64 Questions
Which effector inhibits the activation of the TAK1 kinase, leading to epithelial cell damage and inflammatory response?
VopZ
What is the primary role of VopC in bacterial infection?
Promotes actin bundling
Which effector acts as an acetyltransferase to block MAPKs signaling, suppress cell division, and induce cell death?
VopA
What is the function of VopT in cellular metabolism?
Effects cellular metabolism
Which effector protein's mechanism of cytotoxicity remains unclear?
VPA1380
Why does parahaemolyticus utilize siderophores, heme, and different iron transporters?
To scavenge iron from the environment
Which chromosome contains the Type III Secretion System (T3SS) that contributes to cytotoxicity?
Chromosome 1
What is the role of T3SS2 in Vibrio parahaemolyticus?
Contribute to enterotoxcity
Which iron transporter is utilized by parahaemolyticus along with siderophores to scavenge iron?
Aerobactin
What is the significance of TDH/TRH in Vibrio parahaemolyticus?
Used as diagnostic markers of virulent isolates
What is the main function of VopA, VopC, VopL, and VopT in Vibrio parahaemolyticus?
Translocating into host cells to cause cytotoxicity or enterotoxicity
Which virulence factor is essential for the initial attachment of Vibrio parahaemolyticus to host cells?
MAM7
What is the role of a single flagellum in Vibrio parahaemolyticus?
Required for swimming motility
What type of motility requires the production of flagella along the lateral side of Vibrio parahaemolyticus?
Swarming motility
Which proteins are involved in synergy to cause cytotoxicity or enterotoxicity in Vibrio parahaemolyticus?
T3SS2 effectors (VopA, VopC, VopL, and VopT)
What is the role of VtrA in regulating the expression of T3SS2 in Vibrio parahaemolyticus?
Forms a complex with VtrC to recognize and bind to bile salt
How does bile salt contribute to the expression of T3SS2 in Vibrio parahaemolyticus?
Up-regulates the expression of VtrB
What are the effects of T3SS2 effectors on host cells in Vibrio parahaemolyticus infections?
Destroy the cytoskeleton and disrupt cell signaling
What are two possible explanations for clinical isolates lacking T3SS2 and TDH/TRH discovered by researchers at Health Canada and in Mexico?
Presence of unknown virulence factors or innocence as bystanders
How do growth conditions such as the presence of bile salt affect the regulation of T3SS2 genes in Vibrio parahaemolyticus?
Bile salt up-regulates the expression of VtrB, leading to T3SS2 expression
What is the mechanism by which Cholera Toxin (CTX) triggers acute diarrhea?
Activation of specific ion channels
How does Vibrio cholerae increase its chance of survival and virulence according to the text?
It becomes naturally competent on chitin
What is the role of cyclic AMP (cAMP) in the context of cholera infection?
Triggering efflux of ions from the cell
How does V. parahaemolyticus switch serotypes mid-outbreak, as mentioned in the text?
By undergoing lateral gene transfer rapidly
What is the impact of climate change on the probability of V. cholerae becoming virulent through phage infection?
Increases the probability
What is the significance of V.cholerae serotypes O1 and O139 acquiring the CTX toxin gene?
They acquired the ability to cause cholera
Which statement accurately describes the role of the T3SS in V.parahaemolyticus virulence?
Its exact role is still unclear
What differentiates V.parahaemolyticus isolates with and without the tdh and trh genes?
Isolates without these genes are nonpathogenic
What can happen if the T3SS gets transferred from V.parahaemolyticus to V.cholerae?
V.cholerae gains pathogenicity to humans
How do V.parahaemolyticus isolates lacking tdh and trh genes differ from those with these genes?
They lack the ability to cause illness
What is the generation time of Vibrio parahaemolyticus at 37°C?
8 to 9 minutes
Which type of toxin is produced by pathogenic Vibrio parahaemolyticus that forms tetrameric pore complexes in the host membrane?
Thermostable direct haemolysin
What is the function of the T3SS1 effectors VopQ, VopR, VopS, and VPA0450 in host cells?
Induce cell death
Which of the following statements about Vibrio parahaemolyticus is FALSE?
TDH and TRH toxins promote cell division in host cells
Which virulence factor of Vibrio parahaemolyticus is responsible for cytotoxicity by translocating effectors into host cells?
T3SS1
What are the symptoms that can be observed after ingesting food contaminated with Vibrio parahaemolyticus?
Diarrhea and abdominal cramps
Which Vibrio parahaemolyticus toxin is thermolabile?
tlh
Pathogenic V. parahaemolyticus produces which type of toxins that form tetrameric pore complexes?
Thermostable direct haemolysin (tdh)
What symptoms were experienced by the residents who became sickened in the summer of 2015 in the metro Vancouver area after eating raw oysters?
Diarrhea, abdominal cramping, fever, headache, nausea, and vomiting
When does 'Vibrio' season typically occur in Canadian seafood?
When the water that oysters are harvested from goes above 17°C
What is the most common Vibrio infection from Canadian seafood?
