Emily's Microbio Pre-Winter Midterm

Front 1

Exfoliatins act by

Back 1

targeting desmoglein 1a cadherin in desmosomes of stratum granulosum

Front 2

Where is Exotoxin A encoded, what controls it and what induces it?

Back 2

Chromosomally encoded, under lasR control, induced by iron restriction

Front 3

Where is Staphylokinase encoded?

Back 3

Phage

Front 4

Clostridium histo

Back 4

Gram + rods, large, pleomorphic, FORM SPORES, All but perfringens have peritrichous flagella

Front 5

Dzs caused by Fusobacterium necrophorum

Back 5

liver abscesses

Front 6

Dzs caused by Prevotella melaninogenica

Back 6

necrotizing pneumonia, periodontal disease

Front 7

How is Stenotrophomonas maltophilia spread?

Back 7

Contaminated equipment

Front 8

What Pseudomonad is important in CF and CGD patients?

Back 8

Burkholderia cepacia

Front 9

What type of flagella does Burkholderia pseudomallei have?

Back 9

Multitrichous polar flagella

Front 10

Dz caused by Burkholderia pseudomallei

Back 10

melioidosis: chronic lung dz often misdx as TB

Front 11

What is the only non-motile pseudomonad?

Back 11

Burkholderia mallei

Front 12

How do Pseudomonads respire?

Back 12

Entner Douderoff pathway (2-keto-deoxygluconate pathway). They are obligate aerobes

Front 13

Pseudomonas aeruginosa histo

Back 13

Gram negative rods, Polar flagella

Front 14

Cag pathogenicity island

Back 14

complex outer membrane protein found in most H. pylori isolates from Asia,
loosens TJs,
increases likelihood that H. pylori will cause ulcer and gastric cancer

Front 15

Vascular tropism

Back 15

something that Campylobacter fetus and Pseudomonas aeruginosa do,
attaches to vascular endothelium, causes:
endocarditis,
mycotic aneurysms,
cellulitis and
septic thrombophlebitis

Front 16

Campylobacter fetus sx

Back 16

nonspecific fever, positive culture

Front 17

Distinguish between Campylobacter and Helicobacter pylori

Back 17

Urease test: H. pylori is +, Campylobacter is -

Front 18

STa
(STb may not be active in humans, but would increase secretion)

Back 18

heat-stable E. coli toxin, causes ETEC, plasmid encoded, 19 amino acid peptide,binds guanylate cyclase C (guanylin receptor) on brush border,INCREASES cGMP,causes Cl- secretion

Front 19

Can 1st generation beta lactam antibiotics treat Staph?

Back 19

No

Front 20

Alpha hemolysin

Back 20

Staph aureus virulence factor, most potent of its kind, mushroom structure makes pores in PM of RBCs, WBCs, Platelets (channel size is pH dependent), low MW, chromosomally encoded

Front 21

Coagulase function

Back 21

Staph aureus virulence factor, binds prothrombin to allow Fibrinogen-->Fibrin conversion.

Front 22

F protein

Back 22

Strep pyogenes virulence factor, made under high O2, low CO2 conditions in lieu of M protein, binds to fibronectin, keratinocytes, and possibly respiratory epithelial cells

Front 23

Dzs caused by Enterococcus

Back 23

UTI, esp. in older men with prostate problems, Endocarditis, Abscesses originating from intestines

Front 24

Antibody tests used to detect preceding Strep infection and level of increase required

Back 24

ASO,
Anti-DNAse B,
Antihyaluronidase,
Streptokinase,

4x increase over 2 weeks

Front 25

Symptoms of GBS

Back 25

rapid onset of symmetrical limb weakness, loss of deep tendon reflexes, variable sensory loss, ascending polyneuropathy

Front 26

TSST-1

Back 26

22kD, genes located on pathogenicity island, induces production of IL-1B and TNF by monocytes, controlled by agr-quorum sensing

Front 27

Staph aureus dz by infection in blood stream

Back 27

Osteomyelitis, acute endocarditis, lung abscess, septic arthritis are caused by

Front 28

Pneumococcus virulence factors (6)

Back 28

1. Capsule (repeating oligosacch, 84 types and immunity is type-specific),
2. PDG and teichoic acid release during autolysis,
3. Pneumolysin,
4. Neuraminidase,
5. Hyaluronidase,
6. IgA1 proteases (prevent IgA-mediated immune clearance)

Front 29

Dzs caused by Strep pyogenes

Back 29

Strep pharyngitis (throat), Skin infections (esp. erysipelas), Scarlet fever, Strep Toxic Shock Syndrome, Delayed: Rheumatic Fever, Delayed: Glomerulonephritis

Front 30

Strep pyogenes virulence factors (7)

Back 30

1. M protein, 2. Lipoteichoic acid (LTA) = fibronectin binding molecule, attached to M protein, 3. F protein, 4. Hyaluronic acid capsule, 5. C5a protease, 6. IgG and IgA binding proteins (bind Fc portions),7. Secreted virulence factors

Front 31

Hyaluronic acid capsule

Back 31

Strep pyogenes virulence factor, only 1 kind. resembles human ground substance (may help avoid immune detection).

Front 32

Streptokinase

Back 32

Strep pyogenes secreted virulence factor, hydrolyzes fibrin and other host proteins, antigenic (can be neutralized by Ab)

Front 33

Strep agalactiae virulence factors

Back 33

Polysacch capsule with sialic acid, C5a peptidase, Beta-hemolysin

Front 34

Beta hemolysin

Back 34

Staph aureus and Strep agalactiae virulence factor, sphingomyelinase in 20% S. aureus strains (the ones causing mastitis), toxic to monocytes, pulm. epithel and endothel but NOT PMNs, fibroblasts or lymphocytes.
inhibited by surfactant. Provokes inflamm. response, cytokine release and NO production.

Front 35

Botulism toxin (BoNT) properties

Back 35

from Clostridium botulinum
phage encoded
metalloprotease
binds presynaptic peripheral cholinergic synapses at ganglia and NMJs
heavy chain of toxin binds and light chain enters cell via endocytosis
disrupts ACh release, leading to flaccid paralysis
nonantigenic

Front 36

dx of C. difficile infection

Back 36

endoscopy showing purulent exudates hiding necrotic intestinal tissue, toxin assay of stool (showing enterotoxin types A and B)

Front 37

mechanism of Enterotoxin type B

Back 37

bind receptors on intestinal epithelial cells, glucosylate Rho proteins, disrupt focal adhesions between cells, cause massive fluid secretion and acute inflammatory infiltrate

Front 38

What precipitates infection by Clostridium difficile?

Back 38

Broad-spectrum antibiotics

Front 39

Dz caused by Clostridium difficile

Back 39

Pseudomembranous colitis, Diarrhea

Front 40

Enterotoxin type A

Back 40

heat labile, cause of self-limited gastroenteritis, from Clostridium perfringens

Front 41

Clostridium perfringens virulence factors

Back 41

Alpha toxin (lecithinase), Enterotoxin type A

Front 42

Enzymes secreted by Clostridium

Back 42

collagenase, protease, hyaluronidase, lecithinase, DNAse, neuraminidase, toxins

Front 43

Normal colonization of Actinomyces israelii

Back 43

mouth and GI tract

Front 44

Normal colonization of Prevotella melaninogenica

Back 44

oral pharynx and GI and/or vagina

Front 45

Bacteroides fragilis virulence factors

Back 45

beta-lactamases, capsule (antiphagocytic and CHEMOTACTIC- can cause abscess by itself), deconjugates bile salts

Front 46

Bacteroides histo

Back 46

Gram - rod, nonmotile

Front 47

Distinguish Acinetobacter from Enterobacteriaceae

Back 47

Acinetobacter respires only, and can't reduce nitrate

Front 48

Distinguish Acinetobacter from Neisseria/Moraxella

Back 48

Acinetobacter is oxidase negative

Front 49

Psychrophilic def'n and example

Back 49

grows at 4 degrees Celsius, Ex. Pseudomonas fluorescens

Front 50

Stenotrophomonas maltophilia infects who?

Back 50

CF patients (it has low virulence)

Front 51

What dz does Pseudomonas aeruginosa cause in neutropenics?

Back 51

Pneumonia, bacteremia, ecthyma gangrenosum

Front 52

Pseudomonas aeruginosa's resistance mechanisms

Back 52

beta-lactamase, aminoglycoside inactivating enzymes, enzymes that acetylate chloramphenicol, expulsion of tetracycline, altered drug targets such as PBP (penicillin binding proteins) and gyrase

Front 53

What allows p. aeruginosa to cause ecthyma gangrenosum?

Back 53

Elastase

Front 54

Exotoxin S is... and How does it work?

Back 54

virulence factor made by 90% Pseudomonads, modifies GTP-binding proteins via ADP-ribosylation, stimulates inflammatory cytokines

Front 55

Exotoxin A is... and how does it work?

Back 55

an extracellular toxin of 90% Pseudomonads.
induced by iron limitation
activated by unfolding
enters cell by binding receptors
catalyzes ADP-ribosylation of EF2 (which inhibits protein synth and kills cells -esp. during corneal infections)
convergent evolution with diptheria toxin

Front 56

Alginate fcns

Back 56

exopolysaccharide capsule of Pseudomonas aeruginosa, polymers of D-mannuronic and L-gluronic acid, inhibits ciliary clearance from tracheobronchial tree, antiphagocytic, adheres bacteria to each other, highly antigenic, but Abs ineffective b/c blocking Abs

Front 57

Are Pseudomonads fermenters?

Back 57

No.

Front 58

H. pylori tx

Back 58

Bismuth salts OR Metronidazole OR Macrolides OR Tetracyclines OR Ampicillin AND Omeprazole (direct antimicrobial and synergistic with antibiotics)

Front 59

How does Campylobacter fetus avoid complement lysis?

Back 59

S-protein capsule --> allows it to cause bacteremia

Front 60

Late onset complications of Campylobacter infection

Back 60

GBS, Reactive arthritis

Front 61

Campylobacter jejuni or coli sx

Back 61

Fever, Diarrhea, abdominal cramps

Front 62

Campylobacter and Heliobacter histo

Back 62

Gram - rods, Polar flagella, faint, curved, slender

Front 63

Anti-oxidants

Back 63

compounds that protect agains cell damage by oxygen free radicals, in some Enterobacteriaceae

Front 64

Cytolethal Distending toxin

Back 64

in some E. coli and Salmonella typhi, two component DNAse (nuclear fragmentation and cell cycle arrest)

Front 65

HUS sx

Back 65

Hemolytic Uremic Syndrome, anemia, thrombocytopenia, renal failure, often caused by E.coli 0157:H7

Front 66

Example of invasin

Back 66

from Yersinia, just called "invasin," tightly binds beta1 integrins, rearranges the cytoskeleton and causes the uptake of Yersinia

Front 67

Klebsiella pneumoniae facts

Back 67

produces large goopy capsule in high glucose, nonmotile, causes only extra-intestinal infections, either a primary or opportunistic pathogen

Front 68

E. coli facts

Back 68

green sheen on EMB, primary pathogen or opportunistic pathogen, normal GI flora (made pathogenic by acquiring virulence factors)

Front 69

BFP

Back 69

bundle forming pili, polar, attach E. coli to epithelial cells

Front 70

P fimbriae

Back 70

on nephritogenic E. coli - bind neutral glycolipids of globoside series on human P blood group

Front 71

SPE-B

Back 71

Strep pyogenes secreted virulence factor, chromosomally encoded cysteine protease (tho some strains don't produce active protein), cleaves IL-1B into its active form and degrades fibronectin and vitronectin.

