Bacterial Pathogenesis Flashcards
(196 cards)
1
Q
Infectious and parasitic diseases are a leading cause of (balnK) worldwide
A
death (57,029,000 deaths)
2
Q
(blank) are colonized with bacteria and other microbes (microbiome, microbiota, or microbial flora)
A
humans
3
Q
Bacteria outnumber human cells (blank-fold)
A
3
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
5
Q
T or F
there are thousands of bacterial species though only a small number can be cultures
A
T
6
Q
What kind of relationships does the human microbiome mostly have?
A
mutualistic and commensal relationships (over parasitic)
7
Q
What is the human microbiome composed of?
A
bacteria, viruses, fungi, and protozoa
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
9
Q
What are some conditions associated with the human biome?
A
psoriasis
obesiry
inflammatory bowel disease
colorectal carcinoma
10
Q
THe human genome encodes for about (blank) carbohydrate digesting enzymes
A
20
11
Q
the intestinal tract bacteriume (blank) has around 260.
A
bacteroides thetaitaomicron
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
13
Q
(blank) infections result in about 300 deaths per day in the USA.
A
C. diff (clostridium difficile)
14
Q
What is the first-line therapy for CDI (C. diff infections)?
A
2 week oral antiobiotics (ie. vanocmyocin)
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
16
Q
What has recently starting gaining traction and has a 95% success rate at curing C. diff?
A
fecal micrbiota transplant
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
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
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
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.
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
22
Q
T or F
three year old identical twins have identica skin microbiomes.
A
false, no two individuals microbiomes are identical
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
24
Q
What is this:
time during which nonspecific symptoms occur
A
prodrome period
25
What is this:
| time during which specific clinical signs and symptoms occur
disease period
26
What is this:
| time during which symptoms resolve and health is restored
recovery period
27
Describe the stages of infection
```
incubation period
prodromal period
illness
decline
convalescence
```
28
after the recovery period in the stages of infection what can happen?
some people can become chronic carriers of the organism and in others latent infections develop
29
T or F
some people have subclinical infections during which they remain asymptomatic; the presence of antibodies reveals that a prior infection has occured
T
30
What are the 2 modes of transmission of microbes?
human to human
| nonhuman to human
31
What are some nonhuman sources?
animals, soil, water and food
32
How can animal to human transmission occur?
either by direct contact with the animal or indirectly via a vector
33
Human diseases for which animals are the reservoir are calld (blank) and the pathogens are called (blank)
zoonoses
| zoonotic pathogens
34
The main "portals of entry" into the body are the (blank) (blank) (blank) and (blank)
respiratory tract
GI tract
skin
urogenital tract
35
(blank) is any object capable of carrying infectious organisms
fomite
36
How is gonorrhea passed?
via direct contact
37
How is cholera passed?
no direct contact- through fecal-oral transmission (excreted in human feces, then ingested in food or water)
38
How is congenital syphilis transmitted?
transplacental
| bacteria cross the placenta and infects the fetus
39
How does coagulase-negative staphylococci transmit?
blood-borne
| contaiminated blood products for transfusion
40
How is tetanus transmitted?
```
soil source (trauma)
(spores in soil enter wound in skin)
```
41
How is legionnaires disease transmited?
through water sources (bacteria in water aerosol are inhaled into lungs)
42
How is cat-scratch fever transmitted?
directly from an animal
| bacteria enter in cat scratch
43
How is lyme disease transmitted?
via insect vector (tick bite)
44
How is hemolytic-uremic syndrome cause by enterohemorrhagic escherichia coli transmitted?
via animal excreta (bacteria in cattle feces are injected in undercooked hamburger)
45
How is staphylococcal skin infection transmitted?
```
via fomites (bacteria on an object... i.e a towel are transferred to the skin)
****think about wrestlers and wrestling mats)
```
46
How big of a dose of virbio cholerae will it take to cause disease in a human?
