Bacterial virulence factors US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Bacterial virulence factors. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Bacterial virulence factors US Medical PG Question 1: Part of the success of the Streptococcus pyogenes bacterium lies in its ability to evade phagocytosis. Which of the following helps in this evasion?
- A. Streptolysin S
- B. Streptolysin O
- C. Streptokinase
- D. M protein (Correct Answer)
- E. Pyrogenic toxin
Bacterial virulence factors Explanation: ***M protein***
- The **M protein** is a major virulence factor of *Streptococcus pyogenes* that **inhibits phagocytosis** by binding to factor H, a host complement regulatory protein, preventing C3b deposition.
- It also helps the bacterium adhere to host cells and resist killing by neutrophils.
*Streptolysin S*
- **Streptolysin S** is a **hemolysin** that causes beta-hemolysis on blood agar and contributes to tissue damage by lysing cells.
- While contributing to virulence, its primary role is not direct inhibition of phagocytosis but rather cell lysis.
*Streptolysin O*
- **Streptolysin O (SLO)** is another **hemolysin** that produces pore-forming toxins, leading to cell lysis and tissue destruction.
- It is highly antigenic and often used as a diagnostic marker (ASO titer) for past *S. pyogenes* infections, but it does not directly prevent phagocytosis.
*Streptokinase*
- **Streptokinase** is an enzyme that activates plasminogen, leading to the breakdown of fibrin clots, which helps in the **spread of infection** within tissues.
- Its main function is not to evade phagocytosis but rather to facilitate invasion by dissolving blood clots that would typically wall off the infection.
*Pyrogenic toxin*
- **Pyrogenic toxins** (also known as erythrogenic toxins) are superantigens that cause symptoms like fever and rash (e.g., in scarlet fever) by stimulating a massive, non-specific T-cell activation.
- These toxins contribute to the systemic manifestations of infection but do not directly interfere with the process of phagocytosis.
Bacterial virulence factors US Medical PG Question 2: A 49-year-old male complains of abdominal discomfort that worsens following meals. A gastric biopsy reveals a 2 cm gastric ulcer, and immunohistochemical staining demonstrates the presence of a rod-shaped bacterium in the gastric mucosa. Which of the following is used by the infiltrating pathogen to neutralize gastric acidity?
- A. Mucinase
- B. LT toxin
- C. Flagella
- D. Bismuth
- E. Urease (Correct Answer)
Bacterial virulence factors Explanation: ***Urease***
- The presence of a rod-shaped bacterium in the gastric mucosa causing ulcers points to **Helicobacter pylori**.
- **H. pylori** produces **urease**, an enzyme that converts urea into ammonia and carbon dioxide, creating a more alkaline environment around the bacterium, thus neutralizing gastric acid and allowing its survival.
*Mucinase*
- **Mucinase** is an enzyme produced by some bacteria that breaks down the protective mucus layer, contributing to mucosal damage.
- While contributing to pathogenesis, mucinase does not directly neutralize gastric acidity.
*LT toxin*
- **LT toxin** (heat-labile toxin) is primarily associated with **enterotoxigenic Escherichia coli (ETEC)** and causes watery diarrhea by increasing cAMP.
- This toxin is not produced by **H. pylori** and does not play a role in neutralizing gastric acid.
*Flagella*
- **Flagella** are **locomotor appendages** that allow **H. pylori** to move through the gastric mucus layer and colonize the gastric epithelium.
- While crucial for host colonization, flagella do not directly neutralize gastric acid.
*Bismuth*
- **Bismuth** is a component of some multi-drug regimens used to treat **H. pylori** infection, acting as an antimicrobial and mucosal protectant.
- It is not produced by the bacterium but is a medication given to the patient.