Front 72

Staphylokinase

Back 72

Staph aureus virulence factor, dissolves clots by promoting plasmin activation. phage encoded

Front 73

Non-histo properties that Enterobacteriaceae share

Back 73

Oxidase negative (though they do have an electron transport chain), Facultative (can ferment glucose to pyruvate to something else), Can reduce nitrate to nitrite

Front 74

Group B Strep capsule

Back 74

polysacch, contains sialic acid (inhibits C3 binding, diminishes immune recognition), often only defense in babies is maternal anticapsular IgG

Front 75

Where is Enterococcus' hemolysin encoded?

Back 75

Plasmid

Front 76

Staph aureus virulence factor, binds prothrombin to allow Fibrinogen-->Fibrin conversion.

Back 76

Coagulase

Front 77

Sublytic concentrations induce LTB4 release and IL-8 synthesis, leading to inflammation"

Back 77

Panton Valentine Leukocidin

Front 78

MRSA mutation

Back 78

plasmid-encoded mutation in transpeptidase that's not susceptible to 2nd gen beta lactams

Front 79

Dzs caused by pneumococcus (6)

Back 79

Bacterial pneumonia (most common cause), Otitis media, Sinusitis, Bronchitis, Bacteremia, Meningitis (most common cause)

Front 80

Mechanism of Inflammation related to Pneumococcal infection

Back 80

Released teichoic acid stimulates PAF production, PDG binds CD14 on macrophages, inducing cytokine secretion.(Causes influx of fluid into alveoli, then RBCs, then neutrophils.)

Front 81

Strep pyogenes secreted virulence factors (5)

Back 81

Hyaluronidase, Streptolysin O (SLO), Streptolysin S (SLS), Streptokinase, Streptococcal Pyrogenic Exotoxins (SPE) and Related Superantigens

Front 82

Factors that predispose to Acute Rheumatic Fever (not including previous GAS infection) (8)

Back 82

Age (4-9 year old), Crowding, Winter or Spring, Economic factors (poverty, urban environment), High magnitude of Host response to GAS (high Ab titer), Family history, Previous ARF, Increased frequency of HLA-DR2 and DR4

Front 83

Infections commonly preceding GBS (by 1 month)

Back 83

Diarrheal or Upper Respiratory Infection (found in 2/3 cases): Cytomegalovirus (severe sensory deficit), EBV, Varicella Zoster Virus, Rabies vaccine (if contaminated with myelin), Mycoplasma pneumoniae, Campylobacter jejuni

Front 84

Mechanism for Staph aureusType B Enterotoxin

Back 84

Superantigen, acts at neural receptors in upper GI tract, activating the vomiting center to cause food poisoning

Front 85

Osteomyelitis, acute endocarditis, lung abscess, septic arthritis are caused by

Back 85

Staph aureus dz by infection in blood stream

Front 86

Cerebrosides

Back 86

ceramide with a sugar (usually Glu or Gal) added to the head group

Front 87

Motor only version of GBS, with opthalmoplegia, ataxia, and areflexia. Associated with serotype O19 of Campylobacter jejuni

Back 87

Miller-Fisher variant of GBS

Front 88

What causes the prolonged PR interval in ARF?

Back 88

Myocarditis involving the conduction system

Front 89

What is used to measure the progress of an ARF patient?

Back 89

Acute phase reactants

Front 90

What meds interfere with acute phase reactants?

Back 90

Aspirin and corticosteroids

Front 91

Typical onset of Sydenham's chorea (relative to Strep infection)

Back 91

Gradual onset 4-8 weeks after Strep infection

Front 92

Treatment for arthritis associated with ARF

Back 92

Aspirin and NSAIDs

Front 93

Changes that occur in a heart as a patient heals from ARF carditis

Back 93

Valves thicken and deform, Chordae shorten, Valve commissures fuse (stenosis or insufficiency)

Front 94

Winter and Spring are the peak seasons of:

Back 94

Rheumatic Fever peaks in what seasons?

Front 95

Has glomerulonephritis followed skin infections of GAS?

Back 95

Yes

Front 96

Has glomerulonephritis followed pharyngeal infections of GAS?

Back 96

Yes

Front 97

Growth/Metabolic properties of Enterococcus

Back 97

PCN tolerant, metabolize esculin to a black pigment, can grow in 40% bile, can grow in 6.5% salt

Front 98

How does M protein facilitate the acquisition of bound plasmin for Strep pyogenes?

Back 98

M protein binds fibrinogen, that can then bind plasminogen. Streptokinase cleaves plasminogen.

Front 99

Necrotizing Fasciitis sx

Back 99

Swelling, heat and redness that moves rapidly from the initial infection site. 1 day later skin color changes red- purple - blue and large bullae form. Later skin dies and myositis may develop.

Front 100

What kinds of bacteria can cause necrotizing fasciitis?

Back 100

Strep pyogenes, Staph, Clostridium, Gram Negative Enterics

Front 101

How are Beta-hemolytic Strep classified?

Back 101

By Lancefield antigen aka C carbohydrate surface antigen (A, B, D)

Front 102

Risk factors for severe pneumococcal infection

Back 102

Debilitated health, sickle cell anemia, Hodgkin's dz, multiple myeloma, HIV, splenectomy

Front 103

Treatment of MRSA

Back 103

Vancomycin, Linezolid or Synercid

Front 104

Examples of Beta-lactam antibiotics

Back 104

Penicillins, Cephalosporins, Monobactams, Carbapenems

Front 105

Staph aureus carriers

Back 105

not normal flora, but colonizes nasopharynx, skin or vagina of 30% of population. Higher chance if medical personnel, diabetic, IV drug users

Front 106

Superantigen, acts at neural receptors in upper GI tract, activating the vomiting center to cause food poisoning

Back 106

Mechanism for Staph aureusType B Enterotoxin

Front 107

Dz caused by S. aureus enterotoxins

Back 107

Food poisoning (1-6 hours post-ingestion, NV & diarrhea) is caused by

Front 108

Scalded Skin Syndrome in newborns and Bullous Impetigo in older kids/adults are caused by

Back 108

Dz caused by Exfoliatins

Front 109

Staph aureus virulence factor, most potent of its kind, mushroom structure makes pores in PM of RBCs, WBCs, Platelets (channel size is pH dependent), low MW, chromosomally encoded

Back 109

Alpha hemolysin

Front 110

Staph that causes 10-20% of UTIs in sexually active women 16-35 y.o., 90% of whom have sx

Back 110

Staph saprophyticus

Front 111

22kD, genes located on pathogenicity island, induces production of IL-1B and TNF by monocytes, controlled by agr-quorum sensing

Back 111

TSST-1

Front 112

Staph aureus dz by direct infection

Back 112

Folliculitis, Furuncles, Carbuncles, Abscesses, Cellulitis, Wound infections, Osteomyelitis are caused by

Front 113

Miller-Fisher variant of GBS

Back 113

Motor only version of GBS, with opthalmoplegia, ataxia, and areflexia. Associated with serotype O19

Front 114

Most common antecedent infection to GBS

Back 114

Campylobacter jejuni (esp. serotype O19, which contains neuraminic acid aka sialic acid in the O side chain of LPS, cross reacts with peripheral nerves)

Front 115

Prophyllactic ARF tx (for first 5 years to prevent recurrence)

Back 115

PCN IM monthly, Sulfadiazene qday, Erythromycin BID

Front 116

Tx of ARF

Back 116

PCN, Erythromycin for PCN-allergic, Corticosteroids for acute carditis

Front 117

Acute phase reactants

Back 117

Minor manifestation of ARF. A change in Erythrocyte Sed Rate (ESR), or the presence of C-reactive protein in serum, suggest inflammatory process.

Front 118

Can erythema marginatum occur in a child?

Back 118

Yes, it occurs only in children.

Front 119

Erythema Marginatum

Back 119

Uncommon Major manifestation of ARF. Evanescent (vanishing quickly) pink rash with a clear center and serpiginous (wavy) margins

Front 120

Carditis is more likely to be a symptom of ARF in what population?

Back 120

Children

Front 121

Minor manifestations for dx of ARF (Jones Criteria)

Back 121

Fever, Arthralgia, Previous RF, Acute Phase Reactants, Prolonged P-R interval

Front 122

Major manifestations of ARF (Jones Criteria)

Back 122

Carditis, Polyarthritis, Sydenham's Chorea, Erythema marginatum, Subcutaneous nodules

Front 123

Age group most commonly stricken with Acute Rheumatic Fever (and Strep pharyngitis)

Back 123

4-9 year olds

Front 124

Enterococcus Tx in PCN-allergic patient or PCN-resistant strains

Back 124

Vancomycin + an aminoglycoside. But beware of VRE (Vancomycin resistant enterococci) and cross your fingers they don't spread the ability to MRSA.

Front 125

Growth/Metabolic properties of Strep bovis

Back 125

metabolize esculin to a black pigment, can grow in 40% bile

Front 126

Enterococcal endocarditis Tx

Back 126

a PCN AND an aminoglycoside (ex. ampicillin and gentamycin) - synergistic effect to kill organism (since organism is isolated from host immune system)

Front 127

Group B Strep normal colonization

Back 127

Normally colonizes vagina or intestines of 20-30% adult pop.

Front 128

Group B Strep culture results on blood agar plate

Back 128

Beta-hemolytic, but don't produce large clear zones on blood agar plates. Produce an orange pigment.

Front 129

Strep pyogenes tx

Back 129

PCN. For severe infections, also clindamycin to decrease protein and toxin production. For STSS, IV IgG as adjunctive therapy

Front 130

SPE-A

Back 130

Strep pyogenes secreted virulence factor, encoded on lysogenic phage, associated with scarlet fever, toxic shock syndrome, necrotizing fasciitis.

Front 131

Neuraminidase

Back 131

Pneumococcus virulence factor, unmasks cell-surface binding receptors, may contribute to hemolytic-uremic syndrome.

Front 132

Pneumolysin

Back 132

Pneumococcal virulence factor, cytolysin that forms pores in eukaryotic membrane. Cytotoxic to bronchial epithelial cells, may screw up clearance mechanism, allowing bacteria to grow in lower respiratory tract. Possibly attacks macrophages and neutrophils and makes alveolar-capillary barrier leak.

Front 133

Agr responds ________ to H+ ions

Back 133

positively

Front 134

Agr responds ________ to carbohydrates

Back 134

negatively

Front 135

not normal flora, but colonizes nasopharynx, skin or vagina of 30% of population. Higher chance if medical personnel, diabetic, IV drug users

Back 135

Staph aureus carriers

Front 136

Panton-Valentine Leukocidin

Back 136

Staph aureus virulence factor, found in 5% of strains (mostly causing abscesses), lethal to PMNs via pores.

Front 137

Staph histo

Back 137

Gram Positive Cocci growing in clusters, singly or pairs. Divide perpendicular to plane of last division. Nonmotile.

Front 138

Distinguish Staph aureus from other Staph

Back 138

Staph is coagulase positive, produces a gold pigment (carotenoids) when grown on sheep's blood agar, thermostable nuclease positive, mannitol positive,

Front 139

Staph aureus subtypes

Back 139

5 groups based on lysis patterns with 20 bacteriophages

Front 140

Most common non-aureus Staph

Back 140

Staph epidermidis

Front 141

Is Staph saprophyticus novobiocin sensitive or resistant?

Back 141

novobiocin resistant

Front 142

Is Staph epidermidis novobiocin sensitive or resistant?

