Bacterial Pathogenesis Flashcards

1
Q

what are the key clinical themes of microbiology

A

detection
treatment
prevention

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2
Q

what is a pathogen

A

an organism capable of causing disease

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3
Q

what is a commensal

A

an organism that is part of the normal flora

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4
Q

what is pathogenecity

A

the ability to cause disease

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5
Q

what is virulence

A

the ability to cause severe disease

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6
Q

what is the life cycle of a pathogen

A

enter
attach
colonise
evade host immunity
produce harmful proteins
disseminate
release from host

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7
Q

what are microorganisms

A

agents of infectious diseases that are ubiquitous in nature and in the body
most are harmless
while some are confined to one host, most microbes can live in a wide array of hosts.
plant microbes are harmless to humans

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8
Q

what are microorganisms divided into

A

bacteria
fungi
viruses
prions
parasites

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9
Q

are parasites relevant in dentistry

A

not really

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10
Q

what is microbiology

A

the study of microscopic organisms.

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11
Q

what are the subdisciplines of microbiology

A

virology
mycology
parasitology
bacteriology

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11
Q

describe the pathogenesis of infection

A

when there is colonisation, a balance can develop between colonised microbes and humans to lead to so called normal flora
if the microbe causes a disease it is called an infection

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12
Q

what is colonisation

A

this is when a microbe finds a host and starts to multiply

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13
Q

what is an endogenous infection

A

this is an infection caused by a microbe that is from the patients own flora

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14
Q

what is an exogenous infection

A

this is when the source of the infection is from flora outside of the patients body

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15
Q

what actually is pathogenesis

A

this is when microbes find a host and invade cells

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16
Q

does normal flora cause damage

A

no, not unless the balance is thrown in favour of the microbe

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17
Q

what are primary pathogens

A

microbes that always cause disease in a new susceptible human

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18
Q

what are opportunistic pathogens

A

microbes that only cause disease in immunocompromised patients

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19
Q

what is carrier state

A

the continued presence of an organism in the body that does not cause symptoms, but is able to be transmitted to infect other people

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20
Q

does colonisation mean there is disease

A

no there is no disease causing in colonisation

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21
Q

what is normal flora

A

the presence of bacteria normally found at specific body sites

22
Q

what is infection

A

invasion and multiplication of microorganisms in body tissues especially that causing local cellular injury due to competitive metabolism, toxins, intracellular replication or antigen antibody response

23
Q

what is koch’s postulates

A

the germ theory of disease that argues the microbe must be present in every case of the disease
the microbe must be isolated from the disease host and grown in pure culture
the disease must be reproduced when a pure culture is introduced into a susceptible host
the microbe must be recovered from an experimentally infected host

24
Q

how can microbes spread from person to persn

A

contaminated blood or other bodily fluids
touch
saliva
air

25
Q

how can microbes spread from the environment to the person

A

fomites
insects
water
food

26
Q

explain why UTI colonisation is easy

A

the vagina and the anus are close

27
Q

who is most commonly affected by UTIs

A

females under 10 and 20-40 years olds

28
Q

what do UTIs colonise from

A

faeces or perineal regions

29
Q

what is the main defence against urinary tract infections

A

flushing action of urine

30
Q

where do the bacteria of UTIs bind to

A

bladder mucosal cells

31
Q

what are the functions of capsules around bacteria

A
  • mediate adhesion
  • immune evasion
  • protection from dessication
  • reserves of carbohydrate
  • encapsulated bacteria give rise to smooth colonies
  • capsule material gives rise to capsular antigens
32
Q

what is the function of the outer membrane of the gram negative bacteria

A

act as a permeability barrier
prevents pentrtion of the bacteria by bile salts and other toxic molecules from the gastrointestinal tract
barrier to lysozyme and many antimicrobial agents
impedes destruction of the abcterial cells by serum components

33
Q

where are endotoxins found

A

outer face of the outer membrane of gram negative bacteria

34
Q

what are endotoxins

A

lipopolysaccharides

35
Q

describe lipopolysaccharides

A

lipid A - membrane anchoring region of LPS
R polysaccharide or antigen - indicator in assays for LPS
O antigen or O polysaccharide - provides virulence

36
Q

what do bacterial cells release when they die

A

lipopolysaccharides

37
Q

describe LPS release from cells

A
  • lysis of gram neg bacteria releases LPS
  • LPS bind to LPS binding protein in the blood
  • this complex binds to receptor on the surface of macrophages
  • macrophage triggered to release cytokines
  • cytokines bind to cytokine receptors on target cells and intitiate inflammation
38
Q

which exotoxins have an extracellular action on connective tissue

A

collagenases
hyaluronidases
proteases

39
Q

which exotoxins act on or within membranes, but probably do not enter the cells

A

stable toxins of enterogenic e. coli

40
Q

which exotoxins traverse host cell membrane and kill cells

A

cytotoxin
diptheria toxin

41
Q

which exotoxins traverse host cell membranes and deregulate cell functions

A

cholera toxin

42
Q

which exotoxins are pore forming, thiol activated cytolitic

A

s. alpha, gamma and theta toxins

43
Q

which exotoxins damage membranes

A

phospholipases and surfactant

44
Q

which exotoxins are superantigens

A

staphylococcal toxic shock syndrome toxin

45
Q

do lipopolysaccharides have a high potency

A

no

46
Q

describe the contribution to virulence of pili and other colonisation factors

A

adhesion
antiphagocytic

47
Q

describe the contribution to virulence of capsules and slime

A

adhesion
protection against phagocytosis
camouflage from the immune system

48
Q

describe the contribution to virulence of peptidoglycan

A

immunomodulation
induction of inflammatory mediators

49
Q

describe the contribution to virulence of lipopolysaccharides

A

protection against complement
induction of inflammatory cytokines
endotoxin shock

50
Q

describe the contribution to virulence of teichoic acid

A

adhesion
sequestration of divalent cations
induction of inflammatory mediators

51
Q

describe the contribution to virulence of flagella and axial filaments

A

chemotaxis
penetration of mucous

52
Q

describe the contribution to virulence of outer membrane proteins

A

adhesion
sequestration of iron
invasion
intracellular survival

53
Q

describe the contribution to virulence of surface proteins

A

adhesion
binding Fc region of immunoglobulins