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MoD > L12 - Microorganisms in disease > Flashcards

L12 - Microorganisms in disease Flashcards

1
Q

What are the stages in the chain of infection?

A
  • pathogenic organism
  • reservoir or source
  • exit from source
  • transmission to host
  • entry to host
  • susceptible host
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2
Q

What is virulence?

A

the degree to which a micro-organism is able to cause disease

  • allows description of pathogenic potential
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3
Q

Staphylococcus aureus and streptococcus viridans are both pathogenic. Which is more virulent?

A

Staph. aureus is more virulent than strep. viridans, as it causes disease much more readily

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4
Q

What are the main routes of transmission?

A
  • faecal-oral
  • blood-borne
  • respiratory
  • direct contact (hand-hand, mucous membranes)
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5
Q

What does LD50 mean?

A

Lethal dose

  • the does which will cause death in 50% of hosts
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6
Q

What does ID50 mean?

A

Infectious dose

  • the dose that will cause infection in 50% of hosts
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7
Q

What does infectivity mean?

A

The ability of a microorganism to become established on/in a host

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8
Q

Infectivity is the ability of a microorganism to become established in/on a host. How can this occur?

A

binding of the microbial ligand with the host cell receptor - enables organism to get a footing and then multiply.

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9
Q

Give some examples of ligand-receptor interactions

A
  • E. coli P fimbriae: glycolipids on human uroepithelial cells
  • S. pyogenes protein-F: fibronectin1
  • influenza haemagglutinin: respiratory epithelial sialic acid receptors
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10
Q

What are virulence factors?

A

Components of microorganisms that result in harmful effects

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11
Q

Give some examples of virulence mechanisms

A
  • facilitation of adhesion
  • toxic effect(s)
  • tissue damage
  • interference with host defence mechanisms
  • facilitation of invasion
  • modulation of the host cytokine responses
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12
Q

What are virulence factors sometimes referred to as?

A
  • adhesins
  • aggressins
  • interferins
  • modulins
    etc
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13
Q

An endotoxin is a type of what?

A

Virulence factor

  • Endotoxins are part of the outer membrane of the cell wall of Gram-negative bacteria.
  • Endotoxin acts on neutrophils, platelets and complement to produce, both directly and through mast cell degranulation, vasoactive amines that cause hypotension.
  • Harmful effects incl sepsis
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14
Q

Are endotoxins released from the live or dead bacterial cells?

A

released from damaged/dead cells

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15
Q

Which class of bacteria possess endotoxins?

A

Gram-negative bacteria

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16
Q

What is the active component of endotoxins?

A

Lipopolysaccharide (LPS)

the term LPS often used interchangeably with endotoxin

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17
Q

What do endotoxins do?

A

Binds to a number of host cell receptors

Induces a range of uncontrolled host responses

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18
Q

A host response to an endotoxin is SIRS - systemic inflammatory response syndrome. What is involved in this?

A
  • uncontrolled T-lymphocyte response
  • uncontrolled activation of the clotting cascade
  • uncontrolled activation of complement
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19
Q

One of the components of SIRS is uncontrolled T-lymphocyte response. What is involved in this?

A
  • cytokine release: TNF-a, y-interferon, interleukin-1
  • fever, rigors, hypotension, tachycardia, collapse
  • cardiac and/or renal failure
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20
Q

One of the components of SIRS is uncontrolled activation of the clotting cascade. What is involved in this?

A
  • disseminated intravascular coagulation (DIC)
  • depletion of clotting factors
  • bleeding tendency
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21
Q

SIRS (systemic inflammatory response syndrome) encompasses imprecise terms such as what?

A

Septic shock and endotoxic shock

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22
Q

What is Waterhouse-Friedrichsen syndrome?

A

An example of the catastrophic effects of endotoxin

Meningococcal infection results in bilateral adrenal haemorrhage and subsequent adrenal failure, largely due to endotoxin release from Neisseria meningitidis

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23
Q

what are the consequences of Neisseria meningitidis infection?

A

loss of protein, fluid and plasma into the tissues, with pathological compensatory vasoconstriction

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24
Q

What are exotoxins? What are they produced by?

