Microbiology Comprehensive Flashcards: Bacteriology

Front 1

Staphylococcus are characterized by...?

Back 1

Gram positive cocci, catalase positive, facultative anaerobe

Front 2

Gram positive cocci, catalase positive, coagulase positive

Back 2

Staphylococcus Aureus

Front 3

Gram positive cocci, catalase positive, coagulase negative

Back 3

Staphylococcus (NOT Aureus, e.g. Saprophyticus, Epidermidis, Haemolyticus)

Front 4

Coagulase acts by...?

Back 4

Binding to a serum factor, and this complex converts fibrinogen to fibrin, resulting in clot formation.

Front 5

Capsule and slime layer is important to which species of Staphylococcus?

Back 5

Non-coagulase producing (Aureus) species

Front 6

This antigen is present on the surface of most Staph. Aureus strains. It binds the Fc receptor of IgG1, IgG2, and IgG4 preventing antibody mediated immune clearance.

Back 6

Protein A

Front 7

Protein A is present on what Staphylococcus species?

Back 7

Most strains of Staph. Aureus

Front 8

Protein A acts by...?

Back 8

It binds the Fc receptor of IgG1, IgG2, and IgG4 preventing antibody mediated immune clearance.

Front 9

Clumping factor is present on the surface of...? It acts by...?

Back 9

Staph Aureus. It is a bound form of coagulase. It acts like soluble coagulase, converting fibrinogen to fibrin, causing staphylococci to clump.

Front 10

Superantigens act by...?

Back 10

Binding to MHC-II on macrophages which interact with beta-subunit of T-cell receptor, causing T-cell proliferation and cytokine "storm"

Front 11

Staph Aureus: Alpha Toxin

Back 11

Creates pores in host cell membrane, leading to eflux of K+, influx of Na+ and Ca++, leads to osmotic swelling and lysis. Sensitivity of cell varies by cell type. Produced by most strains of Staph. Aureus.

Front 12

Staph Aureus: Beta Toxin

Back 12

Also called sphingomyelinase C. Heat labile protein that catalyzes the hydrolysis of membrane phospholipids in susceptible cells. Specificity for sphingomyelin and lysophosphatidylcholine. Produced by most strains of Staph. Aureus.

Front 13

Staph Aureus: Delta Toxin

Back 13

Non-specific membrane toxicity. Theorized detergent like mechanism of action. Produced by most strains of Staph. Aureus.

Front 14

Staph Aureus: Gamma Toxin and Panton-Valentine Leukocidin

Back 14

Gamme made by almost all Staph Aureus strains, P-V made by < 5% strains. Form bicomponent toxin of S (slow eluting) and F (fast eluting) chains.

S chains - HlgA (hemolysin gamme A), HlgC, LukS-PV

F chains - HlgB, LukF-PV

All 6 combinations can lyse neutrophils and macrophages.

P-V leukocidin toxin is leukotoxic but has no hemolytic activity.

Cell lysis by ALL these toxins is mediated by pore formation (swelling ~> Lysis)

Front 15

What mediates Staphylococcal scalded scale syndrome (SSSS)?

Back 15

Exfoliative toxins, either ETA or ETB.

ETA - heat stable, chromosomally encoded

ETB - heat labile, plasmid encoded

Both toxins are serine proteases that split intercellular bridges at desmosome.

Front 16

Staphylococcus Aureus: Enterotoxins

Back 16

Heat stable enterotoxins resistant to hydrolysis by gastric and jejunal enzymes. Act as superantigens.

Front 17

Staphylococcus Aureus: TSST-1

Back 17

Toxic Shock Syndrome Toxin-1. Heat and proteolysis resistant, chromosomally encoded. Primarily related to menstruation toxic shock syndrome (TSS), and many other TSS. Causes TSS which leads to hypovolemic shock, multiorgan failure and death.

Front 18

What is the species and toxin associated with menstruation related toxic shock syndrome?

Back 18

Staphylococcus Aureus, TSST-1

Front 19

Catalase acts by...?

Back 19

Converting hydrogen peroxide to oxygen and water.

Front 20

Hyaluronidase acts by...?

Back 20

Hydrolyzing hyaluronic acids, faciliting pathogen spread.

Front 21

Fibrinolysin acts by...?

Back 21

Also called staphylokinase, can dissolve fibrin clots.

Front 22

Lipases act by...?

Back 22

Hydrolyze lipids.

Front 23

Thermostable nuclease is a marker for?

Back 23

Staph. Aureus

Front 24

Penicillinase is...?

Back 24

Also called beta-lactamase. An enzyme that can breakdown the beta-lactam ring of penicillin and other beta-lactam antibiotics, leading to pathogen resistance. Encoded on transmissible plasmids.

Front 25

What are the 7 staphylococcal enzymes?

Back 25

Coagulse, Catalase, Hyaluronidase, Fibrinolysin, Lipases, Nuclease, Penicillinase.

Front 26

What is SSSS also called?

Back 26

Ritter's Disease

Front 27

What is a localized form of SSSS called?

Back 27

Bullous impetigo

Front 28

What is Bullous Impetigo?

Back 28

A localized form of SSSS.

Front 29

What is the pathology of SSSS?

Back 29

Abrupt onset in infants of localized perioral erythema that covers the entire body within 2 days. Slight pressure displaces the skin (positive Nikolsky sign).

The blisters contain a clear fluid that contains no organisms or leukocytes, as the condition is caused by bacterial toxin.

Front 30

What is the Nikolsky sign? Where is it observed?

Back 30

Slight pressure displaces the skin.

Observed in Staphylococcal Scalded Scale Syndrome (SSSS)

Front 31

What is the source of contamination for Staphyloccal food poisoning?

Back 31

Contamination is the result of a human carrier.

~50% with asymptomatic nasopharyngeal colonization

Front 32

What is the time of onset of staphylococcal food poisoning symptoms? What are the symptoms?

Back 32

Mean incubation of 4 hours. Generally lasts less then 24 hours.

Severe vomitting, diarrhea, and abdominal pain or nausea. Diarrhea is watery and non-bloody.

Front 33

What are the clinical manifestations of TSST?

Back 33

Fever, hypotension, diffuse macular erythematous rash.

Skin desquamates, and eventually leads to multi-organ failure.

Front 34

What condition is associated with tampons?

Back 34

Staphylococcal toxic shock syndrome (TSS)

Front 35

What are they cutaneous pyogenic staphyloccal infections?

Back 35

Impetigo, folliculitis, furuncles, carbuncles.

Front 36

What is impetigo?

Back 36

A superficial infection that primarily affects young children, often on the face and limbs.

Begins as a small macule (flattened red spot) that progresses to a pus filled vesicle on an erythematous base. Crusting occurs after the pustule ruptures.

Most often caused by Staph. Aureus, although group A Strep can also cause

Front 37

What isi folliculitis?

Back 37

A pyogenic infection of a hair follicle. The base of a follicle is raised and reddened with a collection of pus beneath the epidermal surface.

In the eyelid, it is called a stye

Front 38

What is a style?

Back 38

Folliculitis of the eyelid

Front 39

What is a furuncle?

Back 39

Also called boils, they are an extension of folliculitis. They are large, painful, raised nodules that have an underlying collection of dead and necrotic tissue.

Front 40

What are carbuncles?

Back 40

They occur when furuncles coalesce and extend to the deeper subcutaneous tissues. Multiple sinus tracts are usually present.

Patients with carbuncles often have chills and fever.

Front 41

Which part of the heart is affected in paraenteral drug abusers suffering from S. Aureus acute endocarditis?

Back 41

The tricuspid valve (right side)

Front 42

What is empyema?

Back 42

A collection of pus in a naturally forming anatomical cavity.

Front 43

What is abscess?

Back 43

A collection of puss in a newly forming anatomical cavity.

Front 44

What is Brodie's abscess?

Back 44

A sequestered focus of staphylococcal osteomyelitis that arises in the metaphyseal area of a long bone and occurs only in adults.

Front 45

What is the most common cause of septic arthritis in children and adults? What is the most common cause in sexually active persons?

Back 45

In children and non-sexually active persons, most common cause is Staphylococcus Aureus.

In sexually active persons, is Neisseria Gonorrhoeae.

Front 46

What is the major cause of endocarditis in artificial heart vales?

Back 46

Coagulase negative staphylococcal species, specifically Staphylococcus Epidermidis.

Front 47

What is the major cause of endocarditis of native heart vales?

Back 47

Most commonly caused by streptococci, can also be caused by staphylococci

Front 48

What is the major clinical disease of S. saprophyticus?

Back 48

Staphylococcus Saprophyticus

Causes urinary tract infections in young, sexually active women.

Front 49

What pathogen causes urinary tract infections in young, sexually active women?

Back 49

Staphylococcus saprophyticus

Front 50

A 23 year old woman presents to your clinic with dysuria and pyuria. Microscopy reveals the presence of numerous organisms in her urine. During questioning the patient reveals that she is sexually active. What organism most likely underlies the presentation?

Back 50

Staphylococcus saprophyticus

Front 51

What mechanism of resistance do staphylococci have against peniccilin?

Back 51

Beta-lactamase

Front 52

How is the resistance of staphylococci to peniccilin coded?

Back 52

The genetic information is encoded on transmissible plasmids.

Front 53

What is MRSA?

Back 53

Methicillin resistant staphylococcus aureus

Front 54

What mediates resistance in MRSA?

Back 54

Acquisition of the gene mecA that codes for PBP2'. This is a penicillin binding protein that is not bound by penicillins, cephalosporins, and carbapenems.

Front 55

P-V leukocidin is associated with what diseases?

Back 55

Necrotizing pneumonia, community acquired MRSA

Front 56

What is the mechanism of low level resistance to vancomycin observed in staphylococcus aureus?

Back 56

A thicker more disorganized cell wall. It is theorized that vancomycin is trapped in the cell wall and unable to reach the cytoplasmic membrane.

Front 57

What is the mechanism of high level resistance to vancomycin observed in staphylococcus aureus?

Back 57

The vanA gene operon acquired from vancomycin resistant enterococci. This produces a modified peptidoglycan layer that does not bind vancomycin.

Front 58

Streptococcus Pyogenes is characterized by...?

