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Second Year Microbiology > Gastrointestinal Pathogens > Flashcards

Gastrointestinal Pathogens Flashcards

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1
Q

What can be classed as enteric pathogens? What do they cause?

A

• Bacteria, viruses, protozoa • Gastroenteritis

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2
Q

What defines gastroenteritis?

A
  • Inflammation of stomach and intestines
  • Results in diarrhoea, vomiting, fever, abdominal pain
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3
Q

What characterises diarrhoea and dysentery and how do they differ?

A

Diarrhoea

  • Abnormal faecal discharge (not just liquid)
  • Frequent and/or fluid stools
  • Forcible expulsion of pathogen (beneficial for pathogen because of dissemination)
  • Watery = secretory
    • Lose water from tissue due to disruption to mucosal ion pumps
    • No damage to mucosal cells, little/no inflammation

Dysentery

  • Bloody diarrhoea
  • Inflammatory disorder of GIT
  • Damages mucosal cells (by pathogen/inflammation preventing water absorption)
  • Sever damage causes the bloody diarrhoea
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4
Q

How does the impact of GE differ between the developing and developed worlds?

A

Developing World

  • Major cause of morbidity and mortality in children under 5
  • Dehydration deaths
  • Long term effects on growth, development, immunity

Developed World

  • Common, not life threatening
  • Annoying, but self-limiting (clears itself up)
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5
Q

What is a reservoir of infection?

A
  • Person/animal/plant/soil/substance which infectious agent normal lives and multiplies
  • Can harbour infectious agent without harm to source
  • Reservoir often needed for survival of pathogen
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6
Q

What are the main 7 sources of GE infection?

A

• Faeces, fluids, fingers, food, flies, fomites, fornication

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7
Q

What can be a source of GE infection with faeces?

A

• Humans, contaminated water/food, animals, contaminated meat

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8
Q

What bacteria are poultry, cattle and pigs sources of?

A
  • Poultry: salmonella, campylobacter
  • Cattle: salmonella, E. coli EHEC ETEC)
  • Pigs : Yersinia
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9
Q

How can GE infection be contracted via fluids?

A

• Drinking, ice, natural disasters, poor sanitation, swimming, pasture runoff, shellfish grown in contaminated water

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10
Q

Why is hand washing important?

A
  • Fingers can convery microorganisms or faeces to the mouth or food
  • Bacteria are shed onto fingers
  • Important for food handling
  • Touching animals can pick up bacteria
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11
Q

What are causes of food associated infections?

A

• Poor food handling, cooking, storage, post cooking contamination

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12
Q

What is intoxication?

A

• Ingest a toxin in food which causes the problem rather than the microorganism

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13
Q

What characterises a microorganism that supplies pre formed toxins in food? What is the main symptom of intoxication?

A
  • Organism contaminates food, multiples in food, produces heat and acid stable toxin
  • Toxin ingested with good and has immediate effect on intestinal mucosa
  • Vomiting main symptom
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14
Q

What must a microorganism do to cause GE infection? Is the affect immediate?

A
  • Survive through stomach
  • Evade host defences (reach intestine)
  • Adhere to intestine and multiply to cause damage
  • Not immediate
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15
Q

What can predispose someone to GE infection?

A
  • pH changes
  • normal flora alterations
  • food provides protection of acidic environment
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16
Q

What is the most common outcome of GE infection?

A

• Diarrhoea

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17
Q

What can cause damage to mucosal cells as a result of GE infection?

A

• Dysentery, not diarrhoea

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18
Q

What can cause the symptoms of GE?

A
  • Toxins
  • Damage during microorganism growth (microorganism needs to multiply after adhering to gut mucosa)
  • Microorganism invading intestinal cells (blood, pus)
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19
Q

How do short and long incubation periods differ?

A

Short

  • 2-6 hours
  • Suggests preformed toxin ingested

Long

  • 12-48 + hours
  • Suggests microorganism needs time to multiply
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20
Q

How do small and large infectious doses differ?

A

Small ID

  • Acid stable usually

Large ID

  • Ensure enough survive to pass through stomach
  • Means need to multiply to big numbers in food to cause disease
  • Relates to food safety
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21
Q

What can act as clues to the cause of GE?

A
  • Symptoms
  • Incubation period (IP)
  • Type of food/food handling or storage
  • Associated activities
  • Patient history
  • Specimens (faecal, food, vomit)
  • Processed to liquid
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22
Q

What kind of pathogens would be examined using electron microscopy?

A

• Viruses

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23
Q

What are examples of routine, specialised and enrichment media?

A

Routine medium (e.g. MAC)

Specialised media (e.g. selective, BCSA)

  • Often has antibiotic to suppress growth of other bacteria

Enrichment media (e.g selenite broth for salmonella)

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24
Q

What are the main families of GIT bacterial pathogens?

A

• Enterobacteriaceae and Vibrionaceae

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25
Q

How are Enterobacteriaceae and Vibrionaceae similar and different?

