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Block 6 Week 3 > Bacterial Pathogenesis > Flashcards

Bacterial Pathogenesis Flashcards

1
Q

Infectious and parasitic diseases are a leading cause of (balnK) worldwide

A

death (57,029,000 deaths)

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2
Q

(blank) are colonized with bacteria and other microbes (microbiome, microbiota, or microbial flora)

A

humans

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3
Q

Bacteria outnumber human cells (blank-fold)

A

3

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4
Q 
T or F
 100 trillion bacterial cells
 3 pounds in weight
 3 pints in volume
 50 bacterial genes for every human gene
A

T

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5
Q

T or F

there are thousands of bacterial species though only a small number can be cultures

A

T

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6
Q

What kind of relationships does the human microbiome mostly have?

A

mutualistic and commensal relationships (over parasitic)

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7
Q

What is the human microbiome composed of?

A

bacteria, viruses, fungi, and protozoa

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8
Q

What all does the human microbiome do?

A

facilitates nutrient acquisition
educates innate defenses and stimulates both innate and adaptive immunity
help to maintain epithelial boundary function and integrity
provides colonization resistance against pathogens

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9
Q

What are some conditions associated with the human biome?

A

psoriasis
obesiry
inflammatory bowel disease
colorectal carcinoma

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10
Q

THe human genome encodes for about (blank) carbohydrate digesting enzymes

A

20

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11
Q

the intestinal tract bacteriume (blank) has around 260.

A

bacteroides thetaitaomicron

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12
Q

Micribiome promotes (blank). Give me an example of this:

A

adaptation
a gene found in the ocean digests seaweeds, most humans dont have this gene, people in japan who eat alot of seaweed do because the bacteria that had that gene incorporated itself into the human genome

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13
Q

(blank) infections result in about 300 deaths per day in the USA.

A

C. diff (clostridium difficile)

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14
Q

What is the first-line therapy for CDI (C. diff infections)?

A

2 week oral antiobiotics (ie. vanocmyocin)

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15
Q

relapsing infections are common in C. diff due to what?

A

resistance of spores to antibiotic therapy and the damaging effects of antibiotics on the gut microbiome

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16
Q

What has recently starting gaining traction and has a 95% success rate at curing C. diff?

A

fecal micrbiota transplant

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17
Q

How do fecal transplants work?

A

homogenize donor stool and place in Gi tract during colonoscopy, via fecal enemas, or via nasal tube

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18
Q

T or F

the diversity and abundance of different bacterial species vary from person to person

A

True, exposure to different microbes or environments alters the microbiome

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19
Q

T or F

The diversity and abundance of different bacteria species vary over time in a single person

A

True, microbiome is constantly changing over time

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20
Q

T or F

H. pylori dramatically alters the diversity of the stomach microbiome

A

True. H pylori infection decreases the number and abundance of other bacterial species.

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21
Q

T or F variation in the gut micriobiome can affect susceptibility to C. difficile infection.

A

True, the microbiome has a major role in protecting against C. difficle and many other infections

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22
Q

T or F

three year old identical twins have identica skin microbiomes.

A

false, no two individuals microbiomes are identical

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23
Q

What is this:
time between the moment the person is expose to the microbe (or toxin) and the appearance of symptoms (note info is an important diagnostic clue).

A

incubation period

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24
Q

What is this:

time during which nonspecific symptoms occur

A

prodrome period

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25
Q

What is this:

time during which specific clinical signs and symptoms occur

A

disease period

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26
Q

What is this:

time during which symptoms resolve and health is restored

A

recovery period

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27
Q

Describe the stages of infection

A 
incubation period
prodromal period
illness
decline
convalescence
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28
Q

after the recovery period in the stages of infection what can happen?

A

some people can become chronic carriers of the organism and in others latent infections develop

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29
Q

T or F
some people have subclinical infections during which they remain asymptomatic; the presence of antibodies reveals that a prior infection has occured

A

T

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30
Q

What are the 2 modes of transmission of microbes?

A

human to human

nonhuman to human

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31
Q

What are some nonhuman sources?

A

animals, soil, water and food

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32
Q

How can animal to human transmission occur?

A

either by direct contact with the animal or indirectly via a vector

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33
Q

Human diseases for which animals are the reservoir are calld (blank) and the pathogens are called (blank)

A

zoonoses

zoonotic pathogens

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34
Q

The main “portals of entry” into the body are the (blank) (blank) (blank) and (blank)

A

respiratory tract
GI tract
skin
urogenital tract

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35
Q

(blank) is any object capable of carrying infectious organisms

A

fomite

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36
Q

How is gonorrhea passed?