Back 58

Gram positive cocci arranged in pairs or chains, Beta-hemolytic, Catalase negative, Lancefield group A antigen

Front 59

Gram positive cocci arranged in pairs or chains, Beta-hemolytic, Catalase negative...is?

Back 59

Streptococcus Pyogenes

Front 60

What is M protein?

Back 60

A major type specific protein associated with virulent streptococci. Can be Class I or II. Class I share exposed antigens, Class II do not.

Only Class I M protein can cause rheumatic fever.

Front 61

What are the classes of M protein?

Back 61

Class I - possess shared exposed antigens. Are the only class capable of causing Rheumatic fever?

Class II - do not possess shared exposed antigens.

Front 62

Which M protein(s) can cause Rheumatic Fever?

Back 62

Only class I

Front 63

What is unique about encapsulated forms of S. pyogenes?

Back 63

Capsule is composed of hyaluronic acid, indistinguishable from mammalian connective tissues. It prevents phagocytosis of the bacteria.

Front 64

What is the biologic effect of M protein?

Back 64

Acts as an adhesin

Mediates internalization by host cells

Antiphagocytic

Degrades complement component C3b

Front 65

What does streptolysin S do?

Back 65

Lyses leukocytes, platelets, and erythrocytes.

Stimulates release of lysosomal enzymes.

Non-immunogenic.

Front 66

What does Strepolysin O do?

Back 66

Lyses leukocytes, platelets, and erythrocytes.

Stimulates release of lysosomal enzymes.

Immunogenic.

Is Oxygen labile.

Front 67

Anti-ASO test is useful for determining which type of infection?

Back 67

S. pyogenes (except skin infections)

Front 68

Why is the Anti-ASO test not useful for identifying S. pyogenes skin infections?

Back 68

Streptolysin O is irreversibly inhibited by cholesterol in skin lipids, patients with S. pyogenes skin infections will not generate antibodies.

Front 69

How does streptokinase act?

Back 69

Cleaves plasminogen, releasing plasmin that cleaves fibrin and fibrinogen, which breaks down blood clots, and facilitates spread of S. pyogenes.

Front 70

What are the 11 virulence factors of S. pyogenes?

Back 70

Capsule
Lipoteichoic Acid
M protein
M-like protein
F protein
Pyrogenic exotoxins
Streptolysin S
Streptolysin O
Streptokinase
DNase
C5a peptidase

Front 71

How do DNases facilitate virulence?

Back 71

DNases are NOT cytolytic.

They depolymerize free DNA present in pus, reducing viscosity of abscess material and facilitating disease spread.

Front 72

How does C5a peptidase act?

Back 72

It clease C5a

Front 73

What produces bacteriocins, and what is their role?

Back 73

They are produced by alpha and gamma hemolytic streptococci. They suppress the growth of group A streptococci.

Front 74

What are the suppurative diseases of S. pyogenes?

Back 74

Pharyngitis, Pyoderma, Erysipelas, Cellulitis, Necrotizing Fasciitis, Streptococcal Toxic Shock Syndrome (STTS)

Front 75

What are the non-suppurative diseases of S. pyogenes?

Back 75

Rheumatic Fever and Acute Glomerulonephritis

Front 76

What is the pathology of Scarlet Fever?

Back 76

A complication of streptococcal pharyngitis. The infecting bacteria is lysogenized by a bacteriophage that stimulates production of pyrogenic toxin.

1-2 days after symptoms of pharyngitis develop, a diffuse erythematous rash appears on the upper chest and spreads to the extremities.

Area around the mouth is not red (Circumoral pallor).

Yellowish-white coat covers the tongue and is then shed, revealing a raw, red surface (Strawberry Tongue).

Rash blanches when pressed, best observed on the abdomen and skin folds (Pastia's lines)

Front 77

What is Scarlet fever?

Back 77

A complication of streptococcal pharyngitis lysogenized by bacteriophage that induces production of pyrogenic exotoxins. Causes chest rash that radiates to limbs, strawberry tongue, circumoral pallor, and Pastia's lines.

Front 78

What is "Strawberry tongue"?

Back 78

Symptom of Scarlet fever. Tongue first has a yellow-white coating, which sheds to reveal a raw, red tongue.

Front 79

What is Circumoral Pallor?

Back 79

The area around the mouth is not affected by rash, a finding in Scarlet Fever.

Front 80

What are Pastia's Lines?

Back 80

Present in Scarlet Fever, skin folds that are ideal locations to demonstrate the rash that blanches when pressed.

Front 81

What is Pyoderma?

Back 81

Also called impetigo, is a confined purulent infection of the skin that primarily affects exposed areas.

Infection begins when S. pyogenes is introduced into the subcutaneous tissue. Vesicles develop, progressing to pustules, and then rupture and crust over.

Common in the warm summer months in children with poor personal hygiene.

Front 82

What is Erysipelas?

Back 82

An acute infection of the skin with localized pain, inflammation, lymph node enlargement, and systemic signs (chills, fever, leukocytosis).

The affected skin is raised and possesses a distinct border from uninvolved skin.

Occurs most commonly in young children and old adults.

Front 83

What is Cellulitis?

Back 83

A skin infection that involves the skin and deeper subcutaneous tissues, with no strong demarcation between infected and non-infected skin.

Front 84

How is Cellulitis different from Erysipelas?

Back 84

Cellulitis involves deeper subcutaneous tissues, whereas Erysipelas is a more superficial infection.

Erysipelas has a sharp border demarcation between infected and non-infect skin. Cellulitis does not.

Front 85

What is Necrotizing Fasciitis?

Back 85

Also called streptococcal gangrene, is an infection that occurs deep in the subcutaneous tissue, spreads along fascia planes, and extensively destroys muscle and fat.

Generally presents with STTS and bacteremia. Requires aggressive surgical debridlement of affected tissues.

Front 86

What is STTS?

Back 86

Streptococcal Toxic Shock Syndrome. Similar to Staphylococcal TTS, except caused by streptococcal species.

Usually presents with bacteremia and necrotizing fasciitis.

Front 87

What is Rheumatic Fever?

Back 87

A non-suppurative complication of S. pyogenes infection. Characterized by inflammatory changes involving the heart, joints, blood vessels and subcutaneous tissue.

Heart - pancarditis (endo, peri, or myocarditis) and associated with subcutaneous nodules. Progressive damage to valves may occur.

Joint - Arthralgias, Arthritis with migratory pattern.

Associated with streptococcal pharyngitis, but not cutaneous streptotococcal infections.

Front 88

What pathology is Rheumatic Fever associated with?

Back 88

Non-suppurative complication of Streptococcal pharyngitis.

Front 89

What is Acute Glomerulognephritis

Back 89

Acute inflammation of renal glomeruli with edema, hypertension, hematuria, and proteinuria.

Front 90

What pathology is Acute Glomerulognephritis with?

Back 90

Non-suppurative complication of streptococcal infection.

Front 91

What is the PYR reaction?

Back 91

Tests for the presence of the enzyme PYR, which is present in S. pyogenes and absent in S. anginosus. Used for rapid differentiation of samples.

Front 92

What species is the PYR reaction used to seperate?

Back 92

S. Pyogenes and S. Anginosus.

Front 93

How can Rheumatic Fever be prevented?

Back 93

If antibiotic therapy is initiated within 10 days of the initial clinical disease.

Front 94

What is used to treat S. pyogenes?

Back 94

Very sensitive to penicillin. In case of penicillin allergy, erythromycin or oral cephalosporin.

Front 95

Gram positive cocci, facultative anaerobe, Catalase negative, beta OR gamma hemolytic...is?

Back 95

Streptococcus Agalactiae (Group B)

Front 96

Streptococcus Agalactiae is characterized by...?

Back 96

Gram positive cocci, facultative anaerobe, Catalase negative, beta OR gamma hemolytic

Front 97

What is the most common cause of septicemia and meningitis in newborns?

Back 97

S. Agalactiae

Front 98

What are the two types of Group B strep disease onsets in newborns?

Back 98

Early onset - Disease occurs in the first 7 days of life

Late onset - Disease occurs between 1 week and 3 months following delivery

Front 99

Early onset neonatal disease caused by S. Agalactiae is caused by what type of exposure?

Back 99

Delivery through colonized genitourinary tract of mother.

Front 100

Group B Streptococcus generally causes infections in...?

Back 100

Neonates, either early or late onset, and debilitated or elderly.

Front 101

What is the CAMP test?

Back 101

S. Agalactiae produce CAMP factor, that enhances beta-hemolysis of S. Aureus.

The test plates a bacteria that is suspected of being group B streptococcus with S. Aureus. Hemolysis patterh determines if the unknown produces CAMP factor.

Front 102

What pathogen is the CAMP test used to differentiate, and which pathogen does the test make use of?

Back 102

The CAMP test uses S. Aureus to identify if a specimen is S. Agalactiae (Group B Strep)

Front 103

What is the drug of choice for S. Agalactiae?

Back 103

Penicillin G with aminoglycoside. MIC using penicillin G is 10x higher then for S. Pyogenes, hence adjuvant drug.

Vancomycin for patients allergic to penicillin.

Front 104

What bacteria is associated with occult malignancy of the colon?

Back 104

Streptococcus Bovis

Front 105

What diseases are Viridans Streptococci usually associated with?

Back 105

Dental caries (S. mutans and S. sobrinus), subacute endocarditis (S. gordonii, S. mitis, S. mutans, S. oralis), and suppurative intraabdominal infections.

Front 106

What pathogen is associated with dental caries?

Back 106

Streptococcus Mutans and Streptococcus Sobrinus

Front 107

Colonies with a dimpled center are characteristic of what pathogen?

Back 107

Streptococcus Pneumoniae

Front 108

Lancet shaped, gram positive, facultative anaerobe, encapsulated cocci, and inhibited by optochin...is?

Back 108

Streptococcus Pneumoniae

Front 109

What pathogen appears alpha-hemolytic when incubated aerobically, and may appear beta-hemolytic when incubated anaerobically?

Back 109

Streptococcus Pneumoniae

Front 110

Streptococcus Pneumoniae is characterized by?

Back 110

Lancet shaped
Gram positive
Facultative anaerobe
Encapsulated
Cocci
Inhibited by optochin

Front 111

The dimpling observed in S. Pneumoniae colonies is due to...?

