Mmi 301 Exam 2

Front 1

define normal flora and state its purpose

Back 1

bacteria that is expected to colonize the body, helps protect from colonization by pathogens, can supplement host nutrition and provides immune stimulation

Front 2

define pathogenic bacteria

Back 2

technically limited to those virulent organisms where common exposure results in disease (Shigella, B. anthracis)

Front 3

define opportunistic pathogen

Back 3

an organism that does not normally cause disease (pseudomonas) causes a disease because the host has a pre-existing condition

Front 4

define and give an example of acute disease

Back 4

rapid onset, usually rapid resolution, e.g. cholera

Front 5

define and give an example of chronic disease

Back 5

slow onset, slow resolution e.g. tuberculosis

Front 6

define and given an example of a recurrent disease

Back 6

usually acute bouts without long lasting immunity, e.g. gonorrhea, E. coli UTI

Front 7

define and given an example of a pyogenic disease

Back 7

fever and large degree of white cell infiltrates (pus), e.g. Staph and Strep wound infections

Front 8

define and give an example of an immune mediated disease

Back 8

antibody or cellular responses to organism cause tissue damage e.g. rheumatic fever

Front 9

List 7 methods by which an organism can enter a host

Back 9

ingestion
inhalation
trauma
needles
arthropod bites
sexual transmission
eyes
Remeber: There Are Some Ewey Nasty Infection Incidents

Front 10

How would organisms like Salmonella, Shigella, Vibrio cholerae, Listeria, and B. anthrasis gain entry into the host

Back 10

ingestion via contaminated food or water

Front 11

How would organisms like M. tuberculosis, Legionella pneumophila, Bordetella, B> anthracis, and Y. pestis gain entery into the host?

Back 11

inhalation

Front 12

Give some examples of species that can gain entry into the host via trauma

Back 12

Clostridia sp, B. anthrasis, Strep, Staph

Front 13

What pathogens commonly gain entry into the host via needlesticks

Back 13

Staph, Pseudomonas

Front 14

What pathogens are often transmited by arthropod bites

Back 14

Rickettsia, Yersinia pestis, Borrelia spp.

Front 15

List some pathogens that can be transmitted sexually

Back 15

Chlamydia trachomatis, Treponema pallidum, Neisseria gonorrhoeae, Shigella spp.

Front 16

List some pathogens that can gain entry into the host via the eyes

Back 16

Chalmydia trachomatis, N. gonorrhoeae, B. cereus, Pseudomonas spp.

Front 17

list the Molecular Koch's postulates

Back 17

1. the phenotype under investigation shoudl be associated with pathogenic members of a genus
2. specific mutagenesis of the gene(s) associated with virulence should lead to a significant decrease in virulence
3. complementation of the mutation should restore pathogenicity

Front 18

What types of mutations are best for proving the molecular koch's postulates

Back 18

inframe deletions or point mutations

Front 19

How might a gene be complemented to restore pathogenicity when trying to prove the molecular koch's postulates

Back 19

on a plasmid or allelic replacement

Front 20

What adherence structures can serve as virulence/ disease mechanisms

Back 20

1. Pili/fimbraie
2. Non fimbrial surface proteins
3. Capsule
4. Lipoteichoic acids
5. flagella
Sticky Pathogens Can Love Forever

Front 21

Describe how a bacteria would normally be destroyed by a macrophage

Back 21

-bacteria becomes bound to cell surface
-induction of cellular events that leads to engulfment and formation of a phagosome
-acidification of the phagosome and fusion with the lysosome
-acid, destructive enzymes, and oxygen radicals destroy the bacteria

Front 22

What are the four methods that bacteria can use to invade a cell and avoid being killed

Back 22

1. Cellular invasion with replication in the cytoplasm
2. invasion with replication in the late endosome
3. Invasion with replication in the phagosome
4. Special parasite vesicle

Front 23

Cellular invasion with replication in the cytoplasm in a mechanism for cell invasion.Given an example of bacteria that do this

Back 23

Rickettsiae, Shigella, Listeria

Front 24

Invasion with replication in the late endosome is mechanism for cell invasion. Given an example of bacteria that do this

Back 24

Salmonella

Front 25

Invasion with replication in the phagolysosome is a mechanism for cellular invasion. Give an example of bacteria that do this

Back 25

Coxiella, Mycobacteria

Front 26

The use of a special parasite vesicle is an example of a cellular invasion mechaism. Give an example of bacteria that do this

Back 26

Chlamydia spp. use inclusion bodies

Front 27

Some intracellular bacteria like Shigella and Listeria spread from cell to cell in the host without an extracellular state. Explain how this occurs

Back 27

1. The cells enter the host and lyse the phagosome and then replicate in the cytoplasm
2. The cells organize polymerization of actin filaments and propel themselves into neighboring cells
3. They enter the new cells encased in a dobule membrane which they lyse for new rounds of replication

Front 28

Describe the general structure of a bacterial exotoxin (AB subunit model)

