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DJ - ESA 3 - Infection > Infection On Surfaces / Allergy > Flashcards

Infection On Surfaces / Allergy Flashcards

1
Q

What is a surface?

A

The interface between a solid and a liquid or gas.

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2
Q

Considering the patient (one of the 4 P’s or determinants of disease), what are some examples of surfaces?

A

Skin: Epithelium, Hair, Nails.

Mucosal surfaces: Gastrointestinal, Respiratory, Genitourinary, Conjunctival.

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3
Q

What are some examples of normal flora on the skin surface?

A

Bacteria: Staph aureus, coagulase negative staphs (gram positive), Enterobacetriaceae (gram negative),
Viruses: Papilloma, herpes simplex,
Fungi: Yeasts, dermatophytes,
Parasites: Mites.

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4
Q

What is an example of normal flora in the nares?

A

The nares (nostrils) normally have staph aureus.

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5
Q

What constitutes the normal flora of the nasopharynx?

A

Neisseria meningitidis, streptococcus pneumoniae, haemophilus influenzae (all cause MENINGITIS; possible septicaemia).

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6
Q

What is an important example of normal flora in the mouth?

A

Strep viridans (infective endocarditis).

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7
Q

What are some examples of normal flora in the stomach?

A

Helicobacter pylori, streps and staphs.

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8
Q

What are some examples of normal flora in the intestines?

A

Bacteroides fragilis, coliforms (E. Coli), clostridium (C. Diff.).

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9
Q

What is an important example of normal flora in the vagina?

A

Lactobacilli.

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10
Q

When is normal flora on skin or a mucosal surface a problem?

A

When these commensals are transferred to other sites.

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11
Q

What are some of the mechanisms in which patients can get infection from surfaces?

A

Invasion (strep pyogenes - pharyngitis).
Migration (UTI - E. Coli via faecal-perineal-urethral route).
Inoculation (coagulase negative staphs, also staph aureus - prosthetic joint infection).
Haematogenous (strep viridans - infective endocarditis).

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12
Q

How can ‘natural surface infections’ be divided?

A

External - pharyngitis, UTI, pneumonia etc.

Internal - endocarditis, vasculitis etc.

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13
Q

What are some important pathogens that may cause infective endocarditis?

A

Strep viridans
Enterococcus faecalis
Staph aureus (more common in IV drug users … and USA…)
Prosthetic valves increase risk - lose natural defence.
Bacteria with good adherence can result in infective endocarditis - E. Coli does not have this.

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14
Q

What are some examples of prosthetic surface infections?

A 
Prosthetic joints,
Prosthetic heart valves & Pacing wires (increase risk of infective endocarditis),
Intravascular lines (catheterisation increases risk of UTIs).
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15
Q

Explain the pathogenesis of infection at surfaces.

A

Adherence of pathogen to host cells or prosthetic surface.
These pathogens form a biofilm (must be able to adhere to surfaces to do this).
The pathogen invades and multiplies.
The host responds: PYOGENIC (neutrophils –> pus) or GRANULOMATOUS (fibroblasts, lymphocytes, macrophages –> nodular inflammatory lesions).

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16
Q

What are important structures in bacteria to increase adherence?

A

The presence of fimbriae (same as pili).

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17
Q

How do bacteria form biofilms?

A

In a deprived state, bacteria can shrink and become spore-like (C. Diff). When no longer starved these bacteria can attach to and grow on a surface. More bacteria attach and encase the colonies with a slimy matrix.

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18
Q

Why is the biofilm so beneficial to the bacteria?

A

Nutrients can diffuse into it and bacteria can easily communicate through molecular signals.

19
Q

Why are biofilms so difficult to get rid of?

A

Antimicrobials can damage the outer layers of cells but the cells within the biofilm are all resistant.

20
Q

What is quorum sensing?

A

How bacteria communicate with each other (communicating gene expression). This can assist them in biofilm formation, virulence and antibiotic resistance.

21
Q

What are the unique challenges of dealing with infections of surfaces?

A

Pathogens may have a high adherence. They may form biofilms or not require much energy to survive.

22
Q

How can we manage infections of surfaces?

A

Antibacterials.
Removing prosthetic material (e.g. heart valve, joint).
Surgery (removal of infected material).

23
Q

How can we prevent infections at surfaces?

A

Natural e.g. maintain surface integrity.

Prosthetic e.g. prevent contamination (sterilising prostheses).

24
Q

What is a hypersensitivity reaction?