A

Enterobacteriaceae

  • Family
  • Gram negative Rods
  • Facultative anaerobes
  • Oxidase negative
  • Grow on simple media
  • Fermentative metabolism of glucose
  • Sometimes motile
  • Differentiated biochemically

Vibrionaceae

  • Genus
  • Gram negative slender curved rods
  • Facultative anaerobes
  • Oxidase positive
  • Need 1% salt in media
  • Fermentative metabolism
  • Motile
  • Differentiated biochemically
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26
Q

What are examples of Enterobacteriaceae pathogens?

A

• E.coli, salmonella, shigella, yersinia

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27
Q

What are examples of Vibrionaceae pathogens?

A

Campylobacter, vibrio cholera

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28
Q

Why does C. jejuni grow well at 42 degrees C?

A

• It’s the temperature of chicken gut

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29
Q

What is a mesophile?

A

• Optimal growth temperature is 37C

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30
Q

What are the main steps involved in the identification process?

A
  1. Culture on selective or specialised media and incubate
  2. Examine for characteristic growth
  3. Relevant biochemical tests from ID charts
  4. Further characterisation and confirmation
  • Serological tests (ELISA, agglutination)
  • Strain comparison (PFGE)
  • Molecular methods (PCR, electrophoresis)
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31
Q

What are characteristics of MacConkey agar?

A
  • Routine media
  • Selective indicator (bile salts, neutral red, lactose)
  • Lactose Fermenters (LF) make acid, pink colonies
  • Lactose Non-Fermenters (LNF) alkali, yellow or colourless colonies
  • Incubate aerobically 35-37°C
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32
Q

What are characteristics of Desoxycholate Citrate Agar?

A
  • Routine media
  • Highly selective indicator (bile salts, citrate, neutral red, lactose)
  • LF pink colonies (E.coli grow poorly because of citrate)
  • LNF yellow or colourless colonies o Has sodium thiosulphate (H2S producers can grow as colonies with black dot in middle)
  • Incubate aerobically 35-37°
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33
Q

What are characteristics of Baird Parker Medium (BP)?

A
  • Specialist medium
  • Very specific selective and diagnostic
  • Isolation of staphylococcus aureus
  • Has egg yolk emulsion and selective agents
  • Colonies would be grey/black, white margin, zone of clearing surround
  • Incubate aerobically 37°C
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34
Q

What are characteristics of B. cereus Selective Agar (BCSA)?

A
  • Specialist medium
  • Indicator, selective
  • Has egg yolk emulsion, polymyxin B antibiotic, mannitol and pH indicator
  • Incubate aerobically at 37°C o Colonies don’t ferment mannitol so are turquoise with precipitate
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35
Q

What are characteristics of Campylobacter Medium (CAMP)?

A
  • Specialist medium
  • Highly selective and enriched (blood)
  • Has blood, pyruvate, vitamin B6, antibiotics
  • Colonies shiny with metallic sheen
  • Incubate 42°C for 48hours in micro-aerophillic conditions
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36
Q

What coloured colonies are produced by lactose fermenters and non-lactose fermenters?

A

• LF pink, LNF yellow/colourless

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37
Q

Which three pathogens are associated as being LNF?

A

• Salmonella, shigella, Yersinia

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38
Q

Are all LNF pathogens?

A

• No, but they are not normal gut flora

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39
Q

What is selenite brother and when is it used?

A
  • Selenite Broth used if no growth on primary culture
  • Enrichment media (enrichment of salmonella)
  • Has sodium biselenite (inhibits growth of many bacteria)
  • Reduction of selenite sometimes causes red precipitate
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40
Q

What do you do if you don’t see a red precipitate in your selenite broth?

A

• If no colour change, subculture on selective medium like DCA and look for LNF

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41
Q

Why are antibiotics put in selective media?

A

• Suppress growth of other bacteria

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42
Q

What happens during an enzyme immune assay? What kind of test is it?

A
  • Serological test
    1. Coat with antibody
    1. Block unbound sites
    1. Capture antigen from sample
    1. Add know antibody conjugated with enzyme
    1. Add substrate for enzyme
    1. Read colour
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43
Q

How does an agglutination reaction test work?

A

• Mix bacteria with antibody against it and visible clumps should form

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44
Q

What are the steps in phage typing? Are the results conclusive?

A
    1. Plate bacteria
    1. Use panel of phage dotted on plate
    1. Incubate
    1. Read the pattern of lysis
  • Can give preliminary conclusions, need more tests
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45
Q

What characterises intoxication by staphylococcus aureus?

A
  • Short IP (2-6 hours)
  • Source from normal human flora or food high in salt/sugar
  • Produce heat stable enterotoxin which causes the issue
  • Only small quantities needed
  • Toxin binds neural receptor in upper GIT, vomiting happens
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46
Q

What characterises intoxication of the emetic type with bacillus cereus?

A
  • Short IP (1-5 hours)
  • Fried rice and starchy foods common source
  • Produce spores, survive boiling and can germinate
  • Heat stable toxin produced
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47
Q

What characterises intoxication of the diarrhoeal type with bacillus cereus?

A
  • Longer IP (6-15 hours)
  • Associated with meat, dried vegetables, milk products contain spores
  • Spores germinate after cooking and grow
  • Heat labile toxin produced
  • Activate adenylate cyclase enzymes (intestinal fluid secretion)
  • Watery diarrhoea
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48
Q

How does Clostridium perfringens cause food poisoning?

