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Medical microbiology > Bacterial pathogens and disease 1 > Flashcards

Bacterial pathogens and disease 1 Flashcards

1
Q

Define a pathogen

A

A micro-organism capable of causing disease

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2
Q

Define pathogenicity

A

The ability of an infectious agent to cause disease

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3
Q

Define virulence

A

The quantitative ability of an agent to cause disease

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4
Q

Define toxigenicity

A

The ability of a microorganism to produce a toxin that contributes to the development of disease

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5
Q

What are example of 4 virulence mechanisms?

A
  • Adherence factors
  • Biofilms
  • Invasion of host cells and tissues
  • Toxins-endotoxins and exotoxins
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6
Q

What are exotoxins and what are they secreted by?

A

• Are a heterogenous group of proteins produced and secreted by living bacterial cells

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7
Q

What type of bacteria are exotoxins produced by?

A

• Produced by both gram negative and gram positive bacteria

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8
Q

What do exotoxins cause?

A

• Cause disease symptoms in host during disease

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9
Q

What mechanisms do exotoxins cause other than there primary function?

A

○ Evade immune response
○ Enable biofilm formation
○ Enable attachment to host cells
○ Escape from phagosomoes

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10
Q

What are the 2 main exotoxins produced by staphylococcus aureus?

A

○Haemolytic toxins

○Phenol soluble modulins

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11
Q

What do haemolytic toxins cause?

A

§ Cause cells to lyse by forming pores in cell membrane

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12
Q

What do phenol soluble modulins aggregate?

A

§ -Aggregate the lipid bilayer of host cells causing lysis of membrane

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13
Q

What can exotoxins be encoded by?

A

○ Can be encoded by chromosomal genes shiga toxin in shigella dysenteriae, TcdA and TcdB in C.difficile
○ Extrachromosomal genes

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14
Q

What are the 3 types of exotoxins?

A

○ Type 1: Membrane acting toxins
○ Type 2:Membrane damaging toxins
○ Type 3:Intracellular toxins

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15
Q

What is the problem involved in the classification of exotoxins?

A

Many toxins have more than one type of activity

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16
Q

Where do type 1 membrane acting toxins act?

A

Act from outside the cell

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17
Q

What do type 1 membrane acting toxins interfere with?

A

○ They interfere with host signalling by inappropriate activation of host cell receptors

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18
Q

What target receptors are included of type 1 membranous acting toxins?

A

§ Guanylyl cyclase:
□ Leads to an increase in intracellular cGMP
§ Adenylyl cyclase
□ Leads to an increase in intracellular cAMP
§ Rho proteins
§ Ras proteins

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19
Q

Steps in the interaction of stable heat toxin and its receptor and its net effect

A

○ Stable heat toxin binds to specific binding receptor(GC-C) on the membrane which causes intracellular part of the membrane to produce cGMP
○ cGMP then geos on to:
§ Act on CTFR pump out cl- and HCO3-
§ Increase levels of cAMP which inhibits pumps out H+ in Na+
§ The net effects of this are that Cl-, HCO3- and Na+ all build up outside the cell and as NaCl is outside the cell, water follows and this leads to diarrhoea

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20
Q

What does type 2 membrane damaging toxin cause?

A

○ Causes damage to the host cell membrane

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21
Q

How many ways is damage to . host cell membrane done in by type 2 membrane damaging toxins?

A
  1. Insert channels in host cell membrane(Receptor mediated)

2. Enzymatical damage(Receptor dependent)

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22
Q

What is an example of receptor mediated damage by type 2 membrane damaging toxins?

A

Alpha toxins bind to receptor which causes polymerase to form defined pores which causes damage to membrane and cell content start to pour out, killing the cell

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23
Q

What is an example of receptor dependent damage by type 2 membrane damaging toxins?

A

□ PSM attaches to membrane causing it to breakdown

24
Q

When are type 3 exotoxins active?

A

○ Active when inside cell hence must gain accesss

25
Q

What are type 3 exotoxins usually made up of?

A

○ Usually made up of 2 components(AB toxins)
§ Receptor binding and translocation function(B)
§ Toxigenic(Enzymatic) (A)
§ May be single or multiple B units

26
Q

What are the 2 ways that exotoxins induce inflammatory cytokine release?

A
  1. Super antigen

2. Activation of the different inflammasome

27
Q

What are the steps involving super antigen?

A

□ Typically, macrophages ingest the bacteria = present the contents of the broken-down bacteria on its’ surface = stimulate T lymphocytes to start producing cytokines
□ Exotoxins over ride this process by attaching to
the surface of the macrophage without bacteria being ingested = stimulate T-cell and produce
Cytokines

28
Q

What are the steps involving activation of the different inflammasome leading to release?

A

□ Detects damage to cells = produces a large structure that produces IL1 Beta and IL18 = two of the most powerful inflammatory cytokines

29
Q

What can exotoxins be inactivated using and what are they used to produce?