Back 28

usually function as two discrete protein subunits or domains within a single protein, one subunit controls the ability to bind to the host cell receptors (B=bind) and the other carries out the toxic activity (A=activity).
There are also discrete elements of the protein necessary for secretion from the cell and for translocation across the plasma or endosomal membrane

Front 29

Describe the 3 ways cytolytic toxins can act and give an example of each

Back 29

1. creation of a membrane pore e.g. alpha toxin of S. aureus
2. Enzymatic destruction of phospholipid bilayer e.g. sphingomyelinase of S. aureus, Beta toxin
3. Surfactant e.g. Delta toxin of S>. aureus

Front 30

T/F hemolytic toxins evovled specifically to lyse RBCs

Back 30

false, they most likely evovled to lyse phagocytes

Front 31

describe type 3 secretion systems

Back 31

-directly delivers bacterial proteins into the host cell cytoplasm by injection
-proteins can affect cytossketal structure and second messenger pathways
-example EHEC and petesal formation/ tight adhesion sites

Front 32

List some examples of mechanisms to evade the host immune response

Back 32

capusles, antigenic variation, anti-immunoglobulin proteases, disruption of complement cascase, inhibition of opsonization, inhibition of phagocyte chemotaxsis, destruction of phagocytes by leucotoxins, intracellular replicaiton

Front 33

Discribe how disease is thought to occur in the three way interaction model

Back 33

When the pathogen enters the host, the homeostasis of the location is interupted and inflmation occurs. If the pathogen survives inflammation better than the normal microbiota, disease occurs

Front 34

Which cytokines are primarily responsible for the acute phase responses

Back 34

IL-6, TNF-a

Front 35

What are the three lines of defense against invasion by bacteria pathogens

Back 35

1. natural barriers like skin, mucous, cilliated epithelium, gastric acid, bile, normal flora
2. innate, pattern recognition and antigen non specific responses (fever, complement, iron binding proteins, antimicrobial peptides, phagocytes)
3. Memory responses based on antigen specificity (antibodies, T cells)

Front 36

What defese mechanism is employed early in infection when bacterial attachement occurs

Back 36

innate defence mechanisms like antibodies to adhesins

Front 37

What defense mechanism is employed early infection when local proliferation occurs

Back 37

phagocytes, complement lysis, blocking of metabolite transport

Front 38

What defense mechanism is employed later in infection if invasion occurs

Back 38

antibody to aggressins, antibody to organism, complement lysis, phagocytes

Front 39

what defense mechaism is employed later in infection if a toxin is produce

Back 39

antibody to the toxin

Front 40

what defense mechaism is employed later in infection if intracelluar growth occurs

Back 40

cell mediated immunity

Front 41

What are the immune barrier defenses associated with the eyes

Back 41

washing of tears and lysozyme (catalyzes hydrolysis of bacterial peptidoglycan)

Front 42

What are the immune barrier defenses of the skin

Back 42

anatomic barrier, antimicrobial secretions

Front 43

What are the immune barrier functions of the digestive tract

Back 43

stomach acidity, normal flora, bile

Front 44

What are the immune barrier functions of the genitourinary tract

Back 44

washing of urine, lysozyme, vaginal lactic acid

Front 45

What are the immune barrier functions to the respiratory tract

Back 45

mucus, ciliated epithelium, alveolar macrophages

Front 46

lysozyme is a nonspecific humoral defense mechanism. What is its function and source

Back 46

function- catalyses the hydrolysis of bacterial peptidoglycan
source-tears, saliva, nasal secretions, body fluids, lysosomal granulas

Front 47

lactoferrin and transferrin are nonspecific humoral defense mechanisms. What is their function and source

Back 47

function-bind iron and compete with MOs for it
source- specific granules of PMNs

Front 48

lactoperoxidase is a nonspecific humoral defense mechanism
what is its source and function

Back 48

function- may be inhibitory to many microorganisms
source-milk and saliva

Front 49

Beta lysin is a nonspecific humoral defense mechanism, what is its function and sourcce

Back 49

function- effective against gram positive bacteria
source- thrombocytes, normal serum

Front 50

chemotactic factors are a nonspecific humoral defense mechanism, what is their function and sourcce

Back 50

function- induce directed migration of PMNs, monocytes, and other cells
source-bacterial substances, products of cell injury, denatured proteins, complement, chemokines

Front 51

properdin is a nonspecific humoral defense mechanism, what is its function and sourcce

Back 51

function- activates complement in the absence of antibody-antigen complex
source-normal plasma

Front 52

cationic peptides (defensins, etc) are a nonspecific humoral defense mechanism, what is their function and sourcce

Back 52

function-disrupt membranes, block cell transport activities
source- polymorphonuclear granules

Front 53

what cell gives rise to all blood cells

Back 53

pluripotent stem cell

Front 54

what % of circulating leukocytes are neutrophils

Back 54

60%

Front 55

what % of circulating leukocytes are B lymphocytes and T cells

Back 55

33%

Front 56

What are PAMPs

Back 56

Pathogen Associated Molecular Patter, a bacterial product like flagella or LPS that trigger immune responses

Front 57

What type of receptors recognize PAMPs

Back 57

toll like receptors (TLRs)

Front 58

When circulating naive Th cells recognize their cognate antigen, they differentiate into one of several effector lineages. What are these lineages?

