Session 7 - Allergies and Infections on surfaces Flashcards

1
Q

Define microbiota

A

Ecological community of commensal, symbiotic and pathogenic MOs that share our body space

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2
Q

How are surfaces within the body infected?

A

Surface infections occur by:

  • Invasion into host
  • Migration – e.g. E. coli UTI
  • Inoculation – Coagulase negative staphylococcus prosthetic join infection
  • Haematogenous – e.g. viridans Strep endocarditis from the mouth
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3
Q

What is an infection of the skin called?

A

cellulitis

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4
Q

infection of pharynx called?

A

pharyngitis

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5
Q

infection of eye called?

A

conjunctivitis

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6
Q

Infection of GI called?

A

gastroenteritis

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7
Q

Infection of Urinary tract called?

A

UTi

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8
Q

Lung infection called?

A

pneumonia

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9
Q

Bone infection called?

A

Osteomyelitis

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10
Q

Infection of plural cavity called?

A

Empyema

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11
Q

Infection of large blood vessels called?

A

Vasculitis

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12
Q

Infection of heart valves called?

A

Endocarditis

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13
Q

Infection of joints?

A

Septic arthrits

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14
Q

What bacterias causes endocarditis in prosthetic valves <1 post-op?

A

Coagulase negative staph aureus

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15
Q

What bacterias cause endocarditis in native and prosthetic valves (>1 yr post op)?

A

Viridans streptococci, staph aureus, HACEK group

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16
Q

Describe the pathogenesis of infections at a surface.

A

1) First step is adherence to host cells or the prosthetic surface – Via use of pili or fimbriae
2) Formation of the biofilm:

  • A mixture of polysaccs and short chain nucleotides produced by bacteria
  • Allows bacteria to survive and multiply on surfaces

3) Invasion and multiplication of bacteria
4) Host response

  • Pyogenic (neutrophils -> pus)
  • Granulomatous – Produces nodular inflammatory lesions.

Some bacteria are better at sticking to certain surfaces than others.

17
Q

How do biofilms form?

A

Formation occurs via quorum sensing:

  • Quorum sensing is communication between bacteria, signalling molecules produced into the bacterial environment with the intention of binding to receptors on other bacteria to signal there are other bacteria of the same type around.
  • If there are a lot of similar types of bacteria around it signals to the bacteria that this is a good place to settle down and reproduce.
  • Positive feedback process.
18
Q

How can you diagnose an infected surface?

A

Difficult but blood cultures and tissue material sonication

19
Q

How can you treat an infected surface?

A

Antibiotics (dont penetrate well into biofilm) or removal of infected tissue

20
Q

How do you prevent infection on a surface?

A
  • Maintain surface integrity
  • Prevent bacterial surface colonisation
  • Remove colonised bacteria
21
Q

Define hypersensitivity

A

Antigen specific immune responses that are either inappropriate or excessive and result in harm to host.

22
Q

How does hypersensitivity develop? What are the names of the 2 phases?

A

1) Sensitisation phase – First encounter with antigen, IgE specific to antigen forms. IgE binds to surface of mast cells
2) Effector phase – Allergen binds to 2 different IgE forming a cross link which activates the mast cell to degranulate. Depending on where the mast cell is different clinical symptoms are experienced.

23
Q

Why do people have allergies? What phenotypes are involved?

A

Hygiene hypothesis:

  • TH1 phenotype – less likely to produce IgE antibodies in response to allergens if raised with low antibiotic use, poor sanitation, with large family sizes and with livestock
  • TH2 phenotype – More likely to produce IgE in response to allergens if raised with high antibiotic use, good sanitation, small family sizes and away from livestock.
24
Q

What is clinical cross-reactivity?

A
  • Allergy to one type of allergen can result in an allergy to another type of structurally similar allergen
  • Depends on structural homology
  • E.g. allergy to cow’s milk carries a 92% risk of being allergic to goat’s milk.
25
Q

What happens in an allergic reaction?

A
  • Mast cells are cells containing a large number of granules which contain chemical mediators
  • When activated degranulation results in the release of mediators • Mediators include histamine, tryptase, TNF-alpha, CCL3 etc etc.

Anaphylaxis results

26
Q

What happens during anaphylaxis?

A

Anaphylaxis results in:

  • Serious hypotension – Lots of blood vessels vasodilate, dropping BP
  • Angioedema
  • Wheezing – Bronchi constrict
27
Q

How do you treat anaphylaxis?

A

Treatment – Adrenaline intramuscular injection:

  • Reverses peripheral vasodilation and reduces oedema
  • Reverses airway obstruction
  • Increases force of myocardial contraction
  • Inhibits mast cell activation
28
Q

What 3 methods can be employed to diagnose an allergy?

A

1) Clinical history – allergens, atopy (predisposition towards hypersensitivity)
2) Blood tests – Serum allergen-specific IgE, serum mast cell histamine
3) Skin prick tests using a range of allergens – Wheel and flare reactions

29
Q

How can you manage an allergy?

A
  • Allergy avoidance
  • Education – how to recognise symptoms, use epipen etc.
  • Medic alert identification – wear a band identifying allergies
  • Drugs – anti histamines, anti-IgE IgG, injectable adrenaline
  • Emerging evidence that slow exposure to very small amounts of allergen increasing over time can desensitise patients
30
Q
A