A
  • Foods have spores and are slowly cooked then not refrigerated. Spores survive cooking, germinate and grow as the food cools to ambient temperature.
  • Stomach acid environment causes heat labile enterotoxin to be produced in intestine
  • Toxin inhibits glucose transport, damages intestinal epithelium and causes protein loss to lumen
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49
Q

What must pathogens do to cause disease?

A
  • Enter body
  • Colonise host
  • Evade defences
  • Multiply (maybe disseminate)
  • Damage host
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50
Q

What role does stomach acid have in regards to pathogens entering the body? What characteristics of organisms let them overcome this?

A
  • Acidic environment, barrier to entry
  • Should be acid resistant, in large numbers, protected by food or stomach has higher than usual pH (antacid) Why are peristalsis and mucous important?
  • Peristalsis can push out pathogens (they must be able to adhere)
  • Mucous provides a barrier that pathogens must penetrate to reach epithelium
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51
Q

Which gastrointestinal disease causing bacteria are extracellular and which are invasive?

A
  • Extracellular: vibrio cholerae, ETEC, EPEC, EHEC
  • Invasive: Shigella, salmonella, campylobacter, Yersinia
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52
Q

What are the two biotypes of serotype O1 Vibrio cholerae?

A

• Classical and el tor

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53
Q

What are characteristics of vibrio cholerae?

A

• Environmental o Free living in water

  • Also human intestinal pathogen
  • Spread in contaminated food or water
  • Voluminous watery diarrhoea
  • Easy to die from dehydration
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54
Q

What happens in the infection cycle by vibrio cholerae?

A
    1. Ingested large numbers
    1. Sensitive to acid so needs large numbers to pass stomach
    1. Colonisation with pili and toxin as virulence factors
    1. Massive fluid and electrolyte loss
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55
Q

What adhesisn is on the pili of vibrio cholerae? Why are they needed?

A
  • Adhesion is TCP (toxin co regulated pili)
  • Need for colonisation of intestine (bacteria bind each other and bind enterocytes)
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56
Q

What is the cholera toxin and how does it cause diarrhoea?

A
  • A-B (A catalytic, B binding)
  • Pentameric (AB5)
  • Bind to GM1 gangliosides on surface of intestinal cells and A subunit internalised
  • Does NOT invade intestine (toxin does)
    1. A1 subunit causes ADP ribosylation of GTPase o Regulates adenylate cyclase activity o GTPase permantely ‘on’
    1. Increased adenylate cyclase activity so increased cAMP levels
    1. Can’t absorb Na, secrete more Cl
    1. Lots of NaCl in lumen so water secreted osmotically
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57
Q

How can v. cholerae be diagnosed in the lab? What colours do other vibrios form on the media?

A
  • Forms yellow colonies on TCBS agar (selective indicator)
  • Other vibrios green
  • Further serological and biochemical identification
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58
Q

What are characteristics of vibrio parahaemolyticus and how does differ to vibrio cholerae?

A
  • Marine waters (e.g. contaminated oysters)
  • IP 12-24 hours
  • Explosive watery diarrhoea
  • Invasive pathogen (not toxin producing)
  • Green on TCBS agar
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59
Q

What type of countries is EHEC most associated with?

A

• Industrialised

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60
Q

What is another common name for ETEC?

A

• Travellers’ diarrhoea

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61
Q

What can cause ETEC?

A

• Food or water contaminated with faecal matter

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62
Q

What is the pathogenesis of ETEC? Is it like cholera?

A
  • Pathogenesis like cholera
  • Adhesin is pilus with colonisation factor antigen (CFA)
  • Makes toxins (heat stable ST and heat labile LT)
  • Pathology resulting from ETEC due to change in cells internal biochemistry
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63
Q

Does ETEC invade cells?

A

• No

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64
Q

How are ST and LT similar and different?

A
  • Heat Labile Toxin (LT)
    • Identical structure and function to cholera toxin
    • Change in cell permanent
    • AB5 toxin which is cytotonic
  • Heat Stable Toxin (ST)
    • Different structure, similar function to cholera toxin
    • Change in cell not permanent
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65
Q

What are the characteristics of EPEC?

A
  • Infant diarrhoea
  • Adults infected if ID high
  • Developing countries
  • Contaminated food and water
  • Extracellular pathogen
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66
Q

What is the pathogenesis of EPEC?

A
  • Extracellular pathogen
  • Adhesin is bundle forming pilus (bfp)
    • Loose attachment to enterocytes
  • No toxins
  • Produces attaching and effacing lesions (A/E lesions)
  • Diarrhoea due to malabsorption (villi damaged), or A/E formation, intestinal permeability
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67
Q

What is T3SS and how does it work? What is characteristic of A/E lesions?

A
  • Type III Secretion System (T3SS)
  • Needle and syringe method to transmit proteins microbe to host cell o Injects virulence/effector proteins
  • Common among gram negative pathogens
  1. BFP loose adhesion
  2. T3SS secretes Tir (receptor protein) into enterocyte
  3. EPEC outer membrane protein Intimin mediates intimate adherence to host cell by binding to Tir
  4. Other effector proteins from T3SS activate actin polymerisation. Host cytoskeleton rearranges and forms pedestal (characteristic of A/E lesions)  A/E lesions have pedestal with intimately adhering EPEC atop
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68
Q

What are the characteristics of EHEC? What is the main reservoir and major serotype?