Back 58

TH1, TH2, TH17

Front 59

What cytokines do TH1 cells produce? What innate immune effector mechanism does this trigger? What type of pathogen does this combat?

Back 59

TH1 cells produce IFN-gamma which stimulates macrophages to fight off intracellular pathogens

Front 60

What innate immune effector mechanism do TH2 cells trigger? What type of pathogen does this combat?

Back 60

TH2 help activate mast cells, basophils, and eosinophils, this helps combat hemolinth infections (parasites)

Front 61

What cytokines do TH17 cells produce? What innate immune effector mechanism does this trigger? What type of pathogen does this combat?

Back 61

TH17 cells produce IL-17 whihc helps recruit neutrophils to conbat extracellular bacteria and fungi

Front 62

What cytokines are important for fighting intracellular bacteria? Extracellular?

Back 62

intracellular-IFN-G (TH1 cells)
extracelllular- IL-17 (TH17 cells)

Front 63

Which cytokine, produce by TH1, TH2, and TH17 cells is important for B cell proliferaiton and antibody production

Back 63

IL-4

Front 64

What cytokines are important in the acute phase response to bacteria?

Back 64

IL-1, IL-6, TNF

Front 65

Describe the immune response in terms of specificity, innateness, memory and cell type at 0-4. 4-96, and after 96 hours

Back 65

0-4 hours, nonspecific, innate, no memory, no specific T cells
4-96 hours- nonspecific and specific, inducible, no memory, no specific T cells
post 96 hrs- specific, inducible, memory, specific T cells

Front 66

Describe the barrier funtions of the immune system at 0-4hrs, 4-96 hrs, and post 96hrs

Back 66

0-4: skin, epithelia
4-96: local inflammation (C5a) and local TNF
post 96:IgA antibody in luminal spaces, IgE antibody on most cells

Front 67

Describe the immune response to extracellular pathogens at 0-4hrs, 4-96 hrs, and post 96hrs

Back 67

early- phagocytes, alternative complement pathway
middle-mannose binding protein, C reactive protien, T cell independent B B cell antibody plus complement
late-IgG antibody and Fc receptor bearing cells, IgG, IgM antibody +, classical complement pathway

Front 68

Describe the immune response to intracellular bacteria at 0-4hrs, 4-96 hrs, and post 96hrs

Back 68

early- macrophages
middle-T cell independent macrophage activation, IL-1, IL-6, TNF-a
late- T cell activation of macrophages by IFN-G

Front 69

Describe the immune response to virus infected cells 0-4hrs, 4-96 hrs, and post 96hrs

Back 69

early-natural killer cells
middle-interferon alpha, Beta, inferon activated NK cells
late- cytotoxic T cells

Front 70

What is the purpose of acute inflammmation and how is this achieved?

Back 70

purpose-contain infection, prevent, signal subsequent immune response.
Achieved by
-capillary expansion to increase blood flow
-increased permeability of microvasculature to allow escape of leukocytes
-exit of leukocytes from capllaries

Front 71

What are the symptoms of acute inflammation? What causes these symptoms

Back 71

rash/warmth- capillary expansion leads to increased blood flow
edema- increased permeabilty of microvasculature allows escapte of fluid, plasma proteins, and leukocytes
pus- exit of leukocytes from capillaries to infection site

Front 72

Where are actue phase proteins produced? What are they produced in response to? Where do these "triggers" come from?

Back 72

Actue phase proteins are produced by liver cells in response to IL-1, IL-6, and TNF, these cytokines are released by macrophages/ dendritic cells in reponse to PAMP ligands

Front 73

What are the acute phase proteins

Back 73

C-reactive protien (CRP), mannose binding protein ,(MBP) and fibrinogen

Front 74

WHat is the structure of CRP? WHat does it bind to? How does it contribute to the acute phase immune response

Back 74

stucture-pentameric disk
binds- phosphorylcholine on bacterial but not host membranes
contribution-opsonizaiton and triggers classical complement pathway

Front 75

What is the strucutre of MBP
WHat does it bind to?
How does it contribute to the acute phase immune response

Back 75

structure- resemebles complement C1q
binds- mannose residues on bacterial cell surfaces common to forms of LPS and capsules
contribution-opsonizatin, activates classical pathway (MBP binds MASP which then activates C4)

Front 76

list the bacterial components that can directly activate protective responses

Back 76

LPS, lipoteichoic acid, lipoarabinomannan, glycolipids and glycopeptides, polyanions, N-formyl peptides

Front 77

list the bacterial components that are chemotactic

Back 77

peptidoglycan fragments,cell surface activation of alternative pathways of complemetn (C3a, C5a)

Front 78

What are the three pathways of complement activation? What triggers them?
Which pathway can begin before the immune response?

