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Microbiology/Immunology > Mechanisms of Bacterial Pathogenesis > Flashcards

Mechanisms of Bacterial Pathogenesis Flashcards

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Biology 101 flashcards
1
Q

Asymptomatic, inapparent, subclinical infection

A

-host defenses clear pathogen before any symptoms of disease are noted

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2
Q

Communicable infection

A

can be passed from host to host

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3
Q

Contagious infection

A

-high communicable

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4
Q

Noncommunicable infection

A

-comes from environment, not a previous host (botulism, Legionnaires Disease)

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5
Q

Latent infection

A

-disease subsides, but microorganisms remain in the body and restart disease later

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6
Q

Chronic carrier state

A

-host survives disease but continues to shed the pathogen indefinitely

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7
Q

Epidemic

A

-much more frequent infection than usual

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8
Q

Pandemic

A

worldwide distribution of infection

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9
Q

Parasitism

A
  • pathogens are parasites in the sense that they harm the host by taking its resources to reproduce themselves
  • all viruses and a few bacteria are obligate intracellular parasites, which must enter host cells to reproduce
  • most bacteria are facultative intracellular parasites, meaning that they can reproduce outside host cells when they need to
  • be careful of confusion with parasites, ie protozoa and helminthes
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10
Q

Nonpathogens

A
  • very unlikely to cause disease
  • most environmental bacteria and normal flora
  • very low virulence: LD50 very high
  • ID50 very high
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11
Q

Opportunistic pathogens

A
  • are very unlikely to cause disease in a healthy person, but will take advantage of a host that is injured or immunosuppressed (pseudomonas, enterobacter, klebsiella)
  • low virulence: LD50 is high
  • ID 50 low- easy to colonize
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12
Q

Highly pathogenic organisms

A
  • likely to cause disease on colonization of even a previously-healthy host
  • STDs
  • Mid-High Virulence Mid-Low LD50
  • Mid low ID50
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13
Q

Pathogenicity

A
  • enhanced by virulence factors, which are gene products needed for causing full-blown disease
  • genes for several of these may be encoded together in pathogenicity islands

Functiions: survival in extreme environments, adhesion to host surfaces, take over host cells, and poison the host, immune evasion

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14
Q

Survive extreme environments

A
  • pH tolerance
  • siderophores- bind iron strongly
  • resistance to drying
  • resistance to detergents
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15
Q

Adhesion to host surfaces

A
  • pili/fimbrae especially in movement
  • slime layer
  • adhesions
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16
Q

Immune Evasion

A
  • capsules for resisting phagocytosis
  • IgA proteases
  • induces of macrophage apoptosis
  • antigenic variation- different antigen for part of the infection, and then switch the antigen keeps the host taxed
  • serum resistance factors for escaping complement
17
Q

Host Cell Takeover

A
  • Endosome Escape Routes- Legionella multiplies in phagosome and becomes motile and escapes, lyse the cell and spreads to another
  • Actin Polymerization Pathways- cell to cell spread, Listeria
  • type 3 and 4 secretion systems- type 3 inject proteins into cytooplasm were type 4 transport DNA and proteins
18
Q

Poison the host

A
  • exotoxins (secreted)
  • endotoxins (cell wall components)- Gram(-)- LPS/LOS, Gram (+)- teichoic acids- symptoms are immunogenic so antibody is not protective and vaccination is not useful
  • tissue degrading enzymes- section off itself a place where it isnt bothered by immune system or Oxygen
19
Q

Stages of Pathogens

A

From previous human host:

1) Respiratory droplets
2) Fecal-oral
3) Direct contact
4) Sexual contact
5) Blood blood
6) Vertical- transplacental, vaginal delivery, breast milk

From animal reservoir: zoonosis (rabies)

Fomite (washcloth, countertop)

Vector (tick, mosquito)

20
Q

Attachment of pathogen to host sufaces

A
  • pili/fimbrae
  • glycocalyx/ slime layer
  • adhesins
  • biofilm formation
  • curli- recently-discovered, similar to pili
21
Q

Invasion of host tissue

A
  • collagenase/hyaluronidase: break down tissue so S pyogenes can penetrate
  • coagulase: breaks down fibrinogen to form a fibrin clot around S. aureus
  • IgA protease: cleaves IgA so N. meningitidis can adhere to mucus membranes
  • leukocidins destroy macrophages
  • capsule and M protein are protect against phagocytosis by macrophages
  • S aureus protein A prevents complement acivation
22
Q

Inflammatory response

A
  • pyogenic: pus-forming, predominately neutrophils

- granulomatous: machrophages kill most of the bacteria but some survive inside macrophages within a granuloma

23
Q

Survival inside host cells

A
  • mycobacteria, legionella, brucella, listeria are facultative intracellular
  • chlamydia and rickettsia are obligate intracellular
  • invasins: virulence factors recognized by cell-surface integrins, docking leads to cell entry
  • inhibit fusion of lysosome with phagosome/endosome, so bacteria continue to multiply rather than being degraded (legionella)
  • allow lysosome fusion but inhibit endosome acidification (Legionella, Chlamydia)
  • allows lysosome fusion and survive acidification (Q fever)
  • escape from the endosome into the cytoplasm (Listeria)
  • actin based motility
  • inhibition of cytokine activation
24
Q

Poisoning the host

A
  • pseudomembrane formation: blocks airway in diphtheria, colon in pseudomembraneous colitis
  • exotoxins
25
Q

Exotoxins

A
  • polypeptides
  • secreted from the cell or injected by T3SS
  • the most toxic substances known
26
Q

Themes of Exotoxins

A
  • often encoded on plasmids or bacteriophage rather than bacterial genome
  • common toxic strategies include superantigenicity, interference with signal transduction, depolymerization of actin
  • several exotoxins have similar A-B subunit structure: B delivers A to site of A’s toxic activity, one common activity for A is ADP-ribosylation
  • almost always heat-liable, inactivated toxoids are often useful vaccines
27
Q

Superantigen exotoxins

A
  • undermine specificity of immune response ( activates up to 25% of T cell repertoire as opposed to normal 0.0001- 0.001%
  • can cause shock and multiple organ failure
  • most common: staph aureus, strep pyogenes- toxic shock syndrome
28
Q

Timeline for infectious disease

A

1) incubation period: lag between colonization by organism or exposure to toxin and onset of symptoms
2) Prodrome period: nonspecific immunogenic symptoms like fever and fatigue
3) Specific illness period- pathogen-mediated symptoms to differentiate
4) Recovery/convalescence- pathogen is cleared and the patient regains strength

Microbiology/Immunology (46 decks)

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