Back 111

Amidase, the pneumococcal autolysin.

Front 112

What is the C polysaccharide, and what pathogen expresses it? What does it do?

Back 112

It is teichoic acid that is exposed on the cell surface, and it is expressed on Streptococcus Pneumoniae.

It precipitates C-reactive protein (CRP) in the presence of calcium.

Front 113

What is the F antigen, and what pathogen expresses it?

Back 113

Lipid bound teichoic acid in the bacterial cytoplasmic membrane, expressed on Streptococcus Pneumoniae.

It is called F antigen because it can cross-react with the Forssman surface antigens on mammalian cells.

Front 114

What pathogen expresses pneumolysin, and what does it do?

Back 114

Streptococcus Pneumoniae.

A cytotoxin that binds cholesterol in the host cell membrane and creates pores. Destroys ciliated epithelial cells and phagocytic cells in pathogenesis.

Front 115

Secretory IgA protease is important to the pathogenesis of what organism? What is it's role?

Back 115

Streptococcus Pneumoniae.

Secretory IgA attaches to bacteria at the antigen binding site, and attatches to mucin at the Fc region, facilitating mucous trapping and clearance.

Front 116

Phosphorylcholine is important to the pathogenesis of what organism? What is it's role?

Back 116

Streptococcus Pneumoniae.

Binds to phosphodiesterase-activating factor, allowing the bacteria to enter host cells.

Front 117

What are the clinical diseases of S. Pneumoniae?

Back 117

Pneumonia, Sinusitis, Otitis Media, Meningitis, Bacteremia.

Front 118

What is the Quellung reaction, and what pathogens is it used to identify?

Back 118

Polyvalent anticapsular antibodies are mixed with bacteria, which is examined microscopically. A positive reaction shows the capsule apparently enlarging and becoming opaque.

The Quellung reaction can be used to identify Streptococcus Pneumoniae, Klebsiella Pneumoniae, Neisseria Meningitidis, and Haemophilus Influenzae.

Front 119

What pathogen is the bile solubility test used to identify?

Back 119

Streptococcus Pneumoniae.

Bacteria are lysed rapidly when autolysins are activated by exposure to bile.

Front 120

What pathogen is sensitive to optochin?

Back 120

Streptococcus Pneumoniae.

Front 121

What is the mechanism of high resistance to penicillin observed in Streptococcus Pneumoniae?

Back 121

Decreased affinity of the antibiotic for penicillin-binding proteins (PBPs) in the cell wall.

Front 122

What are the treatments and preventions for Streptococcus Pneumoniae?

Back 122

Antibiotic sensitivity tests are needed due to recent isolates with high penicillin and other antibiotic resistances. Therapy is guided empirically.

Polyvalent vaccines are available for prevention.

Front 123

Enterococcus are characterized by...?

Back 123

Gram positive, catalase negative cocci, facultative anaerobic, can be gamma, alpha, and rarely beta hemolytic.

Can grow in temperatures ranging from 10-45 degrees Celsius.

Complex nutritional needs; B vitamins, nucleic acid bases, carbon source.

Can grow in harsh conditions, such as 6.5% NaCl and 40% bile salts.

Front 124

Gram positive, catalase negative cocci, facultative anaerobic, can be gamma, alpha, and rarely beta hemolytic are?

Back 124

Enterococcus (Group D streptococci)

Front 125

What are the three most common sites of enterococcus disease?

Back 125

Urinary tract (UTI), peritoneum (peritonitis), heart (endocarditis)

Front 126

Where do most enterococcus infections occur? Why are they dangerous?

Back 126

Most are nosocomial. Common sources can be indwelling catheters, surgical sites, or traumatic wounds.

Most are resistant to many if not all clinically used antibiotics, making them difficult to treat.

Front 127

Spore forming, encapsulated, gram-positive rods, nonmotile, facultative anaerobe, with "ground glass" colonies that are strongly adherent to the agar...is?

Back 127

Bacillis Anthracis

Front 128

Bacillis Anthracis is characterized by?

Back 128

Spore forming, encapsulated, gram-positive rods, nonmotile, facultative anaerobe, with "ground glass" colonies that are strongly adherent to the agar.

Front 129

What are the three exotoxins present in virulent strains of B. anthracis?

Back 129

Protective Antigen (PA), Edema Factor (EF), Lethal Factor (LF).

Front 130

How are the three exotoxins of B. anthracis employed in pathogenesis?

Back 130

Protective antigen (PA) plus edema factor (EF) combine to form Edema Toxin (EdTx).

Protective antigen (PA) plus lethal factor (LF) combine to form Lethal Toxin (LeTx)

Front 131

What is the mechanism of action of EdTx and LeTx in B. Anthracis infection?

Back 131

LF binds to a cell receptor. Host proteases cleave LF, and the larger LF fragments self associate on the cell surface, forming a heptameric complex.

The heptameric complex can then bind 3 molecules of LF and/or EF. Formation of the complex stimulates endocytosis. In this environment, the heptameric complex forms a pore that the LF and EF enter the cytosol through.

LF is a sinc-metalloprotease that cleaves mitogen activated protein (MAP) kinase, leading to cell death.

EF is an adenylate cyclase that raises intracellular cAMP levels, leading to edema.

Front 132

What are the three most important virulence factors to B. antracis?

Back 132

Lethal Toxin, Edema Toxin, and the capsule (inhibition of phagocytosis)

Front 133

What are the three modes of acquisition of B. anthracis disease?

Back 133

Innoculation, ingestion, and inhalation.

Front 134

What is the most common mode of acquisition of B. anthracis disease?

Back 134

Innoculation (~95%). Commonly from either contaminated soil or infected animal products, such as hides, goat hair, and wool.

Front 135

What is wool-sorter's disease?

Back 135

Historic name for inhalation anthrax.

Front 136

What is the presentation of cutaneous anthrax?

Back 136

Development of a painless papule at the site of inoculation that rapidly progresses to an ulcer surrounded by vesicles, then a necrotic eschar.

Front 137

A leather tanner presents with a painless black ulcerated lesion on his hand. He says it developed following a scratch a few days ago. The diagnosis is?

Back 137

Cutaneous anthrax, caused by Bacillus Anthracis.

Front 138

What are the mortality rates for the three types of anthrax?

Back 138

Cutaneous Anthrax - 20% mortality in untreated individuals.

Gastrointestinal - Believed to approach 100%

Inhalation - Nearly 100% of cases progress to shock and death within 3 days of initial symptoms if treatment is not initiated immediately.

Front 139

What is the drug of choice for treating anthrax?

Back 139

Ciprofloxacin is recommended for empirical therapy.

Penicillin and doxycycline are also used, but genes encoding resistance have been transferred to B. anthracis, prompting use of ciprofloxacin.

Front 140

What are the clinically identifiable symptoms of inhalation anthrax?

Back 140

Initial symptoms are non-descript: fever, shortness of breath, cough, headache, vomiting, chills, chest and abdominal pain.

Second stage of disease includes worsening of fever, edema, massive enlargement of the mediastinal lymph nodes resulting in widened mediastinum on chest X-ray.

Meningeal symptoms are seen in half of patients with inhalation anthrax.

Front 141

Spore forming, gram-positive rods, motile, facultative anaerobe, beta-hemolytic...is?

Back 141

Bacillus Cereus.

Front 142

Bacillus Cereus is characterized by?

Back 142

Spore forming, gram-positive rods, motile, facultative anaerobe, beta-hemolytic.

Front 143

What causes the emetic form of B. cereus gastroenteritis?

Back 143

The heat stable, proteolysis resistant enterotoxin.

Front 144

What causes the diarrheal form of B. cereus gastroenteritis?

Back 144

The heat labile enterotoxin.

Front 145

What are the two types of gastroenteritis caused by B. cereus?

Back 145

Emetic and diarrheal form of the disease.

Front 146

What is the mechanism of action of the heat labile enterotoxin in B. cereus? What disease does it cause?

Back 146

It stimulates the adenylate cyclase-cyclic adenosine monophosphate system, leading to profuse watery diarrhea.

It is involved in the Diarrheal form of the disease.

Front 147

What three virulence factors have been implicated in B. cereus ocular infections?

Back 147

Necrotic toxin - a heat labile enterotoxin
Cereolysin - a potent hemolysin named after the species
Phospholipase C - a potent lecithinase

Front 148

The emitic form of B. cereus food poisoning is associated with consumption of what?

Back 148

Contaminated rice.

Front 149

Consumption of contaminated rice is associated with what pathology? What is the incubation time and duration of this disease?

Back 149

The emetic form of B. cereus food poisoning, with an incubation time of 1-6 hours, and a duration of 8-10 hours.

Front 150

The diarrheal form of B. cereus food poisoning is associated with consumption of what? What is the incubation time and duration of this disease?

Back 150

Contaminated meat, vegetables, or sauces. The organism must multiply in the GI tract and produce the heat labile toxin, with an incubation time of 9+ hours, and a duration of a day or longer.

Front 151

What are the two Gram positive rods of uniform shape?

Back 151

Listeria and Erysipelothrix

Front 152

What are the two species of Listeria that are human pathogens?

Back 152

Listeria Monocytogenes and Listeria Ivanovii

Front 153

Gram positive rod, facultative anaerobe, motile at room temperature, weakly beta-hemolytic, growth over broad temperature range (1-45 C)...is?

Back 153

Listeria Monocytogenes

Front 154

What time of motility does L. monocytogenes demonstrate?

Back 154

End over end tumbling observable at room temperature.

Front 155

What species if L. monocytogenes easily confused with?
What pathology do they share?
How can they be differentiated?

Back 155

Streptococcus Pneumoniae or Enterococcus.

S. Pneumoniae and L. Monocytogenes both cause meningitis.

L. Monocytogenes can be differentiated by 3 factors:
- Motile at room temperature
- Weakly beta-hemolytic
- Gram stain morphology

Front 156

Patients with what type of immunity are susceptible to L. monocytogenes infections?

Back 156

Patients with defects in cellular immunity are susceptible, as humoral immunity is largely unimportant to pathogen clearance.

Front 157

L. monocytogenes: internalins?

Back 157

A family of leucine rich proteins that interact with glycoprotein receptors on the surface of the host cells, and mediate entry into nonphagocytic cells.

