Bacterial Pathogens

Which are correct regarding Bacillus anthracis?

Which enzyme allows Yersinia pestis to survive in the midgut of the flea?

There is currently research being done to make an anthrax vaccine. A current candidate for a vaccine is LF (lethal factor) mutant E687C, which induces anti-LF antibody formation but lacks LF enzymatic activity. If a patient was given the E687C mutant as a vaccine but then was exposed to wildtype Bacillus anthracis, what would happen?

Which bacterium does not survive within the host by disabling or killing phagocytic cells?

You are a doctor and have several patients come into your clinic. They have various symptoms: some have skin infections and lesions, some have necrosis of intestines, and some have lung infections. You aren’t concerned because the symptoms don’t seem connected. However, your clinical microbiologist fears an outbreak in your city. What microbe did the clinical microbiologist identify causing infection in all 3 of your patients?

What are the major virulence factors of Bacillus anthracis?

How do the three anthrax toxins participate in pathogenesis?

[blank_start]PA[blank_end] binds to cellular receptors to translocate [blank_start]LF[blank_end] and [blank_start]EF[blank_end] into cells.

What activates the virulence factors in Bacillus anthracis?

[blank_start]Bacillus anthracis[blank_end]: [blank_start]gram-positive[blank_end], [blank_start]spore-forming[blank_end], causes anthrax [blank_start]Yersinia pestis[blank_end]: [blank_start]gram-negative[blank_end], [blank_start]non-sporulating[blank_end], rod shape, [blank_start]causes the plague[blank_end] [blank_start]Treponema pallidum[blank_end]: gram-negative, [blank_start]spirochete[blank_end], [blank_start]causes syphilis[blank_end]

Fill in the blanks for the stages of syphilis. [blank_start]Latent:[blank_end] no signs, but still infected [blank_start]Secondary[blank_end]: skin rashes, mucous membrane lesions, fever, sore throat, headaches, muscle aches, etc. (“The Great Imposter”) [blank_start]Tertiary (years later)[blank_end]: damage to internal organs (heart, eyes, brain) [blank_start]Primary[blank_end]: sores at site of infection

Yersinia pestis rapidly penetrates intact mucous membranes or microscopic dermal abrasions and, within a few hours, enters the lymphatics and blood to produce systemic infection

[blank_start]T. pallidum[blank_end] evades the immune system via antigenic variation of [blank_start]TprK,[blank_end] a surface-exposed protein On contact with host macrophages, [blank_start]Yersinia pestis[blank_end] injects [blank_start]Yops[blank_end] resulting in the silencing of the pro-inflammatory cytokine response and in apoptotic death of the infected macrophages In [blank_start]Bacillus anthracis[blank_end], [blank_start]protective antigen[blank_end] binds to cellular receptors to translocate [blank_start]lethal factor[blank_end] and [blank_start]edema factor[blank_end] into cells. The toxins alter cell signaling pathways in the host to interfere with innate immune responses in early stages of infection and to induce vascular collapse at late stages.

Which transmission routes are possible for Bacillus anthracis?

What are the possible transmission routes for Yersinia pestis?

Which of the following methods of contact would result in transmission of syphilis?

What is the secretion system of Yersinia pestis?

Which of the following pathogens does not have endotoxin?

Yersiniz pestis [blank_start]lesions[blank_end], [blank_start]skin infection[blank_end], [blank_start]lung infection[blank_end] Bacillus anthracis [blank_start]necrosis of intestines[blank_end], [blank_start]lung damage[blank_end], skin infection Treponema pallidum [blank_start]inflamed arteries[blank_end], sores on hands, [blank_start]fever[blank_end], [blank_start]headache[blank_end]