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3rd Year Biomed > Pathogens (Ian) > Flashcards

Pathogens (Ian) Flashcards

1
Q

What is pathogenesis?

A

The process whereby one organism (the pahogen) causes disease in antoher organism (the host)

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2
Q

Simply, how does a pathogen cause disease

A

Usually, a microorganism causes infection (colonisation of, and growth within, the host) that leads to damage of host tissue which manifests as symptoms

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3
Q

Give an example of a microorganism that causes disease without infection

A

Staphylococcal food poisoning via enterotoxins

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4
Q

What usually determines the ‘success’ of a pathogen

A

Its ability to infect the host rather than cause disease

  • Pathogens often evolve from highly pathogenic to less so
  • Common cold good example: being highly infectious not necessarily associated with being highly pathogenic
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5
Q

What are the 7 stages a microorganism must go through to be successful in a host?

A

1) Entry
- airborne, waterborne, food, sexually transmitted etc

2) Attain a niche
- particular part of the body, how it attaches etc

3) Avoid constitutive or non-specific host defences
- Skin, ciliary action etc
- Phagocytosis, complement etc

4) Avoid specific induced defences
T and B cell response, antibodies

5) Grow within the host
- body temp

6) Cause damage to the host
- Toxins and exoenzymes

7) Exit

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6
Q

What are the 3 main reasons for studying pathogenesis?

A

1) Improvements in preventing infection
- Understanding routes of transmission
- Vaccines

2) Better diagnosis
- Identifying causitive agent
- Molecular detail about specific pathogens

3) Improvements in treatment

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7
Q

What are Koch’s postulates?

A

Criteria to establish a link between a pathogen and a disease

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8
Q

What 4 criteria do Koch’s postulates suggest?

A

1) All people with the disease should be infected with the pathogen and the bacterium or its products should be found in the affected body part
2) Should be able to isolate the bacteria from the site of infection
3) Isolated pathogen reintroduced into healthy model should cause the same disease
4) Should be possible to isolate the reintroduced microorganism from the intentionally injected host

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9
Q

Give some reasons why Koch’s postulates have been difficult to fulfil?

A
  • Inability to obtain a pure culture
  • Passage in lab leads to attenuation (loss of pathogenic properties)
  • Some diseases caused by combination of more than one microorganism
  • Different strains of same species have different pathogenic properties
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10
Q

What is a virulence factor?

A

A set of properties that permit a microorganism to infect a host and cause disease

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11
Q

What is Molecular Koch’s postulates?

A

Extention of Koch’s postulates to include not just the organism but its virulence factors

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12
Q

In general, what does characterization of a pathogen involve?

A

A combination of genetic and biochemical approaches using animal models or tissue cultures to investigate virulence factors

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13
Q

What have tissue cultures been particularly useful to study?

A

To study pathogen invasion

- antibiotic gentamycin used to kill extracellular pathogens after initial infection period

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14
Q

How is genetic analysis utilised to determine pathogenicity?

A
  • Identify genes that encode virulence factors
  • E.g isolate (classical genetics) or construct (reverse genetics) mutants that are defective to identify proteins that play a direct role in infection
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15
Q

What is signature-tagged transposon mutagenesis and what is is used to test for?

A

Used to isolate mutants that are defective in pathogenesis

1) Large number of transposon mutants are isolated - each has a unique sequence (the ‘signature tag’)
2) Microtitre dish containing samples of transposons are used to pool together mutants
3) Mutants used to infect a suitable model and also grown in lab as a control
4) Mutants of interest are those that are avirulent and therefore do not grow in the model
5) Identification of transposon mutants that are missing from the pool of microorganisms that grow in the model system (compared to the control)
6) Done by PCR and hybridisation using P2 and P4 universal primers - results in amplificaton of the signature tag region (ST) to identify mutants

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16
Q

Describe the external defences that prevent entry of pathogens into the host?

A

1) Skin forms a continuous protective layer, except for the eyes and mucous membranes

2) Mucosal surfaces form either a tube (gastro-intestinal tract) or envaginations (respiratory and urinary tracts) that seperate internal tissue from outside world by a single layer of cells (mucosal epithelium)
- Mucosal cells have a number of specialized cell types that protect against infection

3) The eye:
- Blink reflects - protects the eye
- Cornea and conjunctiva form physical barriers
- Tears flush out bacteria

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17
Q

Pathogens infect the gastro-intestinal tract, respiratory tract and urinary tract by one or more of these; Waterborne, sexually transmitted, Airborne, Food borne

A

GI tract - Food and water born
Respiratory - Airborne
Urinary - can move up through urethra (STD) or down from the bloodstream

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18
Q

What is the mucosa associated lymphoid tissue?

A

Protective layer of lymphoid tissue found in the mucosal surface of the body containing B and T cells

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19
Q

For a systemic infection to occur, pathogens must breach the skin or mucosal epithelium. How can this occur?