Back 142

sensitive

Front 143

What do S. aureus, saprophyticus, and epidermidis have in their teichoic acid?

Back 143

S. aureus - ribitol, S. saprophyticus and S. epidermidis - glycerol

Front 144

Which non-aureus Staph is commonly nosocomial?

Back 144

S. epidermidis, often from IV catheters and prosthetics, or contaminating blood cultures from needle entering skin

Front 145

Distinguish Staph from Strep

Back 145

Catalase test: drop H2O2, if O2 gas is formed, it's Staph. Catalase is a heme-containing enzyme and Strep doesn't make heme.

Front 146

Virulent factor of Staph epidermidis

Back 146

"Slime" aka biofilm. Viscous, exopolysaccharide, allows it to cling to hospital equipment and is more difficult for host to clear.

Front 147

Bacteremia

Back 147

presence of viable bacteria in blood (positive blood cultures)

Front 148

presence of viable bacteria in blood (positive blood cultures)

Back 148

Bacteremia

Front 149

Septicemia

Back 149

bacteremia with symptoms of systemic response (tachycardia, hypotension)

Front 150

bacteremia with symptoms of systemic response (tachycardia, hypotension)

Back 150

Septicemia

Front 151

Most Gram Positives adhere via...

Back 151

protein-protein interactions

Front 152

Most Gram Negatives adhere via...

Back 152

cell surface appendages interacting with cell surface sugars

Front 153

Staph aureus virulence factors (11)

Back 153

1. Microcapsule
2. Binding proteins (fibronectin, fibrinogen, vitronectin, collagen type II)
3. Clumping factor
4. Coagulase
5. Hemolysins (alpha, beta, gamma, delta)
6. Leukocidins
7. Penicillinase/beta-lactamase
8. Enzymes to tunnel through tissue (Staphylokinase, Hyaluronidase, Lipase)
9. Exotosins (Exfoliatin A&B, Enterotoxins, TSST-1)
10. Release of PDG from cell wall
11. Protein A

Front 154

Staph aureus binding proteins

Back 154

Fibronectin, Fibrinogen, Vitronectin, Collagen type II.

Front 155

Protein A

Back 155

Staph aureus virulence factor, 42 kD, usually linked to PDG, binds Fc of IgG and prevents opsonization/phagocytosis

Front 156

Staph aureus virulence factor, 42 kD, usually linked to PDG, binds Fc of IgG and prevents opsonization/phagocytosis

Back 156

Protein A

Front 157

Staph aureus virulence factor, sphingomyelinase in 20% S. aureus strains (the ones causing mastitis), toxic to monocytes, but NOT PMNs, fibroblasts or lymphocytes

Back 157

Beta hemolysin

Front 158

Staph aureus virulence factor, dissolves clots by promoting plasmin activation. phage encoded

Back 158

Staphylokinase

Front 159

Hyaluronidase

Back 159

Staph aureus virulence factor, drills through proteoglycans in connective tissue

Front 160

Staph aureus virulence factor, drills through proteoglycans in connective tissue

Back 160

Hyaluronidase

Front 161

Lipase

Back 161

Staph aureus virulence factor, dissolves fats and oils, helps disseminate the bacteria

Front 162

Staph aureus virulence factor, dissolves fats and oils, helps disseminate the bacteria

Back 162

Lipase

Front 163

Superantigen

Back 163

A molecule that promotes TH cell and APC (MHCII) attachment regardless of Ag, leading to cytokine release (and thus fever, hypotension, shock, skin lesions, multiorgan faulure, and possibly death)

Front 164

A molecule that promotes TH cell and APC (MHCII) attachment regardless of Ag, leading to cytokine release (and thus fever, hypotension, shock, skin lesions, multiorgan faulure, and possibly death)

Back 164

Superantigen

Front 165

Dz caused by Exfoliatins

Back 165

Scalded Skin Syndrome in newborns and Bullous Impetigo in older kids/adults are caused by

Front 166

Food poisoning (1-6 hours post-ingestion, NV & diarrhea) is caused by

Back 166

Dz caused by S. aureus enterotoxins

Front 167

Sx of toxic shock syndrome

Back 167

fever, desquamative skin rash, hypoTN, multisystem involvement, possibly death

Front 168

fever, desquamative skin rash, hypoTN, multisystem involvement, possibly death

Back 168

Sx of toxic shock syndrome

Front 169

Toxin-mediated Staph aureus dz

Back 169

Scalded Skin syndrome, Bullous impetigo, Gastroenteritis/food poisoning, Toxic Shock Syndrome are caused by

Front 170

Scalded Skin syndrome, Bullous impetigo, Gastroenteritis/food poisoning, Toxic Shock Syndrome are caused by

Back 170

Toxin-mediated Staph aureus dz

Front 171

Folliculitis, Furuncles, Carbuncles, Abscesses, Cellulitis, Wound infections, Osteomyelitis are caused by

Back 171

Staph aureus dz by direct infection

Front 172

Agr is expressed in ______ phase, and causes

Back 172

expressed in stationary phase, and causes upreg. of toxins (alpha, beta hemolysins, serpin, PLC, exotoxin B, C, TSST-1) and downreg. of surface proteins (fibronectin BP, protein A, independent fibrinogen BP, beta-lactamase, collagen)

Front 173

Quorum Sensing mechanism

Back 173

bacteria secrete RAP (RNAIII-activating protein). When a certain concentration threshold is reached (sensed by 2 component system), TRAP (target of RAP) gets phosphorylated, activating it to make RNAIII, which regulates txn of Agr genes.

Front 174

A global regulator

Back 174

A genetic element that controls the transcription of many independent genes (ex. Agr - accessory gene regulator)

Front 175

Penicillins, Cephalosporins, Monobactams, Carbapenems

Back 175

Examples of Beta-lactam antibiotics

Front 176

Can 1st generation beta lactam antibiotics treat Strep?

Back 176

Yes

Front 177

Can 2nd generation beta lactam antibiotics treat Staph?

Back 177

Yes

Front 178

Can 2nd generation beta lactam antibiotics treat Strep?

Back 178

Yes

Front 179

Quorum Sensing definition

Back 179

The ability to sense the number of similar organisms in the vicinity.

Front 180

Coagulase Test

Back 180

Incubate 1-4 hours in rabbit plasma at 37 degrees, watch for clot (positive test)

Front 181

Alpha hemolytic

Back 181

RBCs intact, hemoglobin converted to biliverdin, green color

Front 182

Beta hemolytic

Back 182

Complete RBC lysis, clear blood agar plate

Front 183

Gamma hemolysis

Back 183

no hemolysis

Front 184

Strep histo

Back 184

Gram positive cocci in chains, pairs or singly

Front 185

P disk

Back 185

Optochin, distinguish between Strep pneumoniae (sensitive) and other alpha hemolytic Strep

Front 186

A disk

Back 186

Bacitracin, distinguish between Strep pyogenes (sensitive) and other beta hemolytic Strep

Front 187

Distinguish between Strep pyogenes and other beta hemolytic Strep

Back 187

A disk (bacitracin)

Front 188

Distinguish between Strep pneumoniae and other alpha hemolytic Strep

Back 188

P disk (optochin)

Front 189

Most autolytic of the Strep

Back 189

Pneumococcus. When its autolysin (muramidase) is activated, bacterium destroys itself. In stationary phase, this happens naturally.

Front 190

Method of transmission of pneumococcus

Back 190

Person-to-person only.

Front 191

Most common cause of bacterial pneumonia in adults

Back 191

Pneumococcus

Front 192

Most common cause of meningitis in children and adults

Back 192

Pneumococcus

Front 193

Pneumovax contents and indications

Back 193

23 types of pneumococcal capsule antigens. Indicated for adults >65 y.o., or those with underlying conditions

Front 194

Most important Pneumococcus virulence factor

Back 194

Capsule

Front 195

Children less than 18 mo. old do not raise a good response (only a T-independent response) to a pure oligosacch vaccine. How can we elicit a protective response?

Back 195

Conjugate the oligosacch. to a protein, and a T-dependent response will be raised.

Front 196

Treatment of pneumococcal infections

Back 196

Test for resistance to beta lactams, but generally PCN.

Front 197

Viridans Strep that forms plaque

Back 197

S. mutans

Front 198

Dzs caused by Viridans Strep

Back 198

Endocarditis (usually on previously damaged heart valves), Caries (via lactic acid production and trapping within plaque and tartar)

Front 199

Lancefield Antigen D

Back 199

Now recognized as glycerol teichoic acid, and genus is called Enterococcus

Front 200

Most virulent beta-hemolytic Strep

Back 200

Strep pyogenes, Group A

Front 201

Does Strep pyogenes infect animals?

Back 201

No

Front 202

Necrotizing fasciitis tx

Back 202

surgically excise fascia, rapid antibiotic therapy. Despite best efforts, mortality >50%.

Front 203

Fournier's gangrene

Back 203

Necrotizing Fasciitis of male genital and perineal areas

Front 204

Most important virulence factor of Strep pyogenes

Back 204

M protein

Front 205

C5a protease

Back 205

Strep pyogenes and agalactiae virulence factor, cleaves C5a and inhibits neutrophil chemotaxis

Front 206

Which terminal (C or N) of M protein is attached to PDG?

Back 206

C - this terminal shows little variability, whereas the N terminal shows some variability.

Front 207

How does M protein prevent phagocytosis?

Back 207

By inhibiting C3b deposition.

Front 208

Can we get repeat infections of Strep pyogenes?

Back 208

Yes, because the N terminal of its M protein is what elicits Abs, and the N terminal shows wide variability.

Front 209

How many types of M protein are there?

Back 209

More than 80!

Front 210

What molecule does M protein mimic?

Back 210

Human coiled-coil alpha helical structure

Front 211

Streptolysin O (SLO)

Back 211

###############################################################################################################################################################################################################################################################

Front 212

Streptolysin S

Back 212

Strep pyogenes secreted virulence factor, nonantigenic, oxygen stable, very potent cytotoxin (ex. necrotizing fasciitis), structurally similar to other Gram positive bacteriocin, causes beta hemolysis.

Front 213

Streptococcal Pyrogenic Exotoxins (SPE) - formerly erythrogenic toxins

Back 213

Strep pyogenes secreted virulence factor, ex. SPE-A, SPE-C, SPE-B

Front 214

Strep pyogenes secreted virulence factor, encoded on lysogenic phage, associated with scarlet fever, toxic shock syndrome, necrotizing fasciitis.

Back 214

SPE-A

Front 215

Strep pyogenes secreted virulence factor, chromosomally encoded cysteine protease (tho some strains don't produce active protein), cleaves IL-1B into its active form and degrades fibronectin and vitronectin.

Back 215

SPE-B

Front 216

Mode of mother-baby Group B Strep transmission

Back 216

Colonization in vagina EITHER infects amniotic fluid through placental membranes, then is aspirated, and works its way into the bloodstream, OR acquired during passage through birth canal.

Front 217

Dzs caused by Group B Strep in newborns

Back 217

Pneumonia and Septicemia (RDS and fever in first few days of life, esp for low birth weight or premature water breaking), Bacteremia and Meningitis (usually Capsule type III, can cross BBB via brain capillary cells)

Front 218

CAMP test

Back 218

Test used to ID Group B Strep (Strep agalactiae). Single streak Staph aureus across plate of sheep blood agar, then streak potential Group B Strep perpendicularly (but not crossing the line). If an arrowhead lysis pattern forms pointing to Staph aureus line, it is Strep agalactiae.

