Infection S7 (Done) Flashcards
Give examples of surfaces found on patients
Skin (And accessory nairs, hair)
Mucosa:
GI
Resp
Conjuctiva
Genitourinary
Give examples of viruses found living on the skin under physiological conditions
Papilloma
Herpes simplex
Give examples of normal skin bacterial commensals
Gram positive:
Staph aureus
Coagulase negative staphylococci
Gram negative:
Enterobacteriaceae
Give examples of normal skin fungi and parasites
Fungi:
Yeast
Dermatophytes
Parasites:
Mites
How can commensals become harmful?
Immunocompromise
Spread to another site
By what methods can pathogenic microbes cause infection/enter the body?
Invasion:
Strep pyogenes pharyngitis
Migration:
E. coli UTI
Innoculation:
Coagulase (-) staphylococcus prosthetic joint infection
Haematogenous:
viridans strep endocarditis
Give examples of internal and external surface infections
External:
Cellulitis
Pharyngitis
Conjunctivitis
Gastroenteritis
UTI
Pneumonia
Internal:
Envovascular (Endocarditis, vasculitis)
Septic arthritis
Osteomyelitis
Empyema
Give examples of prosthetic surface infections
Urethral catherter (most common HAI)
Intravascular lines
Peritoneal dialysis catheters
Prosthetic joints
Cardiac valves
Pacing wires (Endocarditis)
Endovascular grafts
What are the common causative organisms of endocarditis?
Native valve or >1yr post operation for prosthetic replacement:
viridans Strep
Enterococci faecalis
Staph aureus
Candida albicans
Prosthetic valve <1yr post op:
Coagulase (-) staph
What are the common causative organisms for infection from prosthetic joints?
Coagulase (-) staph
Staph aureus
What are the common causative organisms for infections from cardiac pacing wires?
Coagulase (-) staph
Staph aureus
What are the processes involved in pathogensis of infection on surfaces?
Adherence to host cells or prosthetic surface
Biofilm formation
Invasion and multiplication
Virulence factors actions and host response
Host response may be pyogenic (Neutrophils/Pus) or granulomatous
What is a biofilm?
What are their functions?
An aggregation of microbes on a surface surounded and encased in a slime matrix
Functions:
Create a favourale environment for growth, replication and exhange of chemical messengers allowing regulation of the colony as a whole
Protection from harmful substances and cells (E.g. Antibiotics and WBCs)
How is a biofilm formed?
Motile bacteria attach to a surface (aided by Pili/Fimbriae in some cases)
Attached bacteria multiply and produce a slimy matrix
Nutrients diffusie into the matrix and chemical gradients are produced that create microenvironments ideal for the bacteria
What is quorum sensing?
The co-ordination of bacteria in a colony to produce behaviours such as biofilm production, incresing virulence and antimicrobial resistance
This is a acheived through local signalling molecules (Autoinducers) and cell surface receptors allowing bacteria to sense the density of the local population and co-ordinate behaviours to adapt to that via changing gene expression
Changes in gene expression made across an entire colony of bacteria allow co-operative behaviours such as those mentioned above
How is diagnosis of surface infections approached?
Aim to identify organism and antimicrobial susceptibilities
This can be achieved through:
Blood cultures
Tissue biopsy
Sonification of prosthetics to disrupt bacterial biofilm and allow accurate diagnoses
What are the challenges of bacterial surface infection diagnoses?
Adherence of organisms to tissue/prosthetic, possibly in a biofilm
Low metabolic state in biofilms
Small colony variants of species in a biofilm amke antibiotic susceptibility harder to assess
Outline a general management plan for a patient with a surface infection
Sterilise tissue and reduce bioburden
Antibacterials
Removal of prosthetic
Surgery (resection of infection/Infected material)
What challenges are presented by surface infections to management of that infection?
Poor antibiotic penetration into the biofilm
Low metabolic activity in biofilm
Dangers/difficulties of surgery
What are the principles of prevention for surface infections?
Natural surface/tissue:
Maintain surface integrity
Prevent colonisation
Remove colonising bacteria
Prosthetic surfaces:
Prevent contaimination
Inhibit surface colonisation
Remove colonising bacteria
Define ‘Hypersensitivity’
An antigen specific immune response that is innappropriate or excessive and results in harm to the host
What are the 2 phases of hypersensitivity development?