A

1) Through healthy epithelium
2) Damaged epithelium
3) Damaged skin
4) Healthy skin following a bite of an insect vector

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20
Q

What areas of the body do pathogens infect?

A

Starts at eyes, skin, mucosal surfaces then can spread to internal organs (heart, spleen etc)

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21
Q

How far can infections spread from the initial site? Give examples of different levels of spread

A

1) Restricted to mucosal surface with no invasion e.g Vibrio chlolerae
2) Invaded but restricted to mucosal cells
e. g Shigella
3) Spread to 1 or more internal organs (systemic infection) e.g Salmonellae typhi

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22
Q

Are most infections specific to one body part or systemic?

A

Most are restricted to specific areas e.g vibrio cholerae in the small intestine
Systemic infections often more serious

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23
Q

Name some other conditions that result from infections in specific areas that can be life threatening

A

1) Cholera - dehydration leading to organ failure
2) Haemolytic uraemic syndrome (mainly E.coli O157:H7) - kidney failure
3) Diphtheria - heart or CNS failure

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24
Q

How is host-pathogen tropism usually determined?

A

Determined by specific adhesins that bind to host receptors. These are often lectins (sugar binding proteins)

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25
Q

How does EPEC influence host-pathogen tropism?

A

Modifies host cells by introducting its own receptor (Tir) for attachment of the bacterial adhesin (lntimin) via a type 3 secretion system

26
Q

What is an opportunistic infection?

A

When the health of the host and its efences are compromised by prior illness (e.g cancer) or trauma (e.g burns), non pathogenic commensal (normal) microorganisms can cause life threatening infections

27
Q

What is a nosocomial infection?

A

Infections that occur in hospitals

28
Q

What are the most common nosocomial infections?

A
  • Clostridium difficile

- Methicilin resistant Staphylococcus aureus (MRSA)

29
Q

Name some features of mucus and skin layers that protect against pathogens

A

1) Physical barrier
2) Sloughing cells
- ‘Shedding of cells’
- Remove bacteria from surfaces
3) Lysosomes
- Found in mucin layer of mucosal surface
- Hair follicles and sweat glands
- Kill bacteria
4) Lactoferrin
- Binds iron to prevent microbial growth

30
Q

How do the normal flora help to prevent infection?

A

Compete with pathogenic bacteria for nutrients, carbon sources etc

31
Q

Give an example of a disease that results from disruption to normal flora

A
  • Psudomembranous (antibiotic-associated) colitis

- Caused by Clostridium difficile following use of broad-spectrum antibiotics

32
Q

Give some ways in which virulence factors allow bacteria to overcome host defences?

A
  • Inactivate secretory IgA to prevent entrapment in mucus
  • Iron acquisition systems (siderophores)
  • Overcoming action of complement (serum resistance)
  • Evading phagocytosis
  • Invade host cells and avoid intracellular killing mechanisms
33
Q

What are the 3 main ways that bacteria overcome the action of complement?

A

1) Modification of the LPS
- Increasing the number of O antigen repeats
2) Production of a capsule
3) Synthesis of a C5a peptidase (C5a usually acts as chemoattractant for neutrophils)

34
Q

What type of damage can pathogens cause?

A
  • Obstruction
  • Cell death (necrosis and/or apoptosis)
  • Tissue destruction
  • Alterations in host metabolism
  • Host responses (inflammation etc)
35
Q

Give some examples of when the hosts response to a microorganism causes damage as opposed to the pathogen products (toxins)

A

1) Septic shock
- Over active cytokine response to presence of LPS or endotoxin in the blood
- Can result in acute respiratory distress syndrome (ARDS), disseminated intravascular coagulation (DIC) and multiple organ failure leading to death
2) Autoimmune diseases
- Auto-reactive antibodies produced
- e.g. autoantibodies produced in response to ganglioside GM1 (similar to LPS in Campylobacter jejuni) leading to Guillian Barre syndrome
Example of bacterial molecular mimicry
3) Shigella
- Release of IL-1 by macrophages following apoptosis by shigella
- IL-1 attracts neutrophils that disrupt tight junctions between enterocytes allowing bacteria to gain access to the sub-mucosa of the intestine

36
Q

What are the main ways in which microorganisms exit the body?

A

Vomit
Coughing
Diarrhoea

37
Q

Questions from here in are on enteric pathogens

What type of organism are the enteric pathogens?

A

Gram negative bacteria

38
Q

What are the 5 main enteric bacteria?

A 
Salmonellae
E.coli
Shigella
Yersinia
Vibrio
39
Q

How many people die of diarrhoea and enteric fever annually?

A

3-5 million

40
Q

How are the 5 main enteric bacteria related?

