damaging agent

BacterioSTATIC

106
Q

Nitromidazoles (Nitrofurantoin)

toxicity (2)

A

1) GI upset

2) Hypersensitivity

107
Q

Nitromidazoles (Nitrofurantoin)

Clinical use (1)

A

1) UTI - e.coli

108
Q

Strep pyogenes is also known as group ______ strep

1) Gram stain and shape?
2) Hemolysis?
3) Catalase?
4) Aerobe or anaerobe?
5) Bacitracin sensitive/resistant?
6) Pyrrolidonyl arylamidase test + or -
7) Penicillin susceptible or no?

A

Group A strep

1) Gram + cocci, form chains
2) Beta hemolytic
3) Catalase -
4) Facultative anaerobic
5) Bacitracin sensitive
6) Pyrrolidonyl arylamidase test positive (differentiate S. pyogenes and enterococci)
7) Penicillin susceptible

109
Q

Disease caused by Strep. Pyogenes

A

1) Streptococcal pharyngitis
2) Scarlet fever
3) Toxic Shock-Like Syndrome
4) Skin/wound infections (non-bullous impetigo, erysipelas, cellulitis, nec. fasc.)
5) Acute rheumatic fever
6) Acute glomerulonephritis
7) Poststreptococcal Reactive Arthritis

110
Q

Streptococcal pharyngitis

A

self-limiting, life long type-specific immunity

Resolution mediated by anti-M protein antibody which allows phagocytosis and rapid killing of bacteria by PMNs/monocytes

**Can have acute RF strains OR acute GN strains

111
Q

When should you culture a throat?

when shouldn’t you?

A

⅔ of sore throats are caused by VIRUSES (cough, runny nose) → don’t culture

Tender lymph nodes, close contact with strep → culture

112
Q

Scarlet fever

A

systemic manifestation of pyrogenic exotoxins A, B, and C

Fever, pharyngitis, strawberry tongue, confluent erythematous “sandpaper like” rash (fine/blanching)

Rash begins on chest and neck, spreads out
-Spares nasolabial triangle and chin

113
Q

Toxic Shock-Like Syndrome

A

systemic release of exotoxin A due to skin infection causes polyclonal activation of T cells

Fever, shock, multi-organ failure

114
Q

How is staph TSS different from strep TSLS?

A

Different from staph because strep has 2 features NOT present in staph

1) Painful pre-existing skin infections
2) Positive blood cultures

115
Q

Strep. Pyogenes skin/wound infections

include what 3 types?
rapid spread due to what?
Can cause what secondary complication?

A
  • rapid spread due to spreading factors (streptokinase, hyaluronidase, etc.)
  • Can cause acute GN (NOT RF)

1) Non-Bullous Impetigo
2) Erysipelas
3) Cellulitis
4) Necrotizing Fasciitis

116
Q

Non-Bullous Impetigo

A

Strep. Pyogenes infection

pustular lesions, honeycomb-like crusts usually around mouth
→ PSGN

117
Q

Erysipelas

A

Strep. Pyogenes infection

superficial infection of skin, well-defined borders
Red, tender, warm

118
Q

Cellulitis due to Strep. Pyogenes infection

A

rapidly spreading skin infection in deeper subcutaneous tissues, ill-defined borders

Red, tender, warm

119
Q

Necrotizing Fasciitis is due to what toxin?

A

Strep pyogenes

Exotoxin B production

120
Q

Acute rheumatic fever

A

non-suppurative (non-pus producing) complications of strep infection

Type II hypersensitivity reaction: cross reaction between S. pyogenes antigens (M protein) and self antigens

Systemic disease 3-6 weeks after S. pyogenes infection (THROAT only, NOT skin infection)

JONES criteria

121
Q

JONES criteria

A

Joints = migratory polyarthritis

O = endocarditis, myocarditis, pericarditis

Nodules = subcutaneous, extensor surfaces

Erythema marginatum rash

Sydenham chorea = neurologic disorder, abrupt, nonrhythmic involuntary movements, muscle weakness

122
Q

Acute glomerulonephritis

A

non-suppurative (non-pus producing) complications of strep infection

Follows strep skin or throat infection by 2-4 weeks

Type III hypersensitivity reaction: circulating immune complex deposition causes glomerular damage

