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Bacterial Diseases > Exposure and Host Adaptation > Flashcards

Exposure and Host Adaptation Flashcards

1
Q

What are the six steps to become a pathogen

A
  1. Exposure (pre infection), surviving in the environment
  2. Adherence, attaching to host cells and colonizing
  3. Cell innovations and immune evasion, persist in the host
  4. multiply in the host, bacterial growth
  5. toxicity and invasiveness disseminate, spread or invade distant sites, within or between hosts
  6. produce symptoms of disease, microbe induced and host response induced
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2
Q

How are people exposed to pathogens

A

some pathogens move from host to host (person to person transmission) and some are unable to survive outside of hosts for extended periods of time

STDs and other blood or bodily fluid transmission by, Neisseria gonorrhoeae, Chlamydia trachomatis, and Treponema palladium

some pathogens are able to survive outside the host in the environment

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3
Q

What must pathogens cope with while surviving in the environment

A

being eating by eukaryotes, prokaryotes, or phages

exposure to noxious chemicals, human and bio made

lack of nutrients, nutrients aren’t everywhere

exposure to sunlight and weather extremes, lack of adherence sites and UV exposure causing mutations and death

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4
Q

What are pathogen survival strategies for pathogens in the environment

A

endospores

desiccation tolerance

secondary metabolites (bacteriocins)

efflux pumps against disinfectants and antibiotics

metabolic diversity so they can grow on diverse substrates

biofilm formation

motility

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5
Q

What are endospores, what are they resistant to, what type of bacteria are they common in

A

a dormant bacterial structure that is coated in thick layers of peptidoglycan

usually form in a response to lack of nutrients

survive desiccation because of cortex area that contains the nucleic acid that is metabolically inert

UV and heat resistance

can survive millions of years, some were found in mummies in egypt

some gram + such as Bacillus and Clostridia

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6
Q

What is desiccation tolerance

A

limit protein oxidation ROS/SOD example

limit DNA damage during dehydration

membrane phospholipid adaptation, increases in saturated fatty acids, increase of cis-trans isomerization, and increase in the proportion of negatively charged phospholipids these all help hold onto water

a pathogen might encounter this is they end up on an empty hospital bed and try to stay alive

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7
Q

What are the four steps of biofilm formation

A
  1. Adhesion: finding a home usually formed at the air liquid layer
  2. Aggregation: secreting extracellular matrix/glycocalyx (polymeric matrix outside cell) and becoming 3D
  3. Maturation: forming the film
  4. Dispersal: continuous release of new microbes

active cells proliferated around the outside of the biofilm and dead cells are in the middle, the dead cells provide DNA and nutrients to the living cells

polysaccharide coat on the outside of the biofilm

channels inside the biofilm to get rid of waste products and receive nutrients inside the biofilm

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8
Q

What are bacteria living inside of biofilms resistant to

A

phagocytosis: predators or phagocytosis, the biofilm is too big for a phagocyte to consume
antibiotics: 100 fold less effective in a biofilm, diffusion rates through the biofilms are limited, metabolically the bacteria in the middle are not susceptible, antibiotics ONLY effect bacteria that are activity dividing

mechanical displacement: its hard to mechanically remove biofilms from tissues think of how hard it is to scrap biofilms off teeth, usually requires surgical removal

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9
Q

When are antibiotics not efficient against bacteria

A

antibiotics ONLY effect bacteria that are ACTIVELY dividing

this is why antibiotics aren’t as effective against bacteria in biofilms or bacteria that divide very slowly

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10
Q

How are bacteria motile and why is it advantageous for bacteria to be motile

A

use a flagella, spirochetes, for motility and chemotaxis

to help bacteria find food and survive conditions inside and outside the hosts

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11
Q

What types of bacteria mainly make flagellas

A

gram - mainly make flagella

some gram + do too

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12
Q

What are spirochetes

What bacteria have them

A

corkscrew shaped internal flagella it is in the periplamsic space between the inner and outer membrane

the flagella never sees the outside world so antibody responses are nullified and TLR 5 cannot detect (innate)