Front 219

Subtypes of Group B Strep

Back 219

Based on surface polysacch capsular Ags (I, II, III ... VI)

Front 220

Group B Strep tx

Back 220

PCN, ampicillin or CEPH

Front 221

Group C Strep hemolysis pattern, dzs

Back 221

beta-hemolytic, uncommon infective agent, syndromes similar to Group A (cellulitis, lymphangitis)

Front 222

Are enterococcus alpha-hemolytic?

Back 222

No

Front 223

Distinguish between Strep bovis and Enterococcus

Back 223

Strep bovis canNOT grow in high salt (6.5%)

Front 224

Cause of Acute Rheumatic Fever

Back 224

Previous Strep pyogenes (GAS) pharyngitis

Front 225

Average time between Strep pharyngitis and onset of Acute Rheumatic Fever

Back 225

2 weeks

Front 226

Most common cause of acquired heart disease

Back 226

Acute Rheumatic Fever

Front 227

Has Acute Rheumatic Fever followed skin infections of GAS?

Back 227

No

Front 228

Can we prevent primary or secondary attacks of Acute Rheumatic Fever?

Back 228

Yes, by prophyllactically treating Strep pyogenes pharyngeal infections.

Front 229

Rheumatic Fever peaks in what seasons?

Back 229

Winter and Spring are the peak seasons of:

Front 230

Chance of developing ARF with a low Ab titer

Back 230

<1%

Front 231

Chance of developing ARF with a high Ab titer

Back 231

3%

Front 232

Which MHC Class II alleles predispose to ARF?

Back 232

HLA-DR2 and DR4

Front 233

Probability of ARF following Strep throat in a person who has a hx of ARF

Back 233

30-50%

Front 234

What is the structure of M protein?

Back 234

alpha helical coiled structure (common in human tissue - myosin, collagen, tropomyosin)

Front 235

True/False: Abs to M proteins conserved region cross-react with human proteins

Back 235

True

Front 236

True/False: Abs to the variable regions of M protein cross-react with human proteins

Back 236

Usually no, but yes in the case of M19 and human sarcolemmal protein

Front 237

Dx of ARF

Back 237

2 major criteria, or 1 major and 2 minor criteria, if supported by evidence of GAS infection

Front 238

What constitutes evidence of a preceding Strep infection in the dx of ARF?

Back 238

One of the following: Increased ASO (antistreptolysin O) titer or increase in other Ab titers, Hx of recent case of scarlet fever, Positive GAS throat culture

Front 239

The most severe manifestation of ARF

Back 239

Carditis (because the heart damage is permanent)

Front 240

Do patients with ARF usually have symptoms referable to the heart?

Back 240

The majority do not.

Front 241

Which valves are most frequently involved in endocarditis?

Back 241

Mitral>Aortic>Tricuspid>>>>>Pulmonic

Front 242

Which layers of heart muscle does ARF's carditis usually affect?

Back 242

All of them (pancarditis)

Front 243

What is MacCallan's patch and what dz is it associated with?

Back 243

In ARF carditis, a rough and thickened area in the left atrium above the base of the post. leaflet of the mitral valve.

Front 244

Arthritis associated with ARF is more likely to be worse in what population?

Back 244

Older, elderly

Front 245

most commonly recognized sympton of ARF

Back 245

arthritis

Front 246

Does ARF arthiritis leave permanent damage?

Back 246

No

Front 247

Another name for Sydenham's chorea

Back 247

St. Vitus' dance

Front 248

Sydenham's chorea

Back 248

Major manifestation of ARF, characterized by sudden, aimless, irregular movement accompanied by muscular weakness and emotional instability. Disappears during sleep.

Front 249

Does Sydenham's chorea continue throughout the night?

Back 249

No, it disappears with sleep.

Front 250

Where does erythema marginatum occur?

Back 250

Trunk or proximal extremities, never face

Front 251

Can erythema marginatum occur in an adult?

Back 251

No

Front 252

Subcutaneous nodules

Back 252

Major manifestation of ARF, also seen in Rheumatoid Arthritis. Pea-sized painless swellings over bony prominences. Only seen with severe carditis.

Front 253

True/False: Subcutaneous Nodules are pathognomic for ARF

Back 253

False- they also occur in RA

Front 254

True/False: Ashoff bodies are pathognomic for RHD

Back 254

True

Front 255

Can subcutaneous nodules occur as the only symptom of ARF?

Back 255

No, they are only seen with severe carditis (and with RA)

Front 256

ARF Subcutaneous nodule histo

Back 256

Spindle shaped interstitial aggregate of large mononuclear cells surrounding an area of fibinous necrosis (Aschoff body)

Front 257

Typical location of Aschoff body

Back 257

Heart, though possibly through the body, incl. subcutaneous nodules

Front 258

Tx of Group A Strep pharyngitis to prevent ARF

Back 258

10 day tx with PCN (Effective even if delayed after symptom onset), Doesn't work with 5 day PCN or 10 day sulfa

Front 259

Guillan Barre Syndrome (GBS)

Back 259

acute polyneuropathy that can lead to motor and sensory deficits

Front 260

Can GBS hit a 1 year old?

Back 260

No, it doesn't occur in children <3 yrs old

Front 261

ceramide with a sugar (usually Glu or Gal) added to the head group

Back 261

Cerebrosides

Front 262

Ganglioside

Back 262

ceramide that has multiple sugars added to the head group

Front 263

ceramide that has multiple sugars added to the head group

Back 263

Ganglioside

Front 264

Biopsies from GBS patients show C3 or Ab bound to...

Back 264

Schwann cells

Front 265

Currently, do people think Chlamydia causes atherosclerosis or ACS?

Back 265

No.

Front 266

Function of Staph aureus binding proteins

Back 266

Bind/adhere to ECM proteins, important for arthritis

Front 267

Pneumococcus histo

Back 267

lancet shaped diplococci

Front 268

% of population normally infected by Pneumococcus

Back 268

20-40% normally colonized in nasopharynx

Front 269

Sublytic concentrations of Panton-Valentine leukocidin induce

Back 269

LTB4 release and IL-8 synthesis, leading to inflammation

Front 270

Enterobacteriaceae histo

Back 270

Gram negative rods, peritrichous flagella (except Klebsiella and Shigella), no spores

Front 271

Outer membrane antigens of Enterobacteriaceae

Back 271

H - flagella, O - somatic antigen (oligosacch side chain of LPS), K - acidic polysacch capsule, Pili (Type 1 or 2) or P fimbriae, X adhesins, BFP

Front 272

K antigen (Vi) functions

Back 272

Enterobacteriaceae Outer Membrane Antigen - acidic polysacch capsule. Vi is the Salmonella typhi capsule.- Evasion of phagocytosis and complement- Adhesion to GI/GU epithelia (ex. E. coli K1 capsule adheres to GU?)

Front 273

Salmonella H Antigen

Back 273

Two different flagella, switch between them.

Front 274

Receptor that senses LPS, systemic symptoms that follow

Back 274

TLR4, fever and shock

Front 275

Type 1 pili

Back 275

mannose sensitive (bind at same site as D-mannose), important for colonization of GI tract, on Enterobacteriaceae

Front 276

Type 2 pili

Back 276

mannose-resistant pili, cause dz outside normal niche

Front 277

X adhesins

Back 277

on nephritogenic E. coli - bind to different globosides

Front 278

3 strains of Enterobacteriaceae that are clinically significant from wherever they are isolated

Back 278

Shigella, Salmonella and Yersinia

Front 279

Highly pathogenic strains of Enterobacteriaceae (6)

Back 279

Escherichia, Shigella, Proteus, Salmonella, Klebsiella, Yersinia

Front 280

selective media

Back 280

made with substances that inhibit the growth of unwanted organisms

Front 281

differential media

Back 281

allows strains to be distinguished based on a metabolic property

Front 282

Normal enteric bacteria are capable of fermenting

Back 282

lactose

Front 283

Differential media for lactose fermentation

Back 283

EMB and MacConkey agar. Suppress Gram + growth also.

Front 284

EMB agar

Back 284

Eosin Methylene Blue agar, Eosin inhibits Gram + growth, Lactose fermentation produces acid that colors the colony (methylene blue), Peptone fermentation leaves the colony clear

Front 285

MacConkey agar

Back 285

Bile inhibits Gram + growth, Lactose fermentation produces acid that colors the colony. Peptone fermentation leaves colonies clear

Front 286

Pyruvate breakdown pathways of Enterobacteriaceae

Back 286

Mixed acid pathway (products = formic acid, acetic acid, lactic acid, succinic acid -->methyl red test), 2,3 -butanediol pathway (products = butanediol, ethanol, acid -->Voges-Proskauer test detects acetoin)

Front 287

Enterobacteriaceae that use the Mixed Acid pathway

Back 287

E. coli, Citrobacter

Front 288

Enterobacteriaceae that use the 2,3 - butanediol pathway

Back 288

Klebsiella, Enterobacter, Serratia

Front 289

Enterobacteriaceae lactose fermenters

Back 289

E. coli, Citrobacter, Klebsiella, Enterobacter

Front 290

Nonmotile Enterobacteriaceae

Back 290

Klebsiella, Shigella

Front 291

Enterobacteriaceae Primary Pathogens (capable of causing dz in anyone)

Back 291

Shigella, Salmonella, Yersinia, Klebsiella pneumoniae, Escherichia coli

Front 292

Enterobacteriaceae Opportunistic pathogens (only cause dz in certain hosts)

Back 292

Escherichia coli, Klebsiella pneumoniae, Proteus, Serratia, Enterobacter, Morganella, Providencia, Citrobacter

Front 293

Enterobacteriaceae that are both Primary and Opportunistic pathogens

Back 293

Escherichia coli, Klebsiella pneumoniae

Front 294

Invasiveness

Back 294

either the ability to enter and survive inside host cells or the ability to invade systemically from an epithelial surface

Front 295

Pathogenicity Island

Back 295

a contiguous set of virulence genes that has been transferred from one bacterial species to another

Front 296

2 component regulators

Back 296

mechanism for sensing environment and respond. A membrane component, under certain conditions, phosphorylates a TF that expresses virulence genes

Front 297

Example of 2 component regulator

Back 297

Salmonella PhoP/PhoQ, senses low Mg2+ in phagosome and allows survival inside a cell

Front 298

Type III secretion system

Back 298

Used by Gram - bacteria to secrete host-destructive proteins into host cells in response to host cell contact, O2 tension, Ca2+, nutrient availability

Front 299

Examples of Type III secretion systems

Back 299

###############################################################################################################################################################################################################################################################

Front 300

E. coli functions in GI

Back 300

synthesizes Vitamin K, deconjugates bile salts and sex hormones, occupies receptors (protects against enteropathogen colonization), produces colicins, stimulates eptihel. cells to synth anti-microbial peptides

Front 301

Shigella facts

Back 301

nonmotile, does not make H2S, primary pathogen, but usually only in colon, ONLY in humans, most virulence factors are plasmid encoded (but Shiga toxin chromosomally encoded, shared via phage with EHEC and EIEC)

Front 302

Salmonella facts

Back 302

all make H2S except S. typhi, primary pathogen, S. typhi and S. paratyphi are ONLY in humans (the others are zoonotic)

Front 303

Proteus: culture, dist. dz

Back 303

swarms on blood agar plates, "ripples" on EMB plates, causes alkaline (pH>8) urine in UTIs (due to urease), opportunistic pathogen

