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infectious disease > 3 damage > Flashcards

3 damage Flashcards

1
Q

bug mediated mech of damage

A
  • intoxication
  • growth outside normal niche
  • overgrowth in normal niche
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2
Q

collaborative mechanisms of damage

A
  • growth inside host cells
  • lytic enzymes
  • toxin mediated
  • cytokine release
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3
Q

host mediated mechanisms of damage

A
  • inflammation
  • immune complex deposition
  • autoimmunity
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4
Q

pseudomonas elastase

A

enters tissue, chews up elastin, disseminates

-bacterial mediated virulence factor

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5
Q

what does elastase chew up

A
  • collagen
  • lysozyme
  • C3b + C5b (affects immune system)
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6
Q

ECM

A
  • collagen
  • elastin
  • hyaluronic acid
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7
Q

example of bacterial mediated factor

A

elastase from pseudomonas

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8
Q

how does elastase help pseudomaonas

A

helps it get access to cells and disseminate

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9
Q

strains lacking in elastase

A

persist locally in burn wounds but fail to disseminate

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10
Q

how is elastase a multitasking enzyme

A

cleaves elastin, collagen, lysozyme, immunoglobulins, and complements C3B + C5a (inhibits opsonization + chemotactic responses)

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11
Q

plasmin

A

chews up fibrins/clots

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12
Q

borelia

A

retains ability to bind so that plasminogen can make plasmin + eat clots

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13
Q

neutrophils

A

elastase allows it to get into the tissue
-psuedomonas deactivates normal neutrophil elastase, allowing plasminogen to plasmin, and then there’s an attack of the host

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14
Q

examples of enzymatic virulence factors that are more “collaborative” involve

A

borrelia hurgdorferi + yesinia pestis

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15
Q

nontoxin mediated damage

A

bug mediated pseudomonas elastase + lytic enzymes

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16
Q

non-toxin-mediated damages

A

collaborative + bug mediated

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17
Q

what facilitates borrelia bind human plasminogen and its activator?

A

spirochetes

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18
Q

What does activated plasminogen do?

A

converts plasminogen to palasmin

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19
Q

plasmin

A

protease that breaks down fibrin clots, eliminating fibrin barriers at wound sites

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20
Q

fibrin

A

protein that form clots during microbial invasion which is triggered by tissue injury

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21
Q

pathogens counter fibrin by producing

A

fibrinolytic enzymes OR subverting host enzymes that dissolve the clots making further dissemination possible

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22
Q

dissemination

A

the act of spreading something, especially information, widely; circulation.

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23
Q

Yersinia Pestis

A

has a pla gene (plasmin activator gene) which has protease activity on its own + can activate host plasmin

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24
Q

pla gene

A

plasmin activator gene from Yersinia Pestis

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25
Q

strep pyogenes (collaborative)

A

makes streptokinase, which binds to and activates plasminogen, converting it to plasmin

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26
Q

staph aureus (collaborative)

A

produces fibrinolysin and a coagulase that lays down a fibrin network that may provide a protected niche

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27
Q

what produces hyaluronidase?

A

strep, staph + clostridia

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28
Q

hyaluronic acid

A

ECM structural component

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29
Q

what causes gas gangrene?

A

clostridia

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30
Q

what does clostridia produce?

A

collagenase, which breaks down tissue supporting collagen matrix, enhancing spread throughout the body

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31
Q

what do enzymatic virulence factors that bacteria make, do?

A

degrade proteins or carbs that maintain tissue integrity, allowing enhanced dissemination

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32
Q

lytic enzymes that are multifunctional

A

modulate immune function

-elastase acting on Ig, C3b, C5a

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33
Q

bug mediated growth outside normal niche can occur during

A

dental treatment

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34
Q

bug mediated overgrowth in normal niche occurs with what two organisms?

A

D. Difficile + candida albicans

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35
Q

What collaborative mechanism of damage involves growth inside host cells?