10 to the 8th
47
How big of a dose of virbio cholerae with bicarbonate will it take to cause disease in a human?
10 the the 4th
48
How big of a dose of salmonella typhi will it take to cause disease in a human?
10 to the 5th
49
How big of a dose of shigella will it take to cause disease in a human?
10 to the 2nd
50
How big of a dose of bacillus anthracis via inhalation will it take to cause disease in a human?
10 to the 4th
51
How big of a dose of mycobacterium TB will it take to cause disease in a human?
1-10
52
What does a bacterial pathogen need to be succesful?
Colonize
immune evasion
reproduce
disseminate
53
What is this:
| enter a human host and become established
colonize
54
what is this:
| avoid innate or adaptive immune defenses
immune evasion
55
What is this:
| acquire nutrients and replicate
reproduce
56
What is this:
| exit host and be transmitted to a new host
disseminate
57
What do you call this:
| host and pathogen usually strike a balance that allows survival of both
pathogen virulence vs. host immunity
58
T or F
| Death of the host is an unusual event
T
59
What is this:
| process whereby microbes attach to host cells or tissues
adherence
60
What is this:
| asymptomatic harboring of microbes on or in the body commensals as well as pathogens
colonization
61
What is this:
| epithelial barrier breached; some host damage caused by a microbe; can be subclinical
infection
62
What is this:
| tissue destruction with specific signs and symptoms
disease
63
What is this:
| a microbe with the inherent capability of causing infection and disease in a host with an intact immune system.
pathogen
64
What is this:
| microbe that usually causes disease only in immunocompromised hosts
opportunistic pathogen
65
What is this:
| the ability of a microorganism to produce infection and disease in a host
pathogenicity
66
What is this:
| term that provides a quantitative measure of pathogenicity, or the likelihood of causing disease
virulence
67
What is this:
| gene products that enable a microbe to establish itself on or in a host (e.g. exotoxins)
virulence factors
68
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.
moderate virulence
69
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.
extremely high virulence
70
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.
high virulence
71
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.
low virulence
72
Salmonella food poisoning causes a bloody diarrhea (blank) after ingestion of contaminated foods.
16 hours to 2 days
73
Shigella food poisoning causes a bloody diarrhea (blank) after ingestion of contaminated foods.
12 hours to 6 days
74
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.
1 to 6 hours
75
C. jejuni causes a diarrheal illness (blank) after ingestion.
2 to 5 days
76
Enterotoxigenic E. Coli causes a diarrheal illness (blank) following ingestion
6 to 48 hours
77
What bacterial virulence factor promotes attachment of bacteria to host cells or tissues
adhesins
78
What bacterial virulence factor prevents phagocytosis?
surface capsules or "slime layers" (aka glycocalyx)
79
What bacterial virulence factor allows for the injection of regulatory molecules and toxins into host cells?
secretion system
80
What bacterial virulence factor allows for the release of things such as cytotoxic proteins, degredative enzymes, and superantigens?
exotoxins
81
What bacterial virulence factor allows for gram-negative bacteria to induce harmful inflammation?
endotoxins
82
(blank) facilitate adherence to human cells.
fimbriae or pili
83
What are fimbriae or pili?
they are fibers that extend from the surface of bacteria that mediate attachment to specific host cell or tissue components
84
(blank) mediate attachment of uropathogenic E. coli strains to uroepithelial cells.
fimbriae
85
Many other virulence factors can promote pathogen adherence, these proteins are termed (blank)
adhesins
86
What are the four types of adhesins?
collagen-binding proteins
fibrinogen-binding proteins
fibronectin-binding proteins
laminin-binding proteins
87
capsules or 'slime layers' can promote (blank)
pathogen adherence
88
(blank) binds epithelial cells through specific recognition of its capsule by the host cell hyaluronic-acid-binding protein CD44
streptococcus pyogenes
89
Most bacterial pathogens produce a polysaccharide capsule or slime layer, which is also called the (blank)
glycocalyx
90
Most bacterial pathogens produce a (blank) which is also called the glycocalyx
polysaccharide capsule or slime layer
91
How can the polysaccharide capsule or slime layer (glycocalyx) enhance immune evasion?
by inhibiting access to pathogen-associated molecular patterns (PAMs) by pattern recognition receptors
AND
inhibiting C3b deposition and access to deposited C3b
92
(blank) formation is part of the infectious cycle for many bacterial pathogens
Biofilm
93
What do biofilms consist of?
bacterial cells embedded in extracellular polymeric substances (EPS).
