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EMS MOD > microorganisms in disease > Flashcards

microorganisms in disease Flashcards

1
Q

what is pathogenicity?

A

the capability of a microorganism to cause infection

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2
Q

what are the requirements to cause infection?

A

transmissibility, establishment in a host cell, harmful effects and persistence

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3
Q

what often causes more harm than the pathogen itself?

A

the harm mediated by the host response

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4
Q

what is virulence often used for?

A

interchangeably to describe pathogenicity - it is sometimes defined as the degree to which a micro-organism is able to cause disease - allows relative description of pathogenic potential

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5
Q

what is an example of virulence?

A

staphylococcus aureus and streptococcus mutans are both found in the mouth - S.aureus is more virulent as causes disease more readily

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6
Q

what is infectivity?

A

the ability of a micro-organism to become established on a host - mediated by microbial ligand and host cell surface receptor

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7
Q

what are virulence factors?

A

components of a micro-organism that aid it’s ability to cause infection - infectivity and virulence

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8
Q

what are virulence factors encoded by?

A

virulence genes

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9
Q

how can you reduce the infectivity or completely stop it?

A

remove the virulence factors

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10
Q

what are examples of virulence factors?

A

tissue damage, facilitation of adhesion and toxic effects, interference with host cell mechanisms, facilitation of invasion, modulation of host cytokine response

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11
Q

what is the cycle of infection?

A

encounter, invade, spread, evade defences, multiply and damage and disperse

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12
Q

what affects the severity and speed of the infection cycle?

A

the status of the host’s immune system

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13
Q

how can you control infection?

A

interrupt at each stage of the infection cycle - understand the processes occurring at each stage is important for this

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14
Q

where can you get infections from?

A

endogenous - microorganisms that get from the wrong place into the host - many individuals who are already in hospital
exogenous - organisms originating from the external environment/infected individuals - receptors on cells can change in level meaning that the pathogen can opportunistically come in

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15
Q

what is bacterial pneumonia?

A

infection of the lower respiratory tract that causes fluid to collect in the alveoli of the lungs

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16
Q

what is the epidemiology of bacterial pneumonia?

A

around 4 million people die annually from pneumonia, mainly the old or young or immunocompromised

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17
Q

what are the main organisms that can cause bacterial pneumonia?

A

streptococcus pneumoniae, staphylococcus aureus, haemophilius influenza - gram positive can survive the environment

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18
Q

what is gonorrhoea?

A

it is a sexually transmitted infection that is caused by neisseria gonorrhoeae

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19
Q

what is the epidemiology of gonorrhoeae?

A

it is the second most common STI in the UK - peak incidence in 15-19y/o for women and 20-24y/o in men

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20
Q

what are the symptoms in gonorrhoea?

A

discharge of pus from the urethra, burning sensation and sterility

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21
Q

what is the sex bias of gonorrohoea?

A

sex bias to symptoms - 90% of men show but only 20% of infected women - untreated can form more severe forms

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22
Q

how can you encounter bacterial pneumoniae?

A

inhalation of air borne droplets containing pathogen - encounter right tissue type, adhere and cause infection, mouth contact with infected individual and contaminated blood

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23
Q

how can you encounter gonorrhoea?

A

sexual contact with infected individuals - horizontal transmission - contact with urethral exudate and vertical transmission from mother to child

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24
Q

what types of entry/colonisation are there?

A

ingress or penetration - getting break through and introduction of organism `

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25
Q

how can you get gonorrhoea of the throat?

A

the GD1 ganglioside can be expressed in the respiratory tract and adhesins are involved in determining the tissue tropism of bacterial infection

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26
Q

what are examples of evading defences?

A

pneumococcal surface protein A, capsule, flagella dn IgA protease

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27
Q

what is a capsule?

A

it is a layer of polysaccharide found on the outside of pathogens that prevents the phagocytosis and complement mediated killing of pathogens - they can move through mucus

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28
Q

how will india ink stain show if a bacteria has a capsule?

A

negative test - capsule means ink cannot go up to border so can be seen easily

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29
Q

what is C3b used for?

A

cytolysis and opsonisation

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30
Q

what is C3a used for?

A

degranulation of mast cells

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31
Q

what is the role pf pneumococcal surface protein A?

A

it prevents complement mediated killing - binds to the Fc portion of ABs meaning that they stick out and the immune system cannot recognise them

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32
Q

what is the complement system?

A

part of the innate immune system - enhance phagocytosis, directly kill cells through MAC, or improve immune system and opsonisation

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33
Q

what is IgA?

A

a secretory immunoglobulin that is found in the mucosal secretions of the urogenital and respiratory tract - bind to pathogens and prevent them adhering to tissues

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34
Q

what is the role of IgA protease?