A

The antigen-specific immune responses that are inappropriate or excessive and result in harm to the host.

25
Q

How do hypersensitivity reactions usually present? (Hint: like 1st, 2nd exposure..)

A

Sensitization phase: first encounter with antigen (produce immune response; clinically silent)
Effector phase: re-exposure to same antigen leading to clinical pathology.

26
Q

What are the four types of hypersensitivity reactions?

A

Type I: immediate (<30 min) = ALLERGIES
Type II: antibody mediated (5-12 hours)
Type III: immune complexes mediated (3-8 hours)
Type IV: cell-mediated (T-cells… 24-48 hours) - due to environmental infectious agents and self antigens.

27
Q

What are Type 1 hypersensitivity (or allergic) reactions due to?

A

Environmental non-infectious antigens (allergens). They are driven by the production of IgE.

28
Q

What is a life-threatening result of allergy? How can we prevent this?

A

Anaphylactic shock - treated with epipen (IM epinephrine).

29
Q

What is the hygiene hypothesis?

A

That those with an increased exposure to potential allergens from an early age are less likely to develop allergy. This is represented through two phenotypes: TH1 (non-allergic) and TH2 (allergic: IgE production, increased risk of asthma, eczema, rhinitis).

30
Q

What are some common allergens?

A

House dust mites, dogs, pollen, bee stings, penicillin, peanuts, latex, etc.

31
Q

With regards to allergy, what is clinical cross-reactivity?

A

The likelihood of allergy to one thing, will mean that you’re allergic to another.
Strong links: cow with goat milk; (shell)fish with other (shell)fish; peanuts with tree nuts; latex with certain fruit (banana, kiwi, avocado).

32
Q

Which cell is the mastermind behind allergy?

A

Mast cells - activated by IgE.

33
Q

What mediators do mast cells release when activated?

A

Histamine (increases vascular permeability to WBCs, causes smooth muscle contraction) and Chemokines: CCL3 (attract macrophages/monocytes and neutrophils)

34
Q

How can mast cells be activated?

A

2 mechanisms:
IgE-dependent: Plasma cell produces IgE which binds to the surface membrane on the mast cell in abundance. Cross-linking of the antigen-specific IgE and antigen results in degranulation of the mast cell.
‘Irritants’: C3a, C5a etc. can directly activate the mast cell.

35
Q

What will the mast cell release when it degranulates? How will this affect the body?

A

Histamine and chemokines.
This will increase vascular permeability, vasodilate (hence low BP in anaphylactic shock), or bronchoconstrict (due to uniqueness of lungs, can cause wheezing).

36
Q

How do you diagnose allergy?

A

History: other allergens? seasonal? route of exposure?
Based on the blood or serum levels of mast cell products (tryptase, histamine… allergen-specific IgE could be tested). A skin prick test can also be carried out.

37
Q

What is a skin prick test?

A

Potential allergens are given through the epidermis (there must be a prick) - histamine is used as a control. A wheal and flare reaction >3mm = allergy. There is a risk of anaphylaxis.

38
Q

What is allergy in the epidermis known as?

A

Urticaria (hives).

39
Q

What is allergy in the deep dermis known as?

A

Angioedema. There is swelling of the lips, eyes, tongue and upper respiratory airways.

40
Q

Why is adrenaline used to treat anaphylactic shock?

A

Reverses peripheral vasodilation (can reduce (angi)oedema) - a1. Increases force of myocardial contraction - B1. Reverses airway obstruction - B2. Adrenaline will also inhibit further mast cell activation.
Must be given intramuscularly to be effective and within 30 minutes of exposure.

41
Q

What is allergic rhinitis?

A

Hay fever - usually due to a pollen allergy.

42
Q

How do we manage allergy?

A

Allergen avoidance (cleaning - house dust mites; read food labels); Education (EPIPEN, others to recognise symptoms); Medic alert identification (e.g. penicillin allergic wristband).

43
Q

How do we treat allergy?

A

Drugs: Anti-histamines, corticosteroids (reduce inflammation), anti-IgE IgG (omalizumab), Epipen IM.
Can consider allergen desensitisation in those with high risk of systemic attacks.

44
Q

What is allergen desensitisation (or immunotherapy)?

A

Exposure to increasing doses of allergen extracts over a period of years (via injection or sublingual - drops/tablets under the tongue). Works through increasing number of inhibitory anti-inflammatory cytokines and increasing production of allergen specific blocking IgG,

DJ - ESA 3 - Infection (12 decks)

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