Front 304

Adhesins

Back 304

macromolecule on cell envelope that helps adhere to host cells

Front 305

Examples of adhesins

Back 305

type 1 and 2 pili, F protein of Strep pyogenes, Filamentous hemagglutinin of Bordetella

Front 306

Invasins

Back 306

proteins that act locally to aid in the invasion of the host cell

Front 307

Capsule type K1

Back 307

E. coli's capsule, heavily sialylated (prevents activation of alternative complement pathway by binding factor H)

Front 308

Toxin

Back 308

poisonous substance produced by a microorganism

Front 309

Toxin causing ETEC

Back 309

LT (heat-labile) toxin, ST (heat-stable) toxin

Front 310

Toxin causing EHEC

Back 310

Shiga toxin

Front 311

Toxin causing EIEC

Back 311

Shiga toxin

Front 312

Toxin causing Dysentery

Back 312

Shiga toxin

Front 313

ETEC, sx

Back 313

Enterotoxigenic E. coli: traveler's diarrhea. decreased Na+ and Cl- reabsorption, increased Cl- and HCO3- secretion, Water diarrhea "rice water" resembling cholera

Front 314

EHEC, sx

Back 314

Enterohemorrhagic E. coli, inhibition of 60s ribosome inside intestinal epithelial cells kills them. Bloody diarrhea with severe ab cramps = "hemorrhagic colitis"

Front 315

EIEC, sx

Back 315

Enteroinvasive E. coli, inflammatory reaction- fever, bloody diarrhea with WBCs, resembles Shigellosis

Front 316

LT

Back 316

heat-labile toxin of E. coli, causing ETEC, plasmid-encoded, mechanism similar to cholera toxin, two-components (A and B, where B binds and A ADP ribosylates Galpha, destroying GTPase activity), causes continual secretion of Cl-, Na+ and H2O

Front 317

Shiga toxin

Back 317

employed by Shigella dysenterie, EHEC and EIEC, chromosomally encoded in Shigella, phage encoded in E. coli, two component cytotoxin, cleaves adenosine residue in 23S rRNA part of 60s ribosome (inhibits proteins synth-->death)

Front 318

RTX = hemolysin

Back 318

in some invasive E. coli, pore-forming protein, secreted by ABC transporter (ATP dependent), kills RBCs and phagocytic cells (increases virulence 100x)

Front 319

Iron transporters

Back 319

in some Enterobacteriaceae, Siderophores compete with iron binding proteins, then transport iron-siderophore complexes inside the cell by outer membrane receptors

Front 320

Iron-binding proteins normally in human tissues and mucosal surfaces

Back 320

Transferrin, lactoferrin, ferritin, myoglobin, hemoglobin.

Front 321

Mechanisms for bacteria to obtain iron

Back 321

1. stealing from transferrin/lactoferrin, 2. use broken down heme, 3. siderophores (ex. Enterobacteriaceae)

Front 322

Culture properties shared by Campylobacter and Helicobacter

Back 322

Fastidious and slow growing (requires specific conditions), Microaerophilic (5-10% oxyygen), Capnophilic (4-8% CO2), Peptone fermentation, CAN'T ferment carbohydrates, Oxidase +

Front 323

Distinguish between Campylobacter jejuni and coli and all other species

Back 323

Campylobacter jejuni and coli grow optimally at 42 degrees Celsius, resistance to cephalotoxin, sensitive to nalidixic acid, sensitive to complement lysis, (opposite for all others, including C. fetus)

Front 324

Oxidase test

Back 324

Add phenylethylene diamine dye, if it turns black, it contains cytochrome c oxidase in its electron transport chain

Front 325

Dzs caused by Campylobacter jejuni and coli

Back 325

Enteritis/diarrhea

Front 326

Dzs caused by Campylobacter fetus

Back 326

systemic infections in immunodeficient patients, abortions in sheep and cattle

Front 327

Normal location of Campylobacter

Back 327

GI flora of animals, esp. pigs and birds

Front 328

Campylobacter transmission

Back 328

contact with animals, eating contaminated food (esp. chicken b/c no air chilling involved in processing) or drinking contaminated water. NOT person to person

Front 329

Does Campylobacter have a carrier state?

Back 329

No

Front 330

Who gets Campylobacter infections?

Back 330

In developing countries, children get LOTS of infections. In developed countries, adults get it, and a severe case of it.

Front 331

Who dies from Campylobacter infections?

Back 331

Children and elderly

Front 332

What meds increase chances of Campylobacter infection?

Back 332

Antacids (anything that decreases gastric acid, because Campylobacters are sensitive to gastric acid).

Front 333

What kind of diarrhea do Campylobacter jejuni and coli cause?

Back 333

Bloody diarrhea of the jejunum, ileum and colon.

Front 334

Time course of Campylobacter jejuni/coli infection (if sx)

Back 334

First fever and HA, Then small amount of blood in diarrhea by 2nd/3rd day, end by 4-5 days

Front 335

What is the gold standard for dx of Campylobacter diarrhea?

Back 335

Culture (though this is difficult since it's microaerophilic and capnophilic!)

Front 336

Campylobacter jejuni/coli tx

Back 336

If any (self-limited), erythromycin and fluoroquinolones, because intrinsically resistant to trimethoprim and most beta lactams.

Front 337

Mech for Campylobacter epithelial cell killing

Back 337

cytotoxin = DNAse, breaks DNA and cell-cycle arrests

Front 338

Normal colonization of Campylobacter fetus

Back 338

GI flora of cattle and sheep

Front 339

Best stain to visulaize H. pylori

Back 339

Silver stain

Front 340

What % of people have H. pylori?

Back 340

50%

Front 341

When is H. pylori acquired?

Back 341

Usually childhood, lasts a lifetime.

Front 342

Is H. pylori zoonotic?

Back 342

No

Front 343

Where does H. pylori reside?

Back 343

Near but NOT INSIDE gastric epithelial cells and ectopic gastric mucosa (duodenal ulcers).

Front 344

Can H.pylori occur without gastritis?

Back 344

No, but the gastritis can be asx.

Front 345

Dzs caused by H. pylori

Back 345

Duodenal ulcer (#1), Gastric ulcer (#2 to aspirin), Gastric cancer, MALT lymphoma, chronic/acute antral/corpus gastritis

Front 346

Antral gastritis is precursor to

Back 346

duodenal ulcers

Front 347

Corpus gastritis is precursor to

Back 347

either gastric ulcers, gastric metaplasia and non-cardia gastric cancer

Front 348

Is GERD associated with H. pylori?

Back 348

No

Front 349

True/False: H.pylori's genome is one of the most conserved known.

Back 349

False, it is one of the most variable! Antibiotic resistance is common.

Front 350

H. pylori virulence factors

Back 350

surface urease, epithelial cell adhesins, Cag pathogenicity island (60% of strains), Vac (same strains as Cag+)

Front 351

urease and how does it act as a virulence factor?

Back 351

enzyme that splits urea into ammonia, on surface of H. pylori, protects from acid stress (urea channel is open at low pH, closes at neutral pH)

Front 352

Cytokines/chemokines produced by H.pylori-infected tissue

Back 352

IL-8 (attracts neutros, initiates TH1 inflammatory response), IL-1 (gastritis, gastric atrophy, gastric cancer)

Front 353

Vac

Back 353

vacuolating cytotoxin of H. pylori that disrupts cellular organelles

Front 354

What type of ulcer is preventative of gastric cancer?

Back 354

Duodenal ulcer

Front 355

Gastric cancer is caused by

Back 355

chronic inflammation due to H. pylori

Front 356

H. pylori treatment can cure what cancer?

Back 356

MALT lymphomas

Front 357

Can duodenal ulcers be cured by antacids? Do they recur?

Back 357

Yes, yes

Front 358

Can duodenal ulcers be killed by anti-H.pylori meds? Do they recur?

Back 358

Yes, No :)

Front 359

CLO test

Back 359

test for urease activity (cleaves urea to liberate ammonia) on antral biopsy obtained during endoscopy, dx for H. pylori infection

Front 360

What dx H. pylori?

Back 360

Urease positive by CLO test of antral biopsy obtained during endoscopy OR serology/urea breath test/stool antigen testing

Front 361

Urea breath test

Back 361

give patient labeled carbon isotope of urea by mouth, if H. pylori is present, tagged CO2 can be detected in breath samples

Front 362

How long do anti-H.pylori IgG Abs persist after infection is eradicated?

Back 362

6 months

Front 363

H. pylori cure rates

Back 363

90% on multiple drugs and prolonged therapy

Front 364

Distinguish Pseudomonas from Enterobacteriaceae

Back 364

Pseudomonas has polar flagella, Enterobacteriaceae have peritrichous flagella. Pseudomonas is oxidase positive, Pseudomonas can't ferment

Front 365

Stenotrophomonas maltophilia properties

Back 365

non-fermentative but oxidase negative Gram negative rod. Sensitive only to co-trimoxazole and tigecycline

Front 366

Can Pseudomonas aeruginosa survive in anaerobic conditions?

Back 366

Yes! Although it is an obligate respirer, it can use nitrate as a terminal electron acceptor.

Front 367

Can Pseudomonads grow on minimal media?

Back 367

Yes, they are nutritionally versatile.

Front 368

Why is Pseudomonas aeruginosa so scary?

Back 368

It's resistant to nearly everything and takes advantage of immunocompromised and burn patients.

Front 369

Is Pseudomonas aeruginosa normal flora?

Back 369

Yes, it is a minor component of bowel flora (but cannot ferment lactose, so it may come up on EMB and MacConkey agar).

Front 370

Pseudomonas aeruginosa culture

Back 370

hemolytic on BAP, extra-cellular pigments diffuse into agar, nutritionally versatile

Front 371

Distinguish between Pseudomonas species

Back 371

temperature tolerance and biochemical tests

Front 372

Pseudomonas aeruginosa virulence factors

Back 372

capsule: Alginate
binding proteins (fimbriae, pyochelin siderophore)
Secreted toxins (endotoxin, exotoxin A and S, pyocins)
Pigments (fluorescein, phenazines)
Enzymes and Proteases (gelatinase, collagenase, lecithinase, neutral and alkaline protease, elastase, PLC, cytotoxin)

Front 373

Regulation of Pseudomonas aeruginosa virulence factors

Back 373

Las R coordinates proteases, elastase and Exotoxin A, quorum sensing- When Las I is plentiful, it induces LasR

Front 374

Do all Pseudomonas aeruginosa strains make Alginate constituitively?

Back 374

No, only those strains associated with CF patients

Front 375

Psuedomodad pigment fcn

Back 375

toxic to WBC, antibiotic

Front 376

When does Pseudomonad pigment production increase?

Back 376

minimal media, low iron

Front 377

Fluorescein (aka ___), properties

Back 377

aka pyoverdin, yellow-green pigment, fluoresces with UV light

Front 378

Phenazine pigments and colors

Back 378

pyocyanin = blue green, pyorubin = rust brown, alpha-oxyphenazine = colorless, breakdown product of pyocyanin

Front 379

Differences between Pseudomonas endotoxin and Enterobacteriaceae endotoxin

Back 379

Pseudomonas endotoxin produces O side chains that are not attached to the core, and have Ca2+ pyrophosphate links that help make the outer membrane impenetrable (sometimes even to antibiotics)

Front 380

Pyocins are...

