Lecture 2 - Bacterial Pathogenesis Flashcards by Eleanor Nicklason

Differentiate between pathogens, opportunistic pathogens and normal flora

Pathogens: inherently cause disease

Opportunistic pathogens: only cause disease when given the chance (when host is immunosupressed, antacids etc.)

Normal flora: bacteria that are present in the gut under normal circumstances and do not cause adverse effects

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Describe how a bacterium can be normal flora, opportunistic infection as well as a pathogen

Staphylococcus aureus
It is normally found on the skin - doesn’t cause disease.
However, when an individual is immunosupressed, it may cause disease

Toxin production in food can cause intoxication

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What is a ‘virulent organism’?

This is an organism that is likely to cause disease

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What is an ‘avirulent organism’?

This is an organism that won’t cause disease under normal circumstances (eg. normal physiology)

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What are virulence determinants?

Give some examples

Characteristics that make an organism virulent
eg.
Pilli
Toxins
Capsules
Exzymes
Siderophores

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What are some ‘opportunities’ for commensals to cause disease?

Immuno compromised individual
Antacids taken
Pathogen is moved (site specific)

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Why are commensals important?

They contribute to:

immune system
metabolism

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When does an infection go from asymptomatic to symptomatic?

After replication, when there is damage to host dissue

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What is the generalised process of bacterial replication?

Colonisation
Penetration
Replication
Damage to host
Disease
Dissemination
Immunity

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Describe how colonisation occurs

What are the two types of colonisation

Attachment:
• surface molecule (binding molecule / adhesin) + host receptor

Fimbrial / non - fimbrial

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Why are epithelial cells said to be polarised?

Different ends of the cell have different expression of receptors

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Why is polarisation of epithelial cells important?

Bacteria may need to damage epithelium to gain access to receptors

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What are the two functions of fimbriae?

Adhesion

* Conjugation

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What is the structure of fimbriae?

Hollow protein tube

Adhesin on the tip

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Which part of a pilus binds to the host cells receptor?

The adhesin on the tip

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How do we know fimbriae are involved in colonisation?

Can be used as antigen in vaccines for immunity

* Infection blocked by antibodies to fimbriae

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How does a Urinary tract infection arise?

Bacteria from the rectum ‘ascend’ to cause an infection in the bladder

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Who is more commonly affected by UTIs?

Why?

Women

Shorter urethra

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Which bacterium is responsible for UTIs?

Uropathogenic E. coli

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How do uropathogenic E. coli cause disease?

‘P’ fimbrial attachment to bladder epithelium
Bacteria internalised
Replicate to high levels

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What is non-fimbrial adhesion?

This is when bacteria adhere to the host cell with molecules present on their cell wall
• glycocalyces (slime layer, capsule)
• teichoic acids

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Give an example of non-fimbrial adhesion

Staphylococcus aureus adheres using Teichoic acids of the cell wall to the fibronectin and collagen of the host

Teichoic acid – Fibronectin

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What are the two forms of glycocalyx?

How may they be differentiated?

Slime layer
Capsule

Slime layer can be washed away?

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What is the function of glycocalyx?

Evasion of host defences by masking antigens

- Adhesion

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What is a biofilm?

Any group of microorganisms in which cells stick to each other on a surface

Is penetration required for disease?

No, | some pathogens are extracellular

Describe how bacteria penetrate cells

RME: receptor mediated endocytosis • Invasins Invasin or molecule on bacteria binds to a receptor on the host cell --> taken up into the cell

How do bacteria spread between cells?

When bacteria penetrate a cell, they can alter the features of the cell, such an cellular junctions Tight junctions become more leaky --> bacteria can spread more easily

How does Pseudomonas cause disease, considering that it lacks the ability to invade

It can only invade when there is damage to the epithelium - such as in burns victims

Where are the different locations where bacterial replication can occur?

1. On cells (extracellularly) 2. Intracellularly • endosome • cytoplasm

What are the pros and cons of the different locations of intracellular bacterial replication?

Endosome: pro: more protection from molecules in the cytosol con: less nutrients and vice versa

True of false: penetration and replication are essential for infectious disease?

False Only replication is essential Bacteria can cause disease extracellularly

Describe the features of the bacterial growth curve

Lag phase: Log phase: exponential growth of bacteria, diving by binary fission Plateau: stable numbers Decline: due to competition for resources and quroum sensing

True or false? | There can be many different species of bacteria in a biofilm

True | Normally not just one species

What do biofilms contain?

Bacteria Glycocalyces Metabolites These hold the bacteria together

What controls the formation of a biofilm?

Quorum sensing

What is quorum sensing?

Recognition of bacteria within a colony by chemical signals released by neighbouring bacteria

What happens when there are sufficient numbers of bacteria?

A quorum The signal takes effect

What are the two types of signal in quorum sensing?

Generic | Specific

What are biofilms normally associated with?

Chronic infection

What sort of genes do signals from quroum sensing regulate?

Replication Biofilm production Virulence determinants

What happens to metabolic activity in a biofilm?

Reduced metabolic activity, because the bacteria can rely on their neighbours and become more efficient

Why are microfilms bad?

- Increased expression of virulence determinants - Protection form host defences - Greater opportunity for gene transfer

When does an infection pass from subclinical to disease?

Subclinical: numbers below the threshold Disease: numbers above a certain threshold

How may physical barriers be subverted by bacteria?

Trauma | Surgury

How may the complement system by avoided by bacteria?

Enzymes that destroy C'

How do bacteria evade phagocytes?

- Capsules - Escape phagosome - Survive in phagosome - Kill phagocytes

How do bacteria evade Ab?

Enzymatic destruction

How do bacteria evade APCs?

Down regulate MHC expression to reduce the efficiency of APCs

What are the three ways that bacteria can cause damage to the host?

Endotoxin Exotoxin Immunopathology

In general, how does exotoxin work?

1. Produced by bacteria 2. Gets into host cell (B subunit) 3. Cytotonic, cytotoxinc (A subunit)

When is endotoxin primarily produced?

When cells die

What is the structure of endotoxin?

Polysaccharide | Lipid A

What is the effect of LPS?

* Activates the alternate complement pathway | * Binds and activates macrophages and neutrophils by PRRs

Describe how bacteria disseminate Give some examples

1. They produce compounds that break down: • intercellular matrices • cells For example: • Hyaluronidase • collagenases • elastases 2. Use host physiology • blood • nervous system

Describe how bacteria can use the host's physiology to disseminate

Neuronal transport Blood circulation • intra / extracellular

Why is infection a race? Who are the competitors?

It is a race: Pathogen vs. Host's immune system Immune system wins: recovery Pathogen wins: loss of function, death Pathogen partially wins: chronic infection, latency

How can we affect the outcome of 'The Race'?

* Maintain physical barriers * Maintain innate IR * Maintain adaptive IR * Reduce virulence of organism * Reduce n° of organisms

What are some features of normal flora?

* mutualistic relationship with host (don't cause disease) * cause disease if moved to another area * occupy the niche to prevent pathogens colonising * contribute to immune system and metabolism * Can be transient / stable

``` TRUE / FALSE: In Biofilms there is increased: • metabolic activity • expression of virulence determinants • replication • gene transfer • protection from host and antibiotics ```

* metabolic activity FALSE * expression of virulence determinants TRUE * replication TRUE * gene transfer TRUE * protection TRUE

How do bacteria kill phagocytes?

Leucocidins

Draw a typical AB5 exotoxin

Slide 26

When is endotoxin mainly produced?

When G- bacteria die