A

tuberculosis (inside has access to nutrients)

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36
Q

lytic enzymes collaborative mechanism of damage

A

macrophages cause lysis

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37
Q

Dental work

A
  • growth outside normal nice

- leads to transient bacteremia, allowing viridans group streptococci to damage heart valves

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38
Q

surgery or trauma can lead to

A

spillage of intestinal contents into peritoneal cavity and subseueny abcess formation by bacteroids fragilis

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39
Q

overgrowth in normal niche can lead to

A

antibiotic therapy can lead to overgrowth of C. difficile in the GI tract and fungus candida albicans on mucosal surfaces

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40
Q

when macrophages are infected by mycobacterium

A

lysosomes leak and cause cellular damage with granulomas

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41
Q

growth inside cells

A
  • mycobacterium tuberculosis
  • legionella pneumophila
  • salmonella typhii
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42
Q

tuberculosis

A
  • survive in alveolar macrophages
  • when macrophages are killed by intracellular bacteria, the lysozomal enzymes and other material released from dying cells contribute to chronic infection and granuloma formation
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43
Q

legionella pneumophila

A

survive in alveolar macrophages, subvery normal phagocytic pathway

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44
Q

salmonella typhii (typhoid mary)

A

gall bladder infection (asymptomatic carrier) that sheds bacteria into the intestinal tract and feces

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45
Q

after patient is exposed to broad spectrum antibiotics

A

pseudomembranous colitis

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46
Q

granuloma formation

A
  • macrophage eats bug
  • bug replicates
  • cell lysis
  • activated macrophages and T cells recruited walling off of bugs and cell debris
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47
Q

persistent infections induce persistant immune responses which in addition to failing to eliminate the infectious microorganism

A

cause pathological changes

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48
Q

old thinking granuloma

A

was hosts means of walling off bacteria

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49
Q

new thinking granuloma

A

bacteria induce granuloma to recruit naive macrophages they can then use for dissemination

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50
Q

immune complex deposition e.g. post streptococcal glomerulonephritis

A

1 strep infection is presented
2 anti strep antibody formation
3immune complex formation (antibody + strep fragments + complements)
4 immune complex deposition in glomeruli, leading to inflammation and kidney disfunction= BAD

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51
Q

what can lead to glomerulonephritis

A

microbial antigen in blood that lead to an immune complex function, leading to pathological changes

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52
Q

what is the major disease process that leads to glomerulonephritis?

A

immune complex formation

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53
Q

glomerulonephritis

A

painful kidney disease

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54
Q

strep pyogenes

A

group A strep/ strep throat

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55
Q

what complexes form in the bloodstream during strep throat

A

streptococcal Ag-Ab complexes that lodge in the glomeruli, causing inflammation of the kideny

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56
Q

glomeruli

A

filtration membranes of kidneys

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57
Q

nephritis

A

inflammation of the kidney

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58
Q

diseases that cause infection triggered autoimunity

A

strep + lyme disease

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59
Q

infection triggered autoimmunity

A

1 infection
2 generation of immune response against pathogen copmonents
2 cross reactivity against self antigens

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60
Q

how do autoimmune disorders occur from microbial infections?

A

microbial products somehow alter or unmask self components OR modulate the processes that normally maintain tolerance to self components

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61
Q

what helps in microbial evasion

A

similarities between microbial molecules (often surface) + host molecules
-the host immune response instead of protecting, elicits cross reactivity

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62
Q

autoimunity

A

rheumatic fever
scarlet fever
lyme disease

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63
Q

toxin

A

a protein that kills or alters the function of a host cell

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64
Q

exotoxin

A

a toxin that is secreted into the extracellular milieu by the bacteria

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65
Q

enterotoxin

A

a toxin that works in or is produced in the GI tract

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66
Q

endotoxin

A

the lipopolysaccharide component of the gram-negative outer membrane; NOT a true toxin

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67
Q

enterotoxin

A

an exotoxin that acts on the small intestine causing changes in intestinal permeability that lead to diarrhea

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68
Q

endotoxin

A

we will not consider this a true toxin

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69
Q

what causes death through hemorrhagic shock and tissue necrosis?

A

endotoxin= lipid A portion of LPS in large enough doses

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70
Q

pyrogens

A

endotoxin stimulates host cells to release proteins called pyrogens (cause fever)

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71
Q

medical supplies that are non-pyrogenic indicate

A

no LPS contamination

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72
Q

which toxicity is higher: endotoxins or exotoxins?

A

exotoxin

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73
Q

toxin that kill cells

A

streptolysin O +diphtheria toxin

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74
Q

toxin that act at cell surface

A

streptolysin O

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75
Q

toxin that act inside cells

A

diptheria toxin

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76
Q

toxin that disrupt function

A

toxic shock syndrome toxin (does NOT KILL cell)

+ cholera toxin (type AB toxin)

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77
Q

streptolysin O kills cells at the surface

A

a pore former toxin that binds to cholesteral in host membrane and forms pores upon oligimerization

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78
Q

diptheria toxin kills cells and act inside cells

A

A/B toxin (single polypeptide) that ADP ribosylates host EF2, stopping protein synthesis

79
Q

staph aureus= disrupts cell physiology/function and act at cell surface

A

TSST-1 (Toxic shock syndrome)

  • strep pryogenes, streptococcal pyrogenic exotoxins such as SPE A.
  • specific for T cells
80
Q

cholera toxin = disrupts cell physiology/function and act inside cells

A

A/B toxin with A/B (5) structure, B part binds GM1 ganglioside and A part acts in cells
-CT leads to increased intracellular cAMP, ion loss to gut lumen and poor ion uptake, rice water diarrhea

81
Q

roles of toxins

A
  • promote bacterial growth
  • facilitate dissemination
  • interfere with host defenses
82
Q

how to do toxins promote bacterial growth?