Back 78

classical-antibody antigen complex either IgG or IgM or CRP or MBP

lectin- mannose binding protein (MBSP replaces the C1 in the classical pathway then C4 to C2 the same way)

alternative-directly on pathogen surface, can begin before the immune response because it doesn't require early complement components (C1, C2, C4 etc)

Front 79

What are the three main consequences of complement activation

Back 79

1. opsonization of pathogens
2. recruitment of inflammatory cells via cytokines
3. direct killing of pathogens

Front 80

Where do the three ways of activating complement converge?

Back 80

THey all result in the activation of C3 convertase

Front 81

What is the central step of the complement cascase, which can be reach by either the classical ,lectin, or alternate pathway? What is the result of this step?

Back 81

central step-activation of C3 convertase to cleave C3 to C3a and C3b
Cleavage of C3 and subsequently C5 (triggerd by C3b) genearates anaphylatoxins (C3a and C5a) and MAC (C5-9)

Front 82

which two complement activation pathways are triggered by bacterial surfaces

Back 82

alternative and lectin

Front 83

Which complment activation pathway is triggered by antibody-antigen complexes

Back 83

classical

Front 84

Which proteins of the complment cascade are anaphylotoxic

Back 84

C3a, C5a

Front 85

which complement protein is responsible for opsonization

Back 85

C3b

Front 86

which bacteria are killed by the terminal complement lytic structure

Back 86

gram negative

Front 87

Who discovered phagocytosis

Back 87

Elie Metchnikoff

Front 88

Describe the process by which neutrophils migrate from the bloodstream to the site of bacterial elicited inflammation

Back 88

1. endothelial cells respond to IL-1 and TNF-a which results in upregulation of selectins leading to neutrophil tethering and rolling adhesion
2.ICAM is induced on the endothelial sufrace which is the receptor for neutrophil LFA1, this results in firm adhesion
3. Neutrophil flattens and pseudopods reach between endothelial cells. The cytoskeleton rearragnes and the cells squeezes into the interstitial space
4. A gradient of chemotactic substances results in migraiton to the site of injury

Front 89

What cytokines are important for the expression of selections which are necessary to faciliate neutrophil tethering and rolling adhesion

Back 89

IL-1 and TNF-a

Front 90

Which receptor-ligand system is essential for neutrophil firm adhesion

Back 90

endothelial cell ICAM and neutrophil LFA1

Front 91

What proteins can serve as opsonins

Back 91

mannose binding protein, IgG, C3b

Front 92

list the oxygen dependent antibacterial compounds found within the phagolysosome

Back 92

hydorgen peroxide (NADPH oxidase, and NADH oxidase)
superoxide
hydroxyl radicals
activated halides
nitrous oxide

Front 93

list the oxygen independent compounds of the phagolysosome

Back 93

acids, lysozyme, lactoferrin, defensins and other cationic protiens, proteases, elastase, cathepsin G

Front 94

What does TLR1 recognize and where is it located

Back 94

lipoprotein, located on plasma membrane

Front 95

What does TLR2 recognize, and where is it located

Back 95

petidoglycan, zymosan, LAM (bacteria, fungi), located on plasma membrane

Front 96

What does TLR 6 recognize
Where is it located

Back 96

mycoplasma lipoprotein, located on plasma membrane

Front 97

What does TLR 4 recognize, Where is it located

Back 97

enterobacterial LPS, located on plasma membrane

Front 98

What does TLR5 recognize, Where is it located

Back 98

flagella, located on plasma membrane

Front 99

What does TLR 3 recognize? Where is it located?

Back 99

recognizes dsRNA ( viruses) , located on the endosomal membrane

Front 100

What do TLR7 and TLR 8 recognize, where are they located

Back 100

recognize ssRNA (viruses) located on endosomal membrane

Front 101

What cytokine facilitates the anti-inflammatory function of macrophages

Back 101

IL-10

Front 102

Immune memory is an accessory function of macropahges. What are the two ways this is acheive and what cytokine is invovled in 1 of the pathways?

Back 102

1. antigen processing and presentation
2. T lymphocyte activation via IL-12

Front 103

What are the two pathogen recognition and inflammatory functions of macrophages? What cytokines are involved?

Back 103

1. cehmokines
2. inflamation w/ IL1, IL6, TNFa

Front 104

What are the 4 effector functions of macrophages?

Back 104

1. nitric oxide
2. oxidative burst
3.antimicrobial peptides
4. opsonization via C3b and IgG Fc receptors then phagocytosis
"NAPO" the microbes (nitric, oxidative, antimicrocial, phagocytosis

Front 105

What are the four main categories of macrophage functions?

