TO DO copy 2 Flashcards
What is a distinguishing trait of Enterobacteriaceae compared to other Gram negative bacteria?
a) Oxidase-positive
b) Ferments glucose
c) Produces spores
d) Gram-positive staining
b) Ferments glucose
Explanation:
• Correct: Enterobacteriaceae are glucose fermenters, a key diagnostic feature.
• a: Enterobacteriaceae are oxidase-negative.
• c: They are non-spore-forming.
• d: They are Gram-negative, not Gram positive.
Which selective media is commonly used to differentiate lactose fermenters from non-lactose fermenters?
a) Mannitol Salt Agar
b) MacConkey Agar
c) Chocolate Agar
d) Blood Agar
b) MacConkey Agar
Explanation:
• Correct: MacConkey Agar differentiates based on lactose fermentation, showing pink colonies for fermenters.
• a: Mannitol Salt Agar is used for Staphylococcus species.
• c/d: Chocolate and Blood Agars are nonselective.
Which of the following is a virulence factor associated with serum resistance in Enterobacteriaceae?
a) Capsule
b) Flagella
c) Lipid A
d) O polysaccharide
a) Capsule
Explanation:
• Correct: Capsules prevent complement binding and phagocytosis, enhancing serum resistance.
• b: Flagella contribute to motility, not serum resistance.
• c: Lipid A is an endotoxin causing immune activation, not resistance.
• d: O polysaccharide aids in antigenic variation but does not directly confer serum resistance.
Which of these Enterobacteriaceae is a non lactose fermenter?
a) Escherichia coli
b) Klebsiella pneumoniae
c) Shigella spp.
d) Enterobacter spp.
c) Shigella spp.
Explanation:
• Correct: Shigella spp. are non-lactose fermenters (colorless on MacConkey Agar).
• a, b, d: These are lactose fermenters, producing pink colonies on MacConkey Agar.
Which antigenic component is responsible for endotoxin activity in Enterobacteriaceae?
a) O polysaccharide
b) Core polysaccharide
c) Lipid A
d) K antigen
c) Lipid A
Explanation:
• Correct: Lipid A, part of lipopolysaccharide (LPS), triggers immune responses and endotoxin activity.
• a: O polysaccharide is involved in antigenic variation.
• b: Core polysaccharide is shared across the genus but lacks endotoxin activity.
• d: K antigen is part of the capsule, aiding in immune evasion.
What distinguishes Enterobacteriaceae from Pseudomonas species?
a) Gram-negative staining
b) Glucose fermentation
c) Presence of catalase
d) Presence of peptidoglycan
b) Glucose fermentation
Explanation:
• Correct: Enterobacteriaceae ferment glucose, whereas Pseudomonas species do not.
What bacterial appendage facilitates horizontal gene transfer?
a) Flagella
b) Pili
c) Capsule
d) O polysaccharide
b) Pili
Explanation:
• Correct: Pili (conjugation pili) transfer genetic material.
• a: Flagella aid in motility.
• c: Capsules protect against phagocytosis.
• d: O polysaccharide is antigenic, not involved in gene transfer.
Which structural component of Enterobacteriaceae is responsible for their resistance to bile salts?
a) Capsule
b) Lipopolysaccharide (LPS)
c) Peptidoglycan layer
d) Outer membrane
d) Outer membrane
Explanation:
• Correct: The outer membrane of Enterobacteriaceae provides a selective barrier, protecting them from bile salts and other harmful substances in the gastrointestinal environment.
• a: The capsule primarily protects against phagocytosis, not bile salts.
• b: LPS contributes to immune evasion and septic shock but is not the primary defense against bile salts.
• c: The peptidoglycan layer is thin in Gram negative bacteria and not directly involved in bile salt resistance.
Which of the following Enterobacteriaceae produces a prominent green metallic sheen on EMB agar?
a) Klebsiella pneumoniae
b) Escherichia coli
c) Proteus mirabilis
d) Salmonella spp.
b) Escherichia coli
Explanation:
• Correct: E. coli produces a distinctive green metallic sheen on EMB agar due to strong lactose fermentation.