A

via direct contact

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37
Q

How is cholera passed?

A

no direct contact- through fecal-oral transmission (excreted in human feces, then ingested in food or water)

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38
Q

How is congenital syphilis transmitted?

A

transplacental

bacteria cross the placenta and infects the fetus

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39
Q

How does coagulase-negative staphylococci transmit?

A

blood-borne

contaiminated blood products for transfusion

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40
Q

How is tetanus transmitted?

A 
soil source (trauma)
(spores in soil enter wound in skin)
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41
Q

How is legionnaires disease transmited?

A

through water sources (bacteria in water aerosol are inhaled into lungs)

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42
Q

How is cat-scratch fever transmitted?

A

directly from an animal

bacteria enter in cat scratch

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43
Q

How is lyme disease transmitted?

A

via insect vector (tick bite)

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44
Q

How is hemolytic-uremic syndrome cause by enterohemorrhagic escherichia coli transmitted?

A

via animal excreta (bacteria in cattle feces are injected in undercooked hamburger)

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45
Q

How is staphylococcal skin infection transmitted?

A 
via fomites (bacteria on an object... i.e a towel are transferred to the skin) 
****think about wrestlers and wrestling mats)
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46
Q

How big of a dose of virbio cholerae will it take to cause disease in a human?

A

10 to the 8th

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47
Q

How big of a dose of virbio cholerae with bicarbonate will it take to cause disease in a human?

A

10 the the 4th

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48
Q

How big of a dose of salmonella typhi will it take to cause disease in a human?

A

10 to the 5th

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49
Q

How big of a dose of shigella will it take to cause disease in a human?

A

10 to the 2nd

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50
Q

How big of a dose of bacillus anthracis via inhalation will it take to cause disease in a human?

A

10 to the 4th

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51
Q

How big of a dose of mycobacterium TB will it take to cause disease in a human?

A

1-10

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52
Q

What does a bacterial pathogen need to be succesful?

A

Colonize
immune evasion
reproduce
disseminate

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53
Q

What is this:

enter a human host and become established

A

colonize

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54
Q

what is this:

avoid innate or adaptive immune defenses

A

immune evasion

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55
Q

What is this:

acquire nutrients and replicate

A

reproduce

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56
Q

What is this:

exit host and be transmitted to a new host

A

disseminate

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57
Q

What do you call this:

host and pathogen usually strike a balance that allows survival of both

A

pathogen virulence vs. host immunity

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58
Q

T or F

Death of the host is an unusual event

A

T

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59
Q

What is this:

process whereby microbes attach to host cells or tissues

A

adherence

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60
Q

What is this:

asymptomatic harboring of microbes on or in the body commensals as well as pathogens

A

colonization

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61
Q

What is this:

epithelial barrier breached; some host damage caused by a microbe; can be subclinical

A

infection

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62
Q

What is this:

tissue destruction with specific signs and symptoms

A

disease

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63
Q

What is this:

a microbe with the inherent capability of causing infection and disease in a host with an intact immune system.

A

pathogen

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64
Q

What is this:

microbe that usually causes disease only in immunocompromised hosts

A

opportunistic pathogen

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65
Q

What is this:

the ability of a microorganism to produce infection and disease in a host

A

pathogenicity

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66
Q

What is this:

term that provides a quantitative measure of pathogenicity, or the likelihood of causing disease

A

virulence

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67
Q

What is this:

gene products that enable a microbe to establish itself on or in a host (e.g. exotoxins)

A

virulence factors

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68
Q

What virulence level is this:
Escherichia coli is universally found in the colon, but if displaced to adjacent tissues or the urinary bladder it can cause acute infections.

A

moderate virulence

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69
Q

What virulence level is this:
Yersinia pestis, the cause of plague, is also highly infectious, but in addition leads to death in a few days in over 70% of untreated cases.

A

extremely high virulence

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70
Q

What virulence level is this:
Bordetella pertussis, the cause of whooping cough, is not found in the normal flora, but if encountered it is highly infectious and causes disease in almost every nonimmune person it contacts.

A

high virulence

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71
Q

What virulence level is this:
Streptococcus salivarius is universally present in the oropharyngeal flora of humans. On rare occasions it can cause septicemia in immunocompromised individuals.