Back 380

bacteriocins that kill other Pseudomonads

Front 381

Evidence for convergent evolution of Exotoxin A and diptheria toxin

Back 381

not related immunologically and lack sequence homology, use different receptors, Exotoxin A activated by unfolding, diptheria toxin by cleavage, Diptheria toxin production localized to the throat

Front 382

Pseudomonas enzymes and proteases

Back 382

Gelatinase, Collagenase, Lecithinase, Neutral and alkaline protease, Elastase, PLC, Cytotoxin

Front 383

Elastase

Back 383

Pseudomonas enzyme
one of the nastiest in terms of damaging our bodies
accounts for "vascular tropism" of Psuedomonas
allows P. aeruginosa to cause ecthyma gangrenosum
destroys blood vessel linings, implicated in hemorrhagic and necrotic lesions of the lung and skin

Front 384

Is Pseudomonas aeruginosa a primary pathogen?

Back 384

No, it only causes dz in ppl with damaged defenses.

Front 385

What dz does Pseudomonas aeruginosa cause in chronic lung dz patients?

Back 385

Pneumonia, esp. after intubation

Front 386

What dz can Pseudomonas aeruginosa cause in hospitalized pts?

Back 386

UTI

Front 387

What dz can Pseudomonas aeruginosa cause in IV drug users?

Back 387

endocarditis

Front 388

What dz can Pseudomonas aeruginosa cause in burn victims?

Back 388

Infection of their burns

Front 389

What dz can Pseudomonas aeruginosa cause in puncture wound patients?

Back 389

Osteochondritis (#1 cause) or osteomyelitis.

Front 390

What dz can Pseudomonas aeruginosa cause in CF patients and how?

Back 390

Infection of the respiratory tract with inhibited ciliary clearance. Blocking Abs are made against alginate capsule, Only normal epithel cells (not CF cells) have the receptor to take up Pseudomonas and kill it.

Front 391

Ecthyma gangrenosum

Back 391

necrotic skin lesion in neutropenics caused by Pseudomonas aeruginosa, infection can progress to bloodstream, where elastase destroys vessel (vascular tropism) causing clotting, obstruction and necrosis.

Front 392

infection can progress to bloodstream, where elastase destroys vessel (vascular tropism) causing clotting, obstruction and necrosis"

Back 392

Ecthyma gangrenosum

Front 393

What dz can Pseudomonas aeruginosa cause in contact lens-wearers?

Back 393

Corneal infections

Front 394

What dz can Pseudomonas aeruginosa cause in hot tub users?

Back 394

What causes Hot tub folliculitis?

Front 395

What causes Hot tub folliculitis?

Back 395

What dz can Pseudomonas aeruginosa cause in hot tub users?

Front 396

What causes external otitis?

Back 396

Pseudomonas aeruginosa

Front 397

What can external otitis lead to?

Back 397

Osteomyelitis of the skull and involvement of cranial nerves (only in diabetics)

Front 398

Malignant otitis externa

Back 398

A Pseudomonas aeruginosa-mediated external otitis that progressed to osteomyelitis of the skull and cranial nerve involvement.

Front 399

Burkholderias are in the same genus as

Back 399

Pseudomonads

Front 400

Dz caused by Burkholderia mallei

Back 400

Glanders

Front 401

Glanders is a dz obtained from..

Back 401

Horses

Front 402

Pneumonia, necrosis of mucous membranes, skin and lymphatics is called

Back 402

glanders

Front 403

Where is Burkholderia pseudomallei found?

Back 403

tropical soil of Southeast Asia

Front 404

When do meloidosis sx occur?

Back 404

Burkholderia psuedomallei is dormant for years, then sx appear under stress

Front 405

Burkholderia cepacia tx

Back 405

piperacillin, 3rd gen CEPH, sometimes only polymyxins

Front 406

What type of flagella does Burkholderia cepacia have?

Back 406

Multitrichous polar flagella

Front 407

Stenotrophomonas maltophilia tx

Back 407

Trimethoprim/sulfamethoxazole (TMP/SMX)

Front 408

Psuedomonas fluorescens transmission

Back 408

infected blood transfusions and medications

Front 409

Acinetobacter histo

Back 409

Gram - (tho can be mistaken for + since it has a tendency to retain crystal violet), rods in log phase, coccobaccilary in stationary phase

Front 410

Is Acinetobacter a primary pathogen?

Back 410

No, it is an opportunistic, nosocomial pathogen.

Front 411

Normal colonization of Acinetobacter

Back 411

soil and water, skin and distal urethra of healthy ppl., (only Gram - part of normal skin flora)

Front 412

Major Acinetobacter pathogen

Back 412

Acinetobacter baumanii complex (80% of infections)

Front 413

What type of flagella does Acinetobacter have?

Back 413

None! It's nonmotile.

Front 414

Acinetobacter virulence factors

Back 414

Capsule (can give mucoid appearance, may predispose C' deficient people to infection), LPS, Bacteriocins

Front 415

Acinetobacter resistance mechs

Back 415

beta-lactamases, alterations of PCN-binding proteins and gyrase, loss of porins, efflux pump

Front 416

Risk factors for Acinetobacter infection

Back 416

severe illness, immunocompromised state, ICU extended stay, previous admin of 3rd gen CEPH, intubation, ventilator use, indwelling urinary catheter, neurosurgery

Front 417

What color are Acinetobacter colonies?

Back 417

Colorless, but may be mucoid

Front 418

Are Acinetobacter nutritionally versatile?

Back 418

Yes

Front 419

Dzs caused by Acinetobacter

Back 419

Pneumonia, Meningitis, Bacteremia, UTIs, wound infections, cellulitis

Front 420

What pathogen causes nosocomial pneumonia associated with ventilators?

Back 420

Acinetobacter

Front 421

What % of patients with Acinetobacter bacteremia get septic shock?

Back 421

30%

Front 422

Enzymes that detox superoxide ion

Back 422

superoxide dismutase, peroxidases, catalase

Front 423

obligate anaerobes are normal inhabitants of..

Back 423

mouth, vagina and intestines

Front 424

dz caused by obligate anaerobes tends to involve

Back 424

tissue injury and compromised vasculature

Front 425

host defenses against anaerobic infection

Back 425

increased redox potential (major), phagocytes (minor)

Front 426

Anaerobic infection tx

Back 426

metronidazole (must be reduced to become a DNA synthesis inhibitor)

Front 427

What is the most prevalent bacteria in stool, AND cause of anaerobic infections?

Back 427

Bacteroides, Bacteroides fragilis

Front 428

What are the fermentation products of Bacteroides?

Back 428

Acetate, propionate, succinate

Front 429

Dz caused by Bacteroides fragilis

Back 429

Diverticulitis, Septic abortion, Septic thrombosis, GI infections

Front 430

Normal colonization of Bacteroides fragilis

Back 430

Lower GI and vagina

Front 431

Can Bacteroides fragilis grow in O2?

Back 431

No, but it can survive O2 exposure.

Front 432

What does Bacteroides fragilis produce?

Back 432

Vitamin K

Front 433

Prevotella melaninogenica histo

Back 433

Gram - rod, grows black

Front 434

Prevotella melaninogenica virulence factors

Back 434

capsule, collagenase, leukocyte inhibitory factor, 10-25% are PCN-resistant

Front 435

Fusobacterium histo

Back 435

Gram - rods, pale-staining, slender with tapered ends

Front 436

How does Bacteroides LPS compare to Enterobacteriaceae LPS?

Back 436

Bacteroides' is much less virulent

Front 437

Normal colonization of fusobacterium

Back 437

oral cavity, GI and vagina

Front 438

Fusobacterium virulence factors

Back 438

very potent LPS, NO CAPSULE, necrophorum: hemolysin and leukocidin

Front 439

What is the fermentation product of Fusobacterium?

Back 439

butyric acid

Front 440

Fusobacterium necrophorum histo

Back 440

Gram - rods, broad, rounded ends with bulges in the middle of cells

Front 441

Fusobacterium nucleatum histo

Back 441

Gram - rod, thin pointed ends

Front 442

Dz caused by Fusobacterium nucleatum

Back 442

pulmonary infections

Front 443

Normal colonization of Peptostreptococci

Back 443

mouth and intestine

Front 444

Dz caused by Peptostreptococci

Back 444

Abscesses in brain, liver, breast and lung

Front 445

Peptostreptococci histo

Back 445

Gram + cocci, short chains, pairs or singly

Front 446

Distinguish Actinomyces israelii and Nocardia (identical histo)

Back 446

Nocardia is acid-fast, Actinomyces is anaerobic, Actinomyces is PCN sensitive

Front 447

Dz caused by Actinomyces israelii

Back 447

Actinomycosis: chronic eroding abscesses all over the body and burrowing through with NO regard for tissue planes

Front 448

Normal colonization of Clostridium

Back 448

GI tract, soil

Front 449

Dz caused by Clostridium perfringens

Back 449

Gas gangrene, Soft tissue infections, Food poisoning

Front 450

Will Clostridium perfringens form spores on aritficial culture media?

Back 450

No

Front 451

Clostridium perfringens culture

Back 451

double zone of hemolysis

Front 452

Gas gangrene

Back 452

caused by Clostridium perfringens, rapid infection of injured muscle, gas forms inside muscle tissue

Front 453

What kind of spore does Clostridium perfringens make?

Back 453

Subterminal spore

Front 454

Alpha toxin

Back 454

lecithinase, Ca2+ dependent PLC, strain A makes the most, causes lysis of RBCs and other cells, from Clostridium perfringens

Front 455

What kind of spore does Clostridium difficile have?

Back 455

Subterminal spore

Front 456

C. difficile tx

Back 456

oral vancomycin, metronidazole, STOP ANTIBIOTIC

Front 457

Exotoxin A properties

Back 457

from Pseudomonas aeruginosa (in low iron setting), chromosomally encoded, controlled by LasR, catalyzes ADP ribosylation of EF2, blocking host protein synth, activated by unfolding, convergent evolution with diptheria toxin

Front 458

Tetanus toxin (aka tetanospasmin) properties

Back 458

from Clostridium tetani
plasmid encoded
metalloprotease
reaches spinal cord and brains stem via retrograde axonal transport
blocks neurotransmission by cleaving neuroexocytosis proteins
inhibits inhibitory neurons
Doesn't develop enough of an immune response to cause immunity

Front 459

Dz caused by Clostridium botulinum

Back 459

Adult botulism (flaccid paralysis), Floppy baby syndrome, Wound botulism (usually drug associated)

Front 460

Where is SPE-B encoded?

Back 460

chromosomally encoded

Front 461

Where is SPE-A encoded?

Back 461

Lysogenic phage

Front 462

Where is Shiga toxin encoded?

Back 462

Chromosomally encoded in Shigella, phage encoded in E. coli

Front 463

Where is BoNT encoded?

Back 463

Phage

Front 464

Where is ST encoded?

Back 464

Plasmid

Front 465

What shape is the EB of C. trachomatosis? C. psittaci? C pneumoniae?

Back 465

round, round, pear-shaped

Front 466

Who is the primary host of C. psittaci?

Back 466

birds

Front 467

Dz caused by C. psittaci

Back 467

acute pneumoniae, endocarditis

Front 468

Dz caused by C. pneumoniae

Back 468

pneumonia, pharyngitis, bronchitis

Front 469

Who is the primary host of C. trachomatis?

Back 469

Humans

Front 470

Why are Chlamydia considered parasites?

Back 470

They can't make their own ATP so they are energy parasites and live intracellularly.

Front 471

Life Cycle of Chlamydia

Back 471

Elementary body (EB) passed extracellularly to new host cell, prevents fusion with lysosome, binary fisses with nucleus, replicates as Reticulate body (RB) and makes more EBs.

