Bacillus anthracis & Anthrax

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Questions and Answers

Which virulence factor of Bacillus anthracis is MOST directly responsible for the fluid accumulation observed in cutaneous anthrax?

  • Lethal toxin, stimulating macrophages to release proinflammatory cytokines.
  • The D-glutamate capsule, inhibiting phagocytosis.
  • Protective antigen, facilitating toxin entry into cells.
  • Edema toxin, increasing intracellular cAMP levels. (correct)

Why is the protective antigen (PA) of Bacillus anthracis considered the MOST effective target for vaccine development?

  • Antibodies against PA prevent both edema toxin and lethal toxin from entering host cells. (correct)
  • It inhibits the formation of the characteristic eschar in cutaneous anthrax.
  • It directly neutralizes the lethal toxin's metalloprotease activity.
  • It stimulates a strong cytotoxic T-cell response that clears the bacteria.

A researcher is investigating potential therapeutic targets for Bacillus anthracis. Which of the following mechanisms would MOST effectively inhibit the function of lethal toxin?

  • Preventing the cleavage of MAP-kinase. (correct)
  • Blocking the release of TNF-alpha and IL-1beta from macrophages.
  • Cleaving the D-glutamate capsule.
  • Inhibiting adenylate cyclase activity.

A patient presents with a painless papule that rapidly progressed to a necrotic ulcer surrounded by vesicles. Gram staining is performed. Which additional test would be MOST useful in confirming a diagnosis of cutaneous anthrax?

<p>Spore stain of the lesion sample. (D)</p> Signup and view all the answers

Which factor contributes to the high mortality rate associated with pulmonary anthrax, even with antibiotic treatment?

<p>The delayed onset of specific symptoms, leading to advanced disease at diagnosis. (D)</p> Signup and view all the answers

In a scenario where a large population is potentially exposed to aerosolized Bacillus anthracis spores, what public health intervention would be MOST effective in preventing widespread disease?

<p>Post-exposure vaccination with the anthrax vaccine, combined with antibiotic prophylaxis. (D)</p> Signup and view all the answers

What is the MOST critical difference between cutaneous and inhalation anthrax in terms of disease progression and prognosis?

<p>Inhalation anthrax involves a prolonged latent period and rapid progression to systemic disease, while cutaneous anthrax is localized. (A)</p> Signup and view all the answers

A veterinarian is called to a farm where several sheep have died suddenly. Upon necropsy, the veterinarian suspects anthrax. What immediate steps should the veterinarian take to prevent further spread of the disease?

<p>Burn or bury the carcasses of the dead animals and vaccinate the remaining herd. (D)</p> Signup and view all the answers

How does Bacillus anthracis's mechanism of cell entry differ from that of other toxin-producing bacteria?

<p>It uses a protective antigen to facilitate the entry of edema and lethal toxins into cells. (C)</p> Signup and view all the answers

If a laboratory is culturing Bacillus anthracis for diagnostic purposes, what specific biosafety precautions are MOST critical to implement to prevent accidental exposure?

<p>Performing all procedures within a certified biosafety level 3 (BSL-3) cabinet with appropriate PPE and controlled access. (C)</p> Signup and view all the answers

Flashcards

Bacillus anthracis

A gram-positive, spore-forming, nonmotile bacterium that causes anthrax. Primarily a disease of herbivores, it can infect humans through skin trauma, inhalation, or ingestion.

B. anthracis Capsule

This capsule inhibits phagocytosis by immune cells, enhancing the bacterium's ability to cause infection.

Edema Toxin

Exotoxin that has adenylate cyclase activity that increases cAMP levels, leading to fluid accumulation and edema.

Lethal Toxin

Zinc metalloprotease that cleaves MAP-kinase, causing cellular death, and stimulates macrophages to release TNF-alpha, IL-1beta, and proinflammatory cytokines.

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Protective Antigen (PA)

Binds to host cells, allowing entry of edema and lethal toxins. Antibodies against this protein are protective.

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Cutaneous Anthrax

Starts as a painless papule and progresses to an ulcer surrounded by vesicles, then a necrotic eschar.

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Inhalation Anthrax

Inhaled spores cause initial nonspecific symptoms (fever, myalgia) followed by rapid deterioration, mediastinal lymph node enlargement, respiratory failure and sepsis. Pneumonia is rare.

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Gastrointestinal Anthrax

Ulcers form in the mouth/esophagus or cecum/ileum, leading to regional lymphadenopathy, edema, and sepsis.

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Anthrax Diagnosis

Diagnosis involves Gram-stain, spore detection in smears, nonhemolytic colonies on blood agar, PCR, fluorescent antibody test, and ELISA.

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Anthrax Treatment & Prevention

Treatment with ciprofloxacin or doxycycline. Prevention includes vaccination of animal herds and proper disposal of infected animals.

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Study Notes

  • Bacillus anthracis causes anthrax, a disease more common in animals but rare in humans.
  • It is a Gram-positive, nonmotile, spore-forming bacterium.
  • On sheep blood agar, Bacillus anthracis colonies appear large, dry, with a "ground-glass" surface, irregular edges, sticky, and nonhemolytic.
  • Entry occurs via skin trauma, inhalation of spores into the lungs, or ingestion of contaminated meat.
  • Primarily a disease affecting herbivores.

Virulence Factors

  • Antiphagocytic capsule is composed of D-glutamate.
  • Edema toxin: has adenylate cyclase activity, increases cAMP, and causes fluid accumulation.
  • Lethal toxin: zinc metalloprotease activity cleaves MAP-kinase causing cell death and stimulates macrophages to release TNF-alpha, IL-1beta, and other proinflammatory cytokines.
  • Protective antigen: binds and allows edema toxin and lethal toxin to enter cells and is the most immunogenic component; antibodies against it are protective.

Cutaneous Anthrax

  • If left untreated, there is a 20% mortality rate.
  • Starts as a painless papule at the site of inoculation.
  • Progresses to an ulcer surrounded by vesicles, then to a necrotic eschar (dry, thick, black or dark brown crust).
  • Systemic signs include painful lymphadenopathy and massive edema.

Pulmonary/Inhalation Anthrax

  • Has a prolonged latent period with nonspecific initial symptoms like fever, myalgias, nonproductive cough, and malaise.
  • The second stage involves rapid worsening with fever, edema, massive enlargement of mediastinal lymph nodes, respiratory failure, and sepsis.
  • Pneumonia is rare, but meningeal symptoms occur in about half of the patients.
  • Can progress to shock and death within 3 days.

Gastrointestinal Anthrax: Upper Intestinal Tract

  • Ulcers form in the mouth or esophagus, accompanied by regional lymphadenopathy, edema, and sepsis.

Gastrointestinal Anthrax: Cecum or Terminal Ileum

  • Symptoms include nausea, vomiting, and malaise, rapidly progressing to systemic disease; mortality rate is 100% without treatment.

Diagnosis

  • Gram-stain, spores in smears, nonhemolytic colonies on blood agar, PCR, fluorescent antibody test, ELISA.

Treatment and Prevention

  • Treatment includes ciprofloxacin and doxycycline.
  • Preventative measures include vaccination of animal herds in endemic regions and burning or burial of animals that die of anthrax.
  • Vaccination is recommended for people in endemic areas, those working with imported animal products, and military personnel.

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