Rotation causes twisting of bacterial shape its like one big corkscrew propeller

Treponema pallidum which causes Syphilis
Borrelia burgdorferi which causes Lyme Disease

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13
Q

When a bacteria goes to colonize a host what are the two main barriers they must overcome

A
  1. cross primary barriers such as skin and mucosa
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14
Q

How do bacteria penetrate the skin

A

there are no known pathogenic bacteria that can penetrate the skin without help

bacteria can use an arthropod as a vector

bacteria are opportunists that wait for the skin to be bypassed in some way

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15
Q

Can any know bacteria penetrate the skin

A

no

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16
Q

What are the known arthropods that are used as vectors

A

Borrelia burgdorferi causes lyme disease and is carried by ticks

Yersina pestis causes the bubonic plague and is carried by fleas

Virures use mosquios to carry west nile fever, yellow fever, dengue fever and malaria

Plasmodium spp is a protist that uses mosquitos to transit malaria

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17
Q

What are ways that the skin is bypassed by opportunistic bacteria

A

cuts, surgery, catheters, burns, etc

IV: staphepidermis takes advantage of the breached surface

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18
Q

Recap of the Mucosal defense

A

mucus is highly effective at preventing microbes from reaching the surface fo the underlying epithelial cells

vicious, sticky substance filled with anti microbial peptides
defensins, lysozyme, slgA, lactoferrin, lactoperoxidase

traps bacteria, kills bacteria, and is resistant to degradation by enzymatic attacks

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19
Q

Why is GALT a liability in humans

A

some bacteria exploit the M cells to pass through the epithelial layer and enter the body

bacteria avoid mucus and go for the M cell where antigenic sampling occurs by transferring it to the phagocyte and the bacteria can pass through the epithelial layer

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20
Q

What bacteria use M cells to bypass the epithelial layer and enter the body

A

Salmonella enterica

Yersinia pseudotuberculosis

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21
Q

How do bacteria penetrate or evade the mucin defenses

A

GALT and M cells
using flagella to move and out of
degrade slugs

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22
Q

How to bacteria move away from mucus and what is a bacteria that does this

A

with motility methods

Helicobacter pylori uses a flagella to move through the mucus layer that has a more neutral pH than the above stomach acid which has a more acidic, lower pH

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23
Q

How do bacteria avoid slgAs

A

slgAs have an antigen binding domain and the Fc region has a docking point on the mucin to neutralize the activity of the bacteria

bacteria can produce enzymes to break apart slgAs these enzymes are slgA proteases

we have slgA1 and slgA2 pathogens can degrade igA1 sot they think that our bodies formed IgA2 which cannot be degraded by pathogens

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24
Q

What is the common type of host produced natural antibodies in humans

A

defensins

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25
Q

what are defensins

A

cationic (positively charged) peptides that bind to the negatively charged surface of bacteria and disrupt the bacterial membranes

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26
Q

How do bacteria combat defensins, four main ways

A

bacteria try to make their membrane surface more positively charged so the defensins that are positively charged are not attracted to them

LPS and LTA modification to change the net negative charge, become more positive to not attract defensins

they can make a capsule to protect their membrane, the thick polysaccharide layer protects the bacteria by slowing or preventing defensin diffusion through

microbial proteases can degrade defensins, not allowing the defensins to disrupt the membrane

counteract defensin channels by using cytoplasmic proteins to ‘plug the hole’ that is formed by defensins in the bacterial membrane

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27
Q

What is the main nutrient required by bacteria to proliferate, which bacteria does not use this and what does it use

A

many, but not all, pathogens require iron to proliferate

Borrelia burgodorferi uses Mn2+ lyme disease

free iron is often a limiting factor for growth 10^-18 M of free iron inside the body, so not a lot at all

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28
Q

How much free iron is in the body, where is the other iron found

A

10^-18 M of free iron in the body

almost all iron is bound to a protein this is chelated

considered antimicrobial peptides “nutritional immunity”