Bacterial virulence factors US Medical PG Question 3: A microbiology student was given a swab containing an unknown bacteria taken from the wound of a soldier and asked to identify the causative agent. She determined that the bacteria was a gram-positive, spore-forming bacilli, but had difficulty narrowing it down to the specific bacteria. The next test she performed was the Nagler's test, in which she grew the bacteria on a plate made from egg yolk, which would demonstrate the ability of the bacteria to hydrolyze phospholipids and produce an area of opacity. Half the plate contained a specific antitoxin which prevented hydrolysis of phospholipids while the other half did not contain any antitoxin. The bacteria produced an area of opacity only on half of the plate containing no antitoxin. Which of the following toxins was the antitoxin targeting?
- A. Alpha toxin (Correct Answer)
- B. Exotoxin A
- C. Tetanus toxin
- D. Diphtheria toxin
- E. Botulinum toxin
Bacterial virulence factors Explanation: ***Alpha toxin***
- The scenario describes a **Nagler's test**, which is specifically used to detect the presence of **alpha toxin (lecithinase)** produced by *Clostridium perfringens*.
- The antitoxin prevents the hydrolysis of phospholipids and the formation of opacity, confirming that the opacity is due to the alpha toxin.
*Exotoxin A*
- **Exotoxin A** is a toxin produced by *Pseudomonas aeruginosa* and inhibits protein synthesis.
- It is not associated with the **Nagler's test** or phospholipid hydrolysis on egg yolk agar.
*Tetanus toxin*
- **Tetanus toxin** is produced by *Clostridium tetani* and causes spastic paralysis by inhibiting inhibitory neurotransmitter release.
- It is not involved in phospholipid hydrolysis or detected by the **Nagler's test**.
*Diphtheria toxin*
- **Diphtheria toxin** is produced by *Corynebacterium diphtheriae* and inhibits protein synthesis, leading to cellular death.
- This toxin is not detected by the **Nagler's test** and does not cause phospholipid hydrolysis.
*Botulinum toxin*
- **Botulinum toxin** is produced by *Clostridium botulinum* and causes flaccid paralysis by inhibiting acetylcholine release at the neuromuscular junction.
- It is not associated with the **Nagler's test** or the hydrolysis of phospholipids.
Bacterial virulence factors US Medical PG Question 4: A 35-year-old patient with no significant past medical history arrives to the ED with abdominal cramps, nausea, and vomiting. He has had no recent travel or chemical exposures; however, three other members of his family also arrived concurrently to the ED with abdominal cramps, nausea, and vomiting. When asked about their recent activities, they recall that they had shared a lunch of leftover fried rice and soft boiled eggs about 5 hours earlier. The patients are otherwise afebrile and deny any history of diarrhea. Which of the following toxins is the most likely to have caused these symptoms?
- A. Shiga toxin
- B. Cereulide (Correct Answer)
- C. Endotoxin
- D. Exotoxin A
- E. Toxin B
Bacterial virulence factors Explanation: ***Cereulide***
- The rapid onset (within 5 hours) of gastrointestinal symptoms (nausea, vomiting, abdominal cramps) after consuming **fried rice** and **boiled eggs** is characteristic of intoxication by **cereulide**.
- This preformed toxin is produced by *Bacillus cereus* in improperly stored starchy foods like rice, leading to emetic-type food poisoning.
*Shiga toxin*
- **Shiga toxin** is produced by *Shigella dysenteriae* and Shiga toxin-producing *E. coli* (STEC), typically causing **bloody diarrhea** and **hemolytic uremic syndrome (HUS)**, which are not present here.
- The incubation period for Shiga toxin-mediated illness is usually longer, ranging from 1 to 8 days, making a rapid onset of symptoms unlikely.
*Endotoxin*
- **Endotoxin** (lipopolysaccharide or LPS) is a component of the outer membrane of **Gram-negative bacteria** and causes systemic symptoms like fever, shock, and organ dysfunction when released during bacterial lysis.
- While it can cause some gastrointestinal effects, the rapid onset of isolated emetic symptoms in a food poisoning cluster is not typical for endotoxin as the primary cause.