• a, c, d: These bacteria do not produce the green sheen characteristic of E. coli.
Which Enterobacteriaceae species is most commonly associated with hemorrhagic colitis?
a) Escherichia coli O157:H7
b) Klebsiella pneumoniae
c) Shigella sonnei
d) Salmonella typhi
a) Escherichia coli O157:H7
Explanation:
• Correct: E. coli O157:H7 produces Shiga toxin, leading to hemorrhagic colitis and hemolytic uremic syndrome (HUS).
• b, c, d: These species are associated with other types of infections (e.g., pneumonia, dysentery, typhoid fever).
Which Enterobacteriaceae species produces a swarming motility pattern on agar?
a) Klebsiella pneumoniae
b) Proteus mirabilis
c) Salmonella enterica
d) Shigella dysenteriae
b) Proteus mirabilis
Explanation:
• Correct: Proteus mirabilis exhibits swarming motility due to its highly active flagella.
• a, c, d: These do not show swarming motility.
Which secretion system is responsible for injecting virulence factors directly into host cells?
a) Type II Secretion System
b) Type III Secretion System
c) Type IV Secretion System
d) Type I Secretion System
b) Type III Secretion System
Explanation:
• Correct: T3SS injects virulence proteins into host cells, manipulating their functions.
• a, c, d: These systems have different functions (e.g., secretion into extracellular space).
What role does the K antigen play in Enterobacteriaceae?
a) Mediates serum resistance
b) Contributes to motility
c) Acts as an endotoxin
d) Differentiates lactose fermentation
a) Mediates serum resistance
Explanation:
• Correct: K antigen (capsular polysaccharide) inhibits complement-mediated killing and phagocytosis.
• b: Motility is due to flagella (H antigen).
• c: Endotoxin activity is attributed to Lipid A.
• d: Lactose fermentation is unrelated to the K antigen.
What is the role of siderophores like enterobactin in Enterobacteriaceae?
a) Enhances adhesion to host cells
b) Facilitates iron acquisition
c) Protects against phagocytosis
d) Increases motility
b) Facilitates iron acquisition
Explanation:
• Correct: Siderophores scavenge iron from host proteins, essential for bacterial survival.
• a: Adhesion is mediated by pili or fimbriae.
• c: Capsules protect against phagocytosis.
• d: Motility is unrelated to siderophores.
Which Enterobacteriaceae is the most common cause of urinary tract infections?
a) Klebsiella pneumoniae
b) Proteus mirabilis
c) Escherichia coli
d) Serratia marcescens
c) Escherichia coli
Explanation:
• Correct: E. coli is the leading cause of UTIs, primarily due to its ability to adhere to uroepithelial cells.
• a, b, d: These are less common causes of UTIs.
Which Enterobacteriaceae has the Vi antigen as part of its capsule?
a) Escherichia coli
b) Klebsiella pneumoniae
c) Salmonella typhi
d) Shigella flexneri
c) Salmonella typhi
Explanation:
• Correct: S. typhi has the Vi antigen, enhancing its virulence by resisting phagocytosis.
• a, b, d: These do not possess the Vi antigen.
What is the primary virulence factor responsible for septic shock in Gram-negative infections?
a) Flagella
b) Lipopolysaccharide (LPS)
c) Siderophores
d) Type III Secretion System
b) Lipopolysaccharide (LPS)
Explanation:
• Correct: LPS triggers cytokine release, leading to septic shock, with Lipid A being the toxic component.
• a, c, d: These factors contribute to virulence but are not the primary cause of septic shock.
What mechanism allows Enterobacteriaceae to evade host immunity through antigenic variation?
a) Secretion of exotoxins
b) Switching expression of surface antigens
c) Producing siderophores
d) Triggering complement cascade
b) Switching expression of surface antigens
Explanation:
• Correct: Antigenic phase variation involves switching surface antigen expression to evade immune detection.
