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My Cards- Infection > Week 7 Infections On Surfaces/ Allergy > Flashcards

Week 7 Infections On Surfaces/ Allergy Flashcards

1
Q

Describe the range of normal microbiota

A

Mocosal flora

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2
Q

What is a surface?

A

Interface between a solid and either a liquid or gas

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3
Q

How do people get infections?

A
  • Invasion- strep pyogenes pharyngitis
  • Migration- E. coli UTI
  • Inoculation- coagulase negative staphylococcus prosthetic joint infection
  • haematogenous- virions strep endocarditis- circulates from mouth to bloodstream then to valves- if damaged sticks and multiples
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4
Q

What are surface infections important?

A

Produce biofilms which protect the bacteria from host and AB attack

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5
Q

Describe the ‘patient’ surfaces from the infection model?

A

Surfaces:
Skin- epithelium, hair, nails
Mucosal surfaces- conjunctiva, gastrointestinal- H pylori- peptic ulcers and cancers, respiratory, genitourinary

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6
Q

Describe biofilm formation- 8 steps

A
  1. Starvation of bacteria= shrink, spore like called ultramicrobacteria-> wait in soil, rock, tissue until suitable conditions for growth
  2. Active bacteria attach to anything- change in gene expression- swimmers to stickers
  3. Attached bacteria multiply, encase colonies within slimy matrix
  4. Nutrients diffuse int matrix
  5. Close proximity of cells in matrix aids exchange of molecular signals that regulate behaviouri
  6. Chemical gradients creates micro environments for different species or levels of activity
  7. Antimicrobials damage outer cell layers but biofilm community resistant
  8. Aggregated cells can detach or roll or ripple along a surface in sheets, remaining in protected biofilm state - can embolise- block small blood vessels- necrotic tissue- release nutrients allowing bacteria to grow= multiple abscesses- common on brain from endocarditis
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7
Q

What is quorum sensing, what does it control and what are the 3 principles?

A

communication between bacteria- bacteria actively secrete molecules into environment then sense how much is out there- from themselves and possibly other bacteria- stimulate biofilm formation together by coordinate gene expression according to the density of their local population.
It controls- sporulation, biofilm formation, virulence factor secretion
Three principles
- signalling molecules- autoinducers (AI)
- cell surface or cytoplasmic receptors
- gene expression-> co operative behaviours and more AI production

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8
Q

Give some examples of natural surface infections- internal and external?

A

External- cellulitis- can lead to sepsis- staph aureus in blood, pharyngitis, conjunctivitis, gastroenteritis, UTI, pneumonia in alveoli
Internal- endovascular (endocarditis (valves), vasculitis (vessels)), septic arthritis (joints- spongey bone interacting with bloodstream), osteomyelitis, empyema (between 2 pleural lining)

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9
Q

Give some examples of prosthetic surface infection?

A
  • Intravascular lines- venflon- if left to long bacteria on skin move to plastic- set up local infection- tract along veins and can=systemic infection if enters bloodstream, central lines- bigger and longer use so more chance of infection, hickman line- cancer burried subcutaneously as need high blood flow to dilute
  • peritoneal dialysis catheters, prosthetic joints, cardiac valves, pacing wires, endovascular grafts, ventriculo- peritoneal shunts
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10
Q

What are some common skin microorganisms- viruses, bacteria, fungi and parasites?

A
  • Viruses- papilloma (warts), herpes simplex
  • Gram +ve bacteria- staph aureus (1/3carry it), coagulate negative staphylococci (all carrying), corynebacterium
  • gram -ve bacteria- enterobacteriaceae- coliforms= ecoli, klebsiella pneumonia- facultative aerobes- lactose fermenting for energy source- in L bowel and skin
  • Fungi- yeast, dermatophytes (athletes foot, ringworm)
  • parasites- mites
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11
Q

How do microorganisms cause disease?

A 
Virulence factors
- exotoxins- cytolytic, AB toxins, superantigens, enzymes
- endotoxins 
Host cellular damage
- direct
- consequent to host immune response
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12
Q

What is the difference in causes of prosthetic valve endocarditis >1 year and

A

> 1 year viridans streptococci, enterococcus faecalis, staph aureus (bloodstream infection), HACEK group, candida

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13
Q

How are surface infections treated?

