Yersinia Pestis: Plague Microbiology

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Questions and Answers

Which virulence factor of Yersinia pestis directly inhibits phagocytosis by forming a protective capsule?

  • Plasminogen activator protease
  • Capsular fraction 1 (F1) (correct)
  • LcrV antigen
  • Yersinia outer proteins (Yops)

A patient presents with high fever, chills, and a rapidly developing pneumonia with hemoptysis. His history includes recent travel to a region known for plague outbreaks. Which diagnostic method would provide the most rapid and specific confirmation of pneumonic plague in this acute setting?

  • Sputum Gram stain
  • Blood culture on MacConkey agar
  • Rapid antigen test for capsular F1 antigen on sputum (correct)
  • Chest X-ray

What is the primary mechanism by which the Type III secretion system in Yersinia pestis contributes to its virulence?

  • Degrading complement proteins C3b and C5a
  • Blocking proinflammatory cytokine secretion in macrophages (correct)
  • Capturing iron from the host to facilitate bacterial survival
  • Activating plasminogen to promote bacterial spread

Disseminated intravascular coagulation (DIC) is a severe complication of septicemic plague. Which mechanism directly triggers DIC in this context?

<p>Secretion of endotoxins by the bacteria (A)</p> Signup and view all the answers

A researcher is investigating potential therapeutic targets for plague. Which of the following would be the MOST effective target to simultaneously disrupt multiple stages of Yersinia pestis's infection cycle?

<p>An agent that inhibits the Type III secretion system (B)</p> Signup and view all the answers

Why is prompt treatment with antibiotics crucial in cases of suspected plague, even before definitive diagnostic confirmation?

<p>To halt the progression of the disease and prevent potential complications such as septicemia and pneumonic plague (A)</p> Signup and view all the answers

How does the plasminogen activator protease produced by Yersinia pestis contribute to its virulence?

<p>degrading complement proteins C3b and C5a. (D)</p> Signup and view all the answers

A public health officer is investigating a cluster of plague cases in a rural community. Which intervention strategy would be MOST effective in preventing future outbreaks?

<p>Implementing rodent control measures and educating the community about avoiding contact with wild animals. (B)</p> Signup and view all the answers

What role do V and W antigens play in the pathogenesis of Yersinia pestis infection?

<p>allowing the organism to survive and grow intracellularly (D)</p> Signup and view all the answers

Doxycycline and streptomycin are commonly used in combination to treat plague. What is the MOST likely reason for using this combination therapy?

<p>To target different stages of the bacterial infection and enhance efficacy (A)</p> Signup and view all the answers

Flashcards

Yersinia pestis

Gram-negative coccobacillus that causes plague.

Fraction 1 (F1) antigen

Capsule that evades phagocytosis.

Plasminogen activator protease

Protease that degrades complement proteins C3b and C5a.

Type III secretion system

System injecting yops, blocking proinflammatory cytokine secretion.

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Enzootic (sylvatic) cycle

Cycle between fleas and rodents.

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Epizootic (urban plague) cycle

Cycle that is an outbreak amongst animals.

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Buboes

Swollen, painful lymph nodes, especially in groin or axilla.

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Septicemia plague

Plague form with endotoxins, DIC, tissue necrosis.

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Pneumonic plague

Plague form with rapid pneumonia, hemoptysis.

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Plague treatment

Streptomycin, tetracycline, or levofloxacin.

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Study Notes

  • Plague is caused by the gram-negative coccobacillus Yersinia pestis.
  • Yersinia pestis displays bipolar staining with Wright-Giemsa and Wayson stains.
  • It is non-spore forming and highly motile due to flagella.
  • This bacterium is a facultative anaerobe and can live and multiply both inside and outside of host cells.
  • Yersinia pestis is oxidase and urease negative, and it is a non-lactose fermenter.
  • It grows on MacConkey agar (colorless colonies), sheep blood agar, and chocolate agar.
  • Rodents, prairie dogs, livestock, and rabbits are carriers.
  • Fleas serve as vectors, regurgitating bacteria into the bite wound.
  • Humans are hosts, and transmission can occur through contaminated surfaces and water droplets.
  • The enzootic cycle (sylvatic) takes place between fleas and rats, while the epizootic cycle (urban plague) is an outbreak amongst animals.

Virulence Factors

  • Capsular fraction 1 (F1) and LcrV antigen contribute to virulence allowing survival.
  • F1 is a surface protein that forms a capsule around Yersinia pestis, aiding in the evasion of phagocytosis.
  • LcrV antigen is part of the Type III secretion system.
  • Plasminogen activator protease degrades complement proteins C3b and C5a.
  • The Type III secretion system injects Yersinia outer proteins (Yops) into macrophages, blocking proinflammatory cytokine secretion.
  • Siderophore molecules help Yersinia pestis capture iron for survival.
  • It contains endotoxin and exotoxin.
  • V and W antigens allow the organism to survive and grow intracellularly.
  • Macrophages burst, leading to the spread of bacteria.

Forms of Plague

  • Bubonic, septicemia, and pneumonic are the three forms of plague.

Bubonic Plague

  • The incubation period is under 7 days.
  • Symptoms include high fever, chills, and fatigue.
  • It spreads to cells near lymph nodes, causing swollen lymph nodes (buboes) in the groin or axilla.

Septicemia Plague

  • Septicemia plague starts in lymph nodes and enters the bloodstream.
  • It secretes endotoxins, leading to hypotension, malaise, and purpuric skin lesions.
  • It causes excessive production of thrombin, leading to disseminated intravascular coagulation (DIC).
  • Symptoms include tissue necrosis, multiorgan failure, and death.

Pneumonic Plague

  • Pneumonic plague starts with bacteria spreading to the lungs via the bloodstream or through inhalation of droplets from another patient.
  • The incubation period is 1-3 days.
  • Symptoms include fever, headaches, weakness, and a rapidly developing pneumonia with shortness of breath, chest pain, cough, and hemoptysis.

Diagnosis

  • Rapid development of a swollen and painful lymph gland + flea bite + travel to western U.S. or endemic area are indicators.
  • Collect samples from blood, pus from bubo, or sputum.
  • Diagnosis involves fluorescent staining, rapid antigen test for capsular F1 antigen, and chest x-ray.

Treatment

  • Treatment should begin immediately, before confirming diagnosis.
  • Treatment options include a combination of streptomycin and tetracycline (such as doxycycline), streptomycin alone, or levofloxacin.

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