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Block 6; Week 3-Michelle > Bacterial pathogenesis-Sumby > Flashcards

Bacterial pathogenesis-Sumby Flashcards

1
Q

What composes the human micro biome?

A

it is composed of bacteria, fungi, parasites, & viruses

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2
Q

T/F Parasitic relationships dominate over mutualistic & commensual relationships when it comes to microbe-human interactions.

A

False. Most of these relationships are mutualistic or commensual.

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3
Q

How do the number of bacterial cells compare to the numbers of human cells?

A 
Bacteria outnumber human cells 3-fold:
 100 trillion bacterial cells
 3 pounds in weight
 3 pints in volume
 50 bacterial genes for every human gene
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4
Q

T/F The same types of bacteria are found throughout the body.

A

False. Different types of bacteria are found in different parts of the body.

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5
Q

What are some of the functions of the human micro biome?

A

**Facilitates nutrient acquisition.
**“Educates” innate defenses and
stimulates both innate and adaptive
immune systems.
**Helps to maintain epithelial boundary
functions and integrity.
**Provides colonization resistance
against pathogens.

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6
Q

T/F Bacteria can even help with wound healing.

A

True.

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7
Q

What are some conditions that the human micro biome affects?

A

Psoriasis
Obesity
Inflammatory bowel diseases
Colorectal carcinoma

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8
Q

What is the first line therapy for C diff (clostridium difficile)? What is the treatment for relapsing patients?

A

First Line: antibiotics-vancomycin
Relapsing: Fecal transplants
**often first line fails b/c of spores that remain in the human.

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9
Q

T/F The diversity and abundance of different bacterial species vary from person to person.

A

True.

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10
Q

T/F The diversity and abundance of different bacterial species vary over time in a single person.

A

True.

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11
Q

T/F H. pylori dramatically alters the diversity of the stomach microbiome.

A

True. When you have this–have fewer other bacteria. Can lead to ulcers if it is in the stomach.

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12
Q

T/F Variation in the gut microbiome can affect susceptibility to C. difficile infection.

A

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

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13
Q

T/F Three-year-old identical twins have identical skin microbiomes.

A

False, no two individuals microbiomes are identical.

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14
Q

What are the stages of infection?

A 
Incubation Period
Prodrome Period
Disease Period
Recovery Period
Convalescence
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15
Q

What is the incubation period?

A

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

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16
Q

What is the prodrome period?

A

time during which nonspecific symptoms occur.

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17
Q

What is the disease period?

A

time during which specific clinical signs and symptoms occur.

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18
Q

What is the recovery period?

A

time during which symptoms resolve and health is restored.

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19
Q

What is convalescence?

A

this is when you have no signs or symptoms

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20
Q

What is an example of a chronic carrier of an infection?

A

Mary Mallon was a chronic carrier of typhoid fever. She wasn’t symptomatic herself.

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21
Q

What is a common latent infection to develop?

A

TB

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22
Q

What are the 2 human-human transmission means?

A 
via direct contact (sneezing)
via vector (tick or mosquito)
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23
Q

What are the 2 animal-human transmission means? What is the name of this pathogen? What is the name of this disease?

A

via direct contact or vector

disease: zoonose
pathogen: zoonotic pathogen

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24
Q

What are some nonhuman sources of pathogens?

A

animals
soil
water
food

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25
Q

What are the main portals of entry for pathogens?

A

respiratory tract, gastrointestinal tract, skin, and urogenital tract.

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26
Q

What is a fomite?

A

any object capable of carrying infectious organisms.

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27
Q

What is the mode of transmission for gonorrhea?

A

direct contact
sexual intercourse
going thru the birth canal

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28
Q

What is the mode of transmission for cholera?

A

no direct contact
fecal-oral
getting human feces into water or food

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29
Q

What is the mode of transmission for congenital syphilis?

A

transplacental

bacteria cross the placenta & infect the fetus

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30
Q

What is the mode of transmission for coagulase-negative staphylococcus?

A

blood-borne

contaminated blood products for transfusion

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31
Q

What is the mode of transmission for tetanus?

A 
soil source (trauma)
spores in soil enter wounds in the skin
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32
Q

What is the mode of transmission for Legionnaire’s Disease?

