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BSMS 102 > Theme 4 - professional pathogens > Flashcards

Theme 4 - professional pathogens Flashcards

1
Q

what is the definition of infection?

A

when an organism enters the body, increases in number and damages the host in the process

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2
Q

What is the definition of colonisation?

A

organism is present but doesn’t cause infection (may precede infection and amount an immune response)

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3
Q

what is the definition of a pathogen?

A

an organism that evades immune defences of a normal human host to cause infection

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4
Q

what step may precede infection?

A

colonisation

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5
Q

what is the definition of a commensal?

A

lives on us but doesn’t cause infection

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6
Q

what is symbiosis

A

mutual benefit

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7
Q

what is a parasite

A

unequal benefit - advantage to the micro-organism over the host

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8
Q

how often do professional pathogens cause disease?

A

almost always

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9
Q

how often do opportunistic pathogens cause disease?

A

only in specific situations eg in immunocompromised patients

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10
Q

what type of pathogen can commensals potentially be?

A

opportunistic

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11
Q

why do some organisms cause infections and others dont?

A

because they vary in virulence

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12
Q

what is virulence?

A

the fundamental property of an organism

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13
Q

what sits at either end of the spectrum of pathogenicity?

A

commensal and pathogen

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14
Q

name two commensal organisms

A

lactobacillus case and propionibacterium acnes

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15
Q

name two organisms in between commensal and pathogen on the spectrum of pathogenicity

A

Candida albicans and staphylococcus epidermis

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16
Q

name three organisms at the pathogenic end of the spectrum of pathogenicity

A

staph aureus, malaria, HIV, neisseria meningitidis and strep pneumoniae

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17
Q

in what situation can organisms with low virulence be pathogens?

A

in immunocompromised patients

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18
Q

what is pathogenicity?

A

the probability that an organism is causing disease when its isolated from a patient

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19
Q

what determines pathogenicity?

A

the virulence of the organism and the immune state of the patient

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20
Q

what three factors determine whether a pathogen from a patient is pathogenic or commensal?

A

the immune status of the patient, the site the sample was taken from (is it sterile) and the virulence of the organism

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21
Q

what are four key features of staph aureus

A

commensal of the anterior nares, form golden colonies on agar, gram positive cocci they associate in clusters, very virulent

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22
Q

what three features make staph aureus very virulent?

A

its surface proteins (adhesins), secreted proteins (toxins) and polysaccharide coat (capsule)

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23
Q

what can allow staph aureus to be distinguished from other less virulent staphs?

A

the specific adhesins and excretions that allow the disease to manifest

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24
Q

what three features make staph aureus unique?

A

adhesins that bind to host proteins, cloaking and protein A

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25
Q

what do adhesins on staph aureus do?

A

bind host proteins

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26
Q

what is cloaking?

A

when an organism (eg staph aureus) coats itself in host proteins to evade the immune system

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27
Q

what does protein A on staph aureus cell surface do?

A

binds the fc portion of IgG (wrong way round) and therefore coats itself in the Ig to allow immune escape

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28
Q

what test can be used diagnostically for staph aureus?

A

coagulase test

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29
Q

how and why does the coagulase test for staph aureus work?

A

staph aureus has coagulase enzyme on its cell surface so will coagulate sheep serum

30
Q

what is the purpose of the coagulase enzyme on staph aureus cell surface?

A

is a virulence factor - stimulates blood clotting around an infection to stop WBC getting there are clearing it

31
Q

what type of staph are coagulase negative?

A

staph epidermis

32
Q

what are three key staphylococcal toxins?

A

cytotoxins, exfoliative toxins and enterotoxins

33
Q

how do staph cytotoxins cause damage?

A

form pores in the cell membrane and lyse host cells (PVL blows up macrophages)

34
Q

how do staph exfoliative toxins work?

A

degrade connective tissue in the skin - target epidermal structures so skin falls off (proteases)

35
Q

how do staph enterotoxins work?

A

aka superantigens. stimulate T cells and confuse the immune system

36
Q

where are many staph toxins encoded?

A

on mobile genetic elements - can move between strains and are only present on a proportion of strains

37
Q

what feature of staph aureus allows it to evade the immune system (opsonisation)

A

the thin polysaccharide capsule - covers surface antigens tthat antibodies normally bind to (eg peptidoglycan)

38
Q

name three staph aureus skin infections

A

furunculosis, staph abscess and impetigo

39
Q

what is the most common type of staph aureus infection?

