Infection Flashcards

1
Q

What is the definition of pathogenicity?

A

the capacity of a micro-organism to cause infection

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2
Q

What are the 4 requirements of an organism to have pathogenicity?

A
  1. transmissibility (ability of an organism to be transmitted from one individual from another) 2. establishment in or on a host 3. harmful effects 4. persistence
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3
Q

What is meant by persistence of a micro-organism?

A

the ability to subvert the immune system in some manner so it can persist for long enough to survive, reproduce and be transferred to another individual

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4
Q

What is the definition of virulence?

A

the degree to which a micro-organism is able to cause disease a more virulent organism will cause disease more readily

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5
Q

What is the definition of infectivity?

A

the ability of a micro-organism to become established on/in a host

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6
Q

What factors are involved in mediating infectivity?

A
  1. microbial ligand 2. host cell surface receptor
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7
Q

What is the definition of a virulence factor?

A

components of a micro-organism which aid its ability to cause infection encoded by virulence genes

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8
Q

What are examples of the actions of virulence factors?

A
  1. facilitation of adhesion 2. toxic effects 3. tissue-damage 4. interference with host defence mechanisms 5. facilitation of invasion 6. modulation of the host cytokine response
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9
Q

What are the 6 stages in the cycle of infection?

A
  1. encounter
  2. entry
  3. spread
  4. evade defences
  5. multiply and damage
  6. disperse
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10
Q

What factors can influence the cycle of infection?

A

the status of the host immune system can impact the speed and severity of the cycle

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11
Q

What is the difference between an endogenous and exogenous source of infection

A

Endogenous:

microorganisms already in the host body travel into a priviledge site (somewhere where they shouldn’t be)

Exogenous:

organisms originate from the external environment

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12
Q

What is bacterial pneumonia?

A

it is an infection of the lower respiratory tract that causes fluid to collect in the alveoli

this impairs gas exchange and leads to poor oxygen uptake

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13
Q

Which groups of people are more susceptible to bacterial pneumonia?

A
  1. extremes of age (old and young)
  2. immunocompromised individuals
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14
Q

What are the 3 main microorganisms which can cause bacterial pneumonia?

A
  1. streptococcus pneumoniae
  2. staphylococcus aureus
  3. haemophilus influenzae
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15
Q

What is gonorrhoea and what organism causes it?

What age group is most commonly affected?

A

it is an STI caused by Neisseria gonorrhoeae

peak incidence is 15-19 in women and 20-24 in men

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16
Q

What are the main symptoms of gonorrhoea?

A
  1. discharge of pus from the urethra
  2. burning sensation
  3. sterility
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17
Q

What is meant by gonorrhoea having a sex bias to symptoms?

A

90% of infected men show symptoms, but only 20% of infected women show symptoms

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18
Q

What is involved in the encounter stage when looking at bacterial pneumonia?

A
  • inhalation of air-bourne droplets containing the pathogen
  • contact with mouth of infected individual
  • contaminated blood
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19
Q

What is involved in the encounter stage when looking at gonorrhoea?

A
  • sexual contact with an infected individual
  • contact with urethral exudate
  • vertical transmission
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20
Q

What aids in the entry/colonisation of N. gonorrhoeae?

A

pilli facilitate attachment of the diplococci to the walls of the urogenital tract

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21
Q

What is a common molecule that many microorganisms adhere to?

What does this mean?

A

fibronectin

this is a common receptor on the surface of many cells meaning that the organism can cause infection in multiple parts of the body

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22
Q

What is the adhesin and receptor of N. gonorrhoeae?

A

adhesin - fimbriae

receptor - GD1 ganglioside

GD1 ganglioside is also found in the respiratory tract so it is possible to get gonorrhoea of the RT

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23
Q

What are the 2 different methods of entry of a microorganism?

A

Ingress:

organism gains access through a standard site that is open to the external environment

Penetration:

the breakthrough and introduction of the organism into a priviledge site e.g. through a scratch

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24
Q

What are the main components of a microorganism involved in spreading and evading defences?

A
  1. flagella
  2. capsule
  3. IgA protease
  4. pneumococcal surface protein A
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25
Q

What is a capsule?

How can it aid a pathogen in surviving (3 main ways)?

A

it is a layer of polysaccharide found on the outside of pathogens

it prevents phagocytosis of pathogens by the cells of the immune system

it allows S. pneumoniae to pass through mucus

it prevents complement-mediated killing

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26
Q

What is the role of pneumococcal surface protein A?

A

it prevents complement mediated killing

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27
Q

What are the 2 main roles of the complement system?

A
  1. it enhances phagocytosis through opsonisation
  2. it directly kills cells through the membrane-attack-complex
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28
Q

How does pneumococcal surface protein A interact with antibodies?

A

It can bind to the Fc region of antibodies so that they are facing the wrong way

This prevents them from using their antigen binding site

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29
Q

Where is secretory IgA found and what is its role?

A

found in mucosal secretions of the respiratory tract and urogenital tract

it binds to pathogens to prevent them from adhering to host tissues

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30
Q

What type of compound is IgA protease?