Front 158

L. monocytogenes: Listeriolysin O and Phospholipase C?

Back 158

Listeriolysin O is a bacterial exotoxin, along with two forms of Phospholipase C, are activated by the acidic environment of the phagolysosome. They act together to release the bacteria into the cell cytosol.

Front 159

What is the process by which L. monocytogenes enters cells?

Back 159

First, a family of 6 or more leucine rich proteins called INTERNALINS interact with glycoproteins on nonphagocytic cell surfaces, mediating internalization in a phagolysosome.

The acidic pH of the phagolysosome activate exotoxin LISTERIOLYSIN O and 2 different PHOSPHOLIPASE C enzymes, which act together and release the bacteria into the cytosol of the cell.

Front 160

What are the 3 types of proteins involved in L. monocytogenes entering cells?

Back 160

Internalins - family of 6 or more
Listeriolysin O - exotoxin
Phospholipase C - two different forms

Front 161

How does L. monocytogenes move around inside a cell?

Back 161

The ActA bacterial protein exists on the bacterial surface, and coordinates the assembly of actin, which propels the bacteria through the cell like a rocket ship.

Front 162

Host actin polymerization is an important mechanism of motility for what pathogen?

Back 162

Listeria Monocytogenes

Front 163

What is the mortality rate of symptomatic listeria infections?

Back 163

20-30%, one of the highest for foodborne diseases

Front 164

What is believed to be the primary source of L. monocytogenes?
Outbreaks of the disease are associated with what?

Back 164

Soil and decaying vegetable matter.

Fecal carriage is estimated in 1-5% of healthy people.

Outbreaks are associated with contaminated food products. Because the pathogen can grow at low temperatures, contaminated foods that are refrigerated for prolonged periods can become grossly infected.

Front 165

What are the two forms of neonatal disease caused by L. monocytogenes?

Back 165

Early-onset disease and late onset disease.

Early onset is also called granulomatosis infantiseptica.

Late onset presents is meningitis or meningoencephalitis with septicemia.

Front 166

What is granulomatosis infantiseptica?

Back 166

Another name for early onset neonatal Listeria Monocytogenes disease.

It is characterized by the formation of disseminated abscesses and granulomas in multiple organs. It has a high mortality rate if not treated quickly.

Front 167

What is the presentation of late onset L. monocytogenes neonatal disease?

Back 167

Occurs 2 to 3 weeks following birth, and presents as meningitis or meningoencephalitis with septicemia.

Clinical signs and symptoms are NOT unique, so other potentially causative organisms, such as group B strep, must be ruled out.

Front 168

How is granulomatosis infantiseptica acquired?

Back 168

The early-onset neonatal L. monocytogenes disease is acquired transplacentally in utero.

Front 169

What are the most common forms of L. monocytogenes infection in adults?

Back 169

Infectiosn can present as mild influenza-like illness, with or without gastroenteritis.

Listeria Monocytogenes can also cause Meningitis. Signs and symptoms are not specific for L. monocytogenes.

Front 170

Is a lumbar puncture useful in identifying L. monocytogenes meningitis?

Back 170

Not immediately. The bacteria are generally present in concentrations below the limit of detection (10^4 per mL CSF). The CSF must be cultured to see if organisms grow, which will then be present in sufficient quantities for identification.

Front 171

How can the beta-hemolysis of L. monocytogenes be enhanced?

Back 171

If it is grown next to Staphylococcus Aureus, enhanced hemolysis is observed. This is a positive CAMP reaction.

Front 172

In addition to group B streptococci, what species can demonstrate a positive CAMP reaction?

Back 172

Listeria Monocytogenes

Front 173

How can L. monocytogenes be cultured effectively in the present of many contaminating species?

Back 173

Cold enrichment. The specimen is stored in a refrigerator for prolonged periods.

Listeria Monocytogenes is capable of growth at temperatures as low as 1 degree Celsius.

Front 174

What is the treatment of choice for L. monocytogenes infections?

Back 174

Penicillin or ampicillin alone, or with gentamicin.

In patients with penicillin allergies, erythromycin can be used.

However, Listeria are naturally resistant to cephalosporins.

Front 175

What species of Erysipelothrix is associated with human disease?

Back 175

Erysipelothrix Rhusiopathiae

Front 176

Pleimorphic gram positive rods that form long filaments, microaerophilis, facultative anaerobe, alpha-hemolytic, and a gram stain that can sometimes decolorize looking like gram negative...is?

Back 176

Erysipelothrix Rhusiopathiae

Front 177

Erysipelothrix disease in humans is usually spread how?

Back 177

It is zoonotic, common in butchers, fisherman, and people who work with wild game. Colonization is especially prevalent in swine, some fish, and turkeys.

Front 178

What are the two forms of E. Rhusiopathiae disease?

Back 178

1) A localized skin infection caused an erysipeloid
2) A septicemic disease

Front 179

What is an erysipeloid?

Back 179

A localized skin infection caused by Erysipelothrix Rhusiopathiae. It presents at a site of taruma and appears violaceous with a raised edge. It spread peripherally as tje doscp;pratopm om tje cemter area fades. The painful lesion is pruritic and the patient experiences a burning or throbbing sensation.

Suppuration is uncommon, a distinguishing feature from streptococcal erysipelas

Front 180

A butcher presents with a painful lesion on his left hand. The lesion is purple with a raised edge. The patient indicates that the lesion is pruritic and produces a burning sensation. Upon questioning, it is revealed the patient cut his hand at work 4 days ago.

There is no suppuration from the lesion.

What is the lesion called, and what is the causative organism?
What would be the likely diagnosis if suppuration were present?

Back 180

The lesion is called an erysipeloid, and is caused by Erysipelothrix Rhusiopathiae.

If suppuration were present, the lesion could be streptococcal erysipelas.

Front 181

What is the septicemic form of Erysipelothrix infection associated with?

Back 181

Endocarditis, either with acute onset or sub-acute, commonly with involvement of previously undamaged heart valves, particular the aortic valve.

Front 182

What is the treatment of choice for Erysipelothrix Rhusiopathiae disease?

Back 182

Penicillin. Cephalosporins, erythromycin and clindamycin can be used in allergic patients.

Erysipelothrix Rhusiopathiae is resistant to Vancomycin.

Front 183

Starting from 1 bacteria, how many bacteria replication cycles does it take to reach 1,000,000 bacteria?

Back 183

Approximately 20 cycles

Front 184

Starting from 1 bacteria, how many bacteria replication cycles does it take to reach 500,000 bacteria?

Back 184

Approximately 10 cycles

Front 185

What is the equation of generation time?

Back 185

B(t) = B(0) x 2^n

where:
n = t / g

t - time
g - generation time
n - number of replication cycles
B(t) - number of bacteria at a given time, given a set starting number of bacteria
B(0) - starting number of bacteria

Front 186

What are the approximate generation times of:
E. Coli
P. Putida
S. Aureus
M. Tuberculosis
C. Perfringens

Back 186

Escherichia coli - 20 minutes
Pseudomonas Putida - 45 minutes
Staphylococcus Aureus - 28 minutes
Mycobacterium tuberculosis - 12 hours
Clostridium Perfringens - 10 minutes

Front 187

What is the viable count method?

Back 187

Serial dilutions of a sample are plated, and number of colonies are measured. Initial bacterial concentration is given by:

Number of colonies on plate x reciprocal of dilution of sample = number of bacteria / mL

Front 188

What are the three methods of measuring bacterial growth?

Back 188

Counting methods - viable count, total count
Measuring optical density
Measuring biomass

Front 189

How many and what are the phases of bacterial growth

Back 189

There are four phases. They are:
1) Lag phase
2) Exponential growth phase (logarithmic growth phase)
3) Stationary phase
4) Death phase (logarithmic decline phase)

Front 190

What are phototrophs?

Back 190

Microorganisms that harness energy from light.

Front 191

What are microorganisms that harness energy from light called?

Back 191

Phototrophs

Front 192

What are chemotrophs? What subtypes are there?

Back 192

Chemotrophs harness energy from chemical compounds. There are two subtypes:

1) Chemoroganotrophs (chemoheterotrophs) - get energy from complex organic comopounds.
2) Chemolithotrophs - utilize inorganic compounds for energy

Front 193

What is is chemotroph?

Back 193

An organism that gets energy from chemical compounds.

Front 194

What is a chemoorganotroph?

Back 194

An organism that gets energy from complex organic chemical compounds.

Front 195

What is a chemolithotroph?

Back 195

An organism that gets energy from inorganic compounds.

Front 196

What are the different carbon sources for microorganisms, and what are the organisms called?

Back 196

Carbon can be gained from organic or inorganic sources.

Heterotrophs - Organisms utilizing organic carbon, such as sugar.

Autotrophs - organisms utilizing inorganic carbon, such as CO2

Front 197

All known pathogenic bacteria are what (in terms of growth requirement naming)?

Back 197

Chemoheterotrophs.

Front 198

What is a mixotroph?

Back 198

Also known as chemolithotrophs, organisms that get energy from inorganic compounds but use organic sources for carbon.

Front 199

All microorganisms can be divided into how many categories, based on nutritional requirements?

Back 199

There are 5 subgroups.

The two phototroph groups are:
1) Photoautotrophs
2) Photoheterotrophs

The three chemotrophs are:
3) Chemolithoautotrophs
4) Chemolithoheterotrophs (mixotroph)
5) Chemoorganotroph (Chemoheterotroph)

Front 200

What are the sources of nitrogen for microorganisms?

Back 200

1) Atmospheric N2 fixation
2) Inorganic (NH4+, NO2-)
3) Organic (Glutamate)

Front 201

What are the groups of required organic ions to microorganisms?

Back 201

Major requirements - Phosphate
Minor requirements - Sulfur, magnesium, potassium, iron
Trace elements - Mn, Mo, Zn, Se, Cu, Co

Essential metabolites - growth factors, vitamins. Varies from organism to oragnism.

Front 202

What are the groupings of microorganisms based on temperature preferences, and what are their optimal temperature ranges?

Back 202

Psychrophile - 10-20 C
Mesophiles - 20-40 C (most pathogens)
Thermophiles - 50-80 C

Front 203

What are the groupings of microorganisms based on Oxygen parameters?