A

line sepsis

40
Q

what type of toxins produced by staph aureus cause impetigo?

A

exfoliative toxins

41
Q

what is the most common cause of staph aureus infection?

A

bacteraemia (bacteria in the blood) - causes endocarditis, osteomyelitis and septic arthritis

42
Q

name three common sites of staph aureus infection

A

skin/soft tissue, surgical site, vascular line, blood

43
Q

is staph aureus usually commensal?

A

yes (in anterior nares)

44
Q

what happens in staph aureus food poisoning?

A

rapid brief illness, lots of vomiting and a little diarrhoea (caused by enterotoxins)

45
Q

name four ways that staph aureus demonstrates its virulence

A

adherence to nasal mucosa (adhesins), invasion of tissues (cytotoxins and enzymes), evades immune clearance (protein A and capsule), replicates and disseminates

46
Q

how does staph aureus gram stain?

A

gram positive- purple

47
Q

what additional mechanism of virulence do gram negative bacteria have?

A

lipopolysaccharide

48
Q

how sensitive is the immune system to lipopolysaccharide?

A

very - allows early detection of infection and can recognise it rapidly at very low concentrations

49
Q

what type of receptors does LPS interact with?

A

toll like receptors - especially TLR4 on monocytes and in the endothelium

50
Q

what is the result of interaction between LPS and TLRs?

A

activation of inflammatory pathways, coagulation and clotting pathways, changes in endothelial integrity

51
Q

why do people get so sick with gram negative infections?

A

due to the release of LPS (endotoxin) in the blood - causes systemic activation of immune responses

52
Q

is LPS endogenous or exogenous in bacteria?

A

endogenous

53
Q

do gram positive bacteria have LPS?

A

no - they have lipoteichoic acid and peptidoglycan that stimulate different TLRs to gram negative bacteria

54
Q

what organism causes meningococcal septicaemia?

A

neisseria meningitidis

55
Q

name two key features that contribute to the pathogenicity of neisseria meningitidis in meningococcal septicaemia

A

the pathogen has adhesins the stick to the throat, resp epithelium and meninges, it sheds LPS off the surface and into the surroundings (blebbing)

56
Q

what does blood stained sputum indicate?

A

pneumococcal pneumonia

57
Q

what type of bacteria causes pneumococcal pneumonia?

A

gram positive diplococci - pneumococcus

58
Q

what are the symptoms of pneumococcal pneumonia?

A

cough, breathlessness, consolidated lung (pus filled), haemoptysis (blood stained sputum) - can cause disseminated disease

59
Q

name four factors that contribute to streptococcus pneumoniae virulence

A

specific adhesins for the respiratory mucosa, pneumolysin, secretion of IgA protease (and other toxins), capsule, LPS, lipotechoic acid and peptidoglycan

60
Q

how does pneumolysin convey virulence in streptococcus pneumoniae

A

binds cholestrol on host cell membrane, forms pores and lyses ciliated cells, lyses phagocytic cells

61
Q

how does IgA protease convey virulence in streptococcus pneumoniae

A

breaks down secreted IgA to prevent mucosal clearance

62
Q

how does the bacterial capsule convey virulence in streptococcus pneumoniae

A

prevents complement mediated phagocytosis (need specific antibodies to target it)

63
Q

how many different types of capsule are there in strep pneumoniae?

A

> 100 types

64
Q

where can strep pneumoniae disseminate to?

A

blood, heart valves (endocarditis), upper respiratory tract (sinusitis, Otis media) and meninges (meningitis)

65
Q

name four key features of clostridium difficle

A

gram postive rods, anaerobic, spore forming and cause wound/GI infections

66
Q

name three types of c difficile

A

c. tetani, c. botulinum and c welchii

67
Q

what aspect of c difficile makes it easy to spread between hospital patients?

A

it is spore forming so is resistant to drying, alcohol and antibiotics

68
Q

where are c difficile spores found?

A

in soil and in the gut of humans and animals

69
Q

what is one of the main symptoms of c difficile?

A

diarrhoea - can be mild or severe but may lead to gut perforation and death

70
Q

what infection is severe pseudomembranous colitis a symptom of?

A

clostridium difficile

71
Q

what two key things contribute to c difficile pathogenicity?

A

production of toxins that cause fluid secretion into the gut (diarrhoea and increased infectivity) and spore production (difficult to control and easy to relapse on treatment)

72
Q

what happens in some virulent strains (027) of c difficile

A

loss of regulation and hyper production of toxic genes, production of additional toxins

BSMS 102 (14 decks)

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