*Exotoxin A*
- **Exotoxin A** is a virulence factor produced by *Pseudomonas aeruginosa* and is associated with severe infections in immunocompromised patients, not typically foodborne illness.
- Its mechanism of action involves inhibiting protein synthesis, leading to tissue damage in specific infections, not acute emetic food poisoning.
*Toxin B*
- **Toxin B** is produced by *Clostridioides difficile* and is a major cause of **antibiotic-associated colitis** and **pseudomembranous colitis**, characterized by diarrhea and abdominal pain.
- The patient's presentation of acute onset nausea, vomiting, and abdominal cramps without diarrhea and no history of antibiotic use does not align with *C. difficile* infection.
Bacterial virulence factors US Medical PG Question 5: A 56-year-old woman comes to the emergency department because of worsening pain and swelling in her right knee for 3 days. She underwent a total knee arthroplasty of her right knee joint 5 months ago. The procedure and immediate aftermath were uneventful. She has hypertension and osteoarthritis. Current medications include glucosamine, amlodipine, and meloxicam. Her temperature is 37.9°C (100.2°F), pulse is 95/min, and blood pressure is 115/70 mm Hg. Examination shows a tender, swollen right knee joint; range of motion is limited by pain. The remainder of the examination shows no abnormalities. Arthrocentesis of the right knee is performed. Analysis of the synovial fluid shows:
Appearance Cloudy
Viscosity Absent
WBC count 78,000/mm3
Segmented neutrophils 94%
Lymphocytes 6%
Synovial fluid is sent for culture and antibiotic sensitivity. Which of the following is the most likely causal pathogen?
- A. Staphylococcus aureus
- B. Escherichia coli
- C. Pseudomonas aeruginosa
- D. Staphylococcus epidermidis (Correct Answer)
- E. Streptococcus agalactiae
Bacterial virulence factors Explanation: ***Staphylococcus epidermidis***
- This patient's symptoms (worsening pain and swelling in a knee with a history of **total knee arthroplasty 5 months ago**, increased WBC count and neutrophil predominance in synovial fluid), point towards a **prosthetic joint infection**.
- **Coagulase-negative Staphylococci**, particularly *S. epidermidis*, are the most common cause of **late prosthetic joint infections**, typically occurring months to years after surgery.
*Staphylococcus aureus*
- *Staphylococcus aureus* is a common cause of **acute prosthetic joint infections**, which usually manifest within the **first 3 months post-surgery**. This patient's symptoms began 5 months after surgery.
- While it can cause late infections, *S. epidermidis* is more characteristic for this timeline in prosthetic joint infections.
*Escherichia coli*
- *Escherichia coli* is typically associated with **urinary tract infections** or **gastrointestinal infections**.
- It is an uncommon cause of prosthetic joint infections unless there's a direct spread from a local infection or systemic sepsis, which is not suggested here.
*Pseudomonas aeruginosa*
- *Pseudomonas aeruginosa* is often associated with **healthcare-associated infections**, particularly in immunocompromised patients or those with indwelling catheters or extensive burns.
- While it can cause prosthetic joint infections, it's less common than Staphylococci and usually linked to specific clinical settings or water contamination.
*Streptococcus agalactiae*
- *Streptococcus agalactiae* (Group B Strep) is primarily known to cause serious infections in **neonates** and **pregnant women**, and in adults with underlying conditions like **diabetes** or **immunocompromise**.
- It is an infrequent cause of prosthetic joint infections in otherwise healthy adults without specific risk factors for GBS infection.
Bacterial virulence factors US Medical PG Question 6: A 19-year-old male is found to have Neisseria gonorrhoeae bacteremia. This bacterium produces an IgA protease capable of cleaving the hinge region of IgA antibodies. What is the most likely physiological consequence of such a protease?