94
What is EPS made up of?
extracellular DNA, proteins and polysaccharides
95
What do biofilms allow pathogenic bacteria to do?
- 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
Many (blank and blank) bacteria have the ability to co-opt the functions of the host cell for their own benefit.
Gram-positive and Gram-negative
97
(blank) inject various effector molecules (e.g. toxins and enzymes) into the host cell cytoplasm that alter cellular machinery or cellular communication.
bacterial secretion systems
98
What is the most common bacterial secretion system?
Type 3 secretion system (T3SS) AKA injectosome
99
How does the type 3 secretion system work?
a secretion apparatus is assembled in the bacterial cell wall that polymerizes to form a hollow "needle" that penetrates the host cell membrane
100
Once the secretion system is set up, what now can the bacterium do?
can inject effector proteins into the cytoplasm of the host cell.
101
What is an invasin?
a protein that promotes bacterial invasion of tissues or cells
102
Invasins can be (extracellular/intracellular) proteins?
both
103
What is an example of an extracellular invasin?
hyaluronidase of strep pyogenes
104
What is an example of an intracellular invasin?
IpaB of Shigella flexneri (via a T3SS)
105
Some bacteria bind to cell surface receptors and induce their own (blank); some bacteria escape the (blank) and others multiply in the (blank)
endocytosis
vacuole
phagolysosome
106
Once bacteria enter a cell what can they do?
they can remain in the cell or move through the cell and escape into the submucosa (transcytosis)
107
When a bacteria enters a cell and moves through it and escapes into the submucosa, what do you call this?
transcytosis
108
What are bacterial exotoxins, and what do they do?
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
Exotoxins usually possess some degree of (blank)
host cell specificity
110
Exotoxins are antigenic and induce antibodies called (blank)
antitoxins
111
Exotoxins can be modified to form (blank) which are antigenic but not toxic (e.g. tetanu toxoid vaccine)
toxoids
112
What are the four tyes of exotoxins?
Type I
Type II
Type III
Extracellular damaging
113
What is an example of a type I exotoxin and what is a type I exotoxin?
=cell surface active
| ex. superantigens such as the toxic shock syndrome toxin
114
What is a type II exotoxin and give me an example of this?
membrane damaging
| ex. the clostridial alpha-toxin which has phospholipase activity
115
What is a type III exotoxin and give me an example of this?
intracellular
| ex. AB toxins such as the cholera toxin
116
Give an example of an extracellular damaging exotoxin?
hydrolytic enzymes such as hyaluronidase and colagenase
117
What kind of toxin is the cholera toxin?
AB toxin with ADP-ribosylation
118
What is the mode of action of the cholera toxin?
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
(blank) bind simultaneously to T cell receptors and MHC class II molecules outsides of the normal peptide-binding groove.
superantigens
120
What do superantigens do?
they hyper-stimulate T cells to secrete cytokines (cytokine storm)
121
In a cytokine storm up to (blank) percent of all peripheral T cells can be stimulated
20
122
What are three examples of superantigens?
S. aureus
-causing toxic shock syndrome toxin (TSST)
-staphylococcal enterotoxins (SEA)
S. pyogenes
-sterptococcal pyrogenic exotoxins (SpeA)
123
Endotoxins are made up of (blank). Where are they located?
lipopolysaccharides (LPS)
| located in outer membrane of gram-negative bacteria
124
Are endotoxins SECRETED by bacteria?
no
125
What is the toxic component of LPS?