A
  • Bloody diarrhoea
  • Can cause haemolytic Uraemic Syndrome (HUS)
  • Transmitted from animals (unaffected) via poorly cooked meat or contaminated foods
  • Cattle main reservoir
  • More common in developed countries (factory farmed animals)
  • Major Serotype O157:H7
  • Attaching and effacing pathogen (no invasion)
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69
Q

What is the pathogenesis of EHEC? What are Shiga toxins and what can they do?

A

Attaching and effacing pathogen (no invasion)

  • Unknown colonising antigens/adhesion
  • T3SS injects Tir and other effector proteins (Tir interacts with intimin)
  • Pedestal formation and actin rearrangement

Produce shiga toxins

  • AB5
  • Cytotoxic (same structure to cholera toxin, different function)
    1. Toxin binds receptor Gb3 on Endothelial cells (goes through tight junction of epithelial cells)
    1. A subunit is N-glycosidase that stops protein synthesis
    1. Endothelial cells are damaged in intestine, bloody diarrhoea
    1. Can damage blood vessels in renal glomeruli (HUS)
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70
Q

What does N-glycosidase do?

A

• It is an A subunit in the shiga toxin that removes nucleic acid from ribosomes to stop protein synthesis

71
Q

What lab methods are used to diagnose EHEC, EPEC and ETEC?

A

Lab Diagnosis EHEC

  • Sorbitol MacConket Agar (SMAC)
  • Serological Tests with EIA for shiga toxins
  • PCR for eae gene (intimin)
  • PCR for stx1 and 2 genes

EPEC

  • PCR for BfpA gene
  • Immunofluorescent Microscopy
  • PCR for eae gene

ETEC

  • PCR for LT gene
  • PCR for ST gene
72
Q

What are characteristics of Shigella pathogen?

A
  • Bloody diarrhoea/dysentery
  • LNF (very similar to E.coli except E.coli LF)
  • Non motile
  • Species
    • Shigella dysenteriae
    • Shigella flexneri
    • Shigella boydii
    • Shigella sonnei
  • Low ID o Very acid stable (acid resistant phenotype)
  • Invade gut cells from basal surface, move cell to cell without becoming extracellular
  • Human only
  • Person to person spread, contaminated food water
  • Virulence plasmid
73
Q

How can shigella be distinguished from E.Coli?

A

• Very similar, but shigella is LNF and E.coli is LF

74
Q

Which form of shigella produces the mildest infection?

A

• Shigella sonnei

75
Q

What are the four species of shigella and what are their characteristics?

A

Shigella dysenteriae

  • Developing countries
  • Shiga toxin

Shigella flexneri

  • Young males

Shigella boydii

Shigella sonnei

  • Industrialised countries

Mildest infection

76
Q

Why is a low ID needed to be infected by shigella?

A
  • Very acid stable and has an acid resistant phenotype
  • Can pass through stomach acid
77
Q

What is the benefit of shigella invading the basal surface of epithelial cells?

A
  • It can move cell to cell without becoming extracellular
  • Hidden from immune response
78
Q

What are the characteristics of shigella’s virulence plasmid? What does it encode?

A
  • Large
  • Encodes T3SS
  • Encodes Ipa (invasion plasmid antigens) proteins
    • Translocated via T3SS
    • Cause membrane ruffling
  • Encodes an outer membrane protein
    • IcsA (Intracellular spread)
    • Recruits actin, allows spread
79
Q

How do Ipa proteins enter a host cell and what do they do?

A

• Translocated via T3SS and induce membrane ruffling

80
Q

What is the IcsA protein? What does it do?

A
  • Intracellular spread protein on outer membrane that recruits host cell actin and allows cell to cell spread
  • Produced at pole of cell
81
Q

How do T3SS’s differ between shigella, salmonella, Yersinia and EPEC?

A

Shigella

  • Deliver effector protein (Ipa’s) for uptake by epithelial cells

Salmonella

  • Encodes 2 of them
  • Invasion and intracellular survival

Yersinia

  • Deliver proteins to disrupt innate immune system

EPEC

  • Use Tir to bind intimin on EPEC membrane
82
Q

What is intimin?

A

• Protein on the outer membrane of EPEC that allows it to bind to Tir, thus the host cell

83
Q

What are M cells?

A

• Antigen sampling cells over lymphoid follicles

84
Q

What happens during the infection cycle of shigella?