Back 203

Obligate aerobes - Must have oxygen to survive
Facultative anaerobes - Can use oxygen for respiration, and fermentation when oxygen is not present
Microaerophiles - Require small amount of oxygen, but too much can kill them
Obligate Anaerobes - can be aerotolerant or non-aerotolerant

Front 204

What enzymes do aerobes have to survive from oxygen damage?

Back 204

Catalase - H2O2 to H20 and O2
Superoxide Dismutase (SOD) - O2- to H2O2 and O2

Front 205

Microaerophiles and aerotolerant anaerobes can tolerate oxygen due to what enzyme?

Back 205

Superoxide Dismutase (SOD) - O2- to H2O2 and O2 (or in lactic acid bacteria, peroxidase)

Front 206

Obligate anaerobes are unable to survive in oxygen, due to the lack of what enzymes?

Back 206

Catalase and Superoxide Dismutase

Front 207

What are the two mechanisms of ATP generation available to microorganisms?

Back 207

Aerobic respiration and fermentation.

Front 208

What are the end products of the glycolysis pathway only?

Back 208

2 ATP and 2 NADH

Front 209

Where is the electron transport chain located in bacteria?

Back 209

In the plasma membrane

Front 210

What is the total yield of glycolysis plus respiration in terms of ATP?

Back 210

38 ATP

Front 211

What mechanisms make bacteria capable of such rapid growth?

Back 211

The large surface area to volume ratio. Also, bacteria have numerous efficient **Nutriant Transport Systems**.

Front 212

What are the types of nutrient transport systems?

Back 212

1) Carrier mediated diffusion
2) Active transport
3) Group translocation systems

Front 213

How do active transport systems in microorganisms function?

Back 213

They either exploit the proton gradient using a proton symport, or the protein directly uses ATP to move something against its gradient.

Front 214

How do group translocation systems work?

Back 214

A substrate is modified when it enters the cell, such as phosphorylation of sugars in the PTS system. This leaves the concentration of the unphosophorylated sugar relatively low in the cell, and it continues to diffuse as there is not a gradient for it to move against.

Front 215

What is the replication rate of DNA in bacteria?

Back 215

A replication fork synthesizes at ~ 50,000 bases/minute. Thus, ~ 100,000 bases/minute for the bacteria (2 forks).

Front 216

How is it that optimal growth of bacteria seems faster then would be possible given the speed of DNA synthesis?

Back 216

Daughter cells are born "pregnant". While the bacterial DNA is undergoing a first replication, a second replication can begin midway through the process, thus each daughter cell is "born" already in the process of DNA replication.

Front 217

What are the unique components of the bacterial translational system?

Back 217

30S + 50S ribosomal subunits (40S + 60S in eukaryotes).
70S ribosome (80S in eukaryotes)
First amino acid is Formylmethionine (methionine in eukaryotes)

Front 218

What are the unique features of prokaryotic DNA replication and RNA transcription?

Back 218

DNA Replication:
~One origin of replication (eukaryotes possess multiple origins)

RNA Transcription:
~RNA polymerase of alpha-2, beta, beta prime and a sigma factor, with introns being rare (eukaryotes - multi-component RNA polymerases, introns common)

Front 219

What are the types of flagerllare arrangements?

Back 219

Polar - on a single end of the cell
Peritrichous - Eminating all over the cell

Front 220

What are the types of flagellar movement, and how are they achieved?

Back 220

Flagella can produce either a run or tumble motion. When the flagella turns one way, it adopts a corkscrew motion and produces the run motion. When it turns the other way, it loses its shape and produces a tumbling motion.

Front 221

What is chemotaxis?

Back 221

The movement of bacteria towards attractants of away from repellants.

Front 222

How is gross movement achieved by bacteria?

Back 222

Longer runs when the bacterium is moving towards an attractant or away from a repellant, and shorter runs (more frequent tumbles) when bacterium is moving away from an attractant or towards a repellant.

Movement exploits the chemical gradient.

Front 223

What variables can be used to differentiate microorganisms?

Back 223

Oxygen sensitivity
Ability to utilize specific carbohydrates
Nitrogen source requirements
Requirement for essential nutrients (vitamin, AA)
Ability to catabolize organic compound (urea deamination)
Ferementation products (lactic acid)
Susceptibility to antibacterial agents (antibiotics)
Spore formation
Ability to move

Front 224

What is the enrichment culture technique?

Back 224

Always performed in liquid cultures, provides conditions which favor a specific organism or group of organisms.

Front 225

What is a selective culture?

Back 225

Culturing of organisms on a specialized media which is toxic to all but a specific organism (methylene blue toxis to Gram +, bile salts toxic to all but enteric bacteria)

Front 226

What are the subunits of prokaryotic RNA polymerase, and what do they do?

Back 226

Alpha subunit - Enzyme assembly
Beta subunit - Nucleotide binding
Beta prime subunit - Template binding
Sigma factor - Promoter binding

Front 227

What is the difference between the RNA polymerase core enzyme and holoenzyme?

Back 227

Core enzyme - a2BB' (2 alpha, beta, beta prime)

Holoenzyme a2BB's (2 alpha, beta, beta prime, sigma)

Holoenzyme includes the sigma factor!

Front 228

What is the rate of RNA synthesis in prokaryotes?

Back 228

50 nucleotides per second.

Front 229

What is the effect of variation in the consensus RNA polymerase binding sequence in promoter regions of prokaryotes? What are three examples of variations?

Back 229

It affects the strength of the promoter or requirement for transcription activators.

1) Strong core promote - no need for additional factors
2) Weak core promoter - but, presence of "UP" element, an AT rich region enhances RNA pol. binding via the alpha subunit
3) Weak Core promoter - but presence of activator protein enhances RNA pol. binding via the alpha subunit

Front 230

What is true of most transcription initiations in prokaryotes?

Back 230

They are abortive, and release oligonucleotides 2 to 9 residues long.

Front 231

What happens during transcription as the RNA polymerase proceeds down the template strand of DNA?

Back 231

The RNA polymerase enzyme releases the sigma factor.

Front 232

What causes termination of RNA synthesis in prokaryotic transcription?

Back 232

Formation of a stem and loop structure at the 3' end of the mRNA

Front 233

What are the general types of DNA binding proteins that regulate transcription? How do they act?

Back 233

Activators and Repressors.

An activator must be bound to the DNA for transcription to occur. A repressor binds to the operator of the DNA, stopping transcription from occuring.

Front 234

howis the repressor of the Lactose operon 'neutralized'?

Back 234

An inducer (lactose) binds to the repressor and releases from the operator portion of the DNA.

Front 235

What structurally happens if a single repressor binds to two different operator sites?

Back 235

It causes looping of the DNA

Front 236

What is the full mechanism of transcription of the Lactose operon?

Back 236

~LacI repressor binds to the operator of the DNA.
~Lactose is the inducer that causes the LacI repressor to release from the operator.
~CRP is the activator that binds to the DNA and promotes and binding of RNA polymerase to the promoter

Front 237

What is the mechanism of regulation of the diphtheriae toxin?

Back 237

The gene is regulated by a repressor, DtxR.

DtxR is bound in the presence of Fe2+. It is also a regulator of iron uptake genes.

In the absence of Fe2+, the repressor is released from the DNA, and toxin genes are expressed.

Front 238

What are the components fo the two-component signaling system? How do they act?

Back 238

A sensor, and a transducer.

Sensor - a transmembrane receptor that, in response to a signal, phosphorylates itself and the transducer

Transducer - Upon phosphorylation, binds DNA to activate or repress expression

Front 239

What is a common feature of two component signaling systems?

Back 239

They often use histidine phosphorylation.

Front 240

What is the two component signalisn system of Bordetella Pertussis?

Back 240

The sensor, BvgS, and the transducer, BvgA, which acts as an activator.

Activation of the system promotes transcription of virulence factor genes (pertussis toxin, filamentous hemaglutinin, adenylate cyclase toxin).

Phosphorylation of BvgA is abolished at low temperature or in the presence of sulphate anions or nicotinic acid.

Front 241

Where and how does the prokaryotic ribosome cmomonly bind to mRNA for translation?

Back 241

The ribosome binds to a sequence upstream teh initiation AUg, called the Shine-Dalgarno (SD) box. This sequence is complementary to a sequence on the 16S ribosomal RNA.

Front 242

What is the translational regulation in Listeria monocytogenes?

Back 242

A transcription factor PrfA acts as an activator of gene transcription for many virulence factors. They are only transcribed at 37 C, not 30 C, because at lower temperatures the SD sequence is trapped in a stem-and-loop structure. The structure melts at 37 C, allowing access by PrfA.

Front 243

What is quorum sensing?

Back 243

The ability of a bacteria to sense the local pupulation density in their immediate proximity. It is accomplished through a secreted metabolite (acyl-homoserine lactone in G-, peptide in G+). Binding of the metabolite activates a transcription factor.

Front 244

What are the quorum sensing metabolites of Gram positive and Gram negative bacteria?

Back 244

Gram negative - acyl-homoserine lactone
Gram positive - peptide

Front 245

How is bioluminescence accomplished in Vibrio fischeri?

Back 245

LuxI synthesizes a specific acyl-homoserine lactone that then binds to LuxR, a transcriptional activator of the bioluminescence genes.

Front 246

What is unique about th quorum sensing system of Vibrio cholerae?

Back 246

There are 3 overlapping systems. They collectively regulate virulence factors, so that they are only produced when the bacterial population density is sufficiently high.

Front 247

What is unique about th quorum sensing system of Pseudomonas Aeruginosa?

Back 247

It containes two systems: LasI/LasR and RhlI and RhlR.

The Las system activates the Rhl system. Both systems activate genes important for pathogenicity and biofilm formation.

Front 248

Functionally, what is the difference in quorum sensing between the two signal factors used in Gram positive and Gram negative bacteria?

Back 248

In gram negative bacteria, the acyl-homoserine lactone can diffuse through the membrane of the bacteria and bind to the transcription factor.

In gram positive bacteria, the peptide must bind to a membrane receptor, generally part of a 2-component system. For example, in Streptococcus neumoniae a secreted peptide triggers the ComD/ComE 2-component system.

Thus, gram positive bacteria require more steps to achieve quorum sensing, generally in the form of a 2-component system.

Front 249

What are the unique features of the prokaryotic genome?