• a, c, d: These mechanisms do not involve antigenic variation.
How do Enterobacteriaceae acquire antimicrobial resistance?
a) Horizontal gene transfer
b) Mutation of mitochondrial DNA
c) Loss of peptidoglycan
d) Overexpression of fimbriae
a) Horizontal gene transfer
Explanation:
• Correct: Enterobacteriaceae transfer resistance genes via plasmids, conjugation, transformation, or transduction.
• b: Bacteria lack mitochondria.
• c: Peptidoglycan is unrelated to resistance acquisition.
• d: Fimbriae are used for adhesion, not resistance.
What is the incubation period for diarrheagenic Escherichia coli (DEC) infections?
A. 1–2 hours
B. A few hours up to 2 days
C. 3–5 days
D. 5–7 days
B. A few hours up to 2 days
Explanation:
• Correct: DEC infections typically have an incubation period ranging from a few hours up to 2 days. This aligns with the typical onset of secretory diarrhea.
• Incorrect:
A: Too short for bacterial incubation.
C and D: Longer than the typical range for DEC.
Which toxin is associated with guanylate cyclase activation in ETEC infections?
A. STa
B. LT-I
C. LT-II
D. EAST-1
A. STa
Explanation:
• Correct: STa binds to guanylate cyclase C receptors, increasing cGMP levels and causing fluid hypersecretion.
• Incorrect:
B and C: LT toxins increase cAMP, not cGMP.
D: EAST-1 also increases cGMP but is associated with EAEC, not ETEC.
What is the hallmark feature of EPEC infections?
A. Biofilm formation
B. Shiga toxin production
C. Attaching and effacing (A/E) lesions
D. Heat-stable toxin secretion
C. Attaching and effacing (A/E) lesions
Explanation:
• Correct: A/E lesions result in villi deformation and microvilli loss, a hallmark of EPEC infections.
• Incorrect:
A: Biofilm formation is a feature but not the hallmark.
B and D: Shiga toxin and heat-stable toxins are not relevant to EPEC.
Which diarrheagenic E. coli pathotype forms a “stacked brick” pattern of adherence?
A. EPEC
B. EAEC
C. ETEC
D. STEC
B. EAEC
Explanation:
• Correct: EAEC is characterized by its stacked brick-like aggregative adherence pattern.
• Incorrect:
A, C, and D: These pathotypes do not exhibit this adherence pattern.
What role does dispersin play in EAEC infections?
A. Toxin production
B. Bacterial adherence
C. Biofilm disruption
D. Cell invasion
B. Bacterial adherence
Explanation:
• Correct: Dispersin assists in keeping EAEC attached to the intestinal mucosa.
• Incorrect:
A, C, and D: Dispersin is not involved in toxin production, biofilm disruption, or cell invasion.
Which virulence factor mediates pedestal formation in EPEC?
A. LT-I toxin
B. Intimin-Tir interaction
C. Shiga toxin
D. EAST-1 toxin
B. Intimin-Tir interaction
Explanation:
• Correct: The binding of Tir to intimin triggers actin polymerization and pedestal formation.
• Incorrect:
A, C, and D: These toxins are unrelated to EPEC’s pathogenesis.
What is the primary reservoir for Shiga toxin producing E. coli (STEC)?
A. Humans
B. Pigs
C. Cattle
D. Poultry
C. Cattle
Explanation:
• Correct: Cattle are the main reservoir for STEC, particularly for strains like EHEC.
• Incorrect:
A, B, and D: Though these animals can occasionally harbor STEC, they are not the primary reservoirs.
What is a major complication of STEC infections?
A. Cholera-like diarrhea
B. Hemolytic-uremic syndrome (HUS)
C. Dysentery
D. Severe dehydration
B. Hemolytic-uremic syndrome (HUS)
Explanation:
• Correct: STEC infections can lead to HUS, characterized by acute renal failure and thrombocytopenia.
• Incorrect:
A: More associated with ETEC.
C: Seen in EIEC infections.