A

low virulence

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72
Q

Salmonella food poisoning causes a bloody diarrhea (blank) after ingestion of contaminated foods.

A

16 hours to 2 days

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73
Q

Shigella food poisoning causes a bloody diarrhea (blank) after ingestion of contaminated foods.

A

12 hours to 6 days

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74
Q

S. aureus, a frequent skin colonizer, can contaminate food during preparation and secrete heat-stable enterotoxins. The toxins enter the blood and affect the vomiting control center of the brain, inducing vomiting (blank) following ingestion.

A

1 to 6 hours

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75
Q

C. jejuni causes a diarrheal illness (blank) after ingestion.

A

2 to 5 days

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76
Q

Enterotoxigenic E. Coli causes a diarrheal illness (blank) following ingestion

A

6 to 48 hours

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77
Q

What bacterial virulence factor promotes attachment of bacteria to host cells or tissues

A

adhesins

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78
Q

What bacterial virulence factor prevents phagocytosis?

A

surface capsules or “slime layers” (aka glycocalyx)

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79
Q

What bacterial virulence factor allows for the injection of regulatory molecules and toxins into host cells?

A

secretion system

80
Q

What bacterial virulence factor allows for the release of things such as cytotoxic proteins, degredative enzymes, and superantigens?

A

exotoxins

81
Q

What bacterial virulence factor allows for gram-negative bacteria to induce harmful inflammation?

A

endotoxins

82
Q

(blank) facilitate adherence to human cells.

A

fimbriae or pili

83
Q

What are fimbriae or pili?

A

they are fibers that extend from the surface of bacteria that mediate attachment to specific host cell or tissue components

84
Q

(blank) mediate attachment of uropathogenic E. coli strains to uroepithelial cells.

A

fimbriae

85
Q

Many other virulence factors can promote pathogen adherence, these proteins are termed (blank)

A

adhesins

86
Q

What are the four types of adhesins?

A

collagen-binding proteins
fibrinogen-binding proteins
fibronectin-binding proteins
laminin-binding proteins

87
Q

capsules or ‘slime layers’ can promote (blank)

A

pathogen adherence

88
Q

(blank) binds epithelial cells through specific recognition of its capsule by the host cell hyaluronic-acid-binding protein CD44

A

streptococcus pyogenes

89
Q

Most bacterial pathogens produce a polysaccharide capsule or slime layer, which is also called the (blank)

A

glycocalyx

90
Q

Most bacterial pathogens produce a (blank) which is also called the glycocalyx

A

polysaccharide capsule or slime layer

91
Q

How can the polysaccharide capsule or slime layer (glycocalyx) enhance immune evasion?

A

by inhibiting access to pathogen-associated molecular patterns (PAMs) by pattern recognition receptors
AND
inhibiting C3b deposition and access to deposited C3b

92
Q

(blank) formation is part of the infectious cycle for many bacterial pathogens

A

Biofilm

93
Q

What do biofilms consist of?

A

bacterial cells embedded in extracellular polymeric substances (EPS).

94
Q

What is EPS made up of?

A

extracellular DNA, proteins and polysaccharides

95
Q

What do biofilms allow pathogenic bacteria to do?

A
  • resist antibiotic treatments
  • trap nutrients for bacterial growth
  • adhere to environmental surfaces and resist flushing
  • live in close association with other bacteria
  • enhance immune evasion
96
Q

Many (blank and blank) bacteria have the ability to co-opt the functions of the host cell for their own benefit.

A

Gram-positive and Gram-negative

97
Q

(blank) inject various effector molecules (e.g. toxins and enzymes) into the host cell cytoplasm that alter cellular machinery or cellular communication.

A

bacterial secretion systems

98
Q

What is the most common bacterial secretion system?

A

Type 3 secretion system (T3SS) AKA injectosome

99
Q

How does the type 3 secretion system work?

A

a secretion apparatus is assembled in the bacterial cell wall that polymerizes to form a hollow “needle” that penetrates the host cell membrane

100
Q

Once the secretion system is set up, what now can the bacterium do?

A

can inject effector proteins into the cytoplasm of the host cell.

101
Q

What is an invasin?

A

a protein that promotes bacterial invasion of tissues or cells

102
Q

Invasins can be (extracellular/intracellular) proteins?

A

both

103
Q

What is an example of an extracellular invasin?