A

• Exotoxins can be inactivated using strong chemicals such as formaldehyde or glutaraldehyde
§These are used to produce toxoids

30
Q

What are toxoids?

A

• Toxoids are inactive proteins that are still highly immunogenic (will elicit an immune
response) and form the basis for vaccines = tetanus vaccine, diphtheria, pertussis

31
Q

What can toxin mediated diseases be treated by?

A

• Toxin mediated disease can be treated by administering performed antibodies to the toxin:
○ Diphtheria toxin injected into horses carry out immune response
○ Tetanus
○ Botulism

32
Q

What is the microbiology of clostridium difficile?

A 
○ Gram-positive bacillus
○ Anaerobic
○ Spore forming
○ Toxin-produciing
○ Can be carried asymptomatically in the gut
33
Q

What is the epidemiology of clostridium difficile?

A

○ Common HAI worldwide
○ Spread by ingestion of pores
○ Coloniser of the human gut

34
Q

What are the risk factors of C.difficil?

A

§ Antibiotic use
§ Age
§ Antacids
§ Prolonged hospital stay

35
Q

What does the use of antibiotic do that it causes C.difficile to colonise and grow?

A

○ Antibiotics disrupt the microbial ecosystem within the gut.
○ Provide a competitive advantage to spore forming anaerobes over non-spore forming anaerobes
○ Allow C.difficile colonisation and growth

36
Q

What are the cytopathic and cytotoxic effects of C.difficile?

A

○ Patchy necrosis with neutrophil infiltration
○ Epithelial ulcers
○ Pseudo membranes

37
Q

What can symptoms range from in terms of cytopathic and cytotoxic effects of C.difficile?

A 
○ Can range from:
	§ Asymptomatic
	§ Watery Diarrhoea
	§ Dysentery
	§ Pseudomembranous colitis
        § Toxic megacolon and peritonitis
38
Q

What indicators are used in the diagnosis of C.difficile?

A

○ Clinical signs and symptoms
○ Raised white cell count in blood
○ Detection of organisms and toxins in stool

39
Q

What is the 2 phase test in the diagnosis of C.difficile?

A
  1. Glutamate dehydrogenase-detects if C.difficile organism is present
  2. Toxin enzyme linked immunosorbent assay for TcdA and TcdB toxins
40
Q

What method do we use to detect TcdA and TcdB genes?

41
Q

What do we use for pseudomembranous colitis?

A

○ Use a colonoscopy for pseudomembranous colitis

42
Q

What treatment do we use for C.difficile and depending on what?

A
  • Antibiotics
  • Surgery
  • Recurrent
43
Q

What antibiotics do we use for C.difficile?

A

§ Fidaxomicin
§ Metronidazole
§ Vancomycin

44
Q

What surgical procedures do we use in C.difficile?

A

§ Partial

§ Total colectomy

45
Q

What is Stx(shiga-toxin) carried by?

A

Stx is carried by some E.coli, most commonly O157:H7

46
Q

What is Stx identified usually by?

A

○ Identified usually by growth on MacConkey agar

47
Q

How is E.coli O147:H7 transmitted?

A

§ Predominantly via consumption of contaminated food and water
§ Person to person especially in child care facilities
§ Animal to person

48
Q

What is the gene of the toxin carried on?

A

○ Gene is carried on lysogenic bacteria

49
Q

What type of exotoxin is verocytotoxin?

A

○ Is a type III exotoxin

Enzymatic component A is bound to 5 B subunits(AB5)

50
Q

What is the mechanism of the stx?

A
  1. Toxin binds to receptor Gb3 or Gb4 on host cell membrane
  2. Bound toxin is internalised by receptor mediated endocytosis
  3. Carried by retrograde trafficking via golgi apparatus to the endoplasmic reticulum
  4. The A subunit is cleaved off by membrane bound proteases
  5. Once in cytoplasm, A1 and A2 dissociate
  6. A1 binds to 28s RNA subunit
    §This blocks protein synthesis
51
Q

What does STEC closely adhere to?

A

○ STEC closely adheres to the epithelial cells of the gut mucosa

52
Q

What does STEC bund to?

A

○ STEC bund to glomerular endothelial cells of kidney CVS and CNS

53
Q

What does Stx favour and what does this result in?

A

○ Stx favours inflammation resulting in microvascular thrombosis and inhibition of fibriniolysis

54
Q

What are the symptoms of STEC?

A

○ Abdominal cramps, watery/bloody diarrhoea

55
Q

What are the symptoms in haemolytic uremic syndrome?

A

§ Anaemia
§ Renal failure
§ Thrombocytopenia

56
Q

What are the less common neurological symptoms of STEC?

A

§ Lethargy
§ Severe headaches
§ Convulsions
§ Encephalopathy

57
Q

What is the diagnosis and treatment for STEC?

A

○ Clinical signs and symptoms
○ Haematological and biochemical evidence
○ Stool culture-Growth on Smac
○ PCR for Stx
○ Supportive treatment including renal dialysis and blood product transfusion
§Antibiotics have little or no rule

Medical microbiology (14 decks)

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