A
    1. Approach intestinal cells (non-motile mechanism)
    1. Invade M cells
  • Intestinal epithelial cells resistant to Shigella invasion on luminal surface o Invade via basal surface
  • Can also penetrate through leaky tight junctions
  • Invade by injecting Ipa (invasion plasmid antigen) proteins via T3SS (membrane ruffles)
  • Bacteria taken up via fliopods

• 3. Bacteria released to lamina propria

  • Engulfed by macrophage
  • Can induce macrophage apoptosis
  • Inflammation triggered by stimulation of IL1 and IL8 cytokines and neutrophils migrating

• 4. Gut becomes leaky

  • Neutrophils move through mucosal tissue and separate tight junctions
  • More bacteria can invade

• 5. Some bacteria leave macrophages and invade enterocytes through basal surface by inducing uptake by cell

  • Use phagolysosome then escape it to replicate in cytoplasm

• 6. IcsA protein produced at on pole of cell

  • Intracellular spread protein
  • Cause polymerisation of actin which propels bacteria to neighbour cells

• 7. Adjacent cells die and ulcer can form

85
Q

Which chemokine’s and cytokines are stimulated to trigger inflammation during infection by shigella?

A

• IL-1 (inflammation) and IL-8 (chemokine)

86
Q

What is the role of Ipa proteins in invasion by shigella?

A
  • Ipa (invasion plasmid antigen) proteins injected via T3SS
  • Causes membrane to ruffle and bacteria taken up via filopods
87
Q

How does shigella damage the host?

A
  • Cells die, focal ulcer
  • Inflammatory cells and RBC into lumen causing bloody diarrhoea
  • Polymorphs recruited to contain infection but can destroy tissue
  • Shigella dysenteriae produces shiga toxin
  • Bind Gb3 receptor endothelial cells
  • Inhibit protein synthesis o Intestinal damage
88
Q

How is shigella diagnosed in the lab?

A
  • LNF (distinguish from E.coli)
  • Biochemical tests
  • Serotype O antigens
  • Non motile, no flagella/H antigens
  • No H2S made (unlike salmonella)
89
Q

How do AB5 toxins differ between shiga toxin from EHEC and shigella dysenteriae and toxins from cholera and ETEC (LT)?

A

Identical structure, different functions

Shiga toxin (EHEC, Shigella dysenteriae)

  • Act on endothelial cells (inhibit protein synthesis)
  • Cytotoxic

Cholera toxin and LT toxin from ETEC

  • Act in intestine, increase cAMP (cGMP)
  • Secretory diarrhoea
  • Cytotonic
90
Q

What are the characteristics of Salmonella?

A
  • LNF
  • Human pathogens : Salmonella enterica
  • Serovars typed by O and H antigens
  • Not all equal (human only or cross host)
  • Normal flora in many animals
  • Contaminated food and water
  • Acid labile/sensitive so high ID needed Which serovars cause human GE?
  • Serovar Typhimurium
  • Serovar Enteritidis
91
Q

What kind of ID is needed to be infected by Salmonella? Why?

A

• High because it is acid labile/sensitive

92
Q

What happens in the infection cycle of salmonella? What causes diarrhoea?

A

• 1. Invade M cells AND enterocytes

  • Invasion proteins = Sip
  • Cause membrane ruffling, organism uptake
    1. Mediators for uptake induce electrolytes/NaCl to accumulate in lumen
    1. Bacteria transcytose to basal membrane (vesicular transport)
    1. Escape at basal surface (don’t harm gut cells, just a barrier they need to cross)
  • Can be engulfed by macrophages
  • Can escape to blood (transient bacteraemia)
    1. Dendritic cells capture bacteria and transport to lymph nodes (replication)
  • Pathogenesis
  • Inflammatory response leads to release of prostaglandins and stimulation of cAMP, active fluid secretion
93
Q

What are Sip? What so they do? Where are they encoded?

A
  • Salmonella Invasion Proteins
  • Induces cellular mediators and mobilise intracellular Ca2+
  • Causes membrane ruffling and uptake of organisms
  • Encoded for on pathogenicity island
94
Q

What is a pathogenicity island?

A
  • Large part of bacterial chromosome
  • Encode virulence genes
  • Absent from non-pathogenic
  • Different G/C content to host DNA
  • Discrete genetic unit
  • Unstable
  • Get by HGT
95
Q

What kind of pathogenicity islands does salmonella have? What do they encode?

A
  • SPI-1 for T3SS and Sip proteins for membrane ruffling
  • SPI-2 for T3SS and Salmonella Survival Antigens (SSA) proteins for survival in macrophage vacuoles)
96
Q

What are the roles of Ssa Proteins?

A

• Salmonella Survival antigens, allow survival inside macrophage vacuole

97
Q

Where can salmonella bacteria go after escaping at the basal surface?

A
  • Can be engulfed by macrophages
  • Can escape to blood (transient bacteraemia)
  • Ultimately Dendritic cells capture bacteria and transport to lymph nodes (replication)
98
Q

How is salmonella diagnosed in the lab?

A
  • LNF so yellow colonies on MAC, DCA
  • Grow on DCA selective media and black colonies (H2S production)
  • Biochemical tests (slide agglutination, O/H antigens)
  • Strain comparisons (phage typing, PFGE)
99
Q

What are the characteristics of Yersinia enterocolitica?

A
  • Symptoms mistaken for appendicitis
  • Food borne (cattle)
  • Virulence Factors
  • Complications like post-infectious reactive arthritis
100
Q

How can Yersinia adhere to cells? Which molecules are involved?

A
  • Adhesion using Invasin protein
  • RGD tri-peptide motif, bind host cell β1 integrin
  • Mimic natural binding process
101
Q

What is in the Yersinia plasmid?

