Chapter 25: Host-Pathogen Interactions Flashcards

1
Q

opportunistic pathogens

A

many elements of normal flora act as opportunistic pathogens in susceptible hosts (heart disease, immunosuppression, radiation therapy, chemotherapy, MRSA)

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1
Q

obligate pathogens

A

never part of normal flora, always cause disease, usually require host for multiplication (HIV, hansen’s disease/leprosy)

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2
Q

mucous membrane barrier

A

first line of defense against pathogens
secrets glycoproteins (retain water)
lysozymes
antibodies
averts infection by flushing: sneezing, swallowing, erosion etc.

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3
Q

virulence

A

relative ability to cause disease

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4
Q

virulence factors

A

structures or molecules of an organism that increase its pathogenicity

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5
Q

examples of virulence factors

A

flagella- motility, attachment
frimbriae- attachment
capsule- concealment, attachment
adhesions- receptors of pathogen surface, glycoproteins, lipoproteins
exotoxins
endotoxins

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6
Q

endotoxin

A

structural part of outer membrane
secreted as part of normal physiological activity during membrane vesicle trafficking while also excreting other virulence factors and proteins
set free passively when cells die or disintegrated

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7
Q

lipopolysaccharide (lps) layer

A

replaces most of phospholipids in outer half of outer membrane
lipid a- host receptor recognition, differing chemistry among species
lps/lipid a structure determines immunogenicity
can cause inflammatory reactions
disregulation of: immune system, clotting cascade, blood pressure regulation
results in: fever, wbc count, hemorrhaging/clotting/ lowered bp, shock, death

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8
Q

exotoxins

A

inhibits host cell function or kills host cells
proteins release from pathogen cells as it grows

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9
Q

categories of exotoxins

A

cytolytic toxins, ab-toxins, superantigen toxins

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10
Q

cytolytic toxins

A

work by degrading cytoplasmic membrane integrity causing cell lysis and death

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11
Q

examples of cytolytic toxins

A

hemolysin: lyses RBCs
leukocidin: lyces WBCs
phospholipases: hydrolyze phospholipids into fatty acids

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12
Q

diptheria ab-exotoxin

A

blockage of protein synthesis
causes thick covering in back of throat
leads to difficulty breathing, heart failure, paralysis, death

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13
Q

neurological exotoxins

A

botulinum and tetanus

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14
Q

clostridium tetani and botulinum

A

produce potent AB-exotoxins that affect nervous tissue
botulinum toxins most potent biological toxins known

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15
Q

tetanus

A

opposite effect of botulinum
muscular rigidity/arrest in tension
rigid paralysis

16
Q

enterotoxin

A

ab-exotoxins whose activity affects small intestine
cause massive secretion of fluid into lumen, vomiting and diarrhea
cholera toxin in vibrio cholerae

17
Q

superantigens

A

cause overstimulation of immune sytstem
shock and death
due to localized infecion with systemic effects
can cause bacteremia or septicemia
causes non specific activation of t-cells resulting in polyclonal t-cell activation and massive cytokine release
fever, kidney disruption, liver etc.

18
Q

exo-enzymes as virulence factors

A

invasiveness requires a pathogen break down host tissues, often done with enzymes that attack host cells

19
Q

examples of exo-enzymes as virulence factors

A

enzymes that
break down tissue
manipulate clotting of fibrin

20
Q

measuring virulence

A

not how many factors, bu how aggressively an infection and disease is established
estimated from experimental studies of LD50

21
Q

highly virulent pathogens

A

show little difference in number of cells required to kill 100% of population

22
Q

compromised host

A

one or more resistance mechanisms are inactive:
genetic predisposition
permanent primary infection
temporary condition
medical procedures
predispose individuals to develop disease

23
Q

attenuation

A

decrease or loss of virulence
attenuated strains are valuable to clinical medicine, used as vaccines