Lecture 3: microbial pathogenesis Flashcards

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1
Q

Koch’s postulates

A
  1. suspected germ must be present in every case of disease
  2. germ must be isolated and grown in pure culture
  3. cultured germ must cause disease when inoculated into a healthy host
  4. same germ must be reisolated from the diseased experimental host
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2
Q

gold standard in establishing cause of infection

A

PCR

  • identifies cause of disease using a single copy of DNA or RNA
  • potential problems due to normal flora
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3
Q

colonization

A
  • involves a transient or permanently established microbial growth
  • NO interference with normal body function
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4
Q

Infection

A
  • involves a transient or permanently established microbial growth
  • may manifest disease
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5
Q

disease

A
  • abnormal condition of body structures and function
  • occurs when interaction leads to pathogenesis
  • CAN occur without presence of microbe
    • toxins from microbes can cause intoxications
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6
Q

how can different organisms lead to disease with similar signs and symptoms

A

due to similar pathogenicity mechanisms

  • ex: conjunctivitis
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7
Q

how can the same organims lead to disease with different signs and symptoms

A
  • due to different pathogenicity mechanisms
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8
Q

stages of disease: incubation (preclinical) stage

A
  • pathogen has entered body
  • no signs or symptoms
  • innate immune system has not been activated
  • not contagious
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9
Q

stages of disease: Prodromal (warning) stage

A
  • appearance of signs and symptoms (non specific)
  • activation of innate immune system
  • pathogen numbers increase
  • easily transmitted even before person realizes they are sick
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10
Q

stages of disease: acute stage; clinical illness

A
  • most severe time of illness
  • characteristic signs and symptoms
  • acquired immune system has been activated
  • pathogen numbers are stationary
  • communicable diseases are easily transmitted
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11
Q

stages of disease: decline stage

A
  • illness is still apparent but signs and symptoms dwindle
  • immune system activity is reduced (Antibodies formed)
  • pathogen cleared from host
  • can be contagious if individual becomes carrier
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12
Q

stages of disease: convalescent stage

A
  • patient returns to full health
  • signs and symptoms end
  • no immune system activity
  • not contagious
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13
Q

mechanisms of bacterial virulence

A
  • metabolites
  • invasins
  • adhesins
  • toxins
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14
Q

mechanisms of bacterial virulence: tissue damaging metabolites

A
  • acids, gases, or other byproducts of metabolism formed during bacterial growth
  • serve to directly damage host tissues
  • ex: strep mutans produces lactic acid which results in dental caries
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15
Q

mechanisms of bacterial virulence: invasins or “spreading factors”

A
  • proteins or enzymes that act locally to damage host cells
  • affect tissue matrices and intracellular spaces
    • allow for spread and replication of bacterium
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16
Q

mechanisms of bacterial virulence: adhesins

A
  • bind pathogens to receptors on host cells and tissues
  • most bind to glycoproteins
17
Q

name 3 types of adhesins

A
  1. glycocalyx material
    1. capsule and slime layers
  2. fimbriae and pili
    1. attach to specific host molecules
  3. afimbrial adhesins
    1. proteins associated with cell envelope (wall/membrane)
18
Q

mechanisms of bacterial virulence: toxins

A

proteins with high activity and specificity and are heat labile

19
Q

exotoxins are found in gram cells

A

both gram negative and positive cells

20
Q

exotoxins

A
  • proteins taht are toxic to cells, usually direct in action
  • secreted into the extracellular fluid or assocaited with the bacterial cell surface
  • bind host cell receptors
21
Q

enterotoxins

A

exotoxins that cause GI signs and symptoms

22
Q

what are the two main categories of exo/enterotoxins

A

A-B exotoxins

23
Q

function of A and B in A-B exotoxins

A
  • A- Attacks cells
  • B- binds toxin to host receptor
    • after binding, A is transported into cell
    • can form toxoids
24
Q

toxoids

A

inactivated toxins

25
Q

superantigens

A
  • toxins
  • activate up to 40% T cells in absense of antigen
  • result in massive release of cytokines
26
Q

name three membrane active exotoxins

A
  1. proteases
    1. destroy protein in host cell (cell membrane)
  2. lipases: destroy lipids in cell membranes
  3. hemolysins: form pores in RBC and phagocytes
27
Q

Name endotoxin of gram negative organisms

A
  • LPS (not very toxic until released)
    • O antigen
    • Lipid A
28
Q

virulence mechanisms: encapsulation

A

blocks phagocytosis

  • ex: S. pneumoniae capsule
29
Q

virulence mechanisms: inactivation of antibody

A
  • S. pneumoniae secretes IgA degrading proteases
  • S. aureus binds to Fc region of IgG
30
Q

virulence mechanisms: intracellular growth

A
  • escape detection so host can’t initiate an immune response
31
Q

virulence mechanisms: antigenic variation

A
  • ability of a microbe to
    • change epitopes
    • present new antigens to immune system
    • initiates new cycle of disease
32
Q

Antigenic drift

A
  • accumulation of genetic mutations
  • alters protein products
  • leads to variability in population
  • form antigenically distinct strains
33
Q

Antigenic shift

A
  • reassortment of viral genome
  • in cell infected by 2 strains of influenza A
  • produces a new subtype of virus
    • can create flu pandemics
34
Q

Antigenic switching

A
  • can result from genetic conversion/shuffling
  • due to recombination within group of genes
  • results in new surface antigen, but no change in biological function