A

water source

bacteria in water inhaled into the lungs

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33
Q

What is the mode of transmission for Cat Scratch Fever?

A

directly from an animal scratch or something

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34
Q

What is the mode of transmission for Lyme disease?

A

via an insect vector from an animal, enters thru a tick bite

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35
Q

What is the mode of transmission for Hemolytic-uremic syndrome (from E coli)?

A

bacteria in cattle feces are ingested from undercooked hamburger.

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36
Q

What is the mode of transmission for staph skin infection?

A

fomite source, bacteria on a towel or something.

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37
Q

What is the infectious dose?

A

the amount of a pathogen that you need to become infected

for TB-nothing! For anthrax-just a little. For cholera- a whole bunch!!

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38
Q

What must a bacterial pathogen do to be successful?

A

Enter a human host and become established (colonize) .

  • Avoid innate or adaptive immune defenses (immune evasion).
  • Acquire nutrients and replicate (reproduce).
  • Exit host and be transmitted to a new host (disseminate).
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39
Q

T/F Death of the host of a bacterial pathogen is a common occasion.

A

False. Usually a balance b/w host immunity & pathogen virulence.

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40
Q

What is adherence?

A

process whereby microbes attach to host cells or tissues.

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41
Q

What is colonization?

A

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

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42
Q

What is infection?

A

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

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43
Q

What is a nosocomial infection?

A

– Hospital-acquired infection,

occurs in 1/10 hospital patients.

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44
Q

What is disease?

A

tissue destruction with specific signs and

symptoms.

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45
Q

What is a pathogen?

A

– a microbe with the inherent capability

of causing infection and disease in a host with an intact immune system

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46
Q

What is an opportunistic pathogen?

A

microbe that usually causes disease only in immunocompromised hosts

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47
Q

What is pathogenicity?

A

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

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48
Q

What is virulence?

A

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

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49
Q

What are virulence factors?

A

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

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50
Q

What is an example of a low virulence pathogen?

A

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

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51
Q

What is an example of a moderate virulence pathogen?

A

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

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52
Q

What is an example of a high virulence pathogen?

A

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.

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53
Q

What is an example of an extremely high virulence pathogen?

A

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.

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54
Q

How long does it take to see bloody diarrhea after salmonella food poisoning?

A

16 hours-2 days after ingestion of contaminated foods

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55
Q

How long does it take to see bloody diarrhea after shigella food poisoning?

A

12 hours-6 days after ingestion of contaminated foods

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56
Q

How long does it take to see bloody diarrhea after staph aureus food poisoning? What’s the deal here?

A

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 1 to 6 hours following ingestion.

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57
Q

How long does it take to see diarrheal illness after ingestion of C. jejuni?

A

2-5 days after ingestion

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58
Q

How long does it take to get diarrheal illness after enterotoxigenic E. Coli ingestion?

A

6-48 hours after ingestion

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59
Q

A hospital emergency room reported to the local public health authorities that 30 male and female patients of all ages had presented with nausea, vomiting, abdominal cramps, and diarrhea. Initial epidemiologic investigation revealed that all 30 patients had just flown into the area. All patients indicated that they ordered the fish, not the steak, on the airplane and symptoms appeared within 3 hours of ingestion. Based on this information, which of the following microorganisms is the most likely culprit?

 Salmonella spp.
 Shigella spp.
 Staphylococcus aureus
 Campylobacter jejuni
 Enterotoxigenic Escherichia coli
A

C. Staphylococcus aureus

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60
Q

A 44-year-old woman is being treated with anticancer drugs, which have reduced the production of white blood cells from her bone marrow. She develops an infection with an organism that does not cause disease in immunologically healthy individuals. What
description best fits this infection?

Asymptomatic

(B) Nosocomial

(C) Zoonotic

(D) Opportunistic

(E) Lethal

A

D. Opportunistic

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61
Q

How do nonpathogenic strains of bacteria become pathogenic?

A

thru horizontal gene transfer

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62
Q

How do bacteria communicate?

A

thru quorum sensing

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63
Q

What are some important bacterial virulence factors?

A 
adhesins
surface capsules or slime layers
secretion systems
exotoxins
endotoxins
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64
Q

What is the fcn of adhesins?

A

promote attachment of bacteria to host cells or tissues. usu proteins

65
Q

What is the fcn of surface capsules or slime layers?