Lactoferrin 
Transferrin 
Ferritin 
Heme 
Siderocalin
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29
Q

Where is Lactoferrin found in the body and what is its role

A

mucosal sites and its present in neutrophil granules

has a high affinity for iron so it takes up iron before pathogens can when inside of mucosal sites and around neutrophil granules

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30
Q

Where is Transferrin found and what is its role

A

in the blood serum, induced by IL-6 and produced by the liver

deliver iron from absorption centers in the duodenum and white blood cell macrophages to all tissues

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31
Q

Where is Ferritin found and what is its role

A

intercellular iron storage

30% of bound iron in the body

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32
Q

Where is Heme found and what is its role

A

Hemoglobin

70% of the bodies iron

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33
Q

What are siderocalins

A

siderocalins interfere with the function of bacterial siderophores

the anti siderophore

we produce siderocalins to take away the bacterial siderophore

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34
Q

Iron in the body is highly controlled within the host so how does bacteria get it from the host

A

compete with the host via siderophores or steal the iron

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35
Q

What are siderophores and what are the two primary structural groups

A

low molecular weight compounds that chelate iron with very high affinities

they take a lot of work for bacteria to make them

caterchols: enterbactin have very high affinity for iron and is produced by bacteria, this takes a lot of enzymatic processes to form and can bind to iron better than our host defenses, it outcompetes the host
hydroxamates: angulibactin bind iron with affinity that competes with host iron binding but not as good as catechols

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36
Q

What are other ways that bacteria can get iron without producing siderophores

A

take other bacterias siderophores: easier than making their own

simply steal the hosts iron-chelators: directly take up transferrin, lactoferrin, or heme: they can destroy the protein in the hosts cytoplasms and release the iron for their own use

produce toxins such as hemolysis and other cytolysins that destroy host cells and release their iron stores (ferritin, the intracellular iron storage protein)

37
Q

What are gram + strategies for iron acquisition

A

they can make two siderophores: Staphyloferrin A and Staphyloferrin B they both have binding proteins that bind to iron and push it through a complex below into the bacterial cell for use, this requires ATP

best way to get iron by them is to strip the heme away from the host cell through a complex, staph, strep, listeria

38
Q

What are gram - strategies for iron acquisition

A

they have transferrin and lactoferrin binding proteins along with a hemopore that can bind and uptake hemoglobin through the membrane

they also have two different siderophores one that uses an outer membrane receptor and not that uses TBDT (transmembrane protein)

39
Q

What are stealth siderophores

A

bacteria take their siderophore and coated it in glucose to make it appear different and make it less recognizable by the hosts siderocalin, therefore the siderocalin cannot bind to stealth siderophores

there is an evolutionary tug of war between hosts and bacteria with siderophores and siderocalins

40
Q

What are key detemerinants of bacterial adhesion inside of hosts

A

pili and fimbriae are key parts of binding to cells and tissues inside hosts

41
Q

What are the different ways bacteria can adhere to cells and tissues

A

pili/fimbriae: these are interchangeable

surface adhesions

MSCRAMMS

if you can block attachment you can block infection

42
Q

What are MSCRAMMS, what bacteria uses MSCRAMMS

A

Microbial surface components recognizing adhesive matrix molecules

type of adhesion uses by Staphlyococcus aureus

not the same as pili and fimbriae

43
Q

What is the difference between pili and fimbriae

A

interchangeable terms

pili: generally refers to longer, thicker surface structures
fimbriae: generally refers to shorter, thinner structures

the best understood mechanism of adherence is the attachment of bacteria to the hosts through rod-shaped filamentous structures

first identified in gram - but more recently they also appear prevalent in gram +

pili come in a variety of shapes and types, there are over 30 types identified for E. Coli alone