A 
Aim- sterilise tissue, reduce bioburden
Antibacterial soap
Remove prosthetic material
Surgery- respect infected material
Challenges- poor AB penetration of biofilm, low metabolic activity of biofilm microorganisms, dangers/ difficulties of surgery
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14
Q

How are surface infections prevented- 3 natural and prosthetic?

A

Natural surfaces- maintain surface integrity, prevent bacterial surface colonisation, remove colonising bacteria
Prosthetic surfaces- prevent contamination, inhibit surface colonisation, remove colonising bacteria

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15
Q

What are the common causative organisms of prosthetic joint infections and cardiac pacing wire endocarditis?

A

Both - Coagulase negative staphylococci, staphylococcus aureus

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16
Q

Name the important steps in allergic reactions starting with trigger- use example of beesting?

A

Trigger eg. bee sting,
timing before symptoms- shortly after sting,
symptoms- resp- wheezy, difficulty breathing, cardio- lightheaded BP 80/40, skin- rash, face- swollen
Therapy- IM of epinephrine
Outcome-death
Why? - had been stung 2 yrs ago- local reaction only

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17
Q

What is the pathogenesis of infections on a surface?

A

Adherence to host cells or prosthetic surface- pili or fimbriae
Biofilm formation
Invasion and multiplication
Host response- pyogenic (neutrophils-> pus), granulomatous (fibroblasts, lymphocytes, macrophages-> modular inflammatory lesions)

18
Q

How are surface infections diagnosed?

A

Diagnosis

  • identify organism and its Antimicrobial susceptibility
  • challenges- adherent organisms, low metabolic state/small colony variants
  • blood cultures
  • tissue/ prosthetic material sonics toon and culture
19
Q

how does prosthetic valve endocarditis come about?

A

turbulent blood flow across valve- peel off endothelium
poor oral hygiene- bacteria from mouth to bloodstream- usually removed by phagocytes and spleen- if settles on sub-endothelial tissue around valve= infection

20
Q

What are the different types of hypersensitivity reactions?

A

type 1- immediate

21
Q

What is hypersensitivity?

A

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

22
Q

What are the two stages of hypersensitivity reactions?

A

Sensitisation phase- first encounter with antigen- immune response driven, keeps memory of it but is a silence response
Effector phage- clinical pathology upon re- exposure with SAME antigen

23
Q

What is microbiota?

A

Commensals- microorganisms carried on skin and mucosal surfaces- normally harmless or even beneficial, harmful if transfer to other sites

23
Q

what are the different types of hypersensitivity reactions- time, mediators, process?

A

type 1- immediate

24
Q

What is the significance of TH1 and TH2 phenotype in relation to allergies?

A

Born with TH2 phenotype- favoured in developed countries- IgE production
Want TH1 as this is correct immune response- develops in children growing up in developing countries

25
Q

How can different childhoods affect likelihood of having allergies?

A

Exposure at a young age to allergens and infective microbes would make immune system enter protective stage- more likely to be protected against allergies
- Developing countries where less use of ABs, rural homes, in contact with livestock, poor sanitation and with large family sizes are less likely to have allergies.

26
Q

What are some of the most common allergens?

A 
House dust mites, animals, 
Tree and grass pollen
Insect venom- wasps and bee stings
Medications- penicillin
Chemicals- latex
Foods- peanuts, milk
27
Q

Explain Clinical cross- reactivity

A

Allergies to certain things increase risk of allergies to other things
Different allergens have same proteins that share same homology
Eg cows milk and goats milk, shellfish and other shellfish

28
Q

Which cells are involved in allergic reactions- what is driving it?