Back 105

1. anti-inflammatory
2. accessory
3. pathogen recognistion and inflamation
4. effector functions

Front 106

What 4 important inflammatory cytokines are produces by macrophages

Back 106

IL1, IL6, IL 12,TNFa

Front 107

Which immunoglobulin is produced first after a primary antigen challenge

Back 107

IgM

Front 108

How does the secondary response to a second antigen challenge differe from the primary response to a primary antigen challenge

Back 108

The secondary response consists mainly of IgG whereas the primary response is IgM first. The secondary response (anamnestic response) reaches a higher titer and lasts longer

Front 109

list the 4 postulates of lymphocyte clonal selection

Back 109

1. each lymphocyte beras a single type receptor of a unique specificity
2. inteaction between a foreign molecule and the receptor with high affinity in the proper context triggers activation
3. The activated cell differentiates into clones with the same receptor specificity
4. lymphocytes beraing receptors specific for self receptors are deleted early in lymphoid development

Front 110

What is the structure, site of action and effector functions of IgM antibodies

Back 110

structure- classic Y shape with heavy and light chain, bound in pentameric structure with disulfide bonds joining the 5 induvidual antibodies
site of action- intravascular
effector functions- complement activation, agglutination, important for responses to polysaccharides on bacterial surfaces

Front 111

What is the structure, site of action and effector functions of IgG antibodies

Back 111

structure- Y shpae with heavy and light chains
site- intravascular, intersitial fluid, transplacental
function- complement activation, neutralization, opsonization, neonatal immunity

Front 112

What is the structure, site of action and effector functions of IgA antibodies

Back 112

structure- Y shape with heavy and light chains, dimeric secretory IgA
site- luminal secretions, breast milk, mucosa
function-neutralization at body surfaces, intestinal immunity in neonates

Front 113

What is the structure, site of action and effector functions of IgE antibodies

Back 113

structure- Y shape with heavy and light chains
site- subcutaneous, submucosal
function-mast cell sensitization, eosinophil acitvation

Front 114

What is the structure, site of action and effector functions of IgD antibodies

Back 114

structure-Y shape with heavy and light chain
site- B cell surface
function-unknonw, possibly B cell antigen receptor

Front 115

list 3 bacteria surface structures that antibodies can bind to

Back 115

1. fimbriae
2. lipoteichoic acid
3. capsule

Front 116

How important (-, +, ++, +++) is complement for fighting extracellular bacteria? Intracellular?

Back 116

extracellular +
intracellular -

Front 117

How important (-, +, ++, +++) is interferon for fighting extracellular bacteria? Intracellular?

Back 117

it is not important for either (-) interferons are important in defending against viral infections

Front 118

How important (-, +, ++, +++) are neutrophils for fighting extracellular bacteria? Intracellular?

Back 118

extracellular +++
intracellular -

Front 119

How important (-, +, ++, +++) are macrophages for fighting extracellular bacteria? Intracellular?

Back 119

extracellular ++
intracellular +++

Front 120

How important (-, +, ++, +++) are CD4 TH1 cells for fighting extracellular bacteria? Intracellular?

Back 120

extracellular -
intracellular ++

Front 121

How important (-, +, ++, +++) are CD cytotoxic T cells for fighting extracellular bacteria? Intracellular?

Back 121

extracellular -
intracellular ++

Front 122

How important (-, +, ++, +++) are antibodies for fighting extracellular bacteria? Intracellular?

Back 122

extracellular ++
intracellular +

Front 123

What are the 5 properties of a good candidate for vaccine development

Back 123

1. organism causes significant illness
2.organism exists as only one serotype
3.antibody blocks infection or systemic spread
4. organism does not have oncogenic potential
5. vaccine is heat stable

Front 124

What are the 5 properties of a good vaccine

Back 124

1. generates memory response without disease
2. elicits a strong response (adjuvants)
3. the correct response is elicited (systemic vs mucosal route, antibody vs. T cell)
4. resonable cost
5. safe

Front 125

Compare and contrast live and inactivated vaccines in terms of route of administration

Back 125

live- natural or injection
inactive- injection

Front 126

Compare and contrast live and inactivated vaccines in terms of dose

Back 126

live- low
inactive- high

Front 127

Compare and contrast live and inactivated vaccines in terms of number of doses

Back 127

live- single
inactive- multiple

Front 128

Compare and contrast live and inactivated vaccines in terms of need for adjuvant

Back 128

live-no
inactive- yes

Front 129

Compare and contrast live and inactivated vaccines in terms of duration of immunity

Back 129

live-long term
inactive- short term

Front 130

Compare and contrast live and inactivated vaccines in terms of antibody response

Back 130

live- IgG, IgA
inactive- IgG

Front 131

Compare and contrast live and inactivated vaccines in terms of cell medaited immune response

Back 131

live-good
inactive- poor

Front 132

Compare and contrast live and inactivated vaccines in terms of heat lability

Back 132

live- yes
inactive- no

Front 133

Compare and contrast live and inactivated vaccines in terms of interferance and side effects

Back 133

live- occasional interferance and occasional mild side effects
inactive- no interfereance, occasional sore arm

Front 134

Compare and contrast live and inactivated vaccines in terms of reversion to virulence

Back 134

live- rare
inactive- none

Front 135

What type of immune response is generated from the naked DNA vaccine model? How is this done?

Back 135

A cytotoxic T cell response is illicited by injecting naked DNA coated on gold particles into muscle cells. This resulted in production of the encoded proteins and an immune response towards those proteins

Front 136

What is the gram stain morphology of Staphylococcus?

Back 136

gram positive cocci
two plane division gives grape like clusters

Front 137

Is Staph motile?
Can it form spores?
catalase rxn?
oxygen relationship?