Front 472

Chlamydia histo

Back 472

Gram - (but no PDG), doesn't grow on culture unless inoculated into cells

Front 473

Dz caused by Chlamydia trachomatis

Back 473

Blindness (trachoma), Urethritis, Cervicitis, Salpingitis

Front 474

Dx of Chlamydia trachomatis

Back 474

direct fluorescent monoclonal anti-MOMP or anti-LPS Ab staining of genital exudates, OR nucleic acid hybridization techniques for asx female genital infections

Front 475

Dx of Chlamydia psittaci and Lymphogranuloma Venereum (LGV)

Back 475

complement fixation test to look for genus-specific LPS

Front 476

Chlamydia trachomatis tx

Back 476

long-acting azithromycin, >10 day macrolide or tetracycline

Front 477

How are Chlamydia's biovars divided?

Back 477

Based on target host cells

Front 478

mech of Chlamydia trachomatis biovar trachoma

Back 478

infects squamocolumnar epithelial cells of the eye and GU tract, causes conjunctivitis

Front 479

Mech of Chlamydia trachomatis biovar lymphogranuloma venereum (LGV)

Back 479

infects inguinal lymph nodes to cause LGV

Front 480

What are serovars?

Back 480

Subdivisions of biovars, equivalent to strains, based on different major outer membrane proteins (MOMP).

Front 481

Which Chlamydia serovars cause chronic conjunctivitis?

Back 481

A, B and C

Front 482

Which Chlamydia serovars cause oculogenital dz?

Back 482

D, E, F, G

Front 483

Which Chlamydia serovars cause LGV?

Back 483

L1, L2, L3

Front 484

What is the leading cause of preventable blindness?

Back 484

Trachoma caused by Chlamydia trachomatis

Front 485

How is C. trachomatis spread?

Back 485

common house fly and person to person

Front 486

Pathology of trachoma

Back 486

chronic follicular conjunctivitis due to Chlamydia trachomatis, progresses to scarring, eyelashes turn in and cause corneal scarring

Front 487

Consequences of recurrent Chylamydia trachomatis infections in women's genitals

Back 487

tubal scarring, ectopic pregnancy, infertility

Front 488

Dz caused by Ureaplasma urealyticum

Back 488

genitourinary infections (urethritis, epididymitis)

Front 489

Dz caused by Mycoplasma hominis

Back 489

genitourinary tract and nongenital infections (pyelonephritis, PID, post partum fever)

Front 490

What surrounds the cytoplasm of Mycoplasma?

Back 490

No PDG, just a 3 layered membrane

Front 491

Can Mycoplasma grow on minimal media?

Back 491

No, they have complex nutritional requirements and are dependent on external sources for nucleotides, AAs, fatty acids and sterols

Front 492

What does Mycoplasma have in its membrane?

Back 492

Sterols

Front 493

Mycoplasma histo

Back 493

Gram -, on artificial media, grow into "fried egg" colonies (hemadsorb and hemolyse RBCs)

Front 494

Does PCN clear Mycoplasma infections?

Back 494

No. They have no PDG cell wall and are inherently resistant to beta-lactam ABX

Front 495

Dz caused by Mycoplasma pneumoniae

Back 495

"walking" pneumonia

Front 496

Mycoplasma pneumoniae transmission

Back 496

droplets to the upper respiratory tract

Front 497

If you find cold agglutinins in a pneumonia patients serum, what bacteria would you suspect?

Back 497

Mycoplasma pneumoniae (though this test is not sensitive or specific)

Front 498

Can you get recurrent infections of Chlamydia?

Back 498

Yes, in fact, you will.

Front 499

Can you get recurrent infections of Mycoplasma?

Back 499

No, because there is no antigenic variation

Front 500

Mycoplasma pneumonia tx

Back 500

Erythromycin and doxycycline

Front 501

Mech of Mycoplasma pneumoniae invasion

Back 501

uses P1 adhesin to bind sialic acid on host respiratory tract cells, damages mucosa with hydrogen peroxide and superoxide, causes ciliastasis and epithelial necrosis

Front 502

Extrapulmonary infestations of Mycoplasma pneumoniae

Back 502

myocarditis, pericarditis, encephalitis, neuropathies, rashes, tender joints and muscles, polyarthritis

Front 503

dx of Mycoplasma pneumoniae

Back 503

Complement Fixation Test (measures early IgM and IgG), ELISA (measures IgM and IgG to P1 adhesin), Ag Capture Enzyme Immunoassay (Ag-EIA), PCR (detects genomic DNA)

Front 504

Dz caused by Hib

Back 504

meningitis, pneumonia, epiglottitis, septicemia

Front 505

Dz caused NtHi

Back 505

bronchitis/pneumonia, otitis media, sinusitis

Front 506

Who gets H. flu infections?

Back 506

Children <5 y.o. who have not been immunized

Front 507

What does H. flu require for growth?

Back 507

Media with X (hematin) and V (NAD)

Front 508

H. flu histo

Back 508

Gram - coccobacilli (small), pleomorphic rods

Front 509

Does H. flu grow on chocolate agar?

Back 509

Yes

Front 510

Dz caused by H. ducreyi

Back 510

Chancroid (STD)

Front 511

What strain should you cross-streak on a blood agar plate to allow H. flu growth?

Back 511

Staph aureus, to provide NAD (V factor)

Front 512

H. flu virulence factors (5)

Back 512

Capsule (PRP), IgA1 protease, LPS, Iron-acquiring outer membrane proteins, Pili/adhesins

Front 513

H. flu capsule comp, types, most pathogenic, antigenic?

Back 513

composed of polymers of PRP (polyribosyl ribitol phosphate), 6 serotypes, type b most pathogenic, antigenic (Abs are bacteriocidal) - only after child is 18months old

Front 514

Hib vaccine, time course

Back 514

PRP polymer conjugated to protein (to provoke a protective T-dependent response), 1st dose at 2 months, booster dose at 12-15 months

Front 515

Hib vaccine Abs cross react with

Back 515

E. coli K100

Front 516

Dz caused by Bordetella pertussis

Back 516

Whooping cough, Pertussis

Front 517

Dz caused by Bordetella parapertussis

Back 517

parapertussis (mild to severe respiratory disease)

Front 518

Which is smaller, H. flu or B. pertussis?

Back 518

B. pertussis is smaller.

Front 519

Is H. flu PCN sensitive?

Back 519

Usually yes but some strains have beta-lactamases

Front 520

Bordetella pertussis histo

Back 520

Gram - coccobacilli (small), Pleomorphic rods, "Bisected pearls" on Bordet-Gengou agar

Front 521

Bordet-Gengou agar

Back 521

will grow Bordetella pertussis, made of potato infusion, glucose, glycerol, peptones and 15-30% blood

Front 522

Dist. H. flu and B. pertussis

Back 522

Grow in anaerobic conditions, H. flu is a facultative anaerobe, B. pertussis is a strict aerobe

Front 523

Bordetella pertussis transmission

Back 523

droplets of resp. tract

Front 524

Dz course of Pertussis

Back 524

biphasic, catarrhal: colonization of resp. epithelium with local damage, paroxysmal: systemic intoxication, intense coughing, vomiting and convulsions

Front 525

Is B. pertussis antigenic

Back 525

Yes, survivors are immune

Front 526

bvg controls what?

Back 526

Bordetella virulence gene locus, controls Pertussis toxin, Adenylate cyclase/hemolysin, Pertactin, Filamentous hemagglutinin (FHA)

Front 527

B. pertussis virulence factors

Back 527

Filamentous hemagglutinin (FHA), Pertactin, Pili, Adenylate cyclase/hemolysin, Tracheal cytotoxin, Pertussis toxin, LOS (lipooligosaccharide)

Front 528

Pertactin

Back 528

69 kD outer membrane protein, Bordetella pertussis virulence factor

Front 529

Tracheal cytotoxin

Back 529

Bordetella pertussis virulence factor, tetrapeptide derived from PDG, causes ciliostasis, inhibits DNA synth and cell death

Front 530

Pertussis toxin

Back 530

Bordetella pertussis virulence factor, ADP ribosylates Gi, blocks its inhibition of AC, increased cAMP, inhibition of chemotaxis, and function of neutros, macrophages and lymphocytes

Front 531

ABX only effective against Pertussis in what phase?

Back 531

Catarrhal

Front 532

Development of Pertussis vaccine

Back 532

1st vaccine caused side effects, 2nd one was acellular but req'd 5 doses, recent one is 1 dose

Front 533

Neisseria histo

Back 533

Gram - cocci (diplococci), kidney bean shaped

Front 534

What types of agar can you culture Neisseria on?

Back 534

Chocolate agar, Thayer-martin

Front 535

Why can you culture Neisseria on chocolate agar?

Back 535

The heating released Hb, which binds FFAs. Neisseria cannot tolerate FFAs in media.

Front 536

What temperature can you NOT grow Neisseria?

Back 536

22 degrees

Front 537

What is Thayer-Martin media?

Back 537

chocolate agar plus vancomycin (to kill Gram +), colistin (to kill non-Neisseria Gram -), trimethoprim (broad spectrum antibiotic), nystatin (to kill yeast)

Front 538

Are Neisseria susceptible to heat, cold or drying?

Back 538

Yes to all 3

Front 539

What % CO2 does Neisseria prefer?

Back 539

4-8% CO2 (capnophilic)

Front 540

Does Neisseria have cytochrome c?

Back 540

Yes, oxidase +

Front 541

What morphologically resembles Neisseria?

Back 541

Moraxella, Acinetobacter, Veillonella

Front 542

Is Neisseria gonorrhoeae glucose positive?

Back 542

Yes

Front 543

Is Neisseria gonorrhoeae maltose positive?

Back 543

No

Front 544

Is Neisseria meningitidis glucose positive?

Back 544

Yes

Front 545

Is Neisseria meningitidis maltose positive?

Back 545

Yes

Front 546

Dist. Neisseria gonorrhoeae and meningitidis

Back 546

Neisseria meningitidis is maltose positive

Front 547

Are Neisseria autolytic?

Back 547

Yes, Neisseria is highly autolytic in stationary phase

Front 548

Which Neisseria strain has a capsule, Class 4 surface protein, and porin serotyping Class 1, 2, etc.

Back 548

Meningitis

Front 549

Which Neisseria strain has antigenic pili and LOS, Rmp surface protein, and porins PorA and PorB

Back 549

Gonorrhoeae

Front 550

Neisseria virulence factors

Back 550

IgA protease, pili, steals iron from transferrin, lactoferrin and Hb, LOS, porins

Front 551

Neisseria meningitidis capsule

Back 551

made mostly of sialic acid, antigenic

Front 552

Rmp

Back 552

Neisseria gonorrhoeae surface protein, elicits IgG blocking Ab response

Front 553

Class 4 surface protein

Back 553

Neisseria meningitidis virulence factor, elicits IgA blocking Abs

Front 554

What kind of blocking Abs does each strain of Neisseria elicit?

Back 554

N. meningitidis class 4 surface protein elicits IgA blocking Abs, N. gonorrhoeae Rmp elicits IgG blocking Abs

Front 555

What kind of Ab is elicited by N. gonorrhoeae's LOS?

Back 555

IgM

Front 556

What does each of the Neisseria strains use for adherence?

Back 556

N. meningitidis uses class 5 OM proteins (host cells and leuks), N. gonorrhoeae uses Opa "opacity" protein

Front 557

Opa protein

Back 557

"opacity proteins" from N. gonorrhoeae - makes colony opaque, antigenic variation, colonies lacking opa tend to be disseminated (DGI- disseminated gonococcal infections)

Front 558

Where is cholera toxin encoded?

