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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
What is botulism caused by?
Exotoxins produced by clostridium botulinum (obligate anaerobe) The toxins block the nerve impulse from getting to the muscles at the neuromuscular junction
26
How is botulism caused?
- ingestion of pre-formed toxin (contaminated food) - infection of dirty wounds (may be trivial wounds) - gastrointestinal colonisation (infants)
27
What is the clinical presentation of botulism?
- diplopia - dysphagia - dysarthria - dry mouth - death (respiratory failure)
28
Where does botulism toxins act?
neuromuscular junction
29
What causes tetanus?
Tetanospasmin The toxin released by clostridium tetani (obligate anaerobe)
30
How is tetanus caused?
- infection of dirty wounds (may be trivial wounds) - toxin production - death caused by respiratory paralysis
31
What is the mechanism of tetanospasmin causing tetanus?
- 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
Ultimately, how is death caused in tetanus?
Death is caused by respiratory paralysis
33
What does obligate anaerobe mean?
Means they are poisoned by oxygen
34
What are the main symptoms of tetanus?
- jaw stiffness (lockjaw) - muscle spasms - fever - sweating - tachycardia Developing into muscle rigidity and respiratory failure
35
As well as botulism and tetanus, list some other exotoxin-mediated infections.
- 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
What are the 3 components that viruses consist of?
- genome (RNA or DNA) - capsid (protein) - (envelope - lipid bilayer)
37
Viruses are incapable of what?
Independent existence
38
What do viruses use to satisfy the requirements of growth and replication?
Host mechanisms
39
What are the stages in the generic virus life cycle?
1. adsorption 2. penetration 3. uncoating 4. synthesis 5. assembly 6. release
40
Adsorption is the first stage in the virus life cycle. What is this?
Interaction between host receptor molecule and virus ligand (determines host-specificity of the virus)
41
Penetration is the second stage in the virus life cycle. What is this?
virus has to gain entrance into | host cells by endocytosis or membrane fusion
42
Uncoating is the third stage in the virus life cycle. What is this?
exposes the genetic material for | replication
43
Synthesis is the fourth stage in the virus life cycle. What is this?
virus proteins are synthesised | within host in nucleus or cytoplasm
44
Assembly is the fifth stage in the virus life cycle. What is this?
Assembly of virus components is mediated by host and/or viral enzymes
45
Release is the sixth stage in the virus life cycle. What is this?
Complete virus particles are released by budding off host cell membrane or disintegration of host cell
46
what is a microbial ligand? give an example.
The bacterial ligand, e.g adhesin, is typically a macromolecular component of the bacterial cell surface which interacts with the host cell receptor.
47
examples of gram-negative bacteria that release endotoxins when they have died
- E. coli and other Gram-negative bacilli | - Neisseria meningitides
48
What is Opisthotonos?
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
What is a sardonic smile and what disorder is it a characteristic of?
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
how does the varicella zoster virus manifest?
chicken pox | shingles
51
how does the herpes simplex virus manifest?
herpes labialis | encephalitis
52
how does the human immunodeficiency virus manifest?
- Acute effects: viraemia, cytokine response - Longer term effects: gradual onset of immunosuppression from destruction of CD4+ immune cells
53
what is the main clinical and radiological feature of tuberculosis?
granuloma production
54
how does primary TB present?
Ranke/Ghon complex: solitary granuloma (nodule) with hilar | granulomatous lymphadenopathy
55
Ranke/Ghon complex is a feature of what type of TB?
primary TB
56
what is a Ghon's complex?
- 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
how does post-primary/reactivation TB present?
Widespread granulomatous inflammation +/- cavitation, often apical
58
how does miliary TB present?
Multiple disseminated 1-3 mm pulmonary granulomas
59
how does extrapulmonary TB present?
Diverse manifestations in bone, liver, kidneys, CNS etc.
60
besides tuberculosis, what else can cause granuloma formation?
schistosomiasis | Schistosoma’s eggs of parasite
61
what is schistosomiasis?
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
what is the incubation period?
Period between infection with the organism and manifestation of clinical features
63
what is the impact of infection on the host?
1. inflammation 2. abscess formation 3. excessive host response to endotoxin 4. toxic effects of exotoxin 5. granuloma formation
64
what causes inflammation?
Activation of complement and clotting systems, fibrinolysis and kinin system.
65
what happens physiologically as a result of inflammation?
- leukocyte adhesion - production of inflammatory mediators - local vasodilation - reduction in endothelial barrier function - increased vascular permeability
66
what are the clinical manifestations of inflammation?
- erythema - swelling - pain - heat - loss of function
67
What are the 4 Streptococcus pyogenes syndromes?
- Erysipelas - Streptococcal sore throat - Scarlet fever - Necrotizing fasciitis
68
what are the 5 S. pyogenes virulence factors?
- Hyaluronidase and streptokinase - Toxic shock syndrome toxin - Erythrogenic toxin - C5a peptidase - Streptolysins -O and –H
69
how does Hyaluronidase and streptokinase | act as a virulence factor?
Break down connective tissue components – facilitate tissue invasion
70
how does toxic shock syndrome act as a virulence factor?
Causes a syndrome very similar to that caused by endotoxin release
71
how does C5a peptidase act as a virulence factor?
inactivates complement component C5a
72
how does Streptolysins -O and –H act as a virulence factor?
Lyse red and white blood cells and platelets
73
what is an abcess?
enclosed collection of pus
74
what is an abcess a consequence of?
inflammatory response with phagocytosis of organisms
75
what does pus consist of?
- living and dead white blood cells - exudate - dead tissue - micro-organisms
76
what are superficial accesses mainly caused by?
Staph. aureus and Strep. pyogenes
77
what is the clinical presentation of abcesses?
- lesion itself - surrounding inflammation - non-specific symptoms of infection (e.g. anorexia, sweats, malaise, fatigue)

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