44
Q

How is tissue tropism governed by pili

A

by the piling tip, this establishes the contact between the host and the bacterial surface

contributes to the host-cell or tissue-specificity of the pathogen

some pathogens can interchange the piling tip but keep the same shaft

45
Q

What do UPEC strains of E. coli P Pili attach to

A

attaches to the mannose sugars on the bladder epithelium

idea to put mannose sugars in the bladder to try and get pili of E. coli to bind to that instead of the epithelium on the bladder

46
Q

What are the three types of pili

A

P Pili

Type IV or Bundle forming pili (BFP)

Curli Pili

47
Q

How are Type I Fimbriae aka P Pili formed

A

by chaperone-usher pathway
holds onto the proton with a beta strand to help with stability while it is being moved this beta strand is called the donor chaperone strand

assembly is the tip going out list and then slowly pushes it out

This occurs in the periplasm

Fim C is the donor chaperone strand

chaperone never becomes part of the pili, just helps stability?

48
Q

What type of pili are formed by the chaperone-usher pathway

A

Type I fimbriae and P. pili

49
Q

How are curli pili formed

A

CsgE, F, G dependent assembly, after secretion past outer membrane, pilin subunit CsgA self-polymerizes

CsgD is a transcription factor that regulates expression of the csgBAC operon

CsgC is a chaperone that escorts it to the outer membrane that is located in the periplasmic space, secreted as it self polymerize

Csg: curli specific genes

50
Q

How are type IV aka bundle forming pili formed

A

secretion dependent

monomers in the inner membrane protrude out the cell surface

stable protein protein interactions work to assemble it

to retract they do the opposite, its pulled back through the same opening

51
Q

What type of pili do Neisseria gonorrhoeae use

A

type IV bundle forming pili

52
Q

What type of pili do E. coli use

A

type I aka P pili and curli pili

53
Q

What types of pili are found in both E. coli and Salmonella spp.

A

Curli fibers

54
Q

What are the csg in E. Coli

A

csgBAC and csgDEFG

55
Q

What are the csg in Salmonella

A

curli specific genes
afg: aggregative fimbriae

agfBAC and agfDEFG

Agf: aggregative fimbriae which promotes the aggregation between bacteria, more bacteria bacteria interaction but still impacts the host

56
Q

What are the pili of gram + bacteria like

A

important for biofilm formation and in pathogenic strains: adhesion and invasion

pilin subunits are covalently attached to each other and to the peptiodogylcan layer by enzymes called sortases

57
Q

What are sortases

A

pilin subunits are covalently attached to each other and to the peptiodogylcan layer by enzymes called sortases in gram + pili

sortases recognize sequence motifs in their substrates LPXTG to cleave the substrate at the threonine residue

this cleaved substrate is coupled to pepitdoglycan or the next available pilin subunit through a second sequence motif YPKN

all the pilin subunits will have this signature at the C-terminus and this links it to another monomer or the cell wall itself

58
Q

How are pili assembled in gram + bacteria

A

sortase is how everything can get through the cell wall

59
Q

What are non-fimbrial adhesions of gram + bacteria

A

hair-like protrusions that resemble pili

many of them bind to extracellular matrix and connective tissue such as fibronectin, collagen, fibrinogen, vitronectin, laminin = MSCRAMMs

60
Q

What does Streptococcus pyogenes use to bind to cells

A

gram + bacteria

nonfimbrial adhesion

F protein binds Fibronectin
pilus-like structures made of M protein that binds to factor H

binds factor H, destroying C3 convertase and avoiding C3b opsonization: this is complement and phagocytosis avoidance

has a sortase to bind to cell wall

61
Q

What are afimbrial adhesions

A

InIA and InIB of listeria monocytogenes triggers bacterial uptake by host cells

causes actin cytoskeleton of host cell to rearrange and allow internalization

62
Q

To maintain a persistent infection and to be a successful pathogen what must happen