What is its role?

A

it is an endopeptidase

it degrades IgA

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31
Q

What is an endopeptidase?

A

it targets amino acid chains in the middle of the protein, opposed to at the terminal ends

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32
Q

What part of IgA is targeted by IgA protease?

A

the amino acid sequence Pro-Pro-Y-Pro

Y = threonine, serine or alanine

this is found on the hinge region of the heavy chain

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33
Q

How can IgA protease help S. pneumoniae and N. gonorrhoeae evade the immune system?

A

the breakdown products of IgA stick to the outside of the pathogen

this allows it to evade the immune system

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34
Q

Label the components of secretory IgA

A
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35
Q

What is meant by the ‘incubation period’?

A

the period between infection with the organism and the manifestation of clinical features

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36
Q

What is meant by the ‘period of infectivity’?

A

period during which a transmissable organism may be transmitted to another person

this can happen BEFORE the patient shows the clinical features of the disease

37
Q

What is required for a microorganism to multiply?

How may they elicit damage in the process?

A

they need to acquire nutrients from the host to multiply

they may cause direct or indirect damage to the host in order to do this

38
Q

What is the most common way in which a pathogen will cause indirect damage to a host?

A

by stimulating the host to damage itself through the production of a strong and unnecessary immune response

39
Q

What organism produces pneumolysin?

A

S. pneumoniae

40
Q

What are the stages involved in pore formation by pneumolysin?

A
  1. soluble monomer secreted by S. pneumoniae
  2. multiple monomers come together and multimerise and bind to cholesterol in the host plasma membrane
  3. this produces the prepore
  4. a change in structure forms a pore which punches a hole in the host cell membrane
41
Q

How does pneumolysin cause damage to the host cell?

A

The pore causes the host to release internal contents into the external environment

the host cell dies and nutrients are released for the pathogen

42
Q

What are the roles of hyaluronidase and neuraminidase?

A

they are enzymes which degrade hyaluronic acid and neuraminic acid

these are components of interstitial cement in connective tissue (hyaluronic) or epithelial cells (neuraminic)

43
Q

What can the breakdown of hyaluronic acid/neuraminic acid achieve for the pathogen?

A
  1. provision of nutrients
  2. activation of the immune system
  3. provision of more space for the pathogen to grow
44
Q

What component of a gram-negative bacterial cell envelope is responsible for endotoxic shock?

A

lipopolysaccharide

45
Q

What is an endotoxin?

A

a lipopolysaccharide that is released on cell death/lysis

it is NOT actively secreted

46
Q

What does the release of an endotoxin usually cause in the host cell?

A

uncontrolled activation of the immune response, leading to:

  1. inflammation
  2. severe tissue damage
  3. multiple organ failure (endotoxic shock/sepsis)
47
Q

What are the rough stages that are involved with the host response to an endotoxin?

A

T-lymphocyte response:

cytokine release leads to fever, rigors, hypotension, tachycardia and collapse

Activation of the clotting cascade:

leads to disseminated intravascular coagulation and depletion of clotting factors

Activation of complement

48
Q
A
49
Q

What is the end result of endotoxic shock and what is it brought about by?

A

Initially, warm shock involves the induction of systemic vasodilation and leaky capillaries

There is a period of hypotension

The body then employs compensatory vasoconstriction

This eventually leads to shock, organ dysfunction and DIC

50
Q

What is an example of a host response to an endotoxin released by N. meningitidis?

A
  1. endotoxin-mediated increase in vascular permeability causes loss of protein, fluid and plasma into the tissues
  2. there is pathological compensatory vasoconstriction
  3. this leads to necrosis of the extremities, which requires amputation
51
Q

Which systems are activated in inflammation?

A
  1. complement
  2. clotting
  3. fibrinolysis
  4. kinin
52
Q

What is the result of leukocyte adhesion and production of inflammatory mediators in inflammation?

A
  1. local vasodilation
  2. reduction in endothelial barrier function
  3. these lead to increased vascular permeability
53
Q

What is the result of erythema in host inflammation?

A

vasodilation causes increased blood flow

this allows increased amounts of immune system components to reach the site of infection

54
Q

What causes swelling in host inflammation?

A

increased vascular permeability allows extravasation of serum proteins and leukocytes

55
Q

What causes pain, heat and loss of function in host inflammation?

A

pain is caused by different physical and biochemical changes in the inflamed tissue

heat is caused by increased blood flow

loss of function is a secondary effect of swelling and pain

56
Q

What are the 4 Streptococcus pyogenes syndromes?

A
  1. erysipelas
  2. streptococcal sore throat
  3. scarlet fever
  4. necrotizing fascitis
57
Q

How is S. pyogenes often recognised on a petri dish?

A

when placed on blood, it is capable of producing toxins that cause beta-haemolyisis

58
Q

What is the role of hyaluronidase and streptokinase as a S. pyogenes virulence factor?

A

they break down connective tissue components, facilitating tissue invasion

59
Q

What is the role of the toxic shock syndrome toxin as an S. pyogenes virulence factor?