A

Salmonellae and E.coli are closely related
E.coli and Shigella are same species
Yersinia and Vibrio more distantly related

41
Q

What main feature is shared between these 5 bacterium?

A

All require adhesins (fimbrial and non fimbrial) for attachment to host

42
Q

What are the characteristics of Vibrio cholerae? (pathogenesis, attachment etc)

A
  • Most strains do not cause disease in humans
  • Colonies the small intestine
  • Uses a type IV pilus (toxin cooregulated pilus or TCP) that sttaches to host receptors
  • Diarrhoea is caused primarily through the action of cholera toxin (CT), an AB type toxin (A1B5) onto host cells
  • CT secreted by a type 2 secretion system
43
Q

What are the 3 distinct layers of gram negative bacteria cell membrane?

A

1) Cytoplasmic (inner) membrane
2) Periplasm containing the peptidoglycan layer
3) Outer membrane
Peptidoglycan and outer membrane = cell wall

44
Q

How are some pathogenicity factors (including cholera toxin) exported across the inner membrane into the periplasm?

A

By the general secretory pathway

45
Q

How is cholera toxin excreted moved from the periplasm out of the cell?

A

Requires the extrecellular protein secretion machinery (EPS)

  • Is a type 2 secretion system
  • Known as the main terminal branch of the general secretory pathway
46
Q

What are the characteristics of the type IV pilus such as the TCP?

A
  • Span both the inner and outer membrane

- Dynamic, can be disassembled and reassembled

47
Q

How does cholera toxin cause diarrhoea?

A

1) B subunit binds to a GM1-ganglioside receptor on the colonic mucoda
2) A subunit internalised by endocytosis
3) A subunit is an ADP ribosylating enzyme:
- A1 subunit activates G protein Gsalpha to stimulate cyclase to produce cAMP
- High cAMP activates cystic fibrosis transmembrane conductance regulator (CFTR)
- CFTR activation causes efflux of ions and water from infected enterocytes resulting in diarrhoea

48
Q

How does vibrio cholerae obtain the genes for TCP and cholera toxin?

A
  • Gene for TCP contained in pathogenicity island on the genome of bacteriophage TCP(uppercase phi)
  • Also cholera toxin gene from bacteriophage CTX(uppercase phi)
  • TCP is receptor for CTX(uppercase phi) attachment so to become pathogenic must be first infected with TCP bacteriophage then CTX bacteriophage
49
Q

What does enteropathogenic E.coli (EPEC) cause?

A

Severe diarrhoea in children in some areas of the third world

50
Q

Is EPEC invasive or non-invasive?

A

Non-invasive

51
Q

What type of pilus does EPEC have?

A

Bundle forming pilus (BFP)

  • another type IV pilus
  • needed for attachment and forms dynamic fibred that promote the formation of aggregates
52
Q

By what 2 ways does EPEC promote the formation of attaching and effacing structures on the mucosal surface of the small intestine?

A

1) Causes loss of microvilli

2) Fomation of actin rich structures on the cell surface

53
Q

Genes required for attachment and effacement are found where?

A

On the pathogenicity island called Locus Enterocyte Effacement (LEE)

54
Q

What does the LEE also encode?

A

A type III secretion system

55
Q

What are the main proteins secreted by the type III secretion system in EPEC?

A

1) Tir
- localised to the host cell membrane
- acts as receptor for non-fimbrial adhesin lntimin
2) Wiscott-Aldrich syndrome proteins (WASP) and AP2/3
- promote actin polymerisation and attaching and effacing lesions

56
Q

What does Shigella cause?

A

Severe, bloody diarrhoea with fever

57
Q

Is Shigella invasive or non-invasive?

A

Invasive but restricted to the mucosal area of colon and rectum

58
Q

What host response to Shigella causes the disease to a large extent?

A

Excessive inflammation induced by presence of bacteria

59
Q

What type of secretion system does Shigella have and what is it encoded by?

A

Type II secretory apparatus

Encoded on a plasmid

60
Q

Where are Shigella outbreaks common

A

In the west, in day care centres

Highly infective

61
Q

Describe how Shigella invades epithelial cells

A

1) Shigella first invades the M cells of the MALT
- involves type II secretion system translocated proteins IpaB and IpaC
2) Invades and induces apoptosis in macrophages attracted to site of infection
- IpaB binds to caspase-1, a macrophage protein that controls the induction of apoptosis and maturation of IL-1
3) IL-1 and IL-8 released by macrophages (and IL-8 by epithelial cells) attract neutrophils
4) Neutrophils loosen tight junctions between adjacent enterocytes, allowing influx of bacteria from gut to sub-epithelium area
5) Shigella enters enterocytes by invasion of basolateral surface (underside)
6) Moves from cell to cell by formation of pseudopodia (finger like projections) that move into cytoplasmof adjacent cells
- also involves alterations in host cell cytoskeleton

3rd Year Biomed (44 decks)

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