A

produced by S. pneumoniae and N.gonorrhoeae that degrades IgA - targets the amino acid sequence pro-pro-Y-pro in the hing region of the heavy chain

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35
Q

what does Y stand for in the amino acid sequence targetted by IgA protease?

A

serine, threonine or alanine

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36
Q

what is IgA protease?

A

it is an endopeptidase - not specific or complete

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37
Q

what is the incubation period?

A

it is the period between infection with the organisms and manifestation of clinical features - chicken pox is 10-21 days and may need isolation to stop spread

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38
Q

what is the period of infectivity?

A

the period during which a transmissible organism may be transmitted to another person - chicken pox is from 48 hours before rash appears to when all lesions have crusted over - the age and health of patients will also determine this and infectivity can start to happen before patient can show any outward symptoms of disease

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39
Q

how can pathogens retrieve the host nutrients they require to multiply?

A

cause direct or indirect damage - when they elicit a huge immune response so they stimulate host to damage itself - examples are endotoxin, neuraminidase, hyaluronidase and pneumolysin

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40
Q

what is pneumolysin?

A

it is a multimeric protein that is secreted by s pneumoniae - multiple monomers are brought together and multimerise and bond to cholesterol in the plasma host membrane

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41
Q

how does the action of pneumolysin kill the host cell?

A

there is pore formation - structural changes - hole in the membrane so the inside of the host cell can lead out and release internal contents - nutrients - death

42
Q

what are hyaluronidase and neuraminidase?

A

enzymes that are capable of breaking of hyaluronic acid or aialic / neuraminic acid

43
Q

what is the significance of hyaluronic acid and neuramin?

A

they are both target components of interstitial cement - hyaluronic in connective tissue and neuraminic in epithelial cells

44
Q

what does breakdown from enzymes do?

A

it provides more space for organisms to grow, provides nutrients and activates the immune system

45
Q

what is broken down?

A

links in the basement membrane - leaky

46
Q

what is the difference between endo and exo?

A

endo -part of cell membrane

exo - something that is released

47
Q

what is endotoxin?

A

it is a component of the outer cell membrane is N. gonorrhoeae that isnt actively secreted but is released on cell death or lysis

48
Q

what does endotoxin do?

A

it causes an uncontrollable immune response with severe tissue damage, inflammation and multi-organ failure which is known as endotoxic shock or sepsis

49
Q

where is LPS found?

A

it is a component of the cell envelope made of a disaccharide fatty acid complex attached to an oligosaccharide core and a polysaccharide O antigen

50
Q

what is the host response to endotoxin?

A

severe sepsis/septic shock - T lymphocyte response, activation of the clotting cascade and activation of the complement

51
Q

what is the T lymphocyte response?

A

cytokine release - TNF-a, y-interferon and interleukin-1, fevers, rigors, hypotension, tachycardia and collapse - cardiac and renal failure

52
Q

what happens in the activation of the clotting cascade?

A

disseminated intravascular coagulation and depletion of clotting factors - deficiency

53
Q

how can compensatory vasoconstriction occur?

A

low BP - patient collapses - can become pathological

54
Q

what is the presenting features of warm shock?

A

warm, systemic vasodilation and leaky capillaries

55
Q

give an example of pathological vasoconstriction?

A

when a patient has N.meningitidis - endotoxin-mediated increase in vascular permeability causes loss of protein, fluid and plasma into tissues so there is compensatory vasoconstriction

56
Q

what impacts are there of infection on the host?

A

granuloma and abscess formation, inflammation, endotoxin response and exotoxin response

57
Q

what happens in inflammation?

A

it is the response to invasion/tissue damage with the activation of complement, clotting and kinin system and fibrinolysis - there is leukocyte adhesion and production of inflammatory mediators resulting in local vasodilation, reduced function of endothelial barrier and increased vascular permeability and phagocytosis of foreign material

58
Q

what are the effects of inflammation?

A

swelling - increased vascular permeability - extravasation of serum proteins and leukocytes, consequent physical and osmotic effects and vasodilation
erythema - vasodilation - increased blood flow
pain - physical and biochemical changes
heat - vasodilation - increased blood flow
loss of function - secondary effect of pain and swelling

59
Q

what in abscess?

A

enclosed collection of pus - consequence of inflammatory response with phagocytosis of organisms

60
Q

what is effects of abscess?

A

localised or systemic inflammation and can be external or internal

61
Q

what is pus?

A

it is dead and living white blood cells, exudate, dead tissue and micro-organisms

62
Q

why are abscess associated with the manifestations of inflammation?

A

they are surrounded by inflammation

63
Q

what are the clinical features of abscesses?