A

aka glycocalyx

prevents phagocytosis

66
Q

What is the fcn of secretion systems?

A

inject regulatory molecules and toxins into host cells.

67
Q

What is the fcn of exotoxins?

A

such as cytotoxic proteins, degradative enzymes, and superantigens.

68
Q

What is the fcn of endotoxins?

A

Gram-negative bacteria can induce harmful

inflammation.

69
Q

What are some types of adhesins? What is their function?

A 
Collagen-binding proteins
Fibrinogen-binding proteins
Fibronectin-binding proteins
Laminin-binding proteins
**fcn: they all target proteins found in the basement membrane of the ECM--then cell adhesion!
70
Q

Aside from adhesins, what are some other things that promote cell adhesion?

A

fimbriae or pili

capsules or slimy layers

71
Q

What is the function of fimbriae or pili?

A

facilitate adherence to human cells. They are fibers that extend from the surface of bacteria that mediate attachment to specific host cell or tissue components: e.g. fimbriae mediate attachment of uropathogenic E. coli strains to uroepithelial cells.

72
Q

How do capsules or slimy layers function in cell adhesion?

A

Capsules or “slime layers” can promote pathogen adherence,
e.g. Streptococcus pyogenes binds epithelial cells through specific recognition of its capsule by the host cell hyaluronic-acid-binding protein CD44

73
Q

How do capsules or a glycocalyx on a pathogen inhibit phagocytosis?

A

**Inhibiting access to pathogen-associated molecular patterns (PAMs) by pattern recognition receptors.
**Inhibiting C3b deposition and access to deposited
C3b.

74
Q

What composes biofilm?

A

Biofilms consist of bacterial cells embedded
in extracellular polymeric substance (EPS).
EPS is mixture of extracellular DNA, proteins,
and polysaccharides.

75
Q

What is the fcn of biofilm?

A

Bacteria can:

  • 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.
76
Q

How does a biofilm form?

A

single bacteria attaches to a surface. Get more bacteria adhesion & growth & EPS deposition. Get polyp-like things. Then dispersion of bacteria alone or in clumps (w/ or w/o EPS).

77
Q

What are some examples of biofilm or things that biofilm can grow on?

A

plaque on teeth

can grow in catheter or on any body implants

78
Q

Once again, what is the idea behind secretion systems? Which type of bacteria use this?

A

**bacteria have the ability to co-opt the functions of the host cell for their own benefit.
Bacterial secretion systems: inject various effector molecules (e.g., toxins and enzymes) into the host cell cytoplasm that alter cellular machinery or cellular communication.
**can be gram negative (usually) or gram positive

79
Q

What is the most common type of bacterial secretion system? How does it work?

A

The most common type is the Type 3 Secretion System (T3SS). A secretion apparatus is assembled in the bacterial cell wall that polymerizes to form a hollow “needle” that penetrates the host cell membrane.

80
Q

If your secretion system involves proteins in a host cell that allow effectors to be injected…what is it called?

A

an injectosome

81
Q

Where are the effectors secreted in the following secretion systems?
Type 1
Type 2
Type 3

A

Type 1: out of bacterial cell but not into host cell
Type 2: into periplasmic space
Type 3: into host cell cytoplasm w/ the help of chaperone proteins

82
Q

What is an invasin?

A

a protein in bacteria that encourages & equips them to invade other tissues or cells

83
Q

Give some examples of invasins.

A

Ex: extracellular proteins (hyaluronidase)-strep pyogenes
intracellular proteins (IpaB)-shigella
collagenase
**hyaluronidase & collagenase would help to get b/w cells & thru the basement membrane for invasion

84
Q

Aside from going b/w cells–what is another way to invade tissues?

A
  • *bind to cell surface receptors & endocytose. Bacteria will either escape the vacuole or multiply in the phagolysosome
  • *transcytosis–when bacteria escape the cell & get into the submucosa
85
Q

What are exotoxins?

A

proteins (sometimes enzymes) that are toxic to their hosts
possess some degree of host cell specificity
antigenic

86
Q

What secretes exotoxins? Where are they secreted?

A

microorganisms synthesize & secrete these proteins

they are secreted into the environment & are found associated w/ a microbial surface

87
Q

What are antitoxins?