Back 137

non-motile, non spore forming, catalase positive, facultative anaerobe

Front 138

What are the three staph species that are important to humans

Back 138

S. aureus
S. epidermidis
S. saprophyticus

Front 139

How is Staph normally grown? How can S. aurues be selected?

Back 139

Can grow Staph species on blood agar plates at 37, colonies form within 24 hrs
S. aureus can be selected for with manitol salts agar which contains 7.5% salt as a selective agent. Fermentation of the mannitol turns the media yellow (differential and selective media)

Front 140

What are the two important diagnostic enzymes for Staphylococcus

Back 140

1. coagulase- S. aureus is coag +
2. catalase- all are catalse + , differ from strep wich are calatase negative

Front 141

What are the 4 staphylococcol tissue destryoing enzymes

Back 141

1. hyaluronidase
2. lipase
3. nuclease
4. fibrinolysin (staphylokinase)
Staph Never Have Love

Front 142

What is staphylokinase and how does it help Staph avoid the immune response

Back 142

Staphylokinase is a Staph enzyme that activates plasminogen to form plasmin which digests fibrin clots. This disrupts the fibrin meshwork which is used to localize an infection. Staphlyokinase also cleaves C3b and IgG which prevents the bacteria from being opsonized efficicently

Front 143

How does fibrinogen protect Staph from the host immune response?

Back 143

It binds C3b and prevents lysis by complement

Front 144

What are 3 mechanisms used by Stahylococcol species to evade the host immune response

Back 144

1. staphylokinase
2. fibrinogen
3. protein A

Front 145

What are the 5 ways protein A functions as a virulence factor?

Back 145

1. binds to Fc fragment of antibodies
2.Binds to TNFa receptor
3. Binds von Willebrand factor
4. Binds B cell surface IgM variable regions
5. Aids in cell agglutinatino/ biofilm formation
"A Fears Very Tiny Bugs" (Aggultination, Fc binding, Von Willebrand, TNF, B Cells)

Front 146

One of the ways that protein A acts as a virulence factor is by binding the Fc portion of antibodies. Explain the net effect of this process

Back 146

-twarts accute immunity by tying up the antibodies in an unproductive way
-prevents opsonization

Front 147

One of the ways that protein A acts as a virulence factor is by binding the TNFa receptor. Explain the net effect of this process

Back 147

binding of the TNFa receptor leads to induction of cytokines and subsequent inflammation

Front 148

One of the ways that protein A acts as a virulence factor is by binding von Willebrand factor. Explain the net effect of this process

Back 148

von Willebrand factor is a serum glycoprotein that mediates platelet aggregation at sites of endothelial damage. Protein A can bind to this factor which facilitates infection and adhesion at invaded sites like catheters etc

Front 149

One of the ways that protein A acts as a virulence factor is by binding to vraible regions of B cell surface IgM. Explain the net effect of this process

Back 149

This induces B cell apoptosis and thus poor antibody response

Front 150

How is protein A used commercially?

Back 150

IT can be coupled to small beads and Ig specific for a target protein can be added. An antigen-antibody- bead complex is formed which can then be centrifuged out of a lysate

Front 151

What is cogulase's (bound and free) function and how does it benefit S. aureus?

Back 151

converts fibrinogen to fibrin
bound form causes staphylococci to clump, free form reacts with globulin plasma factor to form staphylotrhombin
may form a protective layer of fibrin around stahylococcal abscesses

Front 152

How are S. epidermidis and S. saprophyticcus differentiated?

Back 152

novobiocin suceptibilit, S. saprophyticus is resistant

Front 153

Which portion of LPS is antigenic? Which is toxic?

Back 153

the o antigen is antigenic
lipid A is toxic

Front 154

Describe the alpha and beta toxins associated with S. aureus? What do they do?

Back 154

alpha- disrupts smooth muscle in blood vessels, oxic to many different cells types, forms pore in host cell emembrane resulting in an influx of ions and cell lysis
beta (sphingomyelinase C)-catalyses hydrolysis of membrane phospholipids (sphignomyelin)
together the two toxins are responsible for tissue descrtion and abscess formation

Front 155

Describe the Staphylococcal toxin Panton-Valentine Leukocidin
Why is the dose significant?
How is it aquired by the strain? What is unique about is strain distribution

Back 155

-PVL leads to the secretion of two proteins LukS and LukF. These combine on the phagocyte cell membrane and form a pore that leads to leukotoxicity (signifiance in pathogenesis is controversial)
-low dose leads to apoptosis but high dose leads to lysis releasing inflammatory mediators and ROS which cause tissue necrosis
-it is encoded by a prophage
-PVL is made by 5% of S. auerus strains but nearly all MRSA strains

Front 156

What are Phenol-soluble modulins (PSMs)

Back 156

small (20-25 AA) surfactant peptides produce by MRSA ans some S. epidermidis.
At high conentration they can lyse neutrophils and RBCs
at low concentrations their "modulin" activity stimulates neutrophils to produce cytokines and to positivley chemotax towards a loal inflammatory site
(example is delta toxin)