Back 249

Prokaryotes are haploid, with a single circular chromosome and, optionally, extrachromosomal plasmids. Plasmids are able to replicate autonomously.

Front 250

What is the rate of spontaneous mutations in bacteria?

Back 250

10^-7 - 10^-8 per nucleotide per generation.

Front 251

What was the importance of the Lederberg & Lederberg experiment?

Back 251

It was used to determine whether mutations arise at random or in response to environment.

Front 252

How do alkylating agents affect DNA?

Back 252

Alkylated guanine will pair with thymine rather than with cytidine, and alkylated thymine will pair with guanine rather then with adenine.

Front 253

What are the normal base pairings? What occurs with alkylating agents?

Back 253

C with G, and A with T.

Alkylated G prefers T, instead of normally C
Alkylated T prefers G, instead of normally A

Front 254

What is the Ames test?

Back 254

It looks for the existence of a rare His+ (prototrophic for histidine) revertants in a Salmonella Typhimurium mutant strain that is auxotrophic for histidine.

In this way, it can be used to determine if a tested compound is mutagenic.

Front 255

How can it be determined if a compound is mutagenic?

Back 255

Use the Ames test.

Front 256

What will a positive Ames test look like?

Back 256

there will be two distinct zones around the disc containing the mutagen. First, there will be an immediate ring with no growth. This is associated with a concentration of mutagen that causes too many mutations for bacterial proliferation to occur.

Secondary, there will be a ring of intense bacterial growth, that subsides as the distance from the disc increases. This correlated with the concentration gradient of the mutagen. Higher concentrations lead to more effective mutations that can grow on His- media.

Front 257

How can foreign DNA be integrated into another DNA molecule in bacteria?

Back 257

Homologous recombination
Non-homologous recombination
Site specific (phages)
Non-site specific (transposons, phages)

Front 258

What is transformation?

Back 258

DNA released from a lysed bacteria is taken up by a recipient cell and integrated, provided the recipient is competent for transformation (Neisseria, pneumococci)

Front 259

What is conjugation?

Back 259

A method of horizontal DNA transfer in bacteria.

In this, a specialized plasmid called the F-factor directs the formation of F-pili from F+ bacteria to F- bacteria. This pili forms a channel through which DNA is transferred through and integrated into the recipient genome.

If the F-factor is on an extra-chromosomal plasmid, only the plasmid is transferred to the recipient bacteria.

If the F-factor is encoded in the chromosome, DNA of the F-factor plus some chromosomal DNA is transferred. This is termed an Hfr strain (High Frequency Recombination)

Front 260

What is special about conjugation with Hfr?

Back 260

During conjugation, the whole bacterial chromosome is transferred starting with DNA adjacent to the F-factor integration site. This transfer occurs over time, so interruption of transfer at different times will allow for different amounts of DNA to be transferred.

Front 261

What are the two lifecyles of bacteriophages?

Back 261

Lytic and Lysogenic.

Lytic - Infection, high level of replication, cell bursts releasing new viruses

Lysogenic - Phage inserts it's genome into host chromosome and remains silent.

Front 262

How are phages grown?

Back 262

They are grown on a lawn of bacteria. A plaque is a hole in the lawn of bacteria created by growth and propogation of an infecting phage.

Front 263

What is phage transduction?

Back 263

When the phage genome is packaged into the phage head, occasionally a fragment of bacterial genome is packaged instead. Such a phage is termed a **transducing phage particle**, and upon infecting a new bacteria will inject the bacterial genomic fragment into the recipient.

Front 264

What are the mechanisms of horizontal DNA transfer in bacteria?

Back 264

Transformation
Conjugation
Phage Transduction

Front 265

What are the two types of phages?

Back 265

Virulent and Temperate.

Virulent - only capable of the lytic cycle

Temperate - can choose between teh lytic and lysogenic cycle

Front 266

What causes a phage infected bacteria in a lysogenic cycle to enter the lytic cycle?

Back 266

It can occur stochastically at a low frequency, or in response to environmental insults to the host cell.

Front 267

How does the genome of a lysogenic phage survive in a bacteria host?

Back 267

The lysogenic phage DNA can remain as a plasmid in the cytoplasm or it can integrate into the bacterial chromosome.

Front 268

What protects a bacterium in the lysogenic state from superinfection?

Back 268

The presence of the phage repressor protein, which is expressed by the lysogenic prophage protects from superinfection with the same phage type.

Front 269

What is the phage repressor protein?

Back 269

It is expressed by a lysogenic prophage in a infected bacteria in the lysogenic state. It protects the bacteria from superinfection with the same phage.

Front 270

What are some roles of phages in clinical microbiology?

Back 270

Phage typing plays a role in diagnostics.

Virulence factors are often carried on lysogenic prophages.

Front 271

What is transposition?

Back 271

Movement of a genetic element from one location to another on a given bacterial chromosome. There are two types; replicative and non-replicative.

Front 272

What is movement of a genetic element from one location to another on a given bacterial chromosome called?

Back 272

Transposition.

Front 273

What are transposable genetic elements?

Back 273

Mobile genetic elements that can move from a chromosome to a plasmid, between plasmids, or frome one location on a chromosome to another (transposition)

Front 274

What are the types of transposition?

Back 274

Replicative and Non-replicative

Front 275

What are insertion sequences?

Back 275

They encode transposase, which recognizes the extremities of the IS element and catalyzes its transposition.

Front 276

What mobile genetic element encodes Transposase?

Back 276

Insertion Sequences.

Front 277

What is a transposon?

Back 277

A selectable marker flanked by two IS elements of inverted orientation, which confer mobility on the transposon.

The selectable marker in transposons are commonly genes that encode antibiotic resistance.

Front 278

What is conjugative transposition?

Back 278

Upon conjugation, a transposon excises from the donor chromosome and is transferred to the recipient cell, where it integrates into the recipient's chromosome.

The conjugative transposition can only be perofmred by transposons taht carry function of an F-factor.

Front 279

How can a gene encoding tetracycline resistance jump from one bacteria to another?

Back 279

Conjugative transposition.

Front 280

Genes for virulence are often found on...?

Back 280

Transmissible genetic elements such as bacteriophages, plasmids, or transposons.

They are also associated with specific regions of the bacterial chromosome called pathogenicity islands.

Front 281

What are the features of pathogenicity islands?

Back 281

Flanked by tRNA sequences, Insertion Sequence (IS) elements, or other direct repeats.
Are unstable - have a tendency to delete with high frequency
Often have a different C+G content from the rest of the genome, indicating foreign source
Large, usually containing virulence genes

Front 282

What are the 4 types of genomic islands?

Back 282

Ecological Island - environmental adaptation
Saprophytic Island - saprophytic interaction
Symbiosis Island - symbiosis
Pathogenicity Island - parasitism

Front 283

What are 5 feature products of the bacterial core gene pool?

Back 283

1) Ribosomes
2) Cell envelope
3) Key metabolic pathways
4) DNA replication
5) Nucleotide turnover

Front 284

What is phase inversion?

Back 284

An invertable DNA fragment which can promote transcription of two antigenically different products.

Example: Salmonella flagellin. Inversion allows expression of two antigenically different flagellin genes.

Front 285

What are the mechanisms of antigenic variation in bacteria?

Back 285

Phase inversion, phase variation by recombination, and phase variation by frameshift.

Front 286

What is phase variation by recombination? How does this function in N. gonorrhoeae?

Back 286

Antigenically distinct silent genes can be substituted for the expressed gene, producing an effective gene prodoct of the same type that is antigenically distinct.

N. gonorrhoeae has a single expressed pilin gene, PilE, and 8 promoterless silent pilin genes located upstream. The flanking region of all pilin genes are homologous, whereas the contents are not. During homologous recombination, one of the promoterless pilin genes can be swapped in to the space for the expressed pilin gene.

Front 287

How many reading frames can a molecule of DNA be read in for transcription/translation?

Back 287

6 reading frames (bi-directional, or complementary strand...probably bi-directional)

Front 288

How does phase variation by frameshift occur in N. gonorrhoeae?

Back 288

The bacterium possesses 11 opa genes (opacity) which code for surface proteins. Tandem repeats in the 5' end of the coding regions are prone to frameshifting mutations due to slippage during replication.

Front 289

What are the three domains of life?

Back 289

Eubacteria, Archae, Eukaryotes

Front 290

What are the four kingdoms of eukaryotes?

Back 290

Animals, Plants, Fungi, Protists

Front 291

What si the definition of a species?

Back 291

A group of organisms which can interbreed and yield live, fertile offspring.

Front 292

What are the problems with bacterial taxonomic classification?

Back 292

~No sexual reproduction, thus usual definition is inapplicable
~Few morphological characteristics available

Front 293

What have bacterial systematics traditionally relied on, and what have they been replaced with recently?

Back 293

Traditionally relied on metabolic characteristics.

More recently this has been superceded by molecule sequence data, particularly rRNA (16S rRNA subunit).

Front 294

What is the difference between classification and identification?

Back 294

Classification attempts to reflect phylogeny using evolutionally conserved features. Identification is based on easily performed and as few as possible lab tests.

Front 295

What is classification based on?

Back 295

Using conserved characteristics (low rate of evolutionary change), such as wall structure, and sequence data (16S rRNA)

Front 296

What organization scheme is based upon evolutionarily conserved characteristics?

Back 296

Classification

Front 297

What is Identification (diagnostic) based on?

Back 297

Using procedures that are easily performed in the laboratory and as few tests as possible to identify the bacteria.

Front 298

What is sequencing of rRNA (16S) used for?

Back 298

Classification

Front 299

What scheme is sequence detection (PCR) used for?

Back 299

Identification (diagnostic)

Front 300

What scheme is phage typing used for?

Back 300

Identification (diagnostic)

Front 301

What scheme is biochemical testing used for?

Back 301

Identification (diagnostic)

Front 302

What class of antibiotics are sulfonamides?

Back 302

Antimetabolites

Front 303

What class of antibiotics is trimethoprim?

Back 303

Antimetabolites

Front 304

What class of antibiotics is isoniazid?

Back 304

Antimetabolites

Front 305

What antibiotics act as antimetabolites?

Back 305

Sulfonamides, trimethoprim, isoniazid

Front 306

What antibiotics act as inhibitors of bacterial DNA gyrase?