Elevated ASO or anti-DNase B titers

123
Q

Poststreptococcal Reactive Arthritis

A

NSAID unresponsive
Evidence of recent strep infection
Arthritis in small and big AXIAL joints

124
Q

Main structural and pathogenic features of Strep. Pyogenes (7)

A

1) Hyaluronic acid capsule
2) Attachment factors
3) M protein
4) Streptolysin O
5) Streptolysin S
6) Pyrogenic exotoxins A-C
7) Spreading factors

125
Q

Hyaluronic acid capsule of strep. pyogenes

A

Antiphagocytic, non-immunogenic

126
Q

Attachment factors of strep. pyogenes

A

pili, fibronectin-binding protein

Pili → mediate adhesion to epithelial cells (site specificity varies)

127
Q

M protein (strep pyogenes)

A

surface fimbriae

> 80 serotypes, each strain expresses only a single type

Major virulence determinant:
ANTI-PHAGOCYTIC - prevent interaction of bacterial cell with complement components

Adherent to epithelial cells

If strain lacks M protein → avirulent

Immunity to strep based on development of antibodies, serotype specific

128
Q

Streptolysin O

A

destroys RBCs

Inserts pores into RBCs causing lysis

Does not lyse neutrophils

Can measure ASO antibodies as indicator of infection

129
Q

Streptolysin S

A

non antigenic, destroys RBCs and WBCs

130
Q

Pyrogenic exotoxins A-C (strep pyogenes)

A

bacteriophage encoded toxin, subject to LYSOGENIC CONVERSION
-act as superantigens

Exotoxin A: causes toxic-shock like syndrome

Exotoxin B: protease precursor activated by cysteine protease → necrotizing fasciitis

Exotoxin A, B, and C → scarlet fever

131
Q

4 main spreading factors present in strep pyogenes

A

1) Streptokinase
2) Hyaluronidase
3) DNase
4) Proteinase

132
Q

Streptokinase

A

activates plasminogen to plasmin → fibrinolysis

spreading factor of strep. pyogenes

133
Q

Hyaluronidase

A

degrades ground substance of connective tissue, facilitates spread through tissue

spreading factor of strep. pyogenes

134
Q

DNase

A

nuclease which digests DNA, found in large concentrations in pus

Can get ab titers to DNase B

spreading factor of strep. pyogenes

135
Q

Pathogenesis of strep pyogenes infection

  • normal flora where?
  • transmitted how?
A

Carried in normal flora of throat and skin

Transmitted via respiratory droplets, food, or direct inoculation to skin

136
Q

Strep agalactiae

1) Group _____ strep
2) Gram stain? shape?
3) Bacitracin sensitive/resistant?
4) Hemolysis?
5) Two special tests that will be positive?
6) 6.5% NaCl Tolerance?

A

1) group B strep
2) Gram positive cocci
3) Bacitracin resistant
4) None/Beta hemolytic (weaker)
5) CAMP test +, Hippurate +
6) Variable 6.5% NaCl Tolerance

137
Q

Strep agalactiae is normal flora where?

A

vagina

138
Q

Treatment of Strep agalctiae?

A

penicillin G

Pregnant women with + culture → intrapartum penicillin prophylaxis (prevent neonatal disease)

139
Q

Main virulence and structural features of strep agalactiae (4)

A

1) Lipoteichoic acid (LTA) - part of cell envelope, mediate adherence
2) Polysaccharide capsule (antiphagocytic) - mediates ab immunity
3) Neuraminidase (extracellular product)
4) CAMP factor (extracellular product)

140
Q

Neuraminidase

A

Extracellular produce of strep agalactiae

enzyme cleaves sialic acid from polysaccharide and glycoprotein substrates

141
Q

CAMP factor

A

enhances hemolysis of staph aureus

Used for identification

Extracellular produce of strep agalactiae

142
Q

Vaccines for strep agalctiae

A

composed of purified HMW polysaccharides, can be given to high risk women to prevent GBS disease

143
Q

Disease caused by strep agalactiae (3)

A

Most common cause of:

1) neonatal meningitis (<6 mo)
2) sepsis
3) pneumonia

(very high mortality)

144
Q

Group D strep includes what two groups of bugs?

A

Enterococci and non-enterococci

145
Q

Enterococci

1) gram stain?
2) hemolysis?
3) growth in bile?
4) growth in NaCl
5) Hydrolyzes ________
6) normal flora where?