Vibrio parahaemolyticus
How are Vibrio parahaemolyticus infections serotyped?
According to its LPS (O) antigen and capsular polysaccharide (K) antigen
What are the names of the T3SS2 effectors translocated into host cells by Vibrio parahaemolyticus?
VopA, VopC, VopL, and VopT
Where are the flagella produced in Vibrio parahaemolyticus during growth in semi-solid media?
Along the lateral side of the bacterium
What is the name of the multivalent adhesion protein in Vibrio parahaemolyticus that binds to fibronectin and phosphatidic acid for initial attachment to host cells?
MAM7
What are the symptoms of Vibrio vulnificus infection?
Symptoms include fever, chills, nausea, and hypotension.
What is the fatality rate for wound infections caused by Vibrio vulnificus?
20-25% fatality rate.
What are the risk factors associated with primary septicemia from Vibrio vulnificus?
Consumption of Raw Oysters and Wound exposure to seawater or seafood.
What are some of the virulence factors of Vibrio vulnificus?
Polysaccharide capsule (K-antigen), LPS (O-antigen), and vvhA.
What is the mechanism by which Cholera Toxin (CTX) triggers acute diarrhea?
By causing an efflux of ions from the cell membrane, leading to water being drawn from cells and tissues via osmosis
What is the role of cyclic AMP (cAMP) in the context of cholera infection?
cAMP activates specific ion channels in the cell membrane, leading to an efflux of ions and drawing water into the intestinal lumen via osmosis
How does Vibrio cholerae increase its chance of survival and virulence according to the text?
By becoming naturally competent when grown on chitin, allowing it to readily take up DNA from the environment
What is the impact of climate change on the probability of V. cholerae becoming virulent through phage infection?
Climate change increases the probability of V. cholerae becoming virulent through phage infection
Vibrio is a nonspore-forming, Gram-negative, Vibrio shaped ______
bacterium
Most Vibrio isolates, in each of the potentially pathogenic species, are ______
non-pathogenic
In the summer of 2015, 72 residents of the metro Vancouver area became sickened after eating raw oysters and experiencing symptoms such as diarrhea, abdominal cramping, fever, headache, nausea, and vomiting. These residents had all eaten out within the two days preceding their illness. Each sick person reported eating ______.
raw oysters
The most common Vibrio infection from Canadian seafood occurs when the water that oysters are harvested from goes above ______C.
17
Vibrio parahaemolyticus infections are almost exclusively linked to the consumption of ______ or undercooked seafood.
raw
Vibrio parahaemolyticus is serotyped according to its LPS (O) antigen and capsular polysaccharide (K) antigen – On the Canadian West Coast, its commonly seen as O4:K______.
12
What is the role of T3SS2 effectors in Vibrio parahaemolyticus infections?
T3SS2 effectors destroy the cytoskeleton and manipulate cell signaling transduction.
How do T3SS1 effectors VopQ, VopR, VopS, and VPA0450 affect host cells in Vibrio parahaemolyticus infections?
These T3SS1 effectors cause cytotoxicity and enterotoxicity in host cells.
What are the potential explanations for clinical isolates lacking T3SS2 and TDH/TRH in Vibrio parahaemolyticus?
- Emerging virulence factors unknown to researchers. 2. Innocent bystanders to another Vibrio infection.
What is the significance of the flagellum structure in Vibrio parahaemolyticus?
The single flagellum in Vibrio parahaemolyticus aids in motility and attachment to host cells.
What are the pathogenic characteristics of Vibrio parahaemolyticus haemolytic toxins?
Vibrio parahaemolyticus haemolytic toxins form tetrameric pore complexes in host cell membranes.
Study Notes
Vibrio parahaemolyticus
- Has a single flagellum at one pole, required for swimming motility, and produces flagella along its lateral side for swarming motility in semi-solid media
Adhesion and Iron Uptake
- MAM7 is a multivalent adhesion protein that binds to fibronectin and phosphatidic acid, required for initial attachment to host cells
- Utilizes siderophores (vibrioferrin, ferrichrome, and aerobactin) and heme to scavenge iron from the environment, causing haemolysis
- Iron transporters are internalized by different membrane receptors on the outer membrane and transported to the cytoplasm by ABC complexes
Type III Secretion Systems (T3SS)
- T3SS is a major virulence factor, injecting effector proteins into host cells through a syringe-like transmembrane device
- T3SS1 is on chromosome 1, found in environmental and clinical isolates, contributing to cytotoxicity
- T3SS2 is on chromosome 2, found in clinical isolates, contributing to enterotoxicity and involved in negative regulation of cellular inflammatory response
- T3SS2 effectors (VopA, VopC, VopL, and VopT) are translocated into host cells, causing cytotoxicity and enterotoxicity
- TDH/TRH are on the T3SS2 regulon, used as diagnostic markers of a virulent isolate
Explore the evolutionary history of Vibrio cholerae and Vibrio parahaemolyticus in relation to their acquisition of virulence genes and the ability to cause illness in humans. Learn about the specific serotypes and genes involved in the evolution of these pathogens.
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