A

antibodies to exotoxins

88
Q

What are toxoids?

A

modified exotoxins
antigenic but not toxic
Ex: tetanus toxoid vaccine

89
Q

What are Type I exotoxins? Give an example.

A

Type I: cell surface active

e.g. superantigens such as the toxic shock syndrome toxin.

90
Q

What are Type II exotoxins? Give an example.

A

Type II: membrane damaging

e.g. the Clostridial a-toxin which has phospholipase activity.

91
Q

What are Type III exotoxins? Give an example.

A

Type III: intracellular

e.g. AB toxins such as the cholera toxin.

92
Q

Give an example of an extracellular damaging exotoxin.

A

Extracellular damaging

e.g. hydrolytic enzymes such as hyaluronidase and collagenase.

93
Q

Describe the structure of the cholera (AB) exotoxin. Which type is it?

A

Type III-intracellular.
2 subunits. A & B
A has 2 parts (A1 & A2). A1 is the enzymatically active one.

94
Q

Describe the process by which the cholera toxin gets into the host cell & causes watery diarrhea.

A

AB exotoxin.
B subunit binds the toxin to the host cell & A gets in via endocytosis.
A is cleaved into A1 & A2.
A1 ADP-ribosylates Gs protein.
A bunch of adenylate cyclase is activated.
cAMP rises in the cell.
Cystic Fibrosis Transmembrane Conductance Regulator activated.
Dramatic efflux of ions & water.
DIARRHEA

95
Q

What are super antigens? What do they do?

A

Superantigens bind simultaneously to T cell receptors and MHC class II molecules outside of the normal peptide-binding groove.

Hyper-stimulate T cells to secrete cytokines
(cytokine storm).

Up to 20% of all peripheral T cells can be
stimulated.

96
Q

What are some examples of super antigens?

A

S. aureus
The Toxic Shock Syndrome Toxin (TSST)
Staphlyococcal Enterotoxins (e.g. SEA)

S. pyogenes
Streptococcal pyrogenic exotoxins (e.g. SpeA)

97
Q

Exotoxins & Endotoxins

Which are more antigenic?

A

Exotoxins.

Endotoxins are weakly antigenic.

98
Q

What are endotoxins? How are they released?

A

These are the LPS (lipopolysaccharide) found on the outer membrane of gram negative bacteria.
They aren’t secreted by bacteria, but are released via bacterial lysis or membrane blebbing.

99
Q

Which part of the LPS endotoxin is toxic?

A

Lipid A (the part on the inside of the LPS-hidden in the bacterial cell)

100
Q

Describe the structure of LPS.

A

Outside–>Inside

O antigen-outer oligosaccharide-membrane-core glycolipid/inner oligosaccharide-Lipid A

101
Q

What is the effect of Lipid A?

A

Lipid A is the toxic component of LPS. It induces the overproduction of cytokines (e.g. TNF-a) and other inflammatory mediators from macrophages.

102
Q

What symptoms do the inflammatory mediators released via the action of Lipid A cause?

A

Inflammatory mediators cause the symptoms of sepsis and septic shock; fever, hypotension, disseminated intravascular coagulation (DIC), and multi-organ system failure (MOSF).

103
Q

Which cascades does LPS activate? What does this result in?

A

Coagulation Cascade-disseminated intravascular coagulation (DIC)
Complement Cascade–increased vascular permeability

104
Q

A 30-year-old woman complains of difficulty in voiding urine during a gynecologic office visit. A positive urine leukocyte esterase test prompts her physician to order a urine culture. The bacterial species that was isolated in clinically significant numbers grew profusely on MacConkey agar and fermented lactose. The data points to the pathogen being uropathogenic Escherichia coli. Which of the following virulence factors make this E. coli uropathogenic?

A. b-lactamase
B. Fimbriae
C. Flagella
D. Glycocalyx
E. Urease
A

B. Fimbriae–this causes E coli to attach to uroepithelial cells.

105
Q 
Which of these things does E Coli have? 
A. b-lactamase
B. Fimbriae
C. Flagella
D. Glycocalyx
E. Urease
A

A-D.
Doesn’t have Urease.
Only the fimbriae cause its uropathogenicity, however.