A

the lesion itself, surrounding inflammation and the non-specific systemic features

64
Q

what are superficial abscesses caused by?

A

pyogenic microorganisms - S aureus and Strep pyogenes

65
Q

what causes deep abscesses?

A

any organisms

66
Q

what is the fibrous capsule for?

A

to stop the spread of infection - forms a barrier

67
Q

what causes the impact of the infection on the host caused by?

A

exotoxin

68
Q

what is the point of the binding component?

A

it will bind to receptor and facilitate the active component to reach the site to cause damage

69
Q

what are some exo-toxin mediated infections?

A

cholera, diptheria, C difficile, staohylococcal scaled skin syndrome, E coli haemorrhagic colitis, whooping cough, scarlet fever

70
Q

what is scalded skin syndrome?

A

caused by staph aureus epidermolysin - do not fully understand mechanism but is to do with the separation of the dermal layer from the exfoliant toxin

71
Q

what is a well known potent toxin?

A

botulinum

72
Q

what is a granuloma?

A

a focal compact collection of inflammatory cells, mononuclear cells predominating, usualyl as a result of the persistence of non-degradable product and of active cell mediated hypersensitivity

73
Q

what is granuloma formed in response to?

A

inflammatory stimuli - TB, mycobacteria, histoplasmosis, taxoplasmosis, cryptococcosis

74
Q

what are the radiological manifestations of granuloma?

A

nodules

75
Q

what are clinical manifestations of granuloma?

A

tissue necrosis - caseation

76
Q

what are the virulence factors of S pyogenes?

A

C5a peptidase, streptolysins - O and H, erythrogenic toxin, toxic shock syndrome toxin and hyaluronidase and streptokinase

77
Q

what is TSS toxin?

A

it is a superantigen that is bound specifically on the cell membrane resulting in systemic activation of strong immune response and simialar symptoms to endotoxin release

78
Q

what is erythrogenic toxin?

A

it causes the scarlet fever rash and is produced by a piece of DNA transferred by a bacteriophage

79
Q

what do streptolysins O and H do?

A

lyse red and white blood cells and platelets

80
Q

what will fever inducing toxins result in?

A

can develop erysipelas, streptococcal sore throat, scarlet fever and necrotising fasciitis

81
Q

what does tetanus result in?

A

rigid paralysis from clostridium tetani which is an obligate anaerobe

82
Q

how can you contract tetanus?

A

toxin production - produced on the germination of spore and binds to nerves synapses to inhibit the release of inhibitory neurotransmitters in CNS and infection of dirty wounds that may be trivial

83
Q

how is death caused by tetanus?

A

respiratory paralysis

84
Q

what is mycobacterium tuberculosis?

A

it is an intracellular pathogen that results in granuloma formation that accounts for the clinical and radiological features

85
Q

what does a primary TB infection result in?

A

Ranke/Ghon complex - solitary granuloma with hilar granulomatous lymphadenopathy

86
Q

what does post-primary reactivation result in?

A

wide spread granulomatous inflammation and cavitation that is often apical

87
Q

what does miliary TB result in?

A

multiple disseminated 1-3mm pulmonary granulomas that look like rice seeds on Xray

88
Q

what does extrapulmonary TB result in?

A

diverse manifestations in the bone, liver, kidney and CNS

89
Q

why is granuloma formed in TB?

A

associated respiratory burst is not enough to kill TB so granuloma stops the spread around the body

90
Q

what happens with granuloma when the immune system is impaired?

A

there is escape of organisms from granuloma so spread round body and can result in pulmonary TB

91
Q

how does dispersion occur?

A

damage to the host can promote dispersal

92
Q

what are the three main effects of dispersion?

A

inflammation of lung tissue, damage to tissues of the genital tract and induction of the immune response and induction of coughing

93
Q

what happens in inflammation of lung tissue?

A

production of fluid containing pathogen, induction of coughing and dispersal of pathogen via respiratory droplets

94
Q

what happens to tissues of the genital tract?

A

production of urethral discharge and transmission through sexual contact

95
Q

what are the main characteristics in routes of transmission?

A

diarrhoeal disease and production of liquid faeces, skin infection and production of vesicular fluid, pathogens are capable of gaining access to the circulatory system and the infectious dose

96
Q

how does liquid faeces contribute to route?

A

greater dispersal through contamination of food and water

97
Q

how are pathogens able to get into the circulatory system?

A

blood transfusion and needle sharing

98
Q

what is infectious dose?

A

number of organisms required to cause an infection

99
Q

how can infection be reduced?

A

cleaning and sterilisation to reduce proportion of infectious dose

100
Q

how can one infection be easier to share than others?

A

easier to share if less are needed to cause infection - lower infectious dose

EMS MOD (28 decks)

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