Front 157

What two forms of hemolysis can S. aureus display

Back 157

beta and non-hemolytic

Front 158

Describe the staphylococal exotoxin exfoliatin

Back 158

-causes splitting of the epidermnal layers of skin via disruptionof the intracellular junctions, results in desqumation of the epidermis
~%5 of S. aureus
-the cause of staphylococcal scalded skin syndrome

Front 159

What Staphylococcal product causs SSSS

Back 159

exfoliatin

Front 160

Describe the Staphylococcal exotoxin Toxic Shock Syndrome Toxin (TSST)

Back 160

-associated with TSS cuausing S. aureus strains
-binds host cells and induces cytokine and inflamatory produces
"cytokine storm" IL-1, IL-6, IL-12, TNFa

Front 161

Describe the Staphylococcal enterotoxin. What disease does it cause? How does it act?

Back 161

-heat and acid stable
-ingestion of toxin without bacteria is sufficient to cause illness
-leads to food poisioning
-binding of toxin to host cells leads to release of cytokines and inflammatory products
-example of a super antigen

Front 162

What is a super antigen?

Back 162

A superantigen acts as a polyclonal T cell activator. In contrast to the normal pathway where an antigen leads to the activation of one specific T cell population, superantigens can activate many different types of T cells beause they facilitate binding of TCR and MHC2 outside of the antigen binding domain

Front 163

How does the immune response ellicited by a superantigen differ from that induced by a "normal" antigen

Back 163

when a normal antigen is presented to a T cell, recongition leads to cytokine (IL-2) secretion and proliferation of that specific type of T cell. The T cell then ineracts with the B cell resulting in antibody production. When a superantigne activates a T cell the same pathway occurs but in addition, excess IL-2 stimulates the produciton of TNF and other cytokines, eventually leading to shock

Front 164

Toxic shock syndrome is caused when a localized staphylococci infection produces TSST-1. What are the symptoms of TSS? What can cause the disease to reoccur? How is the disease caused?

Back 164

Sxs- sudden fever, hypotension, diffuse erthematous rash, if untreated can lead to multiple organ failure and death
-disease can reoccur if antibiotics do not clear infection or pt. fails to develop
an antibody to TSS-1
-disease associated with use of hyper-absorbant tampons

Front 165

T/F S. aureus associated food poisoning results from ingesting a bacteria

Back 165

false, the posoning is the result of ingesting a heat resistant enterotoxin not the bacteria itself

Front 166

describe S. aureus associated food poisoning
Cause? Severity? Sxs? Tx and recovery?

Back 166

Caused by ingestion of heat stable enterotoxing. Manifests 4-12 hours after ingestion of contaminated food. Sxs include vomiting, diarrhea, abdomnial pain, and nausea. The disease is self limiting and recovery begins post 24 hrs. Rarely seroius except in elderly

Front 167

Describe Staphylococcal Scalded Skin Syndrome (SSSS) aka Ritter's disease
age group? cause? Sxs? Tx?

Back 167

occurs in small children
abrupt onset of erthema (skin inflammation), large bullae (cutaneous blisters) NO WBCs or bacteria
clears 7-10 days, no lasting scarring
caused by the exofoliatin toxin
note that Bullous impetigo has localized blisters also but these are culture positive

Front 168

What two organisms can cause impetigo

Back 168

S. aureus and Group A Strep (S. pyogenes)

Front 169

Describe impetigo

Back 169

result of Group A strep or Staph aureus infection. Formation of multiple pustules on the skin which often rupture and form crusty lesions

Front 170

Describe Folliculitis

Back 170

result of S. aureus infection. Pus filled infection of hair follicules. Folliculitis of the eyelash is called a stye

Front 171

What organism causes furuncles/boils/ carbuncles. Describe these infections. Are there any serious complications?

Back 171

S. auerus. Furuncles/ boids are a progression of folliculitis where larger reddened nodules develop. Carbuncles are groups of furuncels that join togeter and progress deeper into the subcutaneous tissue. This progression canlead to bacterimia.

Front 172

S. aureus is a common cause of bacterimia. What are two ways this organism can get introduced into the blood?

Back 172

-indwelling catheters
- IV drug use

Front 173

Describe S. aureus associated pneumonia

Back 173

life threatening infection. Can result from aspiration of oral secretions or by spread from the blood (hematogenous). Especially probelmatic consequence of viral influenza or cystic fibrosis

Front 174

Staph epidermidis is coagulase negative (diff from S. aureus). What are the most common sites of infection by this organism

Back 174

-infection of replaced heart valves
-infection of catheters and prosthetic joints

Front 175

What type of infection is commonly associated with Staph Saprohyticus? (coagulase negative)

Back 175

Uriniary tract infection (cystitis= bladder, urethritis= urethra)

Front 176

What is the significance of small colony varients

Back 176

A strain of S. aureus that may live intracellulary. Allow the bacteria to avoid host immune response and resist antibiotics

Front 177

What is the purpose of lancefield grouping?

Back 177

serological groupping of streptococci based on cell wall carbohydrages (C groups), note that some species do not have C group antigens (like S. pneumoniae)

Front 178

What speicies belongs to group A strep and gives a Beta hemolytic reacion?