106
Q

A 48-year-old woman has been hospitalized for a month following a skiing accident. She develops a fever due to colonization of an intravenous line with Gram-positive bacteria that are catalase-positive and coagulase-negative. The lab suggests coagulase-negative Staphylococci. In this scenario, what is the major virulence factor?

A. Biofilm production
B. Panton-Valentine leukocidin
C. Pyrogenic exotoxin
D. Streptokinase
E. Vancomycin resistance
A

A. Biofilm production
Here, we are dealing with staph epidermis (everywhere on the skin!)
**biofilm helps it adhere to medical devices
also protects organisms from opsonins & phagocytes

107
Q

Where is Panton-Valentine leukocidin found?

A

Panton–Valentine leukocidin is a cytotoxin found in some strains of S. aureus, particularly community-acquired MRSA.

108
Q

What is an example of a microorganism that is both pyrogenic exotoxin positive & streptokinase positive?

A

group A streptococcus

109
Q

What is an example of a microorganism that is both catalase positive & coagulase positive?

A

Staph aureus

**only one that is coagulase positive.

110
Q

A 79-year-old female nursing home patient with a history of alcoholism suddenly developed a flu-like illness. She complained of chills and fever and had frequent coughing spells productive of a thick, bloody sputum (“currant jelly sputum”). The attending physician diagnosed bronchopneumonia, but despite aggressive antibiotic therapy, the patient died within a week. The lab identified Klebsiella pneumoniae as the offending microorganism. What is the function of the K. pneumoniae virulence factor depicted in the photograph (arrow)?

A. Degrades secretory IgA on mucosal surfaces
B. Inhibits phagocytosis by neutrophils
C. Lyses neutrophils and macrophages
D. Disrupts host cell membranes
E. Cleaves plasminogen into the protease plasmin
**picture points to the bacterial capsule.

A

B.

111
Q

What are some environmental factors that control the production of virulence factors?

A

temp
pH
osmolarity
conc’n of certain things

112
Q

What’s the deal with Corynebacterium diphtheria & virulence regulation?

A

regulated by the iron conc’n in the body

**this is the diphtheria toxin

113
Q

What’s the deal with Borrelia burgdorferi & virulence regulation?

A

regulated by temp
**so the bacteria in the tick does one thing b/c it is colder. But in the mouse or human it produces virulence factors b/c it is at 37 dC.

114
Q

What’s the deal with Vibrio cholera & virulence regulation?

A

regulated by pH & temp

**low pH of the stomach activates it.

115
Q

What is quorum sensing?

A

Quorum sensing is the production and release by individual bacteria of molecules called autoinducers that modulate gene expression in response to the density of a bacterial population

116
Q

What are some examples of coordinated responses from bacteria thru quorum sensing?

A

biofilm formation
virulence factor secretion
sporulation
competence for DNA uptake

117
Q

Describe the Agr system of Staph Aureus.

A 
AgrD--> AIP via AgrB
AIP gets high enough (b/c so many staphs are producing it) to activate cell membrane AgrC.
AgrC phosphorylates AgrA.
AgrA binds DNA.
RNA III transcribed. 
Favors dissemination of the bacteria.
118
Q

What types of things does RNAIII promote to allow for the dissemination of staph aureus?

A

decreased production of adhesins

increased production of factors that allow the bacteria to spread to the site of infection–like hyaluronidase

119
Q

What is something that other bacteria release to inhibit RNAIII actions in staph aureus?

A

RNAIII inhibiting peptide

120
Q

You are working with a Biotech company to try and identify Yersinia pestis surface antigens that may make effective vaccine targets. The approach you are using is to grow Y. pestis in lab media, shave the surface proteins of the cells, and I.D. and quantify the proteins via mass spectrometry. Under what conditions should you grow the bacterium prior to analysis of the cell surface proteins?

A. At 37C in high iron-containing media.
B. At 23C in high iron-containing media.
C. At 4C in low iron-containing media.
D. At 37C in low iron-containing media.
E. At 23C in low iron-containing media.

A

D. Because these are the conditions that most mimic the experience of human infection.

121
Q

T/F The complete gene sequence (genome) of virtually every human pathogen is known

A

True.

122
Q

Where are the genes for these virulence factors found?