Sensitisation:
First encounter with antigen
Effector:
Clinical pathology results from second exposure to same antigen
List the types of hypersensitivity reaction and the time frame within which it occurs post exposure
Type 1 - Immediate (<30mins)
Type 2 - 5-12hrs
Type 3 - 3-8hrs
Type 4 - 24-48hrs
Give a brief describption of type 1 hypersensitivity
Typically known as ‘Allergic reaction’
Environmental, non-infectious antigens trigger mast cell response
IgE mediated
Give a brief description of type 2 hypersensitivity
IgG or IgM mediated
IgG or IgM bind to antigen on a target cell which is in fact a host cell
Cell mediated immune response occurs
Give a brief description of type 3 hypersensitivity
Reaction to the formation of Immune complexes (Soluble antigen and antibody)
When not adequately cleared from circulation by macrophages can be deposited in tissues giving rise to an inflammatory reaction
Give a brief description of type 4 hypersensitivity
Cell mediated immune response to environmental antigens and self antigens
In the case of self antigens, this can lead to the distruction of tissues via cytotoxic action of T cells
‘Autoimmune disease’
Why do people have allergies?
Hygiene hypothesis:
In areas a good sanitation, High antibiotic use and as a result a population with a low helminth and faeco-oral burden Allergic disorders are more likely to occur as a result of the immune system not developing as it should
Conversely, in area of low sanitation, low antibiotic use etc there is a lower prevalence of allergy
Genetics:
Genetic factors seem to contribute to the production of TH1 phenotype (allergy resistant) and TH2 phenotpye (allergy prone)
TH2 phenotype is characterised by increased IgE levels, the mediator of Type 1 hypersensitivity reaction
List some common allergens
House mites, dust, Animals (pets in particular)
Tree and grass pollen
Insect venom (stings)
Medicines (Penicillin)
Chemicals such as Latex
Foods (Milk, Peanuts, nuts)
What is Allergic cross-reactivity?
Give an example
Often people with one allergy have an increased chance of having a related allergy
If someone is allergic to cow’s milk, there is 92% risk of reaction to goat’s milk
What are some of the mast cell mediators involved in type 1 hypersensitivity reactions?
Enzymes (tryptase)
Histamine, Heparin
Cytokines (IL-1, TNF-a)
Leukotrienes
Describe the 2 immune system mechanisms of allergic reactions
Indirect:
Allergen has 1st exposure and antibodies are created
Plasma cells persist production of specific IgE after antigen cleared
IgE binds to cell surface receptors of Mast cells ‘sensitising’ them
Second exposure causes crosslinking of mast cell bound IgE
Mast cell degranulation occurs triggering release of granules content (Histamine/Chemokines) and the synthesis of new mediators (Prostaglandins/Leukotrienes)
This leads to local or systemic effects such as increased vascular permeability, vasodilation and bronchial constriction
Direct:
As above however mast cell doesn’t need to be desensitised, Degranulation occurs in respinse to ‘irritants’ (E.g. C3a, C5a)
Outline the skin prick test for allergy
Allergen is introduced in small amounts into patients skin via a pinprick on the skin
A wheal and flare reaction indicative of local allergic reaction is looked for
Size of reaction indicates severity of allergy
Needs trained personnel due to risk of anaphylaxis
Give 2 skin manifestations of allergic reaction
Urticaria:
Raised, itchy wheals appear on the skin as a result of allergic reaction in the upper dermis
Angioedema:
rapid swelling (oedema) of the dermis, subcutaneous tissue, mucosa and submucosal tissues of the skin
Can lead to airway obstruction
What are the effects of systemic activation of mast cells?
Anaphylaxis:
Hypotension (Cardiovascular collapse)
Generalised urticaria
Angioedema
Bronchial constriction (Wheezing and suffocation may result)
What is the first line treatment for anaphylaxis?
List it’s actions
IM Adrenaline (Epipen):
Reverses peripheral vasodilation and reduces oedema
Reverses airway constriction/bronchospasm
Increases contractile force of myocardium
Inhibits mast cell activation
Give 2 examples of respiratory allergic reactions and their common allergens
Allergic rhinitus:
Pollen
Dust mite faeces
Asthma:
Danders (cat)
Pollen
Dust mite faeces
How is diagnoses of an allergy made?
Clinical history:
Atopy, allergens, seasonality, route of exposure
Blood tests:
Serum IgE
Serum Mast cell tryptase, histamine
Skin prick test:
Wheal and flare over >3mm
Challenge tests:
Give them the thing they’re allergic to and just see what happens
Give some techniques for allergy management
Avoidance:
Read food packaging
Avoid high risk situations
Education:
EPIpen use (and calling the ambulance after!)
Parents to recognise symptoms
Medic alert ID
Densensitisation:
Repeat exposure to allergen to desensitise (highly controlled, highly effective)
Drugs:
Anti-histamines
Corticosteroids
Anti-IgE, IgG
Epipen
Define Desensitisation
Administration of increasing dose of allergen extracts over a period of years given IV, Oral or Sublingual
90% effective in patients with Insect venom Anaphylaxis