A

by providing access to nutrients sequestered inside host cells

83
Q

how do toxins facilitate dissemination

A

by breaking down epithelial carriers

84
Q

how do toxins interfere with host defenses

A

by disrupting actin function in phagocytic cells

85
Q

mechanisms for being active at cell surface

A
  • pore formation
  • phospholipase (chew through phospholipids)
  • superantigen
  • lysins
86
Q

examples of pore formers

A

aerolysin, staph alpha toxin, streptolysin, listeriolysin O

87
Q

examples of phospholipase

A

C perfingens alpha

88
Q

examples of superantigen

A

staph TSST

89
Q

TSST

A

toxic schock syndrome

90
Q

lysins

A

hemolysins

91
Q

hemolysins

A

lyse RBCs

92
Q

pore formers

A

disrupt target cell membrane by causing formation of unregulated channels

93
Q

how are channel pores formed?

A
  • multimer of one bacterial protein that inserts into membrane
  • complex of two or more bacterial proteins that inserts into membrane
  • binding to target cell membrane protein leading to unregulated opening of pore
94
Q

phospholipases

A
  • cleave phosphatidylcholine (lecithin) or spingomyelin (all over cell so it will affect lots of cell types)
  • due to the abundance of substrate, can affect virtually all cell types
  • one or more forms expressed by a large number of bacterial species
  • probably facilitate bacterial dissemination and allow bacteria access to nutrients normally found only in the host cell cytoplasm
95
Q

cholera toxin, botox, tetox

A

high level of target cell specificity

96
Q

phospholipases

A

promiscuous, low cell specificity

97
Q

alpha toxin of C. perfringens

A

phoshpolipase

98
Q

beta toxin of staph aureus

A

sphingomyleinase

99
Q

superantigens

A

staphylococci

100
Q

what grows if tampons are kept in too long

A

irritated the vaginal environment to that favoring staph aureus

101
Q

what caused toxic shock syndrome

A

many strains of staph + strep

102
Q

patients most commonly affected by toxic shock syndrome

A
  • menstruating women

- post surgical, either gender if you allow staph aureus to get through a barrier during surgery/injury

103
Q

clinical features of toxic shock syndrome

A
  • high fever
  • hypotension
  • chills
  • nausea, vomiting, diarrhea
  • erythematous rash all over leads to desquamation especially on hands and feet
104
Q

classic pyrogen

A

LPS

105
Q

pyrogenic

A

causing fever

106
Q

many strains of strep make SPEs

A

streptococcal pyrogenic exotoxins such as SpE A + C

107
Q

TSST-1

A

damage due to superantigen activation of T cells, TSST-1 activates 20 to 25% of T cells

108
Q

superantigens

A

interact with T cell receptors inappropriately

-they bind to a site on the TCR outside of the AG specific TCR binding site

109
Q

superantigen binds to all TCRs with a

A

shared structure, and many TCRs share the same structure outside the Ag binding site

110
Q

superantigens binds to class

A

Class II MHC molecules on APCs

111
Q

cell surface interactions with T cells and APCs during TSST mimic

A

normal Ag presentation and stimulate large numbers of T cells

112
Q

TSST

A

toxic shock syndrome toxin

113
Q

Toxic shock syndrome toxin

A
  • superantigen
  • activates up to 1 in 5 T cells
  • causes massive release of cytokines, TNFa, IL-1, IL-2, IL-6
  • contrast to conventional antigen: approximately 1 in 10,000 T cells activated
  • made by many staph, strep strains
114
Q

toxic shock syndrome

A

desquamation of hands and feet

115
Q

A-B toxins

A

activity + binding domain

116
Q

mechanism of AB toxins active in cytoplasm

A
  • protease
  • nuclease
  • ADP-robosyl transferase
  • adenylate cyclase
117
Q

A-B toxin entry

A
  1. binding
  2. receptor mediated endocytosis
  3. acidification release of a subunit across membrane
118
Q

A-B toxin entry= diptheria

A

directly transits cell or it can undergo receptor mediated endocytosis

119
Q

A/B toxins

A

A is active domain B is binding domain

120
Q

what are exotoxins that act at a distance

A

A/B toxins- B domain may deliver toxin to host cell surface for damaging effects or may permit internalization of toxin such that it acts inside cells

121
Q

“A” domains

A

proteases, nucleases, ADP-ribosyl transferases, adenylate cyclases

122
Q

Are A/B toxins homologous?

