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microorganisms in disease Flashcards

(100 cards)

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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
how can you get gonorrhoea of the throat?
the GD1 ganglioside can be expressed in the respiratory tract and adhesins are involved in determining the tissue tropism of bacterial infection
26
what are examples of evading defences?
pneumococcal surface protein A, capsule, flagella dn IgA protease
27
what is a capsule?
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
28
how will india ink stain show if a bacteria has a capsule?
negative test - capsule means ink cannot go up to border so can be seen easily
29
what is C3b used for?
cytolysis and opsonisation
30
what is C3a used for?
degranulation of mast cells
31
what is the role pf pneumococcal surface protein 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
32
what is the complement system?
part of the innate immune system - enhance phagocytosis, directly kill cells through MAC, or improve immune system and opsonisation
33
what is IgA?
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
34
what is the role of IgA protease?
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
35
what does Y stand for in the amino acid sequence targetted by IgA protease?
serine, threonine or alanine
36
what is IgA protease?
it is an endopeptidase - not specific or complete
37
what is the incubation period?
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
38
what is the period of infectivity?
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
39
how can pathogens retrieve the host nutrients they require to multiply?
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
40
what is pneumolysin?
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
41
how does the action of pneumolysin kill the host cell?
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
what are hyaluronidase and neuraminidase?
enzymes that are capable of breaking of hyaluronic acid or aialic / neuraminic acid
43
what is the significance of hyaluronic acid and neuramin?
they are both target components of interstitial cement - hyaluronic in connective tissue and neuraminic in epithelial cells
44
what does breakdown from enzymes do?
it provides more space for organisms to grow, provides nutrients and activates the immune system
45
what is broken down?
links in the basement membrane - leaky
46
what is the difference between endo and exo?
endo -part of cell membrane | exo - something that is released
47
what is endotoxin?
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
what does endotoxin do?
it causes an uncontrollable immune response with severe tissue damage, inflammation and multi-organ failure which is known as endotoxic shock or sepsis
49
where is LPS found?
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
what is the host response to endotoxin?
severe sepsis/septic shock - T lymphocyte response, activation of the clotting cascade and activation of the complement
51
what is the T lymphocyte response?
cytokine release - TNF-a, y-interferon and interleukin-1, fevers, rigors, hypotension, tachycardia and collapse - cardiac and renal failure
52
what happens in the activation of the clotting cascade?
disseminated intravascular coagulation and depletion of clotting factors - deficiency
53
how can compensatory vasoconstriction occur?
low BP - patient collapses - can become pathological
54
what is the presenting features of warm shock?
warm, systemic vasodilation and leaky capillaries
55
give an example of pathological vasoconstriction?
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
what impacts are there of infection on the host?
granuloma and abscess formation, inflammation, endotoxin response and exotoxin response
57
what happens in inflammation?
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
what are the effects of inflammation?
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
what in abscess?
enclosed collection of pus - consequence of inflammatory response with phagocytosis of organisms
60
what is effects of abscess?
localised or systemic inflammation and can be external or internal
61
what is pus?
it is dead and living white blood cells, exudate, dead tissue and micro-organisms
62
why are abscess associated with the manifestations of inflammation?
they are surrounded by inflammation
63
what are the clinical features of abscesses?
the lesion itself, surrounding inflammation and the non-specific systemic features
64
what are superficial abscesses caused by?
pyogenic microorganisms - S aureus and Strep pyogenes
65
what causes deep abscesses?
any organisms
66
what is the fibrous capsule for?
to stop the spread of infection - forms a barrier
67
what causes the impact of the infection on the host caused by?
exotoxin
68
what is the point of the binding component?
it will bind to receptor and facilitate the active component to reach the site to cause damage
69
what are some exo-toxin mediated infections?
cholera, diptheria, C difficile, staohylococcal scaled skin syndrome, E coli haemorrhagic colitis, whooping cough, scarlet fever
70
what is scalded skin syndrome?
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
what is a well known potent toxin?
botulinum
72
what is a granuloma?
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
what is granuloma formed in response to?
inflammatory stimuli - TB, mycobacteria, histoplasmosis, taxoplasmosis, cryptococcosis
74
what are the radiological manifestations of granuloma?
nodules
75
what are clinical manifestations of granuloma?
tissue necrosis - caseation
76
what are the virulence factors of S pyogenes?
C5a peptidase, streptolysins - O and H, erythrogenic toxin, toxic shock syndrome toxin and hyaluronidase and streptokinase
77
what is TSS toxin?
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
what is erythrogenic toxin?
it causes the scarlet fever rash and is produced by a piece of DNA transferred by a bacteriophage
79
what do streptolysins O and H do?
lyse red and white blood cells and platelets
80
what will fever inducing toxins result in?
can develop erysipelas, streptococcal sore throat, scarlet fever and necrotising fasciitis
81
what does tetanus result in?
rigid paralysis from clostridium tetani which is an obligate anaerobe
82
how can you contract tetanus?
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
how is death caused by tetanus?
respiratory paralysis
84
what is mycobacterium tuberculosis?
it is an intracellular pathogen that results in granuloma formation that accounts for the clinical and radiological features
85
what does a primary TB infection result in?
Ranke/Ghon complex - solitary granuloma with hilar granulomatous lymphadenopathy
86
what does post-primary reactivation result in?
wide spread granulomatous inflammation and cavitation that is often apical
87
what does miliary TB result in?
multiple disseminated 1-3mm pulmonary granulomas that look like rice seeds on Xray
88
what does extrapulmonary TB result in?
diverse manifestations in the bone, liver, kidney and CNS
89
why is granuloma formed in TB?
associated respiratory burst is not enough to kill TB so granuloma stops the spread around the body
90
what happens with granuloma when the immune system is impaired?
there is escape of organisms from granuloma so spread round body and can result in pulmonary TB
91
how does dispersion occur?
damage to the host can promote dispersal
92
what are the three main effects of dispersion?
inflammation of lung tissue, damage to tissues of the genital tract and induction of the immune response and induction of coughing
93
what happens in inflammation of lung tissue?
production of fluid containing pathogen, induction of coughing and dispersal of pathogen via respiratory droplets
94
what happens to tissues of the genital tract?
production of urethral discharge and transmission through sexual contact
95
what are the main characteristics in routes of transmission?
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
how does liquid faeces contribute to route?
greater dispersal through contamination of food and water
97
how are pathogens able to get into the circulatory system?
blood transfusion and needle sharing
98
what is infectious dose?
number of organisms required to cause an infection
99
how can infection be reduced?
cleaning and sterilisation to reduce proportion of infectious dose
100
how can one infection be easier to share than others?
easier to share if less are needed to cause infection - lower infectious dose

EMS MOD (28 decks)

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