A 
in a variety of places
core chromosome
plasmids
bacteriophages
pathogenicity islands
123
Q

Describe the different virulence factors that E coli exhibits. Where are they found?

A

Plasmid: Heat-labile and heat-stable enterotoxins that cause diarrhea
Plasmid: Adherence factors and gene products involved in mucosal invasion
Phage: Shiga-like-toxin inhibits host cell protein synthesis
PAI: Type III secretion system and effector proteins

124
Q

Describe the different virulence factors that Shigella species exhibit. Where are they found?

A

Plasmid: Adherence factors and gene products involved in mucosal invasion

125
Q

Describe the different virulence factors that bacillus anthracis exhibits. Where are they found?

A

Plasmid PXO2: Capsule essential for virulence (pXO2)
Plasmid PXO1: Edema factor, lethal factor, protective antigen all essential
for virulence (pXO1)

126
Q

Describe the different virulence factors that Vibrio cholera exhibits. Where are they found?

A

Phage: Cholera toxin that can cause a severe watery diarrhea

127
Q

Describe the different virulence factors that strep pyogenes exhibits. Where are they found?

A

Phage: Streptococcal pyrogenic exotoxins (SpeA, SpeC, SpeH, SpeI, SpeK, and SpeL) are superantigens
PAI: Streptococcal pyrogenic exotoxins (SpeA, SpeC, SpeH, SpeI, SpeK, and SpeL) are superantigens

128
Q

Describe the different virulence factors that staph aureus exhibits. Where are they found?

A

PAI: Toxic shock syndrome toxin (TSST) is a superantigen

129
Q

How do plasmids usually replicate?

A

usu extrachromosomally

130
Q

How large are plasmids?

A

1-hundred kB

131
Q

What types of genes are found in plasmids?

A

May contain genes that encode for virulence factors and/or antibiotic resistance genes.

132
Q

Do all cells have plasmids?

A

Not necessarily
Some have many
others have none–varies!

133
Q

Describe the role of plasmids in bacillus anthracis.

A

pXO1 (182 kb), toxin component genes

pXO2 (96 kb), capsule biosynthesis genes

134
Q

Some lysogenic phage encode key virulence factors. Give an example.

A

the Shiga-like-toxin of Enterohemorrhagic Escherichia coli from a lysogenic phage–incorporated into host genome

135
Q

T/F Lysins & Lysogenic phages need to be studies for bacterial therapy.

A

TRUE

136
Q

What are pathogenecity islands? How are they acquired? Why are they important?

A

Pathogenicity islands (PAIs) are collections of genes, many of which encode virulence factors, that are clustered together on the bacterial chromosome.

PAIs play an important role in pathogenicity and are usually
acquired by horizontal gene transfer via conjugation.

137
Q

What’s the deal with LEE PAI?

A

locus of enterocyte effacement
present in 2 different E coli genomes
encodes multiple virulence factors

138
Q

What’s the deal with Enterotoxigenic E. coli (ETEC)? What types of mobile genetic elements does it have?

A

the leading bacterial cause of diarrhea in the developing world, as well as the most common cause of travelers’ diarrhea.
has the pENT plasmid

139
Q

What’s the deal with Enteropathogenic E. coli (EPEC)? What types of mobile genetic elements does it have?

A

defined as diarrhea-causing E. coli whose virulence mechanism is unrelated to the excretion of typical E. coli enterotoxins
plasmid: pEAF = EPEC adherence factor
PAI: LEE

140
Q

What’s the deal with Enterohemorrhagic E. coli (EHEC)? What types of mobile genetic elements does it have?

A

can cause diarrhea or hemorrhagic colitis in humans. Hemorrhagic colitis occasionally progresses to hemolytic uremic syndrome (HUS), an important cause of acute renal failure in children and morbidity and mortality in adults
Phage: Stx phage = Shiga-toxin encoding phage
PAI: LEE

141
Q

What’s the deal with Enteroinvasive E. coli (EIEC)? What types of mobile genetic elements does it have?

A

cause a syndrome that is identical to Shigellosis, with profuse diarrhea and high fever
black hole = deleted genes
invasion plasmid

142
Q

What’s the deal with Uropathogenic E. coli (UPEC)? What types of mobile genetic elements does it have?

A

infections account for more than 80% of uncomplicated UTIs.