A

1) Gram +
2) Alpha hemolytic
3) Grow well in 40% bile
4) Grow well in 6.5% NaCl
5) Hydrolyze esculin
6) Normal bowel flora

146
Q

Diseases caused by enterococci (4)

A

1) UTI
2) Biliary infections
3) Bacteremia
4) Subacute bacterial endocarditis

147
Q

Treatment of enterococcus is complicated by what?

A

High prevalence of ampicillin and vancomycin resistance

VRE = Vancomycin Resistant Enterococci: alter cell wall dipeptide d-ala, d-ala → d-ala, d-lac

148
Q

2 important enterococci bugs

A

E. Faecalis, E. Faecium

149
Q

Non-enterococci include…

A

Strep. Bovis (aka strep gallolyticus)

150
Q

Non enterococci

1) gram stain? shape?
2) growth in bile?
3) growth in NaCl
4) uses _______
5) catalase
6) hemolysis

A

1) Gram + cocci
2) Grow in presence of 40% bile
3) Cannot grow in 6.5% NaCl
4) Uses Esculin
5) catalase -
6) non hemolytic (variable)

151
Q

Are non-enterococci (S. Bovis) part of normal human flora?

A

NOT part of normal flora, enters humans via lower GI or oropharynx

152
Q

Treatment of Strep bovis (3)

A

penicillin G, vancomycin, cephalosporins

153
Q

Pathogenesis of strep bovis infection

A

Escapes immune detection using encapsulation while in lamina propria → penetrates bloodstream → bacteremia

Attaches to collagen-rich structures in blood (e.g. valves) via pilus-like structures

154
Q

Diseases caused by strep bovis (3)

A

1) Infective endocarditis - CORRELATED WITH COLORECTAL NEOPLASM
2) Biliary system infection
3) Urinary tract infection

155
Q

Viridans streptococci

1) normal flora?
2) gram stain?
3) hemolysis?
4) capsule?
5) optochin sensitive/resistant?
6) Bile sensitive or resistant?

A

1) commensal (non-pathogenic)
2) gram + bacteria
3) Alpha hemolytic
4) No capsule
5) Optochin resistant
6) Not bile soluble (bile resistant)

156
Q

Common viridans streptococci bugs

A

Strep salivarius, Strep pyogenes sanguis, S. mitis, and S. mutans

157
Q

S. Mutans causes ________

A

dental caries

158
Q

S. Sanguinis causes ____________

A

subacute endocarditis

159
Q

Viridans streptococci produce ________ which allows them to adhere to _______ and _________

A

dextrans

tooth surface and previously damaged heart valves

160
Q

Strep pneumoniae

1) gram stain?
2) shape?
3) aerobe/anaerobe?
4) optochin sensitive/resistant?
5) hemolysis?
6) catalase?
7) positive _______ reaction

A

1) Gram +
2) Lancet shaped diplococci growing in chains
3) Facultative anaerobic
4) Optochin sensitive
5) Alpha hemolytic
6) Catalase -
7) Positive quellung reaction

161
Q

Main virulence factors of strep pneumoniae (2)

A

1) IgA protease: cleaves secretory IgA allowing colonization of nares
2) Polysaccharide capsule (antiphagocytic): increase susceptibility to asplenic patients → prophylactic vaccination

162
Q

Diseases caused by strep pneumoniae (5)

A

C-MOPS

1) Conjunctivitis: redness, discharge in one eye

2) Meningitis: fever, chills, headache, neck stiffness
- Elevated CSF protein, elevated PMNs, low CSF glucose

3) Otitis media: ear pain
4) Pneumonia
5) Sinusitis

163
Q

Symptoms of strep pneumoniae pneumonia

A

fever, chills, cough, chest pain

Rusty-brown sputum

164
Q

Treatment of strep pneumoniae

A

Respiratory fluoroquinolone (levofloxacin, moxifloxacin)

Beta-lactam + macrolide/doxycycline

165
Q

Vaccines available for strep pneumoniae? (2)

A

1) Prevnar =conjugate vaccine (polysaccharide capsule + protein conjugate)
- Given to children < 5yrs, adults > 65 yrs

2) Pneumovax = polysaccharide vaccine
- Give to adults > 65, immunocompromised, or asplenic patients

166
Q

Staph aureus:

1) gram stain?
2) shape?
3) aerobe/anaerobe?
4) grows on _______ but NOT ___________
5) catalase?
6) hemolysis?
7) _______ pigment
8) coagulase?
9) ferments ________

A

1) Gram +
2) Cocci in Clusters
3) Aerobic
4) Grows on blood agar, NOT MacConkey
5) Catalase +
6) B-hemolytic
7) Golden pigment
8) Coagulase +
9) Ferments mannitol (yellow on mannitol salt agar)

167
Q

Which two types of patients are especially susceptible to staph aureus infections?