A

Proteins produced by living bacteria

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25
Q

What is botulism caused by?

A

Exotoxins produced by clostridium botulinum (obligate anaerobe)

The toxins block the nerve impulse from getting to the muscles at the neuromuscular junction

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26
Q

How is botulism caused?

A
  • ingestion of pre-formed toxin (contaminated food)
  • infection of dirty wounds (may be trivial wounds)
  • gastrointestinal colonisation (infants)
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27
Q

What is the clinical presentation of botulism?

A
  • diplopia
  • dysphagia
  • dysarthria
  • dry mouth
  • death (respiratory failure)
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28
Q

Where does botulism toxins act?

A

neuromuscular junction

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29
Q

What causes tetanus?

A

Tetanospasmin

The toxin released by clostridium tetani (obligate anaerobe)

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30
Q

How is tetanus caused?

A
  • infection of dirty wounds (may be trivial wounds)
  • toxin production
  • death caused by respiratory paralysis
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31
Q

What is the mechanism of tetanospasmin causing tetanus?

A
  • produced on germination of spores
  • binds to nerve synapses
  • inhibits release of inhibitory neurotransmitters (eg. gamma-amino butyric acid) in the central nervous system
32
Q

Ultimately, how is death caused in tetanus?

A

Death is caused by respiratory paralysis

33
Q

What does obligate anaerobe mean?

A

Means they are poisoned by oxygen

34
Q

What are the main symptoms of tetanus?

A
  • jaw stiffness (lockjaw)
  • muscle spasms
  • fever
  • sweating
  • tachycardia

Developing into muscle rigidity and respiratory failure

35
Q

As well as botulism and tetanus, list some other exotoxin-mediated infections.

A
  • cholera (vibrio cholerae)
  • diphtheria (corynebacterium diphtheriae)
  • clostridium difficile infection (causing diarrhoea and colitis)
  • E. coli O157 haemorrhagic colitis (verotoxin)
  • staphylococcal scalded skin syndrome (Staph. aureus)
  • whooping cough/pertussis (bordetella pertussis)
  • scarlet fever (strep. pyogenes)
  • scalded-skin syndrome (staph. aureus epidermolysin)
36
Q

What are the 3 components that viruses consist of?

A
  • genome (RNA or DNA)
  • capsid (protein)
  • (envelope - lipid bilayer)
37
Q

Viruses are incapable of what?

A

Independent existence

38
Q

What do viruses use to satisfy the requirements of growth and replication?

A

Host mechanisms

39
Q

What are the stages in the generic virus life cycle?

A
  1. adsorption
  2. penetration
  3. uncoating
  4. synthesis
  5. assembly
  6. release
40
Q

Adsorption is the first stage in the virus life cycle. What is this?

A

Interaction between host receptor molecule and virus ligand (determines host-specificity of the virus)

41
Q

Penetration is the second stage in the virus life cycle. What is this?

A

virus has to gain entrance into

host cells by endocytosis or membrane fusion

42
Q

Uncoating is the third stage in the virus life cycle. What is this?

A

exposes the genetic material for

replication

43
Q

Synthesis is the fourth stage in the virus life cycle. What is this?

A

virus proteins are synthesised

within host in nucleus or cytoplasm

44
Q

Assembly is the fifth stage in the virus life cycle. What is this?

A

Assembly of virus components is mediated by host and/or viral enzymes

45
Q

Release is the sixth stage in the virus life cycle. What is this?

A

Complete virus particles are released by budding off host cell membrane or disintegration of host cell

46
Q

what is a microbial ligand? give an example.

A

The bacterial ligand, e.g adhesin, is typically a macromolecular component of the bacterial cell surface which interacts with the host cell receptor.

47
Q

examples of gram-negative bacteria that release endotoxins when they have died

A
  • E. coli and other Gram-negative bacilli

- Neisseria meningitides

48
Q

What is Opisthotonos?

A

spasm of the muscles causing backward arching of the head, neck, and spine, as in severe tetanus, some kinds of meningitis, and strychnine poisoning.

49
Q

What is a sardonic smile and what disorder is it a characteristic of?