PAIs galore!

143
Q

Antibiotic treatment of ___________ infection may increase incidence of hemolytic uremic syndrome (HUS).

A

Enterohemorrhagic Escherichia coli (EHEC)

144
Q

What is HUS?

A

Hemolytic Uremic Syndrome. HUS is the 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.

145
Q

How do antibiotics increase shiga-like toxin production in EHEC E coli?

A

increase E coli cell lysis (release a bunch of toxin that wouldn’t otherwise escape)
increased transcription of toxin

146
Q

A 33-year-old male is hospitalized with bloody diarrhea. Lab tests point to an Enterohemorrhagic Escherichia coli (EHEC) infection. Consistent with this diagnosis attaching and effacing intestinal lesions (AE lesions) were observed. Which horizontally transferred element enables EHEC to cause AE lesions?

 Shiga-like-toxin-encoding phage
 Transposon
 LEE pathogenicity island
 Plasmid pENT
 Plasmid pEAF
A

C.

147
Q

What is required for E coli to make AE lesions?

A

the formation of AE lesions (pedestal formation) by E. coli requires the T3SS and effector proteins of the LEE pathogenicity island.

148
Q

What are some bacterial defenses against host immunologic 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 fusion
Resistance to lysosomal enzymes
149
Q

What are some important virulence factors & mechanisms that Group A strep uses to evade the host immune response?

A 
Degradation of NETs
Antimicrobial peptide resistance
Phagocyte uptake impairment
Complement Deposition Interference
Cloaking of Opsonins
Nonopsonic Binding or Antibody Degradation
Chemokine Degradation
Phagocyte Lysis (enzymes to put holes in phagocytes)
150
Q

What are NETs?

A

extracellular traps that kill neutrophils
when the cell dies it makes a net-like structure composed of DNA & bactericidal proteins
net traps bacteria & kills them
DNAse kills the net & neutrophils!

151
Q

What does MAC do to act in phagocyte uptake impairment?

A

it binds to receptors on phagocytes & prevents this uptake

152
Q

What happens with chemokine degradation?

A

C5a peptidase & IL-8 peptidase degrade chemokines & so you don’t get neutrophils at the site of an infection

153
Q

Many bacteria have evolved the means to avoid opsonization by antibodies by modifying their surface proteins.
What are these 2 processes?

A

Phase Variation: expression of surface proteins are switched on & off
Antigenic Variation: surface antigens are switched from on type to another
Ex: of both of these-Neisseria pili

154
Q

What are some mechanisms of Phase variation?

A

Site-specific inversion

Slipped-strand mispairing

155
Q

What are some mechanisms of antigenic variation?

A

Homologous recombination

Slipped-strand mispairing

156
Q

What is slipped strand mispairing?

A

is a mutation process which occurs during DNA replication. It involves denaturation and displacement of the DNA strands, resulting in mispairing of the complementary bases.

157
Q

Intracellular pathogens avoid _____ immunity. Give examples of this.

A

HUMORAL

Mycobacterium spp.
Brucella spp.
Francisella spp.
Rickettsia spp.
Legionella pneumophila
Listeria monocytogenes
Salmonella Typhi
Shigella dysenteriae
Yersinia pestis
Chlamydia spp.
158
Q

Some microorganisms inhibit killing following phagocytosis.

What are some mechanisms of this & examples?

A

Inhibition of phagosome-lysosome fusion (Legionella, Mycobacterium, Chlamydia).

Resistance to lysosomal enzymes (Salmonella, Coxiella, Mycobacteria).

Escape from phagolysosome to cytoplasm (Listeria, Franciscella, Rickettsia).

159
Q

A 27-year-old male is seen at a STD clinic for treatment of gonorrhea. Prior treatments for this disease have successfully eradicated the organism; however, the man has not changed his behavior and has been repeatedly re-infected. What is the most important strategy the organism employs which enables it to cause repeated infections?

A. Antigenic variation
B. Induction of immune suppression
C. Intracellular growth in alveolar macrophages
D. Polysaccharide capsule
E. Secretion of IgG protease
A

A. Neisseria gonorrhoeae spontaneously changes the composition of antigenic surface proteins to aid evasion of the host immune response.

Block 6; Week 3-Michelle (5 decks)

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