- A. Membrane attack complex formation is impaired
- B. Impaired antibody binding to mast cells
- C. Opsonization and phagocytosis of pathogen cannot occur
- D. Impaired adaptive immune system memory
- E. Impaired mucosal immune protection (Correct Answer)
Bacterial virulence factors Explanation: ***Impaired mucosal immune protection***
- **IgA** is the primary antibody mediating **mucosal immunity**, protecting surfaces like the urogenital tract from pathogens.
- Cleavage of IgA by a protease directly compromises its ability to bind to and neutralize pathogens at these mucosal surfaces, facilitating infection.
*Membrane attack complex formation is impaired*
- The **membrane attack complex (MAC)** is primarily formed by components of the **complement system (C5b-C9)**, which is activated by IgG and IgM, not IgA.
- While IgA can activate the alternative pathway of complement, its primary role is not in MAC formation.
*Impaired antibody binding to mast cells*
- **Mast cells** primarily bind **IgE antibodies** via their Fc receptors, leading to degranulation upon allergen binding.
- IgA does not typically bind to mast cells, so IgA protease activity would not directly impact this process.
*Opsonization and phagocytosis of pathogen cannot occur*
- **Opsonization** leading to phagocytosis is predominantly mediated by **IgG antibodies** and **complement proteins (e.g., C3b)**.
- While IgA can contribute to opsonization to some extent, it is not the primary mediator, and its impairment would not completely prevent all opsonization.
*Impaired adaptive immune system memory*
- **Adaptive immune system memory** is largely mediated by **memory B cells** and **memory T cells**, which produce and respond to various antibody isotypes (IgG, IgA, IgM, IgE).
- The cleavage of existing IgA antibodies does not directly impair the generation or function of memory lymphocytes, although it might lead to more frequent infections requiring a new immune response.
Bacterial virulence factors US Medical PG Question 7: A previously healthy 26-year-old woman comes to the physician because of a 2-day history of pain with urination. She has been sexually active with two partners over the past year. She uses condoms for contraception. Vital signs are within normal limits. Physical examination shows suprapubic tenderness. Urinalysis shows neutrophils and a positive nitrite test. Urine culture grows gram-negative, oxidase-negative rods that form greenish colonies on eosin-methylene blue agar. Which of the following virulence factors of the causal organism increases the risk of infection in this patient?
- A. Fimbriae (Correct Answer)
- B. Lecithinase
- C. IgA protease
- D. Biofilm production
- E. Lipoteichoic acid
Bacterial virulence factors Explanation: ***Fimbriae***
- The patient's symptoms (dysuria, suprapubic tenderness), urinalysis findings (neutrophils, positive nitrite), and culture results (gram-negative, oxidase-negative rods, greenish colonies on EMB agar) are highly suggestive of a **urinary tract infection (UTI)** caused by **Escherichia coli**.
- **P-fimbriae (pili)** are crucial virulence factors for *E. coli* in UTIs, enabling the bacteria to **adhere to uroepithelial cells** and colonize the urinary tract.
*Lecithinase*
- **Lecithinase (alpha-toxin)** is a virulence factor primarily associated with bacteria like *Clostridium perfringens*, causing gas gangrene, and some *Bacillus cereus* strains.
- It is not a significant virulence factor for *E. coli* in the context of UTIs.
*IgA protease*
- **IgA protease** is an enzyme produced by bacteria such as *Neisseria gonorrhoeae*, *Neisseria meningitidis*, and *Haemophilus influenzae*.
- It cleaves IgA antibodies, preventing their protective effects at mucosal surfaces, but it is not a primary virulence factor for *E. coli* in UTIs.
*Biofilm production*
- While *E. coli* can form biofilms, particularly in chronic infections or on catheters, **biofilm production** is not the primary mechanism that increases the **initial risk** of acquiring an acute uncomplicated UTI in a healthy individual.
- The *initial* adherence to uroepithelium, facilitated by fimbriae, is key for colonization and infection establishment.
*Lipoteichoic acid*
- **Lipoteichoic acid** is a major component of the cell wall in **Gram-positive bacteria** and contributes to their immune stimulation and adherence properties.