A

hyaluronidase of strep pyogenes

104
Q

What is an example of an intracellular invasin?

A

IpaB of Shigella flexneri (via a T3SS)

105
Q

Some bacteria bind to cell surface receptors and induce their own (blank); some bacteria escape the (blank) and others multiply in the (blank)

A

endocytosis
vacuole
phagolysosome

106
Q

Once bacteria enter a cell what can they do?

A

they can remain in the cell or move through the cell and escape into the submucosa (transcytosis)

107
Q

When a bacteria enters a cell and moves through it and escapes into the submucosa, what do you call this?

A

transcytosis

108
Q

What are bacterial exotoxins, and what do they do?

A

microorganisms synthesize proteins that are toxic to ther host and are secreted into environment or associated with microbial surface. Exotoins are antigenic and induce antbodies.

109
Q

Exotoxins usually possess some degree of (blank)

A

host cell specificity

110
Q

Exotoxins are antigenic and induce antibodies called (blank)

A

antitoxins

111
Q

Exotoxins can be modified to form (blank) which are antigenic but not toxic (e.g. tetanu toxoid vaccine)

A

toxoids

112
Q

What are the four tyes of exotoxins?

A

Type I
Type II
Type III
Extracellular damaging

113
Q

What is an example of a type I exotoxin and what is a type I exotoxin?

A

=cell surface active

ex. superantigens such as the toxic shock syndrome toxin

114
Q

What is a type II exotoxin and give me an example of this?

A

membrane damaging

ex. the clostridial alpha-toxin which has phospholipase activity

115
Q

What is a type III exotoxin and give me an example of this?

A

intracellular

ex. AB toxins such as the cholera toxin

116
Q

Give an example of an extracellular damaging exotoxin?

A

hydrolytic enzymes such as hyaluronidase and colagenase

117
Q

What kind of toxin is the cholera toxin?

A

AB toxin with ADP-ribosylation

118
Q

What is the mode of action of the cholera toxin?

A

A1 domain is catalytically active upon cleavage from A2 and ADP-ribosylates the G-protein Gs which results in continuous activation of adenylate cyclase.
high cAMP levels activate the CF transmembrane conductance regulator (CFTR) causing a dramatic efflux of ions and water

119
Q

(blank) bind simultaneously to T cell receptors and MHC class II molecules outsides of the normal peptide-binding groove.

A

superantigens

120
Q

What do superantigens do?

A

they hyper-stimulate T cells to secrete cytokines (cytokine storm)

121
Q

In a cytokine storm up to (blank) percent of all peripheral T cells can be stimulated

A

20

122
Q

What are three examples of superantigens?

A

S. aureus
-causing toxic shock syndrome toxin (TSST)
-staphylococcal enterotoxins (SEA)
S. pyogenes
-sterptococcal pyrogenic exotoxins (SpeA)

123
Q

Endotoxins are made up of (blank). Where are they located?

A

lipopolysaccharides (LPS)

located in outer membrane of gram-negative bacteria

124
Q

Are endotoxins SECRETED by bacteria?

A

no

125
Q

What is the toxic component of LPS?

A

Lipid A

126
Q

What does Lipid A do?

A

it induces the overproduction of cytokines (i.e TNF alpha) and other inflammatory mediators from macrophages

127
Q

Inflammatory mediators cause the symptoms of (blank) and (blank).

A

sepsis and septic shock

128
Q

What are the symptoms of sepsis and septic shock?

A

fever
hypotension
disseminated intravascular coagulation (DIC)
multi-organ system failure (MOSF)

129
Q

LPS activates the (blank) resulting in DIC and the (blank) resulting in increased vascular permeability.

A 
coagulation cascade
complement cascade (classical and alternative pathway)
130
Q

Endotoxins are (Blank) antigenic.

A

poorly

131
Q

explain how you ends up with the cytokine storm and multi organ system failure via lysis of gram negative bacteria

A

you get lysis of gram negative bacteria-> release of LPS -> LPS binding protein binds LPS and binds this complex to CD14 and TLR4 on macrophages. Macrophages then induce transcription of cytokines which induce coagulation cascade, prostaglandins and leukotrein activation and activation of the complement pathways (classical and alternative)-> which results in ARDS, DIC< damage to blood vessel endothelium and MOSF

132
Q

What virulence factors make E. coli uropathogenic?