D: Severe dehydration is common but not a specific complication of STEC.
Which toxin in STEC infections disrupts protein synthesis by binding to 28S rRNA?
A. LT-II
B. STa
C. Shiga toxin (Stx)
D. EAST-1
C. Shiga toxin (Stx)
Explanation:
• Correct: Shiga toxin cleaves 28S rRNA, halting protein synthesis and causing cell death.
• Incorrect:
A, B, and D: These toxins do not target 28S rRNA.
What is the transmission route of EIEC?
A. Person-to-person
B. Contaminated water only
C. Zoonotic
D. Airborne
A. Person-to-person
Explanation:
• Correct: EIEC spreads via the fecal oral route, often through person-to-person contact.
• Incorrect:
B: Waterborne transmission can occur but is not exclusive.
C and D: EIEC is not zoonotic or airborne.
What is a key distinguishing feature of EIEC from Shigella?
A. Presence of pInv plasmid
B. Ability to ferment lactose
C. Motility
D. Pathogenic mechanism
C. Motility
Explanation:
• Correct: EIEC is non-motile, distinguishing it from Shigella.
• Incorrect:
A, B, and D: EIEC shares the pInv plasmid and pathogenesis with Shigella, and both are lactose-negative.
Which E. coli pathotype is primarily associated with community-acquired UTIs?
A. EPEC
B. ETEC
C. Uropathogenic E. coli (UPEC)
D. EAEC
C. Uropathogenic E. coli (UPEC)
Explanation:
• Correct: UPEC accounts for approximately 80% of community acquired UTIs due to its ability to invade and colonize the urinary tract.
• Incorrect:
A, B, and D: These pathotypes are not associated with UTIs; they primarily cause diarrheal diseases.
What is the role of CRISPR in E. coli?
A. Enhances motility
B. Protects against viral DNA
C. Facilitates lactose fermentation
D. Produces shiga toxin
B. Protects against viral DNA
Explanation:
• Correct: CRISPR functions as an immune mechanism to defend against bacteriophage infections.
• Incorrect:
A, C, and D: CRISPR does not enhance motility, fermentation, or toxin production.
Which pathogenic E. coli forms attaching and effacing (A/E) lesions but lacks bundle-forming pili (BFP)?
A. Typical EPEC (tEPEC)
B. Atypical EPEC (aEPEC)
C. STEC
D. EIEC
B. Atypical EPEC (aEPEC)
Explanation:
• Correct: aEPEC lacks BFP but still forms A/E lesions.
• Incorrect:
A: tEPEC contains BFP.
C and D: STEC and EIEC do not form A/E lesions.
Which toxin in ETEC mimics cholera toxin in its mechanism of action?
A. STa
B. LT-I
C. EAST-1
D. Pet toxin
B. LT-I
Explanation:
• Correct: LT-I shares 80% homology with cholera toxin, increasing cAMP to cause watery diarrhea.
• Incorrect:
A: STa increases cGMP.
C and D: EAST-1 and Pet toxin are unrelated to cholera toxin.
Question
Answer & Explanation
- Which E. coli pathotype most commonly causes chronic diarrhea?
A. EPEC
B. EAEC
C. ETEC
D. STEC
Answer: B. EAEC
Explanation:
Correct: EAEC is a major cause of chronic diarrhea due to its biofilm formation and toxin production.
Incorrect:
A, C, and D: These pathotypes are more commonly associated with acute diarrhea.
- What is the mechanism of cell death caused by the A subunit of Shiga toxin?
A. Increases cAMP
B. Halts protein synthesis by cleaving 28S rRNA
C. Disrupts actin cytoskeleton
D. Causes DNA damage
Answer: B. Halts protein synthesis by cleaving 28S rRNA
Explanation:
Correct: The A subunit depurinates 28S rRNA, halting protein synthesis and causing cell death.
Incorrect:
A, C, and D: These mechanisms are unrelated to Shiga toxin.
- Which E. coli pathotype is commonly associated with nosocomial infections?