- The causative organism in this case is a **Gram-negative rod**, making lipoteichoic acid an irrelevant virulence factor.
Bacterial virulence factors US Medical PG Question 8: While testing various strains of Streptococcus pneumoniae, a researcher discovers that a certain strain of this bacteria is unable to cause disease in mice when deposited in their lungs. What physiological test would most likely deviate from normal in this strain of bacteria as opposed to a typical strain?
- A. Quellung reaction (Correct Answer)
- B. Hemolytic reaction when grown on sheep blood agar
- C. Bile solubility
- D. Optochin sensitivity
- E. Motility
Bacterial virulence factors Explanation: ***Quellung reaction***
- The **Quellung reaction** tests for the presence of the **polysaccharide capsule**, which is the primary virulence factor of *S. pneumoniae*.
- An **avirulent strain** that cannot cause disease would most likely lack the capsule and show a **negative Quellung reaction** (no capsular swelling), deviating from the **positive reaction** seen in typical encapsulated pathogenic strains.
- The capsule enables *S. pneumoniae* to evade phagocytosis and complement-mediated killing, which is essential for establishing infection in the lungs.
*Hemolytic reaction when grown on sheep blood agar*
- Both virulent and avirulent strains of *S. pneumoniae* typically exhibit **alpha-hemolysis** (partial hemolysis, producing a greenish discoloration) on sheep blood agar due to the production of pneumolysin.
- This characteristic does not differentiate between pathogenic and non-pathogenic strains in terms of disease-causing ability.
*Bile solubility*
- *S. pneumoniae* is characteristically **bile-soluble** due to the presence of autolysin enzymes that are activated by bile salts, leading to cellular lysis.
- This property is a **species characteristic** present in both virulent and avirulent strains, thus it would not explain the inability to cause disease.
*Optochin sensitivity*
- *S. pneumoniae* is universally **sensitive to optochin**, a chemical agent that inhibits its growth and is used for laboratory identification.
- This characteristic is used for **species identification** but does not correlate with strain virulence or disease-causing ability.
*Motility*
- *Streptococcus pneumoniae* is a **non-motile** bacterium; it lacks flagella.
- This characteristic is consistent across all strains and is not a virulence factor for this species.
Bacterial virulence factors US Medical PG Question 9: A 54-year-old woman comes to the physician because of lower back pain, night sweats, and a 5-kg (11-lb) weight loss during the past 4 weeks. She has rheumatoid arthritis treated with adalimumab. Her temperature is 38°C (100.4°F). Physical examination shows tenderness over the T10 and L1 spinous processes. Passive extension of the right hip causes pain in the right lower quadrant. The patient's symptoms are most likely caused by an organism with which of the following virulence factors?
- A. Proteins that bind to the Fc region of immunoglobulin G
- B. Protease that cleaves immunoglobulin A
- C. Polysaccharide capsule that prevents phagocytosis
- D. Surface glycolipids that prevent phagolysosome fusion (Correct Answer)
- E. Polypeptides that inactivate elongation factor 2
Bacterial virulence factors Explanation: ***Surface glycolipids that prevent phagolysosome fusion***
- The patient's symptoms (low back pain, night sweats, weight loss, fever, spinal tenderness, and hip pain) in a patient on **adalimumab** (a TNF-alpha inhibitor) suggest **disseminated tuberculosis** (Pott disease).
- *Mycobacterium tuberculosis* uses **mycolic acids** and other surface glycolipids to prevent phagolysosome fusion, allowing it to survive and replicate within macrophages.
*Proteins that bind to the Fc region of immunoglobulin G*
- This virulence factor is characteristic of bacteria like *Staphylococcus aureus* (Protein A) and *Streptococcus pyogenes* (Protein G), which is not consistent with the clinical picture.
- These proteins interfere with opsonization and antibody-mediated immunity, but are not the primary mechanism of *Mycobacterium tuberculosis* survival within macrophages.
