Host Microbe Interactions Flashcards

1
Q

Infection is…

A

the process whereby a microbe enters into a relationship with the host. It may or may not cause disease.

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2
Q

An infectious disease is a

A

disease caused by an infection with a microbe. Some infections are communicable (transmitted from patient to patient); others are not communicable and are not

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3
Q

Define pathogenicity and virulence

A

Pathogenicity is the ability to cause disease, and virulence is the degree

Contemporary view: microbial AND host factors contribute to the outcome of an ID. From this “damage-response” framework…
pathogen = microbe capable of causing host damage
virulence = relative capacity of a microbe to cause damage in a susceptible host,
virulence factor = microbial component that can damage a susceptible host.

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4
Q

Explain how a microbe is shown to be the cause of a specific disease

A
  1. Specific microbes are present regularly in characteristic lesions of the disease.
  2. The specific microbes can be isolated and grown in vitro.
  3. Injection of the cultured microbes into animals reproduces the disease seen in humans.
  4. The specific microbes can be re-isolated from lesions of the disease in animals.
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5
Q

Describe typical stages in pathogenesis of an infectious disease and explain their importance.

A

How does the agent…

  1. Encounter: What is the ROA? What is the dose?
  2. Entry: Cross epithelium? Active or passive? Consider colonization of surface and adherence
  3. Spread: Spreading factors (-ase) move through tissue. Coagulase does opposite (wall off)
  4. Multiplication: rate must be > clearance. Thus, in vivo rate may be < in vitro rate
  5. Tissue damage: how by agent or host? virulence factors? Possibilities: direct damage or interfere w/ defense via surface molecules, secreted products, injected products (all targets for vaccine)
  6. Outcome: who wins or coexist? what are the consequences? “survival of obligate parasites depends on a satisfactory portal of exit from the infected host as well as on a portal of entry.”
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6
Q

Compare mechanisms of innate and acquired host defense against infections.

A

Multiply inside tissue cell? make Ab to prevent virus entry (not attachment) then maybe kill the cell
Multiply inside phagocytes? activate (and maybe kill) the phagocyte via T cells
Multiply outside cells? Kill microbe extracellularly via complement or intracellularly with opsonization

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7
Q

Describe the composition of the normal flora of the body.

A

Skin: Staph, Coryne, Enteric bacilli
Oropharynx: a-hemolytic strep, gaffyka, coryne, neisseria, hemophilus bacteroides, mycoplasma spirochetes
Large intestine: micrococcus, strep, lactobacilli, enteric bacilli, clostridia, bacteroides
Vag: strep, lactobacilli, bacteroides, mycoplasma

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8
Q

Describe the importance of the normal flora of the body.

A
  1. Effects on tissue/organ differentiation (normal vs. germfree animals).
  2. Production of vitamins by gut flora.
  3. Biochemical conversions (e.g., bilirubin degradation, drug metabolism, production of potential carcinogens, etc.)
  4. Competition with pathogens for colonization of body surfaces. Source of agents for endogenously acquired infections.
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9
Q

Compare several disease paradigms that illustrate selected mechanisms of pathogenesis

A

Cholera: typical of non-invasive bacteria. It’s ingested, it adheres to small intestine, and then it secretes toxins that case diarrhea. TOXIN damages cells, not the bacterium.

Pneumococcal pneumonia: typical of bacteria that multiply extracellularly. It replicates outside cells (and can get away with it because it has an anti-phagocytic capsule), it grows, and it eventually causes tissue damage in the lung. The host eventually produces antibodies that coat its capsule and cause it to be destroyed.

Tuberculosis: typical of bacteria that multiply intracellularly. Invades macrophages and replicates inside their vacuoles. The host defends itself by T-cell-mediated response, activating the affected macrophages to develop internal granules which kill microbes.

Rheumatic fever: typical of a pathology mediated by an immune response. Occurs after streptococcal infection– the immune response to the strep infection is the thing that causes an autoimmune fever to sprout up a couple of weeks later. Here, the microbe is not directly (although indirectly) responsible for the fever.
Compare mechanisms of innate and acquired host defense against infections

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