A. EPEC
B. EAEC
C. UPEC
D. EIEC
Answer: C. UPEC
Explanation:
Correct: UPEC is a leading cause of nosocomial UTIs due to its ability to colonize the urinary tract.
Incorrect:
A, B, and D: These pathotypes are not typically associated with nosocomial infections.
- Which ExPEC variant is the leading cause of neonatal meningitis?
A. UPEC
B. NMEC
C. SEPEC
D. EPEC
Answer: B. NMEC
Explanation:
Correct: Neonatal meningitis associated E. coli (NMEC) is the leading cause of neonatal meningitis due to its K1 polysialic acid capsule, which enhances survival after crossing the blood-brain barrier.
Incorrect:
A and C: UPEC and SEPEC do not primarily cause neonatal meningitis.
D: EPEC causes diarrhea, not meningitis.
- What virulence factor allows NMEC to evade phagocytosis?
A. Hemolysin
B. Type 1 fimbria
C. K1 polysialic acid capsule
D. Shiga toxin
Answer: C. K1 polysialic acid capsule
Explanation:
Correct: The K1 capsule protects NMEC from phagocytosis and enhances its survival in host tissues.
Incorrect:
A and B: Hemolysin and fimbria are associated with UPEC.
D: Shiga toxin is produced by STEC, not NMEC.
- What is the primary source of UPEC in urinary tract infections?
A. Contaminated food
B. Host vaginal or fecal microbiota
C. Bloodborne transmission
D. Environmental water sources
Answer: B. Host vaginal or fecal microbiota
Explanation:
Correct: UPEC originates from the host’s own vaginal or fecal flora and ascends the urinary tract to cause infection.
Incorrect:
A, C, and D: These are not typical sources of UPEC.
- Which ExPEC toxin promotes bladder hemorrhage in UTIs?
A. Shiga toxin
B. Hemolysin
C. Enterotoxin
D. EAST-1
Answer: B. Hemolysin
Explanation:
Correct: Hemolysin forms pores in epithelial cells, causing cell death and bladder hemorrhage.
Incorrect:
A: Shiga toxin is not involved in UTIs.
C and D: These are toxins from diarrheagenic E. coli.
- What phylogenetic groups do most ExPEC strains belong to?
A. A and B1
B. B2 and D
C. E and F
D. B1 and C
Answer: B. B2 and D
Explanation:
Correct: ExPEC strains often derive from B2 and D phylogroups, which encode virulence genes on plasmids or pathogenicity islands.
Incorrect:
A, C, and D: These groups are less commonly associated with ExPEC.
- Which of the following is the hallmark symptom of typhoid fever caused by Salmonella Typhi?
A. Bloody diarrhea
B. Remittent fever with bradycardia
C. Severe dehydration
D. Bladder hemorrhage
Answer: B. Remittent fever with bradycardia
Explanation:
Correct: Typhoid fever is characterized by a gradual onset of fever with bradycardia, unlike most infections where tachycardia predominates.
Incorrect:
A and C: These are more common in Shigellosis or severe gastroenteritis.
D: This is associated with UPEC.
- What is the primary receptor for Shiga toxin in hemolytic uremic syndrome?
A. GM1 gangliosides
B. Globotriaosylceramide (Gb3)
C. Mannose-binding lectin
D. Fimbrial adhesins
Answer: B. Globotriaosylceramide (Gb3)
Explanation:
Correct: Gb3 is the receptor for Shiga toxin, facilitating its entry into endothelial cells.
Incorrect:
A, C, and D: These receptors are unrelated to Shiga toxin.
- What mechanism allows Shigella to spread from cell to cell?
A. Actin filament rearrangement
B. Fimbrial adhesion
C. Capsule formation
D. Biofilm production
Answer: A. Actin filament rearrangement
Explanation:
Correct: Shigella uses actin filaments to propel itself through the cytoplasm into adjacent cells.
Incorrect:
B, C, and D: These mechanisms are not involved in intracellular spread.
