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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
How do hypersensitivity reactions usually present? (Hint: like 1st, 2nd exposure..)
Sensitization phase: first encounter with antigen (produce immune response; clinically silent) Effector phase: re-exposure to same antigen leading to clinical pathology.
26
What are the four types of hypersensitivity reactions?
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
What are Type 1 hypersensitivity (or allergic) reactions due to?
Environmental non-infectious antigens (allergens). They are driven by the production of IgE.
28
What is a life-threatening result of allergy? How can we prevent this?
Anaphylactic shock - treated with epipen (IM epinephrine).
29
What is the hygiene hypothesis?
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
What are some common allergens?
House dust mites, dogs, pollen, bee stings, penicillin, peanuts, latex, etc.
31
With regards to allergy, what is clinical cross-reactivity?
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
Which cell is the mastermind behind allergy?
Mast cells - activated by IgE.
33
What mediators do mast cells release when activated?
Histamine (increases vascular permeability to WBCs, causes smooth muscle contraction) and Chemokines: CCL3 (attract macrophages/monocytes and neutrophils)
34
How can mast cells be activated?
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
What will the mast cell release when it degranulates? How will this affect the body?
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
How do you diagnose allergy?
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
What is a skin prick test?
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
What is allergy in the epidermis known as?
Urticaria (hives).
39
What is allergy in the deep dermis known as?
Angioedema. There is swelling of the lips, eyes, tongue and upper respiratory airways.
40
Why is adrenaline used to treat anaphylactic shock?
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
What is allergic rhinitis?
Hay fever - usually due to a pollen allergy.
42
How do we manage allergy?
Allergen avoidance (cleaning - house dust mites; read food labels); Education (EPIPEN, others to recognise symptoms); Medic alert identification (e.g. penicillin allergic wristband).
43
How do we treat allergy?
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
What is allergen desensitisation (or immunotherapy)?
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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