Back 178

Group A- S. pyogenes

Front 179

What species belongs to group B strep and gives a Beta and occasionally alpha and non hemolytic reaction

Back 179

S. agalactiae

Front 180

What lancefield group does S. pneumoniae belong to?

Back 180

none, it does not have a C antigen

Front 181

What is the viridans strep group? What disease do they cause

Back 181

Oral commensal speceis that are alpha hemolytic
usually not pathogenic but can cause endocarditis if they are introduced into the blood stream

Front 182

List the 8 virulence determineants of Group A strep, S. pyogenes

Back 182

1. capsule
2. M protein
3. Lipoteichoic Acid
4. F protein
5. Streptolysin O and S
6. C5a peptidase
7. Ig binding protein
8. tissue destroying enzymes

Front 183

What sugar is the group A C antigen?

Back 183

rhamnose, N-acetylglucosamine

Front 184

List 6 suppurative group A streptococcal diseases

Back 184

1. pharyngitis
2. Scarlet fever
3. Streptococcoal toxic shock
4. impetigo
"Strep Is Careful Never to Pass" (scarlet, impetigo, cellulitis, necrotizing faciitis, toxic shock, pharyngitis)
5. cellulitis
6. nercrotizing fasciitis

Front 185

T/F Group A strep can be carried in teh throat without disease

Back 185

True, 15 to 20% of children and adults are carriers

Front 186

List two non suppurative group A streptococcal diseases

Back 186

1. rheumatic fever
2. Acute glomerular nephritis

Front 187

Describe rheumatic fever
cause?
age group?

Back 187

believe to be casused by antibodies to group A strep that cross react with connective tissue leading to local complement activation and destructuion, usually mannefests on hear valves
-usually occurs in children ages 5-15

Front 188

Describe acutue glomerular nephritis
cause?
sxs?

Back 188

inflammation of the glomeruli, loss of filtering ability, accumulation of waste in system and loss of protein in the urine
-believe to be caused by an accumulation of antibody-antigen compelxes to group A strep in the glomeruli

Front 189

How is group A strep cultured and presumptivley identified

Back 189

-culture on BAP plate
-ID- recongize hemolytic colonies, sensitive to bacitracin

Front 190

How is group B strep culture and presumptivley identified

Back 190

-culture on BAP with beta hemolysis
-resistant to bacitracin
-hydrolyses hippurate

Front 191

What two diseases are associated with group B strep

Back 191

neonatal sepsis and meningitis
postpartum sepsis

Front 192

List 4 diseases that are caused by Streptococcus pneumoniae

Back 192

1. pneumonia
2. otitis media and sinusitis
3. meningitis
4. bacteremia

Front 193

T/F S. pneumoniae is a strict human parasite

Back 193

true

Front 194

How is S. pneumoniae cultured and presumptivley identified

Back 194

-readily grown
-forms large goey colonies (capsule) that exhibit alpha hemolysis,
-sensitive to optocin
-note that serological identification of the capsular type is not a routine laboratory test

Front 195

What type of hemolysis?
Group A strep (S. pyogenes)
Group B strep (S. agalactiae)
S. pneumoniae

Back 195

Group A- beta
Group B- beta
S. pneumonaie- alpha

Front 196

What does the S. pneumoniae vaccine consist of and who is it recomended for?

Back 196

-consists of the most common types of capusular carbohydrates
-recomended for elderly

Front 197

What is the difference between active and passive immunity?

Back 197

active- result of an infection,a person forms their own antibodies
passive- a person is given antibodies from anther source (IV, injection etc)

Front 198

Is MBP an opsonin?

Back 198

Yes

Front 199

What are the 4 steps of phagocytosis

Back 199

1. formation of the phagosome
2. acidification of the phagosome
3. fusion with the lysosome
4. killing

Front 200

What are the antigen presenting cells?

Back 200

macrophages, dendritic cells, B cells

Front 201

Listeria monocytogenes is motile intracellularly in infected cells and the motility results in the infection of neighboring cells. What host molecule is rearranged and what listerial protein mediates the rearrangement?

Back 201

Actin, ActA

Front 202

What are the Staphylococcal immune evasion enzymes / binding proteins

Back 202

1. stahylokinse- activates plasminogen to form plasmin which digests fibrin clots and allows the infection to spread. Also cleaves C3b and IgG
2. fibrinogen binding protein- binds C3b and IgG
3. Protein A

Front 203

List 2 Staph virulence factors that can bind IgG

Back 203

Staphylokinase, Protein A

Front 204

List2 Staph virulence factors (enzymes or binding proteins) that interfere with complement

Back 204

1. Staphylokinase cleaves C3b
2. Fibrinogen binding protein binds C3

Front 205

Which streptococcal virulence factors interfere with complement?

Back 205

1. M protein degrades C3b
2. C5a peptidase degrades C5a

Front 206

Which steptococcal virulence factors have lytic activity?

Back 206

Streptolysin S and O
Streptokinase

Front 207

Which streptococcal virulence factors are antiphagocytic

Back 207

1. capusle
2. M protein