A

NO, they contain a great variety of enzymatic activities that are delivered to host cells by a common strategy

123
Q

type III secretion system -dependent intoxication

A

bacteria bind to host cell, then inject toxin into cytosol

124
Q

legionella

A

use a lysosomal pathway + keep cells from undergoing apoptosis

125
Q

type III, IV, V, + VI secretion systems deliver non A/B toxins directly into

A

cytosol of host cells

126
Q

NON A/B toxins

A

similar to A/B toxins

  • enzymes that work in the cytoplasm to subvert host cell phsyiology, protecting themselves from host immune response
  • antibiotics are irrelevant to toxin if bacteria grow intracellularly
127
Q

legionella pneumophila

A

> 150 effector molecules
that prevent endosome-lysozomal fusion and lead to the production of a unique compartment where legionella can grow intracellularly
-some effectors prevent programmed cell death

128
Q

vibrio cholerae

A

gram neg rods

129
Q

what organism causes cholera?

A

vibrio cholerae

130
Q

what kind of environment is vibrio cholerae found?

A

aquatic environments

131
Q

how do we acquire vibrio cholerae?

A

contaminated water or food like uncooked shellfish

132
Q

where does the cholera toxin act in our body?

A

small intestine

133
Q

Can cholera be self-limiting?

A

yes, if patient is kept hydrated

134
Q

what leads to rice water diarrhea?

A

cholera

135
Q

does cholera toxin kill its target cells?

A

no, it subverts their physiology such that ionic balance is lost and water move from cells into the lumen of the small intestine

136
Q

How many liters of fluid can a patient lose per day?

A

5 gallons = 20kg= 44 lbs

137
Q

What therapy is used to replace fluid that is lost

A

oral rehydration solution

138
Q

Oral rehydration solution per liter

A

20g glucose, 4.2 g NaCl, 4.0 g NaHC03, and 1.8g KCL

139
Q

If cholera patients are not too bad off

A

replace fluids orally

140
Q

if cholera patient is very ill

A

get IVs of lactated ringer’s solution

141
Q

Cholera’s mechanism of action

A

adenylate cyclase (regulator) is stuck in the “on” due to ADP-ribosylation of bound GTP, which prevents its conversion to GTP which turns it OFF

142
Q

cholera toxin subunits

A

1A subunit + 5B subunits encoded by separate genes in the CTX phage genome

143
Q

What keeps ADPR (ADP ribosylation of bound GTP) on?

A

cholera toxin + NAD with help from an activator

144
Q

what occurs when GSAlpha (adenylate cyclase regulator) remains in the ON position

A
  • continued activation of adenlyate cyclase

- dramatically increased cAMP

145
Q

what happens in the intestine when GSalpha is ON and cAMP increases?

A
  • decreased Na+ absorption by villus cells
  • increased Cl- secretion by crypt cells
  • DRAMATIC WATER LOSS THROUGH LUMEN OF GUT
146
Q

what do cholera patients get when there is RAMATIC WATER LOSS THROUGH LUMEN OF GUT

A

rice water stool

147
Q

does cholera kill cells?

A

NO!

148
Q

cholera

A
  • cholera toxin action in small intestine
  • toxin A subunit is ADP-ribosyl transferase that alters a regulatory subunit of adenylate cyclase
  • results in increased cAMP levels in cells–> decreased Na+ uptake and increased Cl- secretion–> massive water loss and “rice water” stool
  • Na+ / glucose symporter is not affected, allowing oral rehydration with solutions containing salts + glucose
149
Q

is cholera self liminting?

A

yes, if patient is kept hydrated

150
Q

bacillus antracis

A
  • AB toxin
  • clear central spores
  • gram + spore forming abcterium
151
Q

what helped Koch develop the germ theory of disease and derive “Koch’s postulates?”