A

Mast cells- big nucleus and cytoplasm
Has many different granules containing different mediators driving alleged responses
Are close to blood vessels and present on all mucosal surfaces- GI and resp symptoms
- regulate acute and early phases of inflammation
- all granules released near blood vessels

29
Q

What are some important Mast cell mediators in acute reactions

A

toxic mediators- prostaglandins Histamine and heparin

lipid mediators- leukotrienes C4, D4 and E4, and platelet activating actor

30
Q

describe the immune mechanisms of allergic reaction- 1st and 2nd encounters

A

1st encounter sensitisation to allergen - IgE produced but no symptoms
2nd encounter- Cross linking of IgE- mass cells- activate it and triggers release of granules containing- histamine, chemokines and the synthesis of new mediators- leukotrienes and prostaglandins
- increased vascular permeability
- vasodilation- loss of fluid
- Act of muscle in lungs- bronchoconstriction

31
Q

Describe the manifestations of allergic reactions in the skin- dermis and epidermis

A

mast cells in the epidermis- urticaria

mast cell in deep dermis- angioedema- fluid going into tissue- lips,, eyes, tongue, and Upper resp tract

32
Q

How do you treat anaphylactic shock and how does this work?

A

Epinephrine (adrenaline) intramuscular
- Reverse peripheral vasodilation and reduces oedema and alleviate hypotension
- Reverse airway obstruction/bronchospasm- bronchodilation
- Increase force of myocardial contraction
- Inhibits mast cell activation
TREATMENT NEEDS TO BE GIVEN IMMEDIATELY

33
Q

What are some of the key points about epinephrine?

A

Timesaver- lifesaver
IM not SC
Biphasic reaction- Will be second anaphylaxis phases triggered without allergen- multiple doses may be needed- should carry 2 epipens

34
Q

What are some of the common allergic diseases- allergens, route of entry, response?

A
  • Systemic anaphylaxis- drugs, serum, peanuts- IV entry- oedema, increased vascular permeability, circulatory collapse
  • Acute urticaria- animal hair, insect bites- through skin- local increase in blood flow and vascular permeability
  • Allergic rhinitis (hey fever)- pollens, dust- inhalation- oedema of nasal mucosa
  • Asthma- animal danders, pollen- inhalation- bronchiocontriction, >mucus, airway inflammation
    Food allergy- nuts, milk, eggs- oral route- vomiting, diarrhoea
35
Q

what are biofilms and how are they beneficial to bacteria?

A

any group of microorganisms where cells stick to each other on a surface- frequently embedded within a self-produced matrix of extracellular polymeric substance (EPS)- mucopolysaccharides produced and secreted- contains extracellular DNA, proteins, and polysaccharides- creates 3D extracellular biofilm membrane over top
- helps bacteria adhere and protects them from host macrophages, complement and ABs- cannot penetrate film

36
Q

How are allergies diagnosed?

A
  • Clinical history- what driving response (atrophy)- is it there all year- seasonality, route of exposure
  • blood tests- stages of sensitisation- serum allergen- specific IgE
    Serum mast cell tryptase, histamine- systemic degranulation
  • Skin prick test- range of allergens- wheal and flare reaction
  • challenge test- food and drug allergy - risk of anaphylaxis
37
Q

What are some of the common signs of anaphylaxis?

A

Involves more than 1 system-
- CNS- lightheadedness, loss of consciousness, confusion, headache, anxiety
- Resp- SOB, wheezy, hoarseness, pain swallowing, cough
- GI- crampy abdo, diarrhoea, vomiting
- skin- hives, itchiness, flushing
- Heart and vasculature- fast or slow HR, low BP
swelling of lips, runny nose

38
Q

What are the systemic manifestations of allergic reaction- anaphylaxis?

A

Systemic absorption and reaction to allergen- insect, venom
= systemic activation of mast cells = hypotension, cardiovascular collapse, generalised urticaria, angioedema, breathing problems

38
Q

what is involved in the management of allergy?

A
  • allergen avoidance/elimination- read food labels, house dust mite avoidance, avoid high risk situations
  • education- parents recognise symps, correct use of epipen, call 999 when epipen used- often needs to be used more than once
  • medic alert identification
  • drugs- anti histamines, corticosteroids, anti IgE IgG (omalizumab), anaphylaxis- inject adrenaline
  • allergen desensitization- pt with high risk of systemic attacks
39
Q

what is allergen desensitisation?

A

administration of increasing doses of allergen extracts over a period of years- given to pts by injection or drops/tabs under tongue- sublingual
99% effective in pts with bee and wasp venom anaphylaxis

39
Q

what are some possible mechanisms of allergen desesitisation?

A

shift from TH2 to TH1

allergen specific blocking IgG

My Cards- Infection (9 decks)

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