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Questions and Answers
What is the most critical implication of Yersinia pestis's ability to degrade complement proteins C3b and C5a through its plasminogen activator protease?
What is the most critical implication of Yersinia pestis's ability to degrade complement proteins C3b and C5a through its plasminogen activator protease?
- It directly inhibits the adaptive immune response by preventing T-cell activation.
- It promotes bacterial dissemination by inhibiting opsonization and phagocyte migration. (correct)
- It enhances biofilm formation, increasing resistance to antibiotics and host defenses.
- It disrupts the coagulation cascade, leading to uncontrolled bleeding and hemorrhage.
How does the Type III secretion system in Yersinia pestis contribute to its virulence, specifically in the context of macrophage interaction?
How does the Type III secretion system in Yersinia pestis contribute to its virulence, specifically in the context of macrophage interaction?
- By stimulating the release of pro-inflammatory cytokines, causing a localized inflammatory response that attracts more immune cells.
- By enhancing phagocytosis, leading to the rapid clearance of the bacteria from the host's system.
- By injecting Yersinia Outer Proteins (Yops) that block pro-inflammatory cytokine secretion, disabling macrophage-mediated immune response. (correct)
- By directly activating apoptosis in macrophages, inducing rapid cell death and preventing antigen presentation.
In the pathogenesis of septicemic plague, what is the primary mechanism by which Yersinia pestis induces disseminated intravascular coagulation (DIC)?
In the pathogenesis of septicemic plague, what is the primary mechanism by which Yersinia pestis induces disseminated intravascular coagulation (DIC)?
- Direct activation of platelets, leading to the formation of microthrombi throughout the vasculature.
- Inhibition of natural anticoagulants, such as antithrombin and protein C, leading to an imbalance in the coagulation system.
- Secretion of tissue factor, initiating the extrinsic pathway of the coagulation cascade.
- Release of bacterial lipopolysaccharide (LPS), triggering systemic inflammation and activation of the coagulation cascade. (correct)
A patient presents with fever, headache, weakness, and rapidly developing pneumonia with hemoptysis after recent travel to a plague-endemic area. What is the most critical next step in managing this patient?
A patient presents with fever, headache, weakness, and rapidly developing pneumonia with hemoptysis after recent travel to a plague-endemic area. What is the most critical next step in managing this patient?
Why does Yersinia pestis form colorless colonies on MacConkey agar?
Why does Yersinia pestis form colorless colonies on MacConkey agar?
In the context of plague transmission, what distinguishes the enzootic (sylvatic) cycle from the epizootic (urban) cycle?
In the context of plague transmission, what distinguishes the enzootic (sylvatic) cycle from the epizootic (urban) cycle?
What is the significance of the V and W antigens in the virulence of Yersinia pestis?
What is the significance of the V and W antigens in the virulence of Yersinia pestis?
How does the capsular F1 antigen contribute to the virulence of Yersinia pestis?
How does the capsular F1 antigen contribute to the virulence of Yersinia pestis?
What is the rationale behind using a combination of streptomycin and tetracycline (like doxycycline) as the treatment of choice for plague?
What is the rationale behind using a combination of streptomycin and tetracycline (like doxycycline) as the treatment of choice for plague?
A researcher is studying Yersinia pestis and observes that the bacteria exhibit bipolar staining with Wright-Giemsa and Wayson stains. What is the most accurate interpretation of this observation?
A researcher is studying Yersinia pestis and observes that the bacteria exhibit bipolar staining with Wright-Giemsa and Wayson stains. What is the most accurate interpretation of this observation?
Flashcards
Yersinia pestis
Yersinia pestis
Gram-negative coccobacillus bacteria causing plague, characterized by bipolar staining resembling safety pins.
Plague Transmission
Plague Transmission
Wild rodents are reservoirs; fleas transmit the bacteria via regurgitation into the bite wound.
Y. pestis Virulence Factors
Y. pestis Virulence Factors
Capsule (F1 antigen), plasminogen activator protease, and Type III secretion system that injects Yops.
