Enteric Bacteria (EXAM III) Flashcards
1
Q
Shape & gram stain of enteric bacteria:
A
Gram negative bacilli
2
Q
Some enteric bacteria are common members of:
A
Human & animal flora
3
Q
Some enteric bacteria are members of commensal groups that have become ______ due to _____
A
Pathogenic due to acquired virulence factors
4
Q
What are some of the acquired virulence factors causing some commensal enteric bacteria to become pathogenic?
A
- Toxins from plasmids
- Toxins from bacteriophages
- Pathogenicity islands
5
Q
Most enteric bacteria can be motile due to:
A
Peritrichous flagella (H-antigen)
6
Q
Some enteric bacteria are non-motile such as:
A
- Shigella
- Klebsiella
- Yersinia
7
Q
Most enteric bacteria have _____ on the surface
A
Surface pili
8
Q
Responsible for adherence in enteric bacteria:
A
Fimbriae
9
Q
Responsible for plasmid conjugation in enteric bacteria:
A
Sex pili
10
Q
Some enteric species have ____ such as K or Vi antigen
A
Capsules
11
Q
Some enteric species have capsules such as:
A
K or Vi antigen
12
Q
List the enteric bacterial species that contain capsules:
A
- Most Klebsiella species
- Some enterobacter species
- Somen Ecoli species
13
Q
All enteric bacterial species contain:
A
Outer membrane LPS
14
Q
The outer membrane LPS found in all enteric bacterial species may be referred to as:
A
Heat-stable endotoxin
15
Q
All enteric bacterial species contain LPS (heat-stable endotoxin) with:
A
Enterobacterial common antigen and serotype-specific O-antigen
16
Q
Because enteric bacteria are ______ they can survive when expelled in feces
A
Facultative anaerobes
17
Q
The enteric bacterial species that contain a capsule use this as an important:
A
Virulence factor
18
Q
Why do all enteric bacterial species contain an outer membrane with LPS?
A
Because they are gram NEGATIVE bacteria
19
Q
The characterization of various pathogenic E. coli strains is based on:
A
Toxins produced
20
Q
A lot of pathogenic enteric bacterial species result in:
A
GI issues
21
Q
When enteric bacteria have a toxin like _____ toxin it leads to watery diarrhea
A
Cholera toxin
22
Q
When enteric bacteria have a toxin like _____ toxin it leads to bloody diarrhea
A
Shiga
23
Q
When enteric bacterial infection also involves neutrophils & inflammation, what may result?
A
Pus in diarrhea
24
Q
When enteric bacterial infection results in pus in diarrhea caused by neutrophil & inflammatory involvement:
A
Dysentery
25
Transmission of pathogenic enteric bacterial species causing diarrhea, bloody diarrhea & dysentery are transmitted by:
Person-to-person
The "seven F's"
26
What are the seven F's of transmission?
Feces, food, fluids, fingers, flies, fomites & fornication
27
What is the enterobacterial common antigen:
Outer- and inner-core sugars
28
The outer- and inner-core sugars of enterobacterial species is referred to as:
Enterobacterial common antigen
29
The LPS found in enterobacteria is also referred to as:
Heat-stable enterotoxin
30
When must we consider that the LPS found in enterobacteria is a heat-stable enterotoxin?
Becomes important when considering sterilization
31
Is present in many bacteria like Yersinia, Salmonella, Shigella, Enteropathogenic EPEC (E. coli); also present other species like Pseudomonas and Chlamydia:
Type III secretion system
32
List the enterobacterial pathogenic species that utilize the a Type III secretion system:
1. Yersinia
2. Salmonella
3. Shigella
4. Enteropathogenic EPEC E. coli
33
List the non-enterobacterial pathogenic species that utilize the Type III secretion system:
1. Pseudomonas
2. Chlamydia
34
Describe the structure of a Type III secretion system:
A 20-protein system, that looks like a short, hollow flagellum (needle)
35
What is the purpose of a Type III secretion system:
To inject a variety of specific specie-specific toxins into host cells
36
Often times _____ will be delivered from a bacterial cell (enteric bacteria) to a host cell via a Type III secretion system
Virulence factors
37
Translocated intimin receptor deliver through:
A type III secretion system
38
TIR
Translocated intimin receptor
39
What two pathogens both use a translocated intimin receptor that functions through a type III secretion system:
1. Enterohemorrhagic E. coli (O157:H7)
2. Enteropathogenic E. coli (EPEC)
40
List the modes of transmission of Escherichia coli:
- Person-to-person
- Contaminated food
- Human & animal feces (no hand washing; insect vectors)
- the 7 F's
41
A cholera-like AB-exotoxin that performs ADP-ribosylation of G protein leading to increased cAMP levels resulting in loss of water & electrolytes & ultimately watery diarrhea:
Heat-labile enterotoxin "LT"
42
What is responsible for the condition commonly known as "Traveler's diarrhea"
Heat-labile Enterotoxin "LT"
43
What type of toxin is the heat-labile enterotoxin "LT"?