A

fimbriae, they mediate attachment of uropathogenic strains to uroepithelial cells

133
Q

If you have s bacteria that has colonized an IV line, what virulence factor do you think has contributed to this?

A

biofilm!!!

134
Q

What environmental factors may can control expression of virulence genes?

A

temp
pH
osmolarity

135
Q

In corynebacterium diptheria, the gene for diptheria toxin is regulated by (blank) concentration

A

iron

136
Q

In Borrelia burgdorferi, the expression of surface proteins is regulated by (blank)

A

temperature

137
Q

In vibrio cholerae, he gene for cholera toxin is regulated by (blank) and (blank)

A

pH and temperature

138
Q

How does iron regulate diptheria toxin?

A

in high levels of iron, iron will bind to an iron-dependent repressor protein and turn off transcription of diptheria toxin-encoding gene

139
Q

What is quorum sensing?

A

It is the production an release of autoinducers by inidividual bacteria that modulate gene expression in response to the density of a bacterial population

140
Q

What does quorum sensing do?

A

facilitates coordinated responses by bacterial populations

141
Q

What are some things quorum sensing can induce?

A

biofilm formation
virulence factor secretion
sporulation
competence for DNA uptake

142
Q

Pathogens are pathogenic because of the (blank) they express

A

virulence factors

143
Q

What are examples of some mobile genetic elements?

A

plasmids, bacteriophages, pathogenicity islands (PAIs)

144
Q

T or F, different isolates of the same bacterial species can have widely different virulence characteristics>

A

T

145
Q

Explain how virulence factors are found on pathogenic species

A

there are some virulence factors that are part of the core chromosome of a species therefore found on every member of that species, BUT there are also other virulence factors on each membre of these sepcies that may not be found on a different member of that species

146
Q

What is the virulence factor and or/disease that plasmid-encoded E. coli has?

A

heat-labile and heat-stable enterotoxins that cause diarrhea

147
Q

What is the virulence factor and/or disease that plasmid-encoded E. coli and shigella species cause?

A

adherence factors and gene products involved in mucosal invasion

148
Q

What is the virulence factor and/or disease that plasmid-encoded bacillus anthracis causes?

A

capsule essential for virulence (pX02)

edema factor, lethal factor, protective antigen all essential for virulence (pX01)

149
Q

What are some plasmid encoded pathogens?

A

E. coli
E. coli and shigella species
Bacillus anthracis

150
Q

What are some phage encoded pathogens?

A

E. coli
Vibrio cholerae
Streptococcus pyogenes

151
Q

What are some PAI-encoded pathogens?

A

E. coli
staph aureus
strep pygoenes

152
Q

What is the virulence factor and/or disease that phage-encoded E. Coli causes?

A

shiga-like-toxin that inhibits host cell protein synthesis

153
Q

What is the virulence factor and/or disease that phage encoded vibrio cholerae causes?

A

cholera toxin that can cause a severe watery diarrhea

154
Q

What is the virulence factor and/or disease that phage encoded strep pygoenes causes?

A

streptococcal pyrogenic exotoxins (SpeA, SpeC, SpeH, Spel, Spek and Spel) are superantigens

155
Q

What is the virulence factor and/or disease that PAI encoded E. coli causes?

A

type III secretion system and effector proteins

156
Q

What is the virulence factor and/or disease that PAI encoded Staph aureus causes?

A

Toxic shock syndrom toxin (TSST) is a superantigen

157
Q

What is the virulence factor and/or disease that PAI encoded Strep Pygoenes causes?

A

The R28 adhesin promotes attachment to host epithelial cells

158
Q

Most bacterial plasmids replicate (blank)

A

extrachromosomally

159
Q

Plasmids range in size from (blank) to (blank) Kb

A

1 to hundreds

160
Q

(blank) may contain genes that encode for virulence factors and/or antibiotic resistance genes.

A

plasmids

161
Q

Some pathogen isolates have many plasmids, other have (blank)

A

none

162
Q

Plasmids have essential roles in the ability of Bacillus anthracis to cause disease, what are they?

A

pXO1 (182 kb), toxin component gene

pXO2 (96 kb) capsule biosynthesis genes

163
Q

Are bacteriophages lytic or lysogenic?

A

they can be either

164
Q

Some lysogenic phages encode (blank)

A

key virulence factors

165
Q

Do all pathogens have an integrated phage?