A
  • Encodes T3SS
  • Encodes Yop protein (Yersinia outer protein) translocated to host cell
102
Q

What are Yop proteins? What do they do? How do they enter host cells?

A
  • Yersinia outer protein
  • Translocated to host cell using T3SS
  • Cytotoxicity
  • Regulate genes for cell cycle/growth (YopM)
  • Counteract pro-inflammatory response (YopP) which prevents phagocytosis by macrophages
103
Q

What is involved in the infection cycle of Yersinia? What can it do within a macrophage?

A
    1. Invade M cells
    1. Invade epithelial cells, enter macrophage

Different options within macrophage

  • Form pore, inhibit phagocytosis, inhibit TNF production
  • Dissemination
  • Macrophage apoptosis, bacteria released
104
Q

How is Yersinia diagnosed in the lab?

A
  • LNF, urease positive, oxidase negative
  • Psychotroph (likes low temperatures, incubate at 25, think of pasteurised milk)
  • Grow on selective media CIN with “bulls-eyes” colonies
105
Q

What are the characteristics of campylobacter?

A
  • Microaerophillic (lower than normal O2)
  • Curved/bird wing gram negative rods
  • Animal reservoirs
  • Not acid resistant (high ID, long IP)
  • Can produce bloody diarrhoea, Guillain Barre Syndrome
106
Q

Why does campylobacter have a high ID? What is it’s IP like?

A
  • Not acid resistant
  • IP is long (2-4 days possible)
107
Q

How can campylobacter infect humans?

A
  • Grow in chicken gut (42) but chicken not diseased
  • Go to humans via poor cooking
  • Goes to water supply then contaminates then human eats
108
Q

How can campylobacter be diagnosed in the lab?

A

CAMP medium

  • Highly selective, enriched
  • Blood, pyruvate, vitamin B6
  • Antibiotics

Incubate 42 degrees for 48 hours, microaerophillic

109
Q

Who is most likely to be affected by rotavirus?

A

• Infants

110
Q

Who is most likely to be affected by norovirus?

A

• Adults

111
Q

How does the use of symptoms to distinguish GE causes differ between bacteria and viruses?

A

• You can’t distinguish viral sources of GE by symptoms alone

112
Q

What are characteristics of GE causing rotavirus?

A
  • High risk are infants
  • Seasonal (winter)
  • Person to person spread (Low numbers needed)
  • 2 day IP
  • Diarrhoea
113
Q

When can excretion of rotavirus occur?

A
  • With symptoms, in faeces (large amount of virions)
  • Asymptomatic excretors
  • Virions in stool
  • Excretion weeks before and days after symptoms
114
Q

What is beneficial about the structure of Rotavirus? What is it like?

A
  • “wheel with spokes”
  • Reoviridae family
  • Icosahedral, double capsid protein coat (beneficial to withstand stomach acid)
  • Ds RNA and segmented genome What is a segmented genome?
  • Made up of fragments of nucleic acid (not circular genome)
115
Q

How does rotavirus replicate and spread?

A

• Entry

  • Binding, penetration and RME
  • Enhanced by proteolysis of outer capsid protein spikes by stomach enzyme trypsin
  • Exit phagolysosome
  • Un-coating
  • Viral RNA made
  • In cytoplasm NOT nucleus
  • Assembly
  • Transit through RER
  • Infected cell lysis and viral release
116
Q

What enzyme does rotavirus need for replication? Where does it come from?

A
  • Needs RdRp (RNA dependent RNA polymerase) to make mRNA from RNA genome
  • RdRp imported as part of virion
117
Q

What is involved in the pathogenesis of rotavirus?

A
  • Virus infects mature villi cells (tip)
  • Infected cells lyse, virus released to lumen and infects more cells
  • Villi are blunted/shortened as result of lysis (reduced absorption of sugar, water, salt)
  • Virus produces enterotoxin (protein NSPA) that affects enterocytes o Cl and H2O secreted to gut (diarrhoea)
  • Fluid accumulates in lumen

• Virus replication ends and crypt cells repopulate villi restoring function/structure

118
Q

How can rotavirus be diagnosed in the lab?

A
  • Antigen detection assays (ELISA, latex agglutination)
  • Electron microscopy
119
Q

What is needed to see rotavirus microscopically?

A

• High virus titre or virus specific antibody to form clumps of viruses

120
Q

What is used as vaccination for rotavirus? When is it administered?

A
  • RotaTeq
  • Oral live attenuated vaccine
  • Childhood vaccine (12 weeks age)
121
Q

What are the characteristics of GE causing norovirus?

A
  • Caliciviridae family
  • Explosive outbreaks
  • Winter peak
  • IP 1-2 days
  • Very stable in environment
  • Faecal oral transmission (contaminated food and water, aerosols from vomit)
  • Mild, self-limiting
  • Asymptomatic infection common
  • Viral shedding 2-3 weeks after
122
Q

What is the pathogenesis of norovirus?

A

• Bind histo-blood group antigens

  • Carbohydrate epitopes common on mucosal cells in gut
  • Blunt villi but intact intestinal epithelium
  • Diarrhoea because malabsorption of fat and lactose
123
Q

Which histo-blood group antigen is more likely to be bound by norovirus?