Bubonic Plague
Bubonic Plague
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Septicemic Plague
Septicemic Plague
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Pneumonic Plague
Pneumonic Plague
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Plague Rapid Antigen Test
Plague Rapid Antigen Test
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Plague Treatment
Plague Treatment
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Study Notes
- Plague is caused by the Gram-negative coccobacillus Yersinia pestis.
- Yersinia pestis belongs to the Enterobacteriaceae family.
- Wright-Giemsa and Wayson staining shows bipolar staining, with only the poles of the bacteria staining, resembling safety pins.
- Yersinia pestis is non-motile, non-spore forming, facultative anaerobic, and facultative intracellular.
- It tests negative for oxidase and urease but positive for catalase.
- Yersinia pestis produces colorless colonies on MacConkey agar as a non-lactose fermenter.
- On sheep blood agar and chocolate agar, it forms opaque yellow colonies resembling fried eggs.
Epidemiology and Transmission
- Reservoirs include rodents, livestock, rabbits, and prairie dogs, especially in the U.S.
- Fleas act as hosts and vectors, transmitting the bacteria through regurgitation into the bite wound.
- Humans are accidental hosts.
- Infection can occur through handling tissue or body fluids of infected animals.
- Pneumonic plague spreads through respiratory droplets.
- The enzootic (sylvatic) cycle involves transmission among wild rodents by fleas.
- The epizootic (urban plague) cycle refers to outbreaks among animals; humans are more at risk during these outbreaks
- Plague is endemic in wild rodents in the Western United States, but 99% of cases occur in Southeast Asia.
Virulence Factors and Pathogenesis
- Capsule contains F1 antigen with anti-phagocytic properties.
- Plasminogen activator protease degrades complement components C3b and C5a, preventing opsonization and phagocytic migration.
- Type III secretion system injects Yersinia outer membrane proteins into macrophages, blocking secretion of pro-inflammatory cytokines like TNF alpha and IL-8, and inactivates macrophages.
- Virulence factors include Yersiniabactin, endotoxin, exotoxin, V antigen, and W antigen.
- V and W antigens allow the organism to survive and grow intracellularly.
- These virulence factors cause macrophages to burst, spreading bacteria throughout the body and causing three forms of the disease.
Bubonic Plague
- Develops when Yersinia pestis spreads to nearby cells in the lymph nodes, causing swelling (buboes).
- Incubation period is two to more than seven days.
- Symptoms: high fever and painful buboes in the groin or axillary regions.
Septicemic Plague
- Yersinia pestis enters the bloodstream from the lymph nodes.
- The bacteria secretes endotoxins, causing excess thrombin production, leading to disseminated intravascular coagulation (DIC).
- DIC causes tiny clots throughout the body, leading to tissue necrosis.
- Symptoms include hypotension, malaise, purpuric skin lesions, and tissue necrosis (black regions on the limbs).
- Can cause multi-organ failure and death if untreated.
Pneumonic Plague
- Can develop in two ways: bacteria spreading to the lungs from the bloodstream (secondary pneumonic plague) or through inhalation of respiratory droplets from another patient (primary pneumonic plague).
- Incubation period is usually one to three days.
- Symptoms include fever, headache, weakness, and rapidly developing pneumonia with shortness of breath, chest pain, cough, and sometimes bloody or watery mucus.
Diagnosis
- Plague is suspected in people living in or recently traveled to the western United States or other endemic areas.
- Common signs include rapid development of swollen and painful lymph glands, a known flea bite, or the presence of a bubo.
- Smear and culture of blood or pus from the bubo is the best diagnostic procedure.
- Giemsa or Wayson stain reveals the typical safety pin appearance of the bacteria.
- Fluorescent antibody staining can identify the organism in tissues.
- A rise in antibody titer to the envelope antigen can be useful retrospectively.
- A rapid antigen test can identify Yersinia pestis F1 antigen in sputum or serum.
- Chest X-ray can be used for the diagnosis of pneumonic plague.
Treatment
- Should be started immediately.
- Combination of streptomycin and tetracycline (e.g., doxycycline) is the treatment of choice.
- Streptomycin or levofloxacin can also be used.
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