A

1) Chronic Granulomatous Disease

2) Job Syndrome

168
Q

Chronic Granulomatous Disease

A

neutrophil defect in killing due to impaired H2O2 formation (NADPH oxidase deficiency)

169
Q

Chronic Granulomatous Disease are susceptible to which bugs?

A

**Also susceptible to: Need PLACESS

Nocardia, Pseudomonas, Listeria, Aspergillus, Candida, E. coli, S. aureus, Serratia

170
Q

Job Syndrome

A

hyper IgE syndrome

Deficiency of Th17 cells due to STAT3 mutation → impaired recruitment and chemotaxis of neutrophils to sites of infection

Predisposed to staph abscesses

171
Q

Staph aureus is normal flora where?

A

anterior nares

172
Q

Disease caused by staph aureus (9)

A

1) Food poisoning
2) Pneumonia
3) Osteomyelitis
4) Acute endocarditis
5) Septic arthritis
6) Skin infections (impetigo, cellulitis, abscesses, furuncles, carbuncles, wound infections)
7) Otitis and sinusitis
8) Scalded skin syndrome
9) Toxic shock syndrome

173
Q

Staph aureus Food poisoning

Associated virulence factors?

A

preformed toxin ingestion → vomiting/diarrhea

Associated virulence factors: enterotoxins

174
Q

Staph aureus Pneumonia

A

hospitalized acquired pneumonia s/p viral infection, or ventilator-associated pneumonia

Symptoms: abrupt onset fever, chills, LOBAR consolidation, rapid destruction of lung parenchyma → CAVITATIONS, EMPYEMA (pus in pleural space)

175
Q

Staph aureus Osteomyelitis

A

bone infection (usually boys < 12 yrs), due to hematogenous spread

176
Q

Staph aureus Acute Endocarditis

A

violent destruction of heart valves, sudden onset, high fever → endocarditis with thrombophlebitis

IV drug user → tricuspid → pneumonia from bacterial embolization from infected valve

Mitral/aortic valve → embolism of vegetations to brain

177
Q

Staph aureus Septic arthritis

A

invasion of synovial membrane by staph → closed infection of joint cavity

Symptoms: acutely painful, red, swollen joint, decreased ROM → can permanently lose function

Synovial fluid = > 100,000 PMNs, yellow/turbid

178
Q

Staph aureus skin infections? 3 kinds

A

1) Impetigo: contagious, crusty/honey colored, wet flakey typically on face or around mouth
2) Cellulitis: deeper infection (fat), hot, red, shiny skin
3) Local abscess, furuncles, carbuncles, wound infections

**Staph likes to localize in one spot

179
Q

Scalded skin syndrome

associated virulence factors?

A

painful, erythroderma, + Nikolsky sign, Bullous Impetigo

Infant → scalded skin syndrome

Older child → staph scarlet fever (no strawberry tongue)

Associated virulence factors: exfoliatins

180
Q

3 staph exotoxins

A

1) TSST-1 = super antigen
2) Enterotoxin
3) Exfoliant

**can treat infection with abx, but exotoxin mediated effects persist

181
Q

TSST-1

mechanism of action?

1) cross link ______________________ with ______________________
1) → antigen ___________ _______ cell activation
2) → increased _____ and _______ →
4) activate __________ →
5) increased ______, ________, and ________ pro-inflammatory cytokines
6) → SHOCK

A

staph aureus exotoxin

Acts as superantigen:

1) cross link a-chain of MHCII on APCs (macs, DCs) with variable region of B-chain of T-cell Receptors on CD4+ TH cells
1) → antigen independent TH cell activation
2) → increased IL-2, IFN-y →
4) activate macrophages →
5) increased IL-1, IL-6, TNF-a pro-inflammatory cytokines
6) → SHOCK