A

bacillus anthracis

152
Q

What kind of infection is bacillus anthracis

A

zoonotic infection, derived from herbivores such as cattle and sheep

153
Q

woolsorter’s disease

A

derived from catle and sheep; bacillus anthracis

154
Q

domestic terrorism via US mail caused 22 cases of anthrax

A

11 inhalation + 11 cutaneous via envelopes

155
Q

3 ways bacillus anthracis

A

skin, Gi Tract, Lungs

156
Q

anthrax is a

A

multi component A +B toin

157
Q

how anthrax gets in the skin

A

scrape or scratch- scores germinate-anthrax toxin produced-local lesions-tissue necrosis-pustules and ulceres

158
Q

how anthrax is presented in the GI tract

A

ingested spores germinate– anthrax toxin produced-local lesions-possible dysentery

159
Q

what is the most common way disease is presented by anthrax?

A

on the skin

160
Q

how anthrax is presented in the lungs

A

inhaled spores germinate-septicemia-high mortality

161
Q

B subunit of anthrax

A

“PA” for protective antigen, binds to type 1 membrane protein causing receptor mediated endocytosis

162
Q

A subunit of anthrax

A

LF or EF

163
Q

PA + LF anthrax

A

lethal activity

164
Q

PA + EF anthrax

A

edema

165
Q

EF+ LF anthrax

A

inactive

166
Q

LF antrhax

A

letal factor, a Zn++ dependent protease that induces cytokine formation in macrophages + lymphocytes (A2 + B)

167
Q

EF

A

edema factor , an adenylate cyclase enzyme that increases levels of cAMP

168
Q

how does EF cause edema + phagocytic response

A

leads to the formation of ion= increase fluid release, permeable pores in membranes, causing edema and phagocytic response

169
Q

tetanus + botulinum neurotoxins

A

synthesized as a single polypeptide chains

170
Q

what synthesizes tetanus

A

clostridium tetani

171
Q

how do tetanus and botulinum neurotoxins lead to disruption of neurotransmission

A

A subunits cleave proteins involved in docking of synaptic vesicles to plasma membranes

172
Q

BoTox and Tetox

A

homologos + highly sequence similar toxins that affect neural transmission

173
Q

Tetox is transmitted to cranial nerves by

A

intraspinal transmission among involved motor neurons (retrograde transport) OR by bloodstream delivery to neuromuscular junctions

174
Q

TEtox is associated with

A

traumatic wounds/deep puncture (anaerobic)- dreaded “rusty nail”. leads to spastic paralysis (lockjaw)

175
Q

vaccine DDT2

A

tetanus toxoid generated by formalin treatment of TeTox

176
Q

Botox prevents

A

release of neurotransmitter and acts at peripheral cholinergic synapses leading to flaccid paralysis

177
Q

what toxin is heat labile

A

C. botulinum

178
Q

heat labile protein

A

one that can be changed or destroyed at high temperatures.

179
Q

does the C. botulinum toxin grow in the body?

A

rarely, except in infant botulism where there is colonization of the large intestine

180
Q

how is C. botulinum introduced?

A

through contaminated food, and the toxin is heat labile

181
Q

does C. botulinum kill targets?

A

Toxin does NOT act by killing target cells nor does it produce sepsis/fever.

182
Q

How do we treat C. botulinum disease?

A

antitoxin + supportive care

183
Q

What two toxins can damage at extremely low doses?

A

Botox and Tetox

184
Q

How much of botox could kill all the people on earh?

A

.6kg

185
Q

botox (botulinum?) and tetox (tetanus?) attack

A

same targets but different neurons

-you can take A from botulinum and put on B of tetanums and you can retarget

186
Q

how many kDa are Botox and Tetox proteins

A

~150lDa

187
Q

Botox and Tetox

A

Zn++ proteases that cleave proteins in involved in docking of synaptic vesicles to the plasma membrane of neurons

188
Q

What proteins are proteolytically clipped at the hairpin to produce a light chain and a heavy chain that are held by a disulfide bridge

A

botoxin + tetoxin

189
Q

what two toxins block similar steps in neurotransmission but affect different target neurons due to their B domains?

A

botox + tetox

190
Q

locked jaw

A

starts in jaw but then whole body gets rigid

191
Q

how do you die from botulinum neurotoxin

A

flaccid paralysis- you die of suffocation because you can’t breathe

192
Q

tetanus and botulinum neurotoxins A subunits

A

cleave proteins involved in docking of synaptic vesicles to plasma membrane, leading to disruption of neurotransmission; opposite effects on host due to selection of target neurons by B subunits

193
Q

botulinum toxin

A

peripheral neurons, blocks release of stimulatory neurotransmitters, flaccid paralysis

194
Q

tetanus toxins

A

retrograde transport to CNS, blocks release of inhibitory neurotransmitters, spastic paralysis

infectious disease (7 decks)

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