Back 306

Quinolones, nalidixic acid, fluoroquinolones.

Front 307

What class of antibiotics act as inhibitors of RNA polymerase?

Back 307

Rifamycins

Front 308

What class of antibiotics act by affecting cell membranes?

Back 308

Polymyxins

Front 309

How does Isoniazid (INH) work?

Back 309

INH is activated by KatG and then conjugated to NAD. INH-NAD inhibits fatty acid synthesis (FASII), responsible for mycolic acid synthesis in mycobacteria.

Front 310

What is Izoniazid used to treat?

Back 310

Mycobacteria, specifically tuberculosis.

Front 311

What is the mechanism of Daptomycin?

Back 311

A cyclic lipopeptide that affects cell membranes. It is bacteriacidal against Gram Positive bacteria.

Front 312

What drug is bacteriacidal against Gram Positive bacteria and acts by affecting the cell membrane?

Back 312

Daptomycin

Front 313

How does Fosfomycin act?

Back 313

Inhibits NAM synthesis?

Front 314

What drug inhibits NAM synthesis?

Back 314

Fosfomycin

Front 315

How does D-cycloserine act?

Back 315

Inhibits D-ala-D-ala synthesis

Front 316

What drug inhibits D-ala-D-ala synthesis?

Back 316

D-cycloserine

Front 317

How does Bacitracin act?

Back 317

Inhibits dephosphorylation of NAG-carrier phospholipid

Front 318

What drug inhibits dephosphorylation of NAG-carrier phospholipid?

Back 318

Bacitracin

Front 319

How does Vancomycin act? What type of drug is it?

Back 319

Vancomycin is a glycopeptide. It binds the disaccharide precursom, inhibiting transpeptidation and sugar chain elongation.

Front 320

How do beta-lactams act?

Back 320

Inhibit transpeptidase function, and thus, peptidoglycan crosslinking

Front 321

How does penicillins act?

Back 321

Inhibit transpeptidase function, and thus, peptidoglycan crosslinking

Front 322

How do cephalosporins act?

Back 322

Inhibit transpeptidase function, and thus, peptidoglycan crosslinking

Front 323

What drugs inhibit transpeptidase function, and thus, peptidoglycan crosslinking?

Back 323

Beta-lactams, penicillins, cephalosporins.

Front 324

What drugs act as inhibitors of peptidoglycan synthesis?

Back 324

Fosfomycin, D-cycloserine, Bacitracin, Glycopeptides (vancomycin), beta-lactams, penicillins, cephalosporins

Front 325

What drugs act by binding to the 30S ribosomal subunit?

Back 325

Tetracyclines, aminoglycosides. Are bacteriacidal.

Front 326

How do tetracyclines act?

Back 326

By binding to the 30S ribosomal subunit

Front 327

How do Aminoglycosides act?

Back 327

By binding to the 30S ribosomal subunit

Front 328

What class of drugs are Streptomycin, Kanamycin, and Gentamicin and how do they act?

Back 328

Aminoglycosides, by binding to the 30S ribosomal subunit and blocks tRNA binding to A site. At low concentrations reduces accuracy of translation.

Front 329

What drugs act by binding to the 50S ribosomal subunit?

Back 329

Chloramphenicol, Macrolides, Lincosamides, Oxazolidinones, Puromycin

Front 330

How does Chloramphenicol act?

Back 330

By binding to the 50S ribosomal subunit.

Front 331

How do Macrolides act?

Back 331

By binding to the 50S ribosomal subunit.

Front 332

How do Lincosamides act?

Back 332

By binding to the 50S ribosomal subunit.

Front 333

How do Oxazolidinones act?

Back 333

By binding to the 50S ribosomal subunit - inhibiting translation initiation. May inhibit translation by interfering with ternary complex formation and/or binding of the 50S to the ternary complex.

Front 334

How does Puromycin act?

Back 334

It is a charged tRNA analog that acts as a chain terminator.

Front 335

What type of drugs are Erythromycin and Clarithromycin, and how do they act?

Back 335

They are macrolides, and act by blocking the entrance to the peptide exit channel on the 50S unit, thereby indirectly inhibiting peptide chain elongation and ribosomal translocation on the mRNA.

Front 336

What types of drugs are Clindamycin and Lincomycin, and how do they act?

Back 336

They are Lincosamides, and act by binding to the peptidyl transferase site on the 50S ribosomal subunit and inhibit peptide chain synthesis.

Front 337

What type of drugs are Linezolid and Eperozolid, and how do they act?

Back 337

They are Oxazolidinones, and act by inhibiting translation initiation, by interfering with ternary compelex formation and/or binding of the 50S to the ternary complex.

Front 338

How do Fusidic Acid act?

Back 338

Inhibits EF-G function. It locks EF-G on the ribosome after GTP hydrolysis, thereby inhibiting translocation.

Front 339

What is Synercid?

Back 339

A combination of Quinupristin and Dalfopristin. They bind to the ribosome on adjacent sites. Each is bacteriostatic by themselves, but together they are bactericidal.

Front 340

How does Mupirocin act?

Back 340

It inhibits bacterial isoleucyl tRNA synthetase.

Front 341

What drug inhibitsbacterial isoleucyl tRNA synthetase?

Back 341

Mupirocin.

Front 342

What are the three mechanisms of resistance to antibiotics?

Back 342

1) Inactivation of antibiotics
2) Preventing access to the cytoplasm
3) Modification of the target to prevent recognition by the drug

Front 343

How is resistance to Chloramphenicol achieved?

Back 343

Acetylating the drug via Chloramphenicol acetyl-transferase

Front 344

how is resistance to aminoglycosides achieved?

Back 344

By modification and inactivation of the drugs.

By preventing their active transport into the cell.

Front 345

What are the two mechanisms of tetracycline resistance?

Back 345

Expression of an ATP-dependant efflux pump (common), or expression of a protein that blocks access of tetracycline to the 30S subunit of the ribosome (rare)

Front 346

What are two examples of active efflux pump antibiotic resistances?

Back 346

Tetracycline pumps, Macrolide pumps.

Front 347

Resistance to what drug is achieved by preventing their active transport into the cell?

Back 347

Aminoglycosides, Fosfomycin

Front 348

What are two mechanisms of beta-lactam resistance?

Back 348

Expression of beta-lactamase, mutations in the PBPs that prevent binding.

Front 349

How is beta-lactamase mediated resistance overcome clinically?

Back 349

Clavulanic acid is an inhibitor of beta-lactamase.

Front 350

Mutational modifications of which target enzymes provides resistance to which antibiotics?

Back 350

PBPs - Beta-Lactams
Gyrase - Quinolones
RNA Polymerase - Rifampins
Dihydropteroate Synthase - Sulfonamides
Dihydrofolate Reductase - Trimethoprim

Front 351

Enzymatic modification of which targets provides resistance to which antibiotics?

Back 351

Methylation of 23S rRNA - Macrolides, Lyncosamides
Incorporation of D-ala-D-hydroxybutyrate

Front 352

How is resistance to Vancomycin achieved?

Back 352

Incorporation of D-ala-D-hydroxybutyrate

Front 353

How is resistance to Macrolides achieved?

Back 353

Methylation of 23S rRNA.

Front 354

How is resistance to Lyncosamides achieved?

Back 354

Methylation of 23S rRNA.

Front 355

How do Sulfonamides work?

Back 355

By inhibiting Dihydropteroate Synthase.

Front 356

How does Trimethoprim work?

Back 356

By inhibiting Dihydrofolate Reductase.

Front 357

What tetracycline drug evades the two classical resistance mechanisms of bacteria to tetracyclines?

Back 357

Tigecycline.

Front 358

What is clinically important about Tigecycline?

Back 358

It evades the two classical resistance mechanisms of bacteria to tetracyclines.

Front 359

How is the Tetracycline pump regulated?

Back 359

By a Repressor. In the presence of Tetracycline, the Tetracycline-Repressor complex releases the promoter, allowing transcription.

Front 360

The Erythromycin resistance gene is regulated at what level?

Back 360

Translation. In the presence of Erythromycin, the ribosome stalls while translating the leader peptide, thereby allowing access to the initiation codon of the methylase protein.

Front 361

What general mechanisms confer low level resistance to antibiotics?

Back 361

Permeability mutants, such as porin mutations and altered cell wall composition.

Mutants with reduced autolysin activity partially resistant to cell wall synthesis inhibitors.

Certain physiologic states, like biofilm formation and the stationary phase.

Reduced production of target proteins.

Front 362

What is the theorized reason why resistant strains dominate the population following antibiotic exposure?

Back 362

The resistant strains have accumulated second site mutations that increase fitness in thep resence of the resistance mutation, but decrease fitness when the resistant site reverts to sensitive.

Front 363

What are the three steps of the antibiotic screen model?

Back 363

1) Use genomics to identify new essential targets
2) Use high thoroughput screens to identify inhibitors of these targets (Lead compounds)
3) Modify lead compounds to enhance activity and specificity

Front 364

What factors have contributed to reduced efforts in antibiotic research?

Back 364

1) Disappointment - Hundreds of attempts failed. Difficult to go from inhibitor of essential enzyme in vitro to compound that works in vivo
2) Economics - New classes will be last resort, i.e. small number of candidates

Front 365

What are virulence factors?

Back 365

Characteristics of the microorganism that enhance pathogenicity.

Front 366

Characteristics of the microorganism that enhance pathogenicity are?

Back 366

Virulence factors.

Front 367

What are Host Defenses?

Back 367

A series of barriers and mechanisms used by the host to prevent and combat infection.

Front 368

A series of barriers and mechanisms used by the host to prevent and combat infection are known as?

Back 368

Host Defenses

Front 369

The outcomes of an infection can depend upon?

Back 369

1) The host's physical barriers against infection, and the ways they are breached
2) The parasite's ability to evade local host defenses
3) The method used by the organism to spread and cause disease
4) The body's adaptive immune response

Front 370

What innate defenses are present in skin?

Back 370

Dry, acidic, <37C, shedding of cells
Competition with resident flora
Hair follicles, sweat glands - lysozyme and toxic lipids
Beneath the surface: Skin-associated lymphoid tissue (SALT)

Front 371

What innate defenses are present in mucous membranes?