A

• A and O best

124
Q

What is a difference in pathogenesis between rotavirus and norovirus?

A

• No enterotoxin (unlike rotavirus)

125
Q

How can norovirus be diagnosed?

A
  • RT-PCR for viral RNA in stool
  • Electron microscopy
  • EIA for antigen
126
Q

What are the characteristics of GE causing adenovirus?

A
  • Adenoviridae family
  • Non enveloped, dsDNA
  • Stable in environment
  • Faecal oral spread
  • Shed for months after infection
127
Q

How can adenovirus be diagnosed?

A

• Using antigen detection

128
Q

What is the benefit of a virus being non-enveloped?

A

• Survive well in the environment and bile (Hep A)

129
Q

How does Hep A spread and cause infection?

A

• Faecal oral spread • Mouth → GI tract → bloodstream → liver → virions in bile → faeces

130
Q

Does Hep A cause GE?

A

• No

131
Q

What are some common characteristics of rotavirus, adenovirus and norovirus?

A
  • Pathogenesis mechanism not well understood
  • Stable in the environment
  • Can be shed from asymptomatic carriers
132
Q

How are protists characterised?

A

• By motility and replicative cysts

133
Q

How can infection by protists be acquired?

A

• Ingestion of cysts

134
Q

What does Entamoeba histolytica cause? How?

A

• Mild

  • Loose stool, cramps

• Amoebic dysentery

  • Blood stool, fever, pain
  • Can invade deeper tissue (abscess forms)

• Ulcerates small intestine

135
Q

What parts of the word does Entamoeba histolytica dominate?

A

• Developing countries

136
Q

What is the life cycle of Entamoeba histolytica and what are the two stages?

A

Life Cycle

  • Cyst stage (dormant, infectious, resistant)
  • Trophozoite stage (growing, cause disease)
  • Extreme cases: spread to liver, form abscess
  • Ingest mature cyst → spread in faeces
  • Mature cyst → excystation to trophozoite → multiply to more trophozoites or cysts
137
Q

How does Entamoeba histolytica cause infection?

A

• Adhere to Gal-galNAc sugars on intestinal cells using parasite lectin

  • Can be inhibited by mucous
  • Attachment then contact-dependent killing of host cell using pore forming proteins (amebapores)
  • Kill macrophages and neutrophils (less phagocytosis)
  • Make cysteine protease
138
Q

What does cysteine protease do?

A

• Breaks down IgA (mucosal) and IgG (circulatory)

139
Q

How is Entamoeba histolytica diagnosed in the lab?

A
  • Microscopy (cysts, trophozoites, iodine stain)
  • Serology with antigens in stools, antibodies in patient sera (won’t distinguish from past infection)
140
Q

How is Entamoeba histolytica treated? How does the drug work? How does treatment differ between deep infection and gut infection?

A
  • metronidazole
  • Get parasite anaerobic metabolism for invasive deep tissue infection
  • Pro-drug, activated by pathogenic amoebae
  • If just gut infection, need extra anti-parasitic drugs
141
Q

What causes Giardiasis? What are the characteristics of the illness and protist?

A
  • Giardia lamblia
  • Zoonosis
  • Faecal oral route (chlorine resistant)
  • Watery, grumbly diarrhoea
  • Gut malabsorption
  • Non invasive
  • Cysts acid resistant (low ID)
142
Q

What characteristics of Giardia lamblia cysts are beneficial for the organism?

A
  • Acid resistant and chlorine resistant
  • Low ID needed
  • Can spread in water more easily
143
Q

What is the life cycle of Giardia lamblia?

A
  • Cyst stage
  • Trophozoite stage
  • Ingest cyst, form trophozoite in body, cysts (sometimes trophozoites) in faeces
144
Q

How does Giardia lamblia cause infection? What are the symptoms?

A
  • Non invasive
  • Trophozoite adheres to intestinal wall (ventral sucking disc)
  • Decreases absorption capacity
  • Host immune response with infiltration of inflammatory cells
  • Microvilli damaged/shortened
  • Nutrients not absorbed
  • Watery diarrhoea
145
Q

How is Giardia lamblia diagnosed in the lab?

A
  • Microscopy (cysts, trophozoites in stool)
  • Antigen detection (immunoassay)
146
Q

How can Giardia lamblia be treated and prevented?

A
  • Treatment with metronidazole
  • Prevention by filtering/boiling water
147
Q

What does Cryptosporidium cause?

A

• Cryptosporidiosis, watery diarrhoea

148
Q

What is beneficial about the properties of Cryptosporidium cysts?

A

• Highly chlorine resistant (recreational water spread)

149
Q

What are key points about the Cryptosporidium life cycle?

A
  • Complex
  • Sexual and asexual stages
  • Oocyst is dormant, infectious
150
Q

How does Cryptosporidium cause infection?

A
  • Adherence using surface glycoproteins and lectins
  • Non invasive
  • Epithelial damage due to enterocyte disturbance
  • Makes proteases
151
Q

How can Cryptosporidium be diagnosed in the lab?