Lipid A
126
What does Lipid A do?
it induces the overproduction of cytokines (i.e TNF alpha) and other inflammatory mediators from macrophages
127
Inflammatory mediators cause the symptoms of (blank) and (blank).
sepsis and septic shock
128
What are the symptoms of sepsis and septic shock?
fever
hypotension
disseminated intravascular coagulation (DIC)
multi-organ system failure (MOSF)
129
LPS activates the (blank) resulting in DIC and the (blank) resulting in increased vascular permeability.
```
coagulation cascade
complement cascade (classical and alternative pathway)
```
130
Endotoxins are (Blank) antigenic.
poorly
131
explain how you ends up with the cytokine storm and multi organ system failure via lysis of gram negative bacteria
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
What virulence factors make E. coli uropathogenic?
fimbriae, they mediate attachment of uropathogenic strains to uroepithelial cells
133
If you have s bacteria that has colonized an IV line, what virulence factor do you think has contributed to this?
biofilm!!!
134
What environmental factors may can control expression of virulence genes?
temp
pH
osmolarity
135
In corynebacterium diptheria, the gene for diptheria toxin is regulated by (blank) concentration
iron
136
In Borrelia burgdorferi, the expression of surface proteins is regulated by (blank)
temperature
137
In vibrio cholerae, he gene for cholera toxin is regulated by (blank) and (blank)
pH and temperature
138
How does iron regulate diptheria toxin?
in high levels of iron, iron will bind to an iron-dependent repressor protein and turn off transcription of diptheria toxin-encoding gene
139
What is quorum sensing?
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
What does quorum sensing do?
facilitates coordinated responses by bacterial populations
141
What are some things quorum sensing can induce?
biofilm formation
virulence factor secretion
sporulation
competence for DNA uptake
142
Pathogens are pathogenic because of the (blank) they express
virulence factors
143
What are examples of some mobile genetic elements?
plasmids, bacteriophages, pathogenicity islands (PAIs)
144
T or F, different isolates of the same bacterial species can have widely different virulence characteristics>
T
145
Explain how virulence factors are found on pathogenic species
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
What is the virulence factor and or/disease that plasmid-encoded E. coli has?
heat-labile and heat-stable enterotoxins that cause diarrhea
147
What is the virulence factor and/or disease that plasmid-encoded E. coli and shigella species cause?
adherence factors and gene products involved in mucosal invasion
148
What is the virulence factor and/or disease that plasmid-encoded bacillus anthracis causes?
capsule essential for virulence (pX02)
| edema factor, lethal factor, protective antigen all essential for virulence (pX01)
149
What are some plasmid encoded pathogens?
E. coli
E. coli and shigella species
Bacillus anthracis
150
What are some phage encoded pathogens?
E. coli
Vibrio cholerae
Streptococcus pyogenes
151
What are some PAI-encoded pathogens?
E. coli
staph aureus
strep pygoenes
152
What is the virulence factor and/or disease that phage-encoded E. Coli causes?
shiga-like-toxin that inhibits host cell protein synthesis
153
What is the virulence factor and/or disease that phage encoded vibrio cholerae causes?
cholera toxin that can cause a severe watery diarrhea
154
What is the virulence factor and/or disease that phage encoded strep pygoenes causes?
streptococcal pyrogenic exotoxins (SpeA, SpeC, SpeH, Spel, Spek and Spel) are superantigens
155
What is the virulence factor and/or disease that PAI encoded E. coli causes?
type III secretion system and effector proteins
156
What is the virulence factor and/or disease that PAI encoded Staph aureus causes?
Toxic shock syndrom toxin (TSST) is a superantigen
157
What is the virulence factor and/or disease that PAI encoded Strep Pygoenes causes?