A

no!! some have none, others have many

for ex. 10% of the strep pyogenes chromosome is made up of phages

166
Q

(blank) are currently being studied as anti-bacterials

A

lysins

167
Q

What are pathogenicity islands?

A

they are a collection of genes, many of which encode virulence factors

168
Q

Where do you ding pathogenicity islands?

A

clustered together on bacterial chromosomes

169
Q

The genomes of many pathogenic bacteria contain multiple (blank) accounting for up to 10-20% of the genome

A

PAIs

170
Q

The locus of enterocyte effacement (LEE) PAI, which is present in the genomes of 2 different E. coli pathogypes, encodes (blank)

A

multiple virulence factors

171
Q

How big is the LEE PAI?

A

35 kb

172
Q

What determines the E. coli pathotype?

A

mobile genetic elements

173
Q

What are the mobile genetic elements?

A

plasmids, phages, PAIs

174
Q

What makes Enterotoxigenic E. coli?

A

commensal E. coli and pENT

175
Q

What makes up enteropathogenic E. coli?

A

commensal E. coli, pEAF, LEE

176
Q

What makes up enterohaemorrhagic E. coli?

A

commensal E. coli, LEE, and phage

177
Q

What makes up enteroinvasive E. coli and shigella spp.

A

commensal E. coli, black hole, invasion plasmid

178
Q

What makes up uropathogenic E. coli?

A

commensal E. coli, and PAIs

179
Q

Antiobiotic treatment of (enterohemorrhagic E. coli (EHEC) infection may increase incidence of (blank)

A

hemolytic uremic syndrome (HUS)

180
Q

Why does HUS occur?

A

as a result of the rapid and premature destruction of erythrocytes, the remnants of which can clog the filtering system in the kidneys leading to kidney failure

181
Q

How can antibiotics increase Shiga-like-toxin production by EHEC?

A
  • increase release of toxin following EHEC cell lysis

- increased transcription of the toxin genes following phage induction

182
Q

What are the bacterial defenses against host immunlogic clearance?

A 
encapsulation
antigenic mimicry
antigenic variation
anti-Ig proteases
destruction of phagocytes
intracellular replication
inhibition of chemotaxis
inhibition of phagocytosis
inhibition of phago-lysosomal function
resistance to lysosomal enzymes
183
Q

(blank) express an arsenal of virulence factors to thwart the host immune response.

A

GAS (group A strep)

184
Q

What kind of virulence factors does GAS secrete?

A 
degredation of NETs
antimicrobial peptide resistance
phagocyte uptake impairment
complement deposition interference
cloaking of opsonins
nonopsonic binding or antibody degredation
chemokine degredation
phagocyte lysis
185
Q

(blank) has homology to the alpha subunit of a leukocyte B2-integrin, CD(blank), which binds to CD(blank) on the surface of neutrophils inhibiting phagocytosis and activation of the oxidative burst.

A

Mac
CD11b
CD16

186
Q

Many bacteria have evolved the mens to avoid (blank) by antiodies by modifying their surface proteins.

A

opsonization

187
Q

How do bacterial avoid opsonization?

A

Phase variation
and
antigenic variation

188
Q

What is phase variation?

A

expression of surface proteins are switched on or off

189
Q

What is antigenic variation?

A

where surface antigens are switched from one type to another

190
Q

What are the two mechanisms of phase variation?

A

site-specific inversion

slipped-strand mispairing

191
Q

What are the two mechanisms of antigenic variation?

A
  • homologous recombination from silient pilS loci to transcribed pilE
  • slipped-strand mispairing
192
Q

What intracellular bacterial pathogens avoid humoral immunity?

A 
mycobacterium spp
brucella spp
francisella spp
rickettsia spp
legionella penumophilia
Listeria monocytogenes
salmonella typhi
shigella dyseteriae
yersinia pestis
chlyamydia spp
193
Q

What microorganims inhibits phagosome-lysosome fusion?

A

legionella, myobacterium, chlamydia

194
Q

WHat microorganisms resist lysosomal enzymes?

A

salmonella, coxiella, mycobacterium

195
Q

What microorganisms escape from phagolysosome to cytoplasma?

A

Listeria, franciscella, rickettsia

196
Q

What are three ways microorganisms can inhibit killing following phagocytosis?

A
  • inhibition of phagosome-lysosome fusion
  • resistance to lysosomal enzymes
  • escape from phagolysosome to cytoplasma

Block 6 Week 3 (5 decks)

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