A cholera-like AB-exotoxin
44
How does the virulence factor Heat-labile enterotoxin "LT" work?
1. ADP-Ribosylation of G protein
2. increase in cAMP levels
3. loss of water and electrolytes
= watery diarrhea
45
What are two virulence factors of E. coli?
1. Heat-labile enterotoxin "LT"
2. Shiga toxin
46
An AB-exotoxin cytotoxin that functions through the inactivation of 60S ribosome subunit by removal of a specific adenine base from a nucleotide of 28s rRNA that results in the stop of translation, leading to cell death & blood diarrhea:
Shiga toxin
47
lt
48
What kind of toxin is Shiga toxin?
AB-exotoxin cytotoxin
49
Foodborne enterotoxigenic ETEC E. coli may be responsible for ______ and specifically caused by ________
Watery diarrhea; heat-labile enterotoxin "LT"
50
Foodborne enterohemorrhagic EHEC E. coli O157:H7 may be responsible for ______ and specifically caused by _____
Bloody diarrhea; Shiga toxin
51
In addition to bloody diarrhea Shiga toxin may also be responsible for:
Hemolytic uremic syndrome resulting in kidney damage/failure
52
Describe how the virulence factor shiga toxin works:
1. Inactivation of the 60s ribosome subunit by removal of a specific adenine base from a nucleotide of 28S rRNA
2. Stop translation
3. Cell death
= Bloody diarrhea
53
Describe the symptoms of Shigella Dysenteriae:
1. Diarrhea with blood
2. Intestinal cell invasion
3. Apsoptosis of neutrophils to cause pus in diarrhea
54
What disease is responsible for the set of symptoms "diarrhea with blood" combined with intestinal cell invasion, apoptosis and neutrophilic resulting in pus and ultimately dysentery?
Shigella dysenteriae
55
What virulence factors of E. coli often have a seasonal basis to their incidence?
Shiga toxin
56
EHEC:
Enterohemorrhagic E. Coli (O157:H7)
57
Enterohemorrhagic E. coli (O157:H7) clinically appears as:
1. Bloody diarrhea
2. Hemorrhagic colitis
3. Hemolytic uremic syndrome
58
What is the treatment for enterohemorrhagic E. coli (O157:H7)?
Replinish fluids
(antibiotics are contraindicated)
59
How does UroPathogenic E. coli appear clinically?
Cystitis (bladder infection)
60
For what E. coli strain are antibiotic treatment contraindicated?
EHEC (O157:H7)
61
______ % of cystitis are due to an E. coli strain
70-90%
62
In the process of shigella infection, shigellas are taken up by _____ and transported _____
M cells; beneath the epithelium
63
In the process of shigella infection, what happens to the shigellas once below the epithelium?
Taken up by macrophages which will result in macrophage death and release of the shigellas
64
In the process of shigella infection, the bacteria enter the ____ & _____ aspects of epithelial cells via induction of ____
Inferior & lateral aspects; endocytosis
65
In the process of shigella infection, after the shigella enter the lateral & inferior aspects of epithelial cells via endocytosis, what happens to the endosomes?
Endosomes are quickly lysed, leaving shigellas free in the cytoplasm
66
In the process of shigella infection, how do the shigellas spread from cell-to-cell?
The polymerize actin to form a tail that pushes the into the next cell
67
In the process of shigella infection, what is the location of multiplication of shigellas?