*Protease that cleaves immunoglobulin A*
- **IgA protease** is a virulence factor for bacteria such as *Neisseria gonorrhoeae*, *Neisseria meningitidis*, and *Streptococcus pneumoniae*, which colonize mucosal surfaces.
- This mechanism helps these bacteria evade mucosal immunity, but it is not relevant to the pathogenesis of tuberculosis.
*Polysaccharide capsule that prevents phagocytosis*
- A polysaccharide capsule is a major virulence factor for many encapsulated bacteria (e.g., *Streptococcus pneumoniae*, *Haemophilus influenzae*, *Neisseria meningitidis*) that helps them evade phagocytosis.
- However, *Mycobacterium tuberculosis* is not primarily characterized by a polysaccharide capsule for immune evasion; its internal survival within macrophages is more critical.
*Polypeptides that inactivate elongation factor 2*
- Toxins that inactivate **elongation factor 2** are associated with *Corynebacterium diphtheriae* (**diphtheria toxin**) and *Pseudomonas aeruginosa* (**exotoxin A**), leading to inhibition of protein synthesis.
- This mechanism is not involved in the pathogenesis of *Mycobacterium tuberculosis* infection or its ability to cause disseminated disease.
Bacterial virulence factors US Medical PG Question 10: A 12-year-old boy admitted to the intensive care unit 1 day ago for severe pneumonia suddenly develops hypotension. He was started on empiric antibiotics and his blood culture reports are pending. According to the nurse, the patient was doing fine until his blood pressure suddenly dropped. Vital signs include: blood pressure is 88/58 mm Hg, temperature is 39.4°C (103.0°F), pulse is 120/min, and respiratory rate is 24/min. His limbs feel warm. The resident physician decides to start him on intravenous vasopressors, as the blood pressure is not responding to intravenous fluids. The on-call intensivist suspects shock due to a bacterial toxin. What is the primary mechanism responsible for the pathogenesis of this patient's condition?
- A. Inactivation of elongation factor (EF) 2
- B. Inhibition of GABA and glycine
- C. Inhibition of acetylcholine release
- D. Release of tumor necrosis factor (TNF) (Correct Answer)
- E. Degradation of lecithin in cell membranes
Bacterial virulence factors Explanation: ***Release of tumor necrosis factor (TNF)***
- The patient's presentation with **warm limbs** and **hypotension** despite fluid resuscitation in the setting of severe pneumonia is highly suggestive of **septic shock**.
- **Bacterial toxins**, particularly **endotoxins** from gram-negative bacteria or **exotoxins** like superantigens, trigger a massive **inflammatory response** by stimulating immune cells to release pro-inflammatory cytokines such as **TNF-α**, IL-1, and IL-6, leading to systemic vasodilation and capillary leak.
*Inactivation of elongation factor (EF) 2*
- This is the mechanism of action of **diphtheria toxin** and **exotoxin A** from *Pseudomonas aeruginosa*.
- While these toxins can cause severe systemic illness, their primary role is not typically the induction of septic shock characterized by widespread vasodilation and warm extremities.
*Inhibition of GABA and glycine*
- This mechanism is characteristic of **tetanus toxin**, which prevents the release of inhibitory neurotransmitters and leads to spastic paralysis.
- This is not consistent with the patient's presentation of septic shock.
*Inhibition of acetylcholine release*
- This is the mechanism of action of **botulinum toxin**, which causes flaccid paralysis by blocking acetylcholine release at the neuromuscular junction.
- This effect is not associated with the pathogenesis of septic shock.
*Degradation of lecithin in cell membranes*
- This mechanism is associated with **alpha toxin** of *Clostridium perfringens* (lecithinase), which causes gas gangrene and hemolysis.
- While this toxin contributes to tissue damage in certain infections, it is not the primary mechanism behind the systemic inflammatory response and vasodilation seen in septic shock.
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