182
Q

Signs and symptoms of toxic shock syndrome

A

fever, hypotension, nausea, vomiting

RASH: erythema starts on TRUNK, spreads to extremities, erythema on PALMS/SOLES, conjunctival hyperemia, strawberry tongue
-Rash desquamation (peeling) 1-2 weeks later

Elevated ALT, AST, bilirubin

183
Q

Staph aureus Enterotoxin

A

superantigen

  • Heat resistant, acid stabile
  • Rapid onset food poisoning (within 1-6 hrs)
  • -> Nausea, vomiting, watery diarrhea

Mediated by CYTOKINE release (mast cells)

Classic foods: meat, poultry, mayo, milk/egg/dairy products, custards

184
Q

Staph aureus Exfoliant

A

Proteolytic exotoxin → cleaves desmoglein 1 → blister below stratum corneum = Bullous impetigo and staph scalded skin syndrome

185
Q

Staph aureus proteins that disable our immune defenses: (8)

A

1) Protein A
2) Catalase
3) Coagulase
4) Hemolysins
5) Leukocidins (PVL)
6) Beta-lactamase (penicillinase)
7) Novel penicillin binding protein (transpeptidase)
8) Clumping factor

186
Q

Staph aureus: Protein A

A

part of cell wall, binds Fc on IgG → protect from complement fixation (opsonization) and ab-mediated phagocytosis

187
Q

Staph aureus: Catalase

A

catalyzes H2O2 → inhibits PMN killing

188
Q

Staph aureus: Hemolysins

A

destroy RBCs, neutrophils, macrophages, and platelets

189
Q

Staph aureus: Leukocidins (PVL)

A

destroys PMNs → protects from phagocytosis

190
Q

Staph aureus: Beta-lactamase (penicillinase)

A

secreted B-lactamase that destroys B-lactam portion of penicillin molecule → inactivates antibiotic

191
Q

Staph aureus: Novel penicillin binding protein (transpeptidase)

A

protein necessary for cell wall peptidoglycan formation altered conferring resistance to penicillinase-resistant penicillins and cephalosporins

192
Q

Staph aureus: Clumping factor

A

binds fibrin → large clumps, blocks phagocytosis

193
Q

Staph aureus: Coagulase

A

leads to fibrin formation around bacteria → protect it from phagocytosis

194
Q

Staph aureus proteins to tunnel through tissue (4)

A

1) Hyaluronidase
2) Staphylokinase
3) Lipase
4) Protease

195
Q

Staphylokinase

A

protein lyses formed fibrin clots

196
Q

MRSA

A

staph with resistance conferred by altered penicillin binding proteins (MecA)

197
Q

What can you treat MRSA with? (5)

A

1) Vancomycin
2) Linezolid
3) Ceftaroline (5th gen cephalosporin)
4) Daptomycin
5) Tigecycline

198
Q

Vancomycin resistant staph

A

VISA and VRSA
Gets vanA gene from enterococcus

Must treat with alternative abx

199
Q

Erythromycin-induced clindamycin resistance (D-test)

A

Seen with some staph aureus

Exposure to erythromycin causes resistance to clindamycin

200
Q

S. epidermidis

1) Gram stain?
2) coagulase?
3) Novobiocin sensitive/resistant?
4) Urease +/-?
5) Hemolysis?
6) Normal flora where?

A

1) Gram +
2) Coagulase - (aka coag negative staph)
3) Novobiocin sensitive
4) Urease +
5) Non-hemolytic
6) Skin - Often a contaminant of blood cultures

201
Q

S. Epidermidis produces _______ which allows it to do what?

A

biofilm that allows adherence and colonization of prosthetic materials

202
Q

S. epidermidis causes what diseases? (2)

A

Common cause of catheter-associated UTI

Infects prosthetic devices: prosthetic heart valves, peritoneal dialysis catheters, prosthetic joints

203
Q

S. saphrophyticus

1) gram stain?
2) coagulase
3) Novobiocin sensitive/resistant?
4) Urease +/-
5) Catalase +/-
6) Normal flora where?
7) causes what disease?
8) aerobe or anaerobe?

A

1) gram +
2) Coagulase -
3) Novobiocin resistant
4) Urease +
5) Catalase +
6) Normal flora of rectum and vagina
7) UTI in sexually active females
8) Facultative anaerobe

Infectious Disease (9 decks)

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