A

it is a superantigen

it binds to the outside of the MHC class II molecule

this makes it non-specific so that it activates every T-cell within the region

this leads to a strong immune response which can be pathological in itself

60
Q

What is the role of the erythrogenic toxin as an S. pyogenes virulence factor?

A

it causes the rash of scarlet fever

61
Q

What is the role of C5a peptidase as an S. pyogenes virulence factor?

A

it inactivates complement component C5a

62
Q

What are the roles of streptolysins -O and -H as S. pyogenes virulence factors?

A

they are involved with lysis of red and white blood cells and platelets

63
Q

What is an abscess?

A

an enclosed collection of pus

it is a consequence of localised or systemic inflammation with phagocytosis of organisms

64
Q

What does pus consist of?

A
  1. living and dead white blood cells
  2. exudate
  3. dead tissue
  4. microorganisms
65
Q

What are the main clinical manifestations of an abscess?

A
  1. the lesion itself - a fluid-filled fluctuant mass
  2. surrounding inflammation
  3. non-specific signs of infection - e.g. anorexia, sweats, malaise, fatigue
66
Q

What are the main organisms which cause a superficial abscess?

A
  • Staphylococcus aureus*
  • Streptococcus pyogenes*

These are pyogenic organisms

67
Q

What are the 2 types of abscesses?

A

superficial or deep

68
Q

What is the role of the fibrous capsule in abscess formation?

What can interrupt this process?

A

it acts to try and stop the infection from spreading to other sites

organisms can express proteolytic enzymes which can break down the fibrous capsule, allowing them to cause a systemic infection

69
Q

What is the difference between a B and an A component of an exotoxin?

A

B - binding component:

this allows the toxin to bind to a receptor and be endocytosed

A - active component:

this is the part which causes damage to the host cell

The B component facilitates entry of the A component into the host cell

70
Q

How does the botulinum toxin affect the body?

A

it prevents the release of ACh at nerve synapses

this means there is no muscle contraction

it leads to flaccid paralysis and respiratory failure

71
Q

How is wound botulism treated?

A

with penicillin and botulinum antitoxin

ventilation in ICU is needed for the respiratory failure

72
Q

How does Clostridium tetani (tetanus toxin) affect the body?

A

it caauses muscle rigidity and respiratory failure

patients often complain of jaw spasms

73
Q

What is the treatment for tetanus infection?

A

metronidazole and tetanus antitoxin

ventilation in ICU is needed for respiratory failure

74
Q

What is significant about the effects of exotoxins on the host?

A

they tend to have very specific effects on the host body

75
Q

How does someone usually contract an infection with Clostridium tetani?

A

through infection of dirty wounds

76
Q

What is the tetanus toxin called?

How does it affect the body?

A

tetanospasmin

it binds to nerve synapses and inhibits the release of inhibitory neurotransmitters (e.g. GABA)

this leads to severe muscle contraction and death by respiratory paralysis

77
Q

What is a granuloma?

Why does it occur?

A

it is a compact collection of inflammatory cells and mononuclear cells as a result of the persistence of a non-degradable product and of active cell-mediated hypersensitivity

it is the body’s response to an organism that cannot be broken down and killed

78
Q

What infectious agents tend to cause a granuloma?

A
  1. tuberculosis
  2. other mycobacteria as the mycolic acid layer prevents breakdown
  3. histoplasmosis
  4. cryptococcosis
  5. toxoplasmosis
79
Q

What are the radiological and clinical manifestations of a granuloma?

A

radiological - a nodule is present

clinical - tissue necrosis

80
Q

What accounts for the main clinical and radiological features of tuberculosis?

A

granuloma production

81
Q

how is primary tuberculosis identified?

A

By the Ranke/Ghon complex

this is a solitary granuloma (nodule) with hilar granulomatous lymphadenopathy

82
Q

How is post-primary/reactivation TB identified?

A

through widespread granulomatous inflammation +/- cavitation

this is often apical

83
Q

How are miliary and extrapulmonary TBs identified?

A

MIliary - multiple disseminated 1-3mm pulmonary granulomas

Extrapulmonary - diverse manifestations in bone, liver, kidneys, etc.

84
Q

Why are immunocompromised patients more susceptible to Mycobacterium tuberculosis infection?

A

granuloma formation is an active process

if the immune system is impaired, the granuloma cannot be maintained

the organisms escape from the granuloma and disseminate

85
Q

What factor promotes dispersal of a pathogen?

A

damage to the host cells

86
Q

What influences dispersal in pneumonia?

A

inflammation of lung tissue leads to production of fluid containing the pathogen

this induces coughing

this leads to dispersal of the pathogen through respiratory droplets

87
Q

How can damage to the host influence dispersal of gonorrhoea?

A

damage to tissues of the genital tract induces an immune response

this leads to production of urethral discharge

this leads to dispersal via sexual contact

88
Q

What is meant by the ‘infectious dose’?

A

the minimum number of organisms required in order to cause an infection