The R28 adhesin promotes attachment to host epithelial cells
158
Most bacterial plasmids replicate (blank)
extrachromosomally
159
Plasmids range in size from (blank) to (blank) Kb
1 to hundreds
160
(blank) may contain genes that encode for virulence factors and/or antibiotic resistance genes.
plasmids
161
Some pathogen isolates have many plasmids, other have (blank)
none
162
Plasmids have essential roles in the ability of Bacillus anthracis to cause disease, what are they?
pXO1 (182 kb), toxin component gene
| pXO2 (96 kb) capsule biosynthesis genes
163
Are bacteriophages lytic or lysogenic?
they can be either
164
Some lysogenic phages encode (blank)
key virulence factors
165
Do all pathogens have an integrated phage?
no!! some have none, others have many
| for ex. 10% of the strep pyogenes chromosome is made up of phages
166
(blank) are currently being studied as anti-bacterials
lysins
167
What are pathogenicity islands?
they are a collection of genes, many of which encode virulence factors
168
Where do you ding pathogenicity islands?
clustered together on bacterial chromosomes
169
The genomes of many pathogenic bacteria contain multiple (blank) accounting for up to 10-20% of the genome
PAIs
170
The locus of enterocyte effacement (LEE) PAI, which is present in the genomes of 2 different E. coli pathogypes, encodes (blank)
multiple virulence factors
171
How big is the LEE PAI?
35 kb
172
What determines the E. coli pathotype?
mobile genetic elements
173
What are the mobile genetic elements?
plasmids, phages, PAIs
174
What makes Enterotoxigenic E. coli?
commensal E. coli and pENT
175
What makes up enteropathogenic E. coli?
commensal E. coli, pEAF, LEE
176
What makes up enterohaemorrhagic E. coli?
commensal E. coli, LEE, and phage
177
What makes up enteroinvasive E. coli and shigella spp.
commensal E. coli, black hole, invasion plasmid
178
What makes up uropathogenic E. coli?
commensal E. coli, and PAIs
179
Antiobiotic treatment of (enterohemorrhagic E. coli (EHEC) infection may increase incidence of (blank)
hemolytic uremic syndrome (HUS)
180
Why does HUS occur?
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
How can antibiotics increase Shiga-like-toxin production by EHEC?
- increase release of toxin following EHEC cell lysis
| - increased transcription of the toxin genes following phage induction
182
What are the bacterial defenses against host immunlogic clearance?
```
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
(blank) express an arsenal of virulence factors to thwart the host immune response.
GAS (group A strep)
184
What kind of virulence factors does GAS secrete?
```
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
(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.
Mac
CD11b
CD16
186
Many bacteria have evolved the mens to avoid (blank) by antiodies by modifying their surface proteins.
opsonization
187
How do bacterial avoid opsonization?
Phase variation
and
antigenic variation
188
What is phase variation?
expression of surface proteins are switched on or off
189
What is antigenic variation?
where surface antigens are switched from one type to another
190
What are the two mechanisms of phase variation?
site-specific inversion
| slipped-strand mispairing
191
What are the two mechanisms of antigenic variation?
- homologous recombination from silient pilS loci to transcribed pilE
- slipped-strand mispairing
192
What intracellular bacterial pathogens avoid humoral immunity?
```
mycobacterium spp
brucella spp
francisella spp
rickettsia spp
legionella penumophilia
Listeria monocytogenes
salmonella typhi
shigella dyseteriae
yersinia pestis
chlyamydia spp
```
193
What microorganims inhibits phagosome-lysosome fusion?
legionella, myobacterium, chlamydia
194
WHat microorganisms resist lysosomal enzymes?
salmonella, coxiella, mycobacterium
195
What microorganisms escape from phagolysosome to cytoplasma?
Listeria, franciscella, rickettsia
196
What are three ways microorganisms can inhibit killing following phagocytosis?
- inhibition of phagosome-lysosome fusion
- resistance to lysosomal enzymes
- escape from phagolysosome to cytoplasma