Cytoplasm
68
In the process of shigella infection, describe the role of neutrophils:
Cells infected with shigella die & slough off resulting in an intense response of acute inflammatory cells (neutrophils)
69
In the process of shigella infection, in addition to the intense response of acute inflammatory cells, what may also occur in the final stages of shigella infection?
Bleeding & abscess formation; induction of apoptosis
70
Discuss the epidemiology of shigella:
- Tranmission via fecal-oral route
- Sometimes spread through contaminated food or water
- Humans generally the only source
71
What is generally the source of spread of shigella?
Humans generally the only source
72
The virulence factors of shigella include:
1. Shiga toxin
2. Cell invasion
73
What do the virulence factors of shigella ultimately lead to?
Dysentery
74
The shiga toxin virulence factor of shigella is responsible for:
Bloody, watery diarrhea; cell death
75
The cell invasion virulence factor of shigella bacteria is responsible for:
Neutrophil death & pus formation
76
S. Enterica=
Salmonella
77
What illnesses may salmonella cause?
1. Enteric fever
2. Typhoid
78
In extreme cases salmonella may cause as its associated with:
High rate of mortality
79
Salmonella is a species of:
Enteric bacteria
80
What is the reservoir for S. enterica?
Human reservoir
81
Aside from S. Enterica using a human reservoir, many salmonella species have a _____ reservoir:
Poultry
82
The poultry reservoir of many salmonella species include:
The meat, the outside of the egg and sometimes on the inside of the egg
83
Many salmonella species are the cause of a:
Foodborne illness
84
What bacteria species causes gastroenteritis:
Salmonella
85
Describe the virulence factors of salmonella:
1. Type III secretion
2. Intracellular endoscope growth in macrophages
86
Describe the virulence factors of S. Typhi serovars specifically:
1. Invasion into different tissues and organs through macrophages
2. Destruction of Peyer's patches resulting in intestinal rupture
87
Salmonellas ability use type III secretion induces:
Enteric epithelial uptake via M cells
88
The intracellular endosome growth in macrophages seen with salmonella species results in:
Secretion of protein that prevents phagosome-lysosome fusion
89
Salmonella invasion of intestinal epithelia occurs through:
1. M cell uptake through ruffles
2. Electrolyte release to lumen
3. Release of inflammatory exudate
4. Transport to lymph nodes/transient bacteremia
90
Uptake of salmonella into the intestinal epithelia occurs through the induction of membrane ruffling that occurs by the:
remodeling of the actin cytoskeleton
91
When salmonella invoke membrane ruffling through the remodeling of actin cytoskeleton this occurs through:
Secretion of the virulence factors into the host cell
92
What occurs when salmonella invade beyond the intestinal epithelium?
Transport to lymph nodes resulting in a transient bacteremia
93
Entrobacter species that is responsible for causing more systemic symptoms:
S. Typhi
94
In S. Typhi, the bacterium can pass through the epithelia of the gut and spread by:
Surviving inside phagocytes
95
Where is the initial presence of S. Typhi following ingestion:
Small intestin
96
If the S. Typhi spreads beyond the initial infection in the small intestine, it will travel via _____ to the ____
Lymphatics to the mesenteric lymph nodes
97
Once the S. Typhi reaches the mesenteric lymph nodes via the lymphatics, it will travel via _____ to cause _____
Thoracic duct; transient (primary) bacteremia
98
If S. Typhi infection causes transient (primary) bacteremia what will proceed:
Multiplication in macrophages in the liver, spleen & bone marrow
99
When infection of S. Typhi processes to septicemia, what results?
Fever, kidney & other organs infected
100
Why is it significant if S. Typhi infects the gallbladder:
Following initial infection, individuals may maintain the bacteria in their gallbladder which can be shed in the feces and creates a very important carrier state of typhoid fever
101
When S. Typhi infects the gallbladder this results in:
Cholecystitis & carrier state
102
Infection of S. Typhi that is maintained in the small intestines leads to:
Inflammation & ulceration of Peyers patches
103
When S. Typhi causes inflammation & ulceration of Peyer's patches this results in:
Diarrhea, hemorrhage & perforation
104
What is the significance of S. Typhi getting into the kidney?