A
  • Microscopy (oocysts and acid stain)
  • Antigen detection with immunoassay
152
Q

How can Cryptosporidium be treated? How does severity and treatment differ between normal and immunocompromised people?

A

Normal

  • 2-10 days after infection
  • Watery diarrhoea, resolves in couple of weeks
  • Treat with nitazoxanide (like metronidazole)

Immunocompromised

  • Severe dehydration
  • Life threating illness
  • Need supportive therapy too (rehydration, anti-motility drugs)
  • If AIDs, boost immune system
153
Q

Why do cases of GE in Australia seem low?

A

• Lack of reports, don’t often visit doctor for it

154
Q

Who can be affected by the cost of GE?

A

• Individuals, business, healthcare, government

155
Q

What is epidemiology?

A
  • Study occurrence, spread, control of disease
  • Who, where, when, why, how
  • Collect data, aim to limit further spread
156
Q

What is the difference between endemics, epidemics and pandemics?

A

Endemic

  • Always present in community, low frequency

Epidemic

  • More cases of disease than expected in given area for given group of people for particular time period

Pandemic

  • Endemic covering large area (multiple countries/continent) and often affecting large proportion of population
157
Q

How did epidemiology come about?

A

London 1850’s

  • Overcrowding, no sewers, cholera outbreaks
  • Believed in miasmas and spontaneous generation

John Snow linked cholera to water pump

  • Believed human cause of cholera (NOT germ theory)
158
Q

Why was John Snow so important?

A
  • Showed that disease causing agents may come from human body
  • Track cholera to water pump, closed it down
159
Q

How can a disease outbreak be investigated using epidemiology? What steps are involved? Investigating Outbreaks

A

Describe

  • Time
  • Place
    • Use rate calculations
  • Person
    • Demographic, social characteristics
    • Measure of outcome (e.g. death, self-limiting)
  • Pathogen
    • Genotypic, phenotypic analysis

Develop and test hypotheses for cause

  • Analytical epidemiology
    • Case controlled study
    • Identify source, find commonalty
  • Microbiological investigation

Intervene, control outbreak

Prevent future outbreaks by implementing mechanisms

160
Q

What are the types of epidemic curves? What features do they have?

A

Point Source

  • Rapid peak, moderate decline, shorter time frame

Continuing Source

  • Slow to peak and decline, longer time frame, relatively flatter (if no person to person spread)

Person to Person Spread

  • Waves and peaks (IP = gaps between peaks)
  • Earlier cases are sources to infect new people
  • Continue until no more people susceptible or interventions occur
161
Q

Why may an epidemic curve graph fall quickly?

A

• Quick fall if no person-person spread

162
Q

When will a continuing source epidemic curve end?

A

• Ends when fault fixed or all susceptible are infected

163
Q

How does person to person spread affect the way an epidemic curve looks?

A
  • The graph has waves
  • Gaps between peaks due to IP
164
Q

How can an outbreak be described?

A

• In terms of time, place, person and the pathogen

165
Q

How can the responsible pathogen be found?

A
  • Genotypic, phenotypic analysis
  • Molecular (PFGE)
  • Genomic sequencing
166
Q

What is analytical epidemiology? What type of study is used?

A
  • Identify source, find commonalty, use cause and effect
  • Case controlled study
167
Q

At what levels can food borne GE be controlled?

A
  • State health (MDU)
  • National (FSANZ, OzFoodNet)
  • International (WHO, Enternet)
  • ‘Paddock to plate’ (HACCP)
  • Consumer education
168
Q

What is HACCP? What steps are involved?

A
  • Hazard analysis and critical control point
    1. Analyse hazards
    1. Identify critical control points
    1. Establish preventative measures with critical limits for each control point
    1. Establish procedures to monitor critical control points
    1. Establish corrective actions to be taken when monitoring shows critical limit not met
    1. Establish procedures to verify system working properly
    1. Establish effective record-keeping to document HACCP system
169
Q

What are WHO’s rules for safe food preparation?

A
  • Choose foods processed for safety
  • Cook thoroughly
  • Eat cooked foods immediately
  • Store cooked foods carefully
  • Reheat thoroughly
  • Avoid raw and cooked contact
  • Wash hands repeatedly
  • Keep surfaces clean
  • Protect from vermin/animals
  • Use safe water
170
Q

What are the challenges of controlling food borne GE?

A
  • Developing vs developed countries (easier to follow rules)
  • Food production distribution (large, complex)
  • Food industry globalisation (import, export, different standards)
  • Patterns of food consumption changing
  • Vulnerable groups (immunocompromised)
  • Antibiotics in animals (resistant microbes)
171
Q

Where do 99% of deaths by diarrhoea occur?

A

• Developing world

172
Q

What are the common causes of deaths for children under two in developing world?

A

• Dehydration, dysentery, malnutrition

173
Q

How can the effects of food borne GE be prevented in the developing world?

A
  • Better housing, sanitation
  • Less crowding
  • Waste disposal
  • Clean water
  • Improve maternal education and health care
  • Longer breastfeeding
  • Supply oral rehydration therapy, nutrition, vaccination
  • Better food hygiene

Second Year Microbiology (8 decks)

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