A

Risus sardonicus or rictus grin is a highly characteristic, abnormal, sustained spasm of the facial muscles that appears to produce grinning. Risus sardonicus may be caused by tetanus, strychnine poisoning or Wilson’s disease.

50
Q

how does the varicella zoster virus manifest?

A

chicken pox

shingles

51
Q

how does the herpes simplex virus manifest?

A

herpes labialis

encephalitis

52
Q

how does the human immunodeficiency virus manifest?

A
  • Acute effects: viraemia, cytokine response
  • Longer term effects: gradual onset of immunosuppression from destruction
    of CD4+ immune cells
53
Q

what is the main clinical and radiological feature of tuberculosis?

A

granuloma production

54
Q

how does primary TB present?

A

Ranke/Ghon complex: solitary granuloma (nodule) with hilar

granulomatous lymphadenopathy

55
Q

Ranke/Ghon complex is a feature of what type of TB?

A

primary TB

56
Q

what is a Ghon’s complex?

A
  • a lesion seen in the lung that is caused by tuberculosis.
  • The lesions consist of a calcified focus of infection and an associated lymph node.
  • common in children
  • can retain viable bacteria, so are sources of long-term infection and may be involved in reactivation of the disease in later life.
57
Q

how does post-primary/reactivation TB present?

A

Widespread granulomatous inflammation +/- cavitation, often apical

58
Q

how does miliary TB present?

A

Multiple disseminated 1-3 mm pulmonary granulomas

59
Q

how does extrapulmonary TB present?

A

Diverse manifestations in bone, liver, kidneys, CNS etc.

60
Q

besides tuberculosis, what else can cause granuloma formation?

A

schistosomiasis

Schistosoma’s eggs of parasite

61
Q

what is schistosomiasis?

A

also known as snail fever and bilharzia, is a disease caused by parasitic flatworms called schistosomes. The urinary tract or the intestines may be infected. Symptoms include abdominal pain, diarrhea, bloody stool, or blood in the urine.

62
Q

what is the incubation period?

A

Period between infection with the organism and manifestation of clinical
features

63
Q

what is the impact of infection on the host?

A
  1. inflammation
  2. abscess formation
  3. excessive host response to endotoxin
  4. toxic effects of exotoxin
  5. granuloma formation
64
Q

what causes inflammation?

A

Activation of complement and clotting systems, fibrinolysis and kinin system.

65
Q

what happens physiologically as a result of inflammation?

A
  • leukocyte adhesion
  • production of inflammatory mediators
  • local vasodilation
  • reduction in endothelial barrier function
  • increased vascular permeability
66
Q

what are the clinical manifestations of inflammation?

A
  • erythema
  • swelling
  • pain
  • heat
  • loss of function
67
Q

What are the 4 Streptococcus pyogenes syndromes?

A
  • Erysipelas
  • Streptococcal sore throat
  • Scarlet fever
  • Necrotizing fasciitis
68
Q

what are the 5 S. pyogenes virulence factors?

A
  • Hyaluronidase and streptokinase
  • Toxic shock syndrome toxin
  • Erythrogenic toxin
  • C5a peptidase
  • Streptolysins -O and –H
69
Q

how does Hyaluronidase and streptokinase

act as a virulence factor?

A

Break down connective tissue components – facilitate tissue invasion

70
Q

how does toxic shock syndrome act as a virulence factor?

A

Causes a syndrome very similar to that caused by endotoxin release

71
Q

how does C5a peptidase act as a virulence factor?

A

inactivates complement component C5a

72
Q

how does Streptolysins -O and –H act as a virulence factor?

A

Lyse red and white blood cells and platelets

73
Q

what is an abcess?

A

enclosed collection of pus

74
Q

what is an abcess a consequence of?

A

inflammatory response with phagocytosis of organisms

75
Q

what does pus consist of?

A
  • living and dead white blood cells
  • exudate
  • dead tissue
  • micro-organisms
76
Q

what are superficial accesses mainly caused by?

A

Staph. aureus and Strep. pyogenes

77
Q

what is the clinical presentation of abcesses?

A
  • lesion itself
  • surrounding inflammation
  • non-specific symptoms of infection (e.g. anorexia, sweats, malaise, fatigue)

MoD (19 decks)

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