Back 371

Mucin layer - containing lysozyme, lactoferrin, lactoperoxidase, sIgA
Surface - Shedding of cells, tight junctions
Beneath Surface - Mucosa-associated lymphoid tissue (MALT)

Front 372

What are the specific defenses of the Eyes, Mouth, Nose, Intestinal Tract, Lungs, Urogenital Tract?

Back 372

Eyes - Blinking, Tears (lysozyme, sIgA, lactoferrin)
Mouth - Flow of saliva, resident microflora
Nose - Sneeze response
Intestinal Tract - Proteolytic enzymes, bile salts, peristaltic flow, low pH, resident microflora
Lungs - Normally sterile
Urogenital Tract - Lactobacillus (vagina), cervical plug, urethral sphincter, urination

Front 373

What are the nonspecific constitutive defenses in tissue and blood?

Back 373

Transferrin
Mannose-binding protein, LPS-binding protein
Complement

Front 374

What ar ethe two methods of activation of the complement system?

Back 374

Classical and Alternative pathway

Front 375

What mediates the chemotactic function of the complement?

Back 375

C5a

Front 376

What is the inflammatory response?

Back 376

The host response to injury caused by infection or trauma. Results from combination of complement activation and phagocyte attack.

Characterized by swelling, redness, pain, and increased temperature.

Front 377

Innate immunity recognizes what on bacteria?

Back 377

Pathogen-Associated Molecular Patterns (PAMPs)

Front 378

What is a PAMP?

Back 378

Pathogen Associated Molecular Pattern, what is recognized by the innate immune response.

Front 379

What receptors are involved in innate immunity?

Back 379

Toll-like receptors (TLRs)

Front 380

What is the receptor for LPS?

Back 380

TLR4

Front 381

TLR4 is the receptor for what PAMP?

Back 381

LPS and Lipoteichoic Acid

Front 382

What is the receptors for Lipoproteins?

Back 382

TLR2, TLR6

Front 383

TLR2 and TLR6 are the receptor for what PAMP?

Back 383

Lipoproteins

Front 384

What is the receptor for Peptidoglycan?

Back 384

TLR2

Front 385

TLR2 is the receptor for what PAMP?

Back 385

Peptidoglycan

Front 386

What is the receptor for Lipoteichoic Acid?

Back 386

TLR4

Front 387

What is the receptor for Unmethylated CpG?

Back 387

TLR9

Front 388

What is the receptor for Flagellin?

Back 388

TLR5

Front 389

TLR9 is the receptor for what PAMP?

Back 389

Unmethylated CpG

Front 390

TLR5 is the receptor for what PAMP?

Back 390

Flagellin

Front 391

What are cytokines?

Back 391

Secreted elements that mediate the inflammatory response and modulate the adaptive immunity.

Front 392

What pathway induces production of antibacterial peptides?

Back 392

The toll pathway

Front 393

How do the antibacterial peptides induced by the toll pathway act?

Back 393

Either by disrupting the bacterial membrane and causing fragmentation, or diffusing from the membrane into the cell to affect intracellular targets

Front 394

Antibodies secreted by B cells do what 3 things?

Back 394

1) Opsonize bacteria (IgG)
2) Activate complement (IgM > IgG)
3) Neutralize Toxins (IgG, IgM)

Front 395

What are the two types of T-cells, and how do they act?

Back 395

Helper (CD4) stimulate B cells to produce antibodies, and stimulate macrophages with IFN-g
Cytotoxic (CD8) kill infected host cells.

Front 396

What are the differences between colonization, infection, and asymptomatic carriage?

Back 396

Colonization - Establishment of non-disease causing microorganism in the body
Infection - Establishment of disease causing organism in the body
Asymptomatic Carriage - Infection in the absence of disease

Front 397

What are two groupings of portals of entry for a pathogen into the body?

Back 397

Through skin - wounds, insect bites
Through mucosal surfaces - GIT, respiratory tract, etc.

Front 398

What are the two categories of virulence factors of pathogens?

Back 398

Those that promote colonization and invasion of the host, and those that cause damage to the host.

Front 399

What pathogen components mediate adherence and penetration of mucosal surfaces?

Back 399

Pili and nonfimbrial adhesins
Motility and Chemotaxis
sIgA proteases
Binding to and entry of M cells
Bacterial triggering actin rearrangement: forced phagocytosis, movement from one cell to another.

Front 400

What is the role of Pili and nonfimbrial adhesins?

Back 400

Mediate adherence to mucosal surfaces.

Front 401

What is the Type III Secretion System?

Back 401

A protein system that allows for injecting of proteins into the host cell cytoplasm. The structure is evolutionarily related to the flagella.

Front 402

What is EPEC, and how does it make use of the Type III Secretion System?

Back 402

Enteropathogenic E. coli, the Type III system injects receptor molecule, Tir, that acts as a nucleation point for actin. This effectively rearranges the host cell actin and forms a "pedestal" structure on the intestinal epithelial cell.

Front 403

How does Shigella, Salmonella, and Listeria achieve intracellular colonization?

Back 403

Adherence to M cells is followed by forced phagocytosis, also following an induced actin rearrangement.

Front 404

What bacteria can move in the cytoplasm of host cells, both within single cells and between cells, by use of cellular actin?

Back 404

Shigella and Listeria Monocytogenes.

Front 405

What factor aids in bacteria iron acquisition?

Back 405

Siderophores

Front 406

What are Siderophores?

Back 406

Factors that are involved in iron acquisition for bacteria.

Front 407

What are sources of iron for many pathogenic microorganisms?

Back 407

Hemoglobin and Hemin

Front 408

What are some mechanisms of resistance to phagocytosis?

Back 408

1) Capsule - Microbe resists ingestion
2) Toxin secretion - Microbe kills neutrophil
3) Intracellular survival - Microbe grows inside phagocyte

Front 409

What is endotoxin? Where is it found?

Back 409

Lipopolysaccharide (LPS), found only in the outer membrane of Gram Negative bacteria.

Front 410

What are the three parts of LPS?

Back 410

Lipid A
Core
O-Antigen

Front 411

Which component of LPS is responsible for it's toxicity?

Back 411

The Lipid A component

Front 412

What are 4 examples of exotoxins?

Back 412

A-B toxins
Hormone analogs
Membrane-disrupting toxins
Superantigens

Front 413

How is an A-B toxin composed, and how does it act?

Back 413

The toxin is composed of two parts, a B part generally consisting of 5 copies of the B protein, and an attached A protein. They are linked by a disulfide bond.

The B component binds (binding domain) to a cell receptor, and translocates (translocation domain) the A component into the cytosol where it is seperated. The A component is then free in the cytoplasm, where it creates its effect (catalytic domain).

Front 414

What are three examples of A-B toxins?

Back 414

Diphtheria - ADP-ribosylates host EF-2, causing damage to heart and organs
Shiga - Cleaves host rRNA
Botulism - MOST POTENT TOXIN; protease which affects excitatory nerve functions, causing flaccid paralysis

Front 415

How does Botulism toxin act?

Back 415

It is an A-B toxin. The catalytic domain is a metalloprotease which cleaves components of the synaptic vesicle release apparatus at nerve endings.

The end result is no release of Acetylcholine (Ach) and therefore flaccid paralysis.

Front 416

What are two major clinical manifestations of infantile botulism?

Back 416

Hypotonia (from flaccid paralysis), enlarged pupils

Front 417

What is the most potent toxin? What is the second most potent toxin?

Back 417

The most potent toxin is the Botulism A-B toxin.
The second most potent toxin is the Tetanus A-B toxin

Front 418

What type of toxin is the Tetanus toxin, and how does it act?

Back 418

The tetanus toxin is an A-B toxin. The toxin binds to the presynaptic end of neuromuscular junctions, preventing the release of inhibitory neurotransmitters such as GABA and glycine.

The net effect is a spastic paralysis.

Front 419

What type of toxin is the Cholera toxin, what pathogen secretes it, and how does it act?

Back 419

The cholera toxin is an A-B toxin, produced by the pathogen Vibrio Cholerae.

The toxin acts by ADP-Ribosylating the host Gs Adenylate cyclase protein. This causes a massive rise in intracellular cAMP, leading to opening of apical Cl- channels. A large efflux of Chloride occurs, followed by water and other cations. The net result is a profuse, watery diarrhea.

This is also the mechanism of the heat-labile E. coli enterotoxin.

Front 420

What is an example of a hormone analog toxin?

Back 420

The E. coli heat stable toxins (STa)

Front 421

What is STa, and what is it's mechanism of action?

Back 421

E. coli heat stable toxins.

It mimics Guanylin. It acts by binding to and activating guanylate cyclase-C. This causes a rise in intracellular cGMP, leading to opening of apical Cl- channels. The net result is a secretion of chloride, followed by cations and water, leading to watery diarrhea.

It is hypothesized that continuous exposure to STa toxins is the reason for reduced incidence of colon cancer in the third world.

Front 422

How does Listeriolysin O act?

Back 422

It is a pore forming cytotoxin. It creates a pore in the phagocytic vesicle, allowing Listeria Monocytogenes to escape the phagocytic vesicle (phagolysosome).

Front 423

What membrane disrupting toxin is crucial for L. Monocytogenes? How does it act?

Back 423

Listeriolysin O. It is a pore forming cytotoxin. It creates a pore in the phagocytic vesicle, allowing Listeria Monocytogenes to escape the phagocytic vesicle (phagolysosome).

Front 424

What toxin is necessary for C. perfringens disease gas gangrene?

Back 424

Alpha toxin, a membrane disrupting toxin.

Front 425

How does C. perfringens alpha toxin act?

Back 425

It acts as a phospholipase, killing phagocytes and other cell types.

Front 426

How do superantigens act?

Back 426

They crosslink the MHCs on antigen presenting cells (APCs) to T-cell receptors. The result is activation of said T-cells, and production of many cytokine factors, particularly IL-2 and TNF-alpha. This cytokine storm can lead to septic symptoms, including hypotension, fever, organ failure, shock, and death.

Front 427

What pathogens possess superantigens as virulence factors?

Back 427

Staphylococcus Aureus and Streptococcus Pyogenes.

Front 428

Prolonged treatment with what drug will result in clostridial pseudomembranous enterocolitis?

Back 428

Clindamycin