Salmonella can be discharged into urine a couple weeks after initial infection
105
What is the gram stain of enteric bacteria?
Gram negative
106
Vibrio cholera is a type of _____ bacteria
Enteric
107
In terms of virulence factors, vibrio cholera is considered:
Non-invasive (it doesn't actually get inside of host cells, just infects them)
108
Describe the gram stain and shape of vibrio cholera:
Gram negative; curved rods
109
Vibrio cholera is found in:
Estuaries & marine environments
110
Give an example of a host that may carry vibrio cholera:
A crab
111
Vibrio cholera bacteria are _____ tolerant
Salt
112
Virulence factors of vibrio cholera include:
1. Toxin co-regulated pilus (TCP)
2. Cholera toxin
3. ST toxin
113
The vibrio cholera toxin co-regulated pilus (TCP) is a virulence factor responsible for:
Adhesion to the small intestinal epithelia
114
The vibrio cholera's cholera toxin virulence factor is also called:
Heat-labile exotoxin "LT"
115
What is cholera toxin (heat-labile exotoxin "LT") responsible for?
Protein A causes cAMP rise, leading to watery diarrhea
116
The additional virulence factor "ST" toxin contained by vibrio cholera is responsible for:
Raising cGMP levels, contributes to watery diarrhea
117
In virbrio cholera, responsible for adhesion to the epithelium of small intestine:
Toxin co-regulated pilus (TCP)
118
The additional ST toxin found in vibrio cholera contributes to watery diarrhea by:
The raise in cGMP levels causes electrolytes & subsequent outlflow of water from epithelial cells
119
What can cause an increase in cholera toxin binding in vibrio cholera infections?
Neuraminidase
120
How does neuraminidase work to increase cholera toxin binding?
By cleaving sialic acid
121
The cholera toxin is encoded in:
Bacteriophage genome called CTX-Phage
122
The CTX-phage enters the cholera bacteria cell through:
A toxin co-regulated pilus
123
TCP=
Toxin co-regulated pilus
124
TCP production is induced within the _____ while production in other environments appears to be _____
Intestine; minimal
125
What is responsible for encoding the proteins that comprise the cholera toxin?
ctxA & ctxB
126
Describe the vaccine for cholera:
It is formalin-killed meaning its non pathogenic bacteria that has been inactivated but still a whole cell vaccine
127
What are the common epidemic strain of vibrio cholera?
Server O1
128
What is the newer strain of vibrio cholera that has caused recent epidemics?
Serovar O139
129
List the virulence factors for vibrio cholera:
1. Cholera toxin
2. Toxin-coregulated pili
3. Toxins
4. Neuraminidase
130
List the clinical features of infection with virbio cholera:
Severe watery diarrhea (disease is self-limiting as intestinal cells with surface bacteria are shed)
131
What is the treatment for vibrio cholera infection?
Rehydration + electrolytes
132
What is the epidemiology of vibrio cholera?
1. Fecal transmission in developing countries (can get into drinking water)
2. Under-cooked coastal crabs
133
Bacteria that looks very similar to vibrio cholera:
Campylobacter jejune
134
Describe the gram stain & shape of campylobacter jejune:
Gram negative & short "S" or curved/comma shaped rods
135
A major virulence factor of campylobacter jejune includes:
Growth in intestinal tract
136
The growth in the intestinal tract of campylobacter jejune functions to do what? (2)
1. Invade intestinal epithelial cells or grow below the epithelial layer
2. Inflammatory response
137
A more common, but less severe source of gastroenteritis in the US compared to E. coli & Salmonella:
Campylobacter jejune
138
What type of reservoir is seen with campylobacter jejune?
Animal reservoir (intestinal)
139
Because campylobacter jejune utilizes an animal reservoir this is called:
Zoonosis
140
Describe the transmission of campylobacter jejune:
Transmission occurs through contaminated food (poultry, milk)
141
In a study, what percent of raw chicken contained campylobacter?
89%
142
How is campylobacter jejune typically resolved?
Without treatment in less than one week
143
Campylobacter jejune infection being resolved without treatment creates:
Protective immunity