A

the pathogen must be able to combat the immune defenses of the host

the innate and adaptive immunity

innate: complement and phagocytosis
adaptive: antibodies/phagocytosis and CTLs

63
Q

How do bacteria use capsules to avoid complement

A

prevent alternative pathway activation

inhibits formation of the C3 converts binds serum protein H rather than factor B

steric hindrance is used by the capsule to prevent phagocytosis

factor H and protease I inactive C3b prevent the complement in our own tissues

64
Q

How do capsules avoid complement

A

prevent alternative activation: inhibits formation of the C3 convertase by binding factor H instead of factor B and this inhibits phagocytosis

prevents formation of the MAC complex: proteins are unable too get through the capsule of the membrane, this prevent direct lysis

65
Q

How do bacteria use host mimicry

A

make capsules out of sialic or hyaluronic acid

66
Q

What is sialic acid and how is it used by bacteria

A

found in relatively high amounts in all animal tissues

prevents comment

the sialic acid is used by bacteria in host mimicry, they make capsules out of it to avoid detection by the host immune system

67
Q

What is Hyaluronic acid and how is it used by bacteria, what bacteria is an example of it

A

found as glycosaminoglycan found in connective, epithelial, and neural tissue

make capsules out of hyaluronic acid in bacterial host mimicry

streptococcus pyogenes

68
Q

What is the role of C5a peptidase/toxins

A

secrete enzymes (proteases) that destroy the complement proteins, C5a for instance by some gram +, then the neutrophils don’t know where to attach to

produce toxins that kill, inactivate, immobilize, or reduce the strength of immune cells such as phagocytes they can also prevent cytokine signaling

69
Q

What do pathogens avoid if they become intracellular

A

pathogens that live inside the host cells are not directly exposed to the immune system

no antibodies 
no complement proteins 
no defensins 
no lysozyme 
no phagocytes 
no direct exposure to any immune cells 
really advantageous if you can survive inside a macrophage

they could also escape the phagosomes into the cytoplasm before the bacteria are killed, they produce toxins that disrupt, degrade, or make holes in the hosts membrane

70
Q

How do bacteria escape the phagosome

A

alternatively bacteria just escape from the phagosome into the cytoplasm before the bacteria are killed

they produce toxins that disrupts, degrade, or make holes in the hosts membrane

71
Q

What kind of bacteria lyse the phagosome

A

Listeria monocytogenes produces a pore forming hemolysin called listeriolysin O LLO

only active at pH 5.5 as phagosome becomes acidified and it escapes

PlcA result in the lysis of the phagosome membrane

vacuole is lysed and bacteria escapes into cytosol and replicates

72
Q

What is actin-based motility of bacteria and what bacteria use this

A

many pathogens that can direct their own endocytosis and can also manipulate the actin cytoskeleton once inside the host cell

use actin-based motility
able to push themselves around the cell and into neighboring cells

never have to leave the intracellular enivrionemt 
Listeria monocytogenes 
Shigella flexneria (dysentary)
Rickettsia rickettsii (Rocky Mtn Spotted Fever)

don’t every have to exit the cell

cytotoxic T lymphocytes can enter the cell, but this results in inflammation

73
Q

How does Listeria monocytogenes move pithing and between cells

A

uses actin-based motility

74
Q

How does Legionella pneumophilia avoid phagolysosomal fusion

A

removes proteins necessary for membrane fusion from phagosome, LAMP-1 and LAMP -2

  1. Legionella is taken up inside the cell
  2. the phagosome does not become acidified because it does not fuse with the lysosome
  3. phagosome surrounded by the endoplasmic reticulum studded with ribosomes
  4. bacteria multiply in phagosome
  5. phagosome ruptures
  6. host cell lyses and bacteria escape
75
Q

How does Salmonella Typhimurium prevent phagolysomal fusion?