Back 558

Lysogenic phage

Front 559

Vibrio cholerae histo

Back 559

Gram - rod, short, curved, motile

Front 560

Mechanism of cholera toxin

Back 560

enters via 5 B and 1 A subunit, ADP ribosylates G-alpha, blocking GTPase activity, INCREASE cAMP, Cl- leaves cell

Front 561

Where are ST and LT encoded?

Back 561

Plasmid

Front 562

Mechanism of E. coli LT

Back 562

enters cell via 5 B and 1 A subunit, ADP-ribosylates G-alpha, blocks GTPase activity, INCREASE cAMP, Cl- leaves the cell

Front 563

Why is LT's effect smaller than Cholera toxin, despite 80% homology and identical mechanisms?

Back 563

LT toxin is not secreted, and must be cleaved by host cell proteases to be activated

Front 564

What causes traveler's diarrhea?

Back 564

LT toxin of E. coli (ETEC)

Front 565

Why do infants get more severe diarrhea with ST than adults?

Back 565

They have more guanylin receptors.

Front 566

Mech of Pertussis toxin

Back 566

Identical to cholera toxin and LT , (ADP ribosylates G-alpha subunit, INCREASE cAMP), BUT it also secretes it's own AC (adenylate cyclase)

Front 567

Where is pertussis toxin encoded?

Back 567

Chromosomally encoded

Front 568

How is the expression of pertussis toxin controlled?

Back 568

bvg

Front 569

Where is diptheria toxin encoded?

Back 569

Lysogenic phage

Front 570

What toxins are produced in response to iron restriction?

Back 570

Exotoxin A (P. aeruginosa), Diptheria toxin (Corynebacterium diptheriae)

Front 571

Mechanism of Diptheria toxin

Back 571

Identical to Exotoxin A, enters cell by B and A subunits, catalyzes ADP-ribosylation of EF2, blocking protein synthesis

Front 572

Dz caused by C. diptheria

Back 572

throat infection- post. pharynx necrosis, heart failure (if absorbed systemically), wound infections

Front 573

Dz caused by Neisseria meningitidis

Back 573

Meningitis, Meningococcemia, Waterhouse-Friederichsen syndrome, Pneumonia (rare)

Front 574

Risk factors for Neisseria meningitidis infection

Back 574

Age (6-24 months and 10-20 years), Overcrowding, Winter or early Spring, C6, 7, 8 or MB-lectin deficiency

Front 575

How is Neisseria meningitidis transmitted?

Back 575

Nasal droplets

Front 576

Neisseria meningitidis dx?

Back 576

Gram stain of CSF, Culture of CSF, blood or skin lesions

Front 577

Can serum kill Neisseria meningitidis?

Back 577

No, because IgA blocking Ab to Class 4 surface protein, Sialic acid on capsule/LOS

Front 578

Neisseria meningitidis vaccine

Back 578

1) MPSV4 - 3-5yr. immunity to all strains except B (because not immunogenic), 2) MCV4 - should last longer

Front 579

Neisseria meningitidis tx

Back 579

high dose IV PCN or CEPH, Prophyllaxis with rifampin, adjunctive therapy with rBPI21

Front 580

rBPI21

Back 580

fragment of natural proteins from PMNs that bind LOS and kills Neisseria meningitidis, adjunctive therapy

Front 581

Neisseria meningitidis Meningitis sx

Back 581

brain damage (due to cytokines), potentially neuro deficits, SKIN LESIONS (petechiae-->necrotic, due to LOS)

Front 582

Meningococcemia sx

Back 582

low grade fever, skin lesions, arthritis, due to Neisseria meningitidis

Front 583

Waterhouse-Friderichsen syndrome

Back 583

bilateral hemorrhagic destruction of the adrenal glands, fulminating DIC, shock, due to Neisseria meningitidis

Front 584

Dz caused by Neisseria gonorrhoeae

Back 584

Men: urethritis, epididymitis, Women: cervicitis, salpingitis, PID

Front 585

Risk factors for Neisseria gonorrhoeae infection

Back 585

sexually active young adults, age 15-30yrs, C6, 7, 8 deficiency

Front 586

All women with Gonorrhea show sx

Back 586

No, only about 50% do!

Front 587

All men with Gonorrhea show sx

Back 587

Just about, 90% of urethritis has sx

Front 588

Neisseria gonorrhoeae dx

Back 588

men: Gram stain showing Neisseria gonorrhoeae in PMNs, women: culture of cervical pus

Front 589

What Ab can kill Neisseria gonorrhoeae?

Back 589

IgM

Front 590

What Ab can kill Neisseria meningitidis?

Back 590

IgG to capsule

Front 591

Neisseria gonorrhoeae tx

Back 591

Cephtriaxone (injectable CEPH), Cefixime PO, Quinolone if PCN-resistant due to plasmid beta-lactamase

Front 592

Quellung reaction

Back 592

method to type Pneumococcal capsule, mix unknown pnuemococcus with Abs against known capsule type, if swells --> + test, correct capsule type

Front 593

Ziehl-Neelsen stain

Back 593

Acid Fast stain (for Mycobacterium), HOT carbol fuscin, HCl and EtOH decolorize, methylene blue counterstain

Front 594

Why doesn't Mycobacterium stain with Gram's stain?

Back 594

It is acid-fast, cell envelope has mycolic acid, lipids and waxes

Front 595

Kinyoun modification of Ziehl-Neelsen stain

Back 595

dissolve carbol fuscin in phenol (no need for heat), Carbol fuscin in phenol, HCl and EtOH decolorize, methylene blue counterstain

Front 596

Modified acid fast stain

Back 596

Dist. Nocardia and Actinomyces: HOT carbol fuscin, sulfuric acid decolorize, methylene blue counterstain

Front 597

What organism(s) have a long doubling time (and therefore a long log phase)?

Back 597

Mycobacterium TB

Front 598

What organism(s) have a short doubling time (and therefore a short log phase)?

Back 598

E. coli

Front 599

What organism(s) have a long stationary phase?

Back 599

Staph aureus

Front 600

What organism(s) have a short stationary phase?

Back 600

Pneumococcus, Neisseria

Front 601

Aerobactin

Back 601

E. coli's siderophore

Front 602

How does Bacteroides get iron?

Back 602

from heme (once it's broken down)

Front 603

Fermentation product of Streptococcus

Back 603

lactic acid

Front 604

Fermentation product of E. coli

Back 604

mixed acids

Front 605

Fermentation product of Clostridium

Back 605

Butyric acid

Front 606

What does E. coli have that Shigella doesn't

Back 606

"peritrichous flagella

Front 607

What must a cell have in order to respire?

Back 607

Electron transport chain and final electron acceptor (O2 or nitrate...)

Front 608

What uses fumarate as a terminal electron acceptor?

Back 608

Bacillus fragilis

Front 609

Island (as in pathogenicity island)

Back 609

Operon and additional genes

Front 610

Operon

Back 610

cluster of genes encoding enzymes in the same pathway

Front 611

episome

Back 611

nonessential DNA, either integrated in chromosome or free in cytoplasm (ex. F plasmid)

Front 612

Are insertion sequences capable of self-replication?

Back 612

No

Front 613

Do transposons require sequence homology?

Back 613

No

Front 614

Which strains are natural transformers?

Back 614

Pneumococcus, Neisseria, H. pylori, H. influenzae

Front 615

Superantigens

Back 615

TSST-1, Enterotoxin, Exfoliatins, SPEs

Front 616

Which bacteria cannot be cultured?

Back 616

Mycobacterium leprosae

Front 617

Where can Mycobacterium leprosae be grown?

Back 617

armadillos or mouse footpads

Front 618

What is optimal temp for Mycobacterium leprosae?

Back 618

lower than core body temp, grows best by surviving in macrophages and Schwann cells in skin and superficial nerves

Front 619

Where does Mycobacterium leprosae grow best in the infected body?

Back 619

In macrophages and Schwann cells in skin and superficial nerves

Front 620

What cell wall component is specific to Mycobacterium leprosae?

Back 620

PGL-1, M. leprae-specific phenolic glycolipid

Front 621

What cell wall component do Mycobacterium leprosae and tuberculosis share?

Back 621

LAM (lipoarabinomannan)

Front 622

What's Hansen's dz?

Back 622

Leprosy

Front 623

Incubation period for leprosy

Back 623

5-7 years

Front 624

How is M. leprosae transmitted?

Back 624

Household contact, maybe mosquito or bed bug bite

Front 625

What % of ppl infected with M.leprosae develop the dz?

Back 625

10%

Front 626

States with highest M. leprosae rates

Back 626

CA, TX, NY, HI (immigrants from endemic areas)

Front 627

Endemic leprosy areas

Back 627

India, China, Brazil, Nigeria

Front 628

Tuberculoid leprosy aka

Back 628

Paucibacillary dz (since few of the bacilli are found in skin cultures)

Front 629

Treatment for leprosy

Back 629

Dapsone, Rifampin with or without clofazimine

Front 630

Role of IFN-gamma in lepromatous granulomas

Back 630

secreted by CD4 cells to stimulate macrophages to contain M. leprae growth

Front 631

Role of IL-2 in lepromatous granulomas

Back 631

secreted by CD4 cells to recruit more CD4 cells

Front 632

Are CD8 cells present in a lepromatous granuloma?

Back 632

Yes, on the periphery

Front 633

Tuberculoid leprosy sx

Back 633

anesthetic skin plaques, asymmetric peripheral nerve trunk involvement

Front 634

Which form of leprosy has a poor cell-mediated response?

Back 634

Lepromatous

Front 635

What is the role of CD8 cells in lepromatous leprosy?

Back 635

secrete cytokines that ENHANCE bacterial growth and inhibit CD4 function and expansion

Front 636

Which form of leprosy produces well-formed granulomas?

Back 636

Tuberculoid

Front 637

What is the role of IL-4 in lepromatous leprosy infection?

Back 637

secreted by CD8 cells, suppresses CD4 cell proliferation and function

Front 638

Lepromatous leprosy sx

Back 638

symmetric skin nodules, plaques, leonine (lion-like) facies, loss of eyelashes and body hair, loss of digits secondary to trauma, and testicular dysfcn (infertility)

Front 639

Which dz causes leonine facies?

Back 639

Lepromatous leprosy

Front 640

Where is Mycobacterium ulcerans endemic?

Back 640

wetlands of tropical and subtropical Africa, Western Pacific, Asia and South America

Front 641

How is Mycobacterium ulcerans transmitted?

Back 641

Unknown

Front 642

What is the 3rd most common mycobacterial infection in immunocompromised ppl?

Back 642

Buruli ulcer (m. ulcerans)

Front 643

What causes Buruli ulcer?

Back 643

M. ulcerans

Front 644

How long does it take a Buruli ulcer to develop?

Back 644

1-2 months

Front 645

name the organism:single, small, painless, subq nodule on a limb expands to 15cm ulcerated nodule over months, with whole limb edema

Back 645

M. ulcerans

Front 646

What is a Buruli ulcer?

Back 646

single, small, painless, subq nodule on a limb expands to 15cm ulcerated nodule over months, with whole limb edema

Front 647

Does a Buruli ulcer yield inflammatory infiltrate/pus?

Back 647

No!

Front 648

Tx for Buruli ulcer

Back 648

No antibiotics, wide surgical debridement (stop before greater disfiguring/deformity!)

Front 649

Which mycobacteria species are not in the Runyon grouping?

Back 649

M. leprae and M. ulcerans