A

hijacks cell’s actin cytoskeleton to create its own space and make its own vesicle called the SCV the salmonella containing vesicles

  1. bacteria trigger actin rearrangements on the surface of the cell, ruffling occurs and ruffles grow into pseudopods
  2. pseudopods encircle and engulf bacteria and the bacteria are taken up into spacious vacuoles
  3. bacteria remodel the vacuoles creating a growth-conducive environment and the bacteria replicate in the vacuoles
76
Q

How does Mycobacterium tuberculosis prevent phagolysomal fusion

A

uses host protein TACO to coat the phagosome

  1. bacteria bind CR3 on surface of macrophage and the bacteria are taken up in a vesicle
  2. bacteria recruit host protein to surface of phagosome, no fusion of lysosome with phagosome
  3. bacteria prevent endocytic acidification, have reduced bacterial oxidative burst, and bacteria can replicate
77
Q

How does Brucella abortus prevent phagolysomal fusion

A

only replicates upon acidification of vacuole directing it to the ER

  1. Brucella abortus enters the cell and binds and fuses with the lysosome
  2. prefers fusion with the lysosome and the acidification processionals and then it gets sent to the ER to escape from the cell
78
Q

How does Chlamydia replicate inside the cell

A
  1. Chlamydia enters the cell in EB form (non-replicative form)
  2. EB changes into RB form (replicative form)
  3. RBs replicate and some stay RB and others switch back to EBs
  4. EBs are released from the cell to go infect other cells
79
Q

How does Coxiella replicate inside the cell

A

promotes replication upon acidification

  1. Coxiella enters the cell in the SCV form (non-replicative form)
  2. SCV fuses with the lysosome
  3. this fusion changes it to LCV and this is the replicative form producing SCVs and LCVs
  4. the SCVs are released from the cell to go infect other cells
80
Q

How do bacteria resist reactive oxygen species ROE’s, what is an example of a bacteria that does this

A

reactive oxygen species are the primary way the oxidative burst kills bacteria

produce enzymes that neutralize oxygen radicals

catalase H2O2 –> O2 + H2O

superoxide dismutase O2- –> O2+H2O2
Salmonella SodCl enzyme is phage encoded

81
Q

What type of bacteria can avoid nitric oxide (reactive nitrogen compound)

A

Neisseria meningitidis produces nitric oxide reductase that converts NO to N2O (laughing gas) which is less toxic

E. Coli uses nitric oxide dioxygenase to convert NO to NO3- (nitrate)

82
Q

How does Streptococcus pygoenes cope with the adaptive immune system

A

uses protein G

uses it as a surface domain to bind the antibody backwards and not identify the bacterial cell

83
Q

How does Staphylococcus aureus cope with the adaptive immune system

A

uses protein A

bind to the Fc regions of antibodies specifically IgG

coat the antibodies which face outwards

surface domain that binds the antibody backwards

84
Q

What are all the ways that bacteria can cope with the adaptive immune response

A

protein G
protein A

Collagen/fibronectin/fibrinogen which are ECM proteins, clumping factors bind fibrinogen

host mimicry: bind host collagen they can entirely coat their surfaces, host views it as self and doesn’t emit an immune response

85
Q

What are the ways that bacteria can spread cell to cell into new parts of the body

A

actin based motility
flagella or chemotaxis

breakdown pus

secrete spreading factors that break down connective tissue and ECM

secrete blood thinners to escape from blood clots

want to move to different parts of the body so they are harder to find by the immune system and to disseminate through the body

86
Q

How do bacteria breakdown pus, what is the reason for this

A

pus is a thick substance that tends to trap bacteria

pus is composed of proteins, dead cells and DNA, NETS hold onto bacteria while neutrophil is functioning

bacteria secrete DNases to thin it to become untapped and spread

to disseminate through the body

87
Q

What is the role of bacterial spreading factors

A

collagenases, elastases, hyaluronidases and other proteases

break down connective tissue and extracellular matrix proteins to be able to infect different areas and move to new areas

to disseminate through the body

88
Q

Why does bacteria secrete blood thinners

A

secrete blood thinners to degrade fibrin to escape from blood clots and spread to other parts of the body

Streptokinase degrades fibrin

to disseminate through the body

Bacterial Diseases (8 decks)

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