S7: infections at a surface & adaptive immunity Flashcards
Describe the antigen receptor present on both B cells and T cells
T cells = T cell receptor (TCR): alpha & beta chains -helper T cells (CD4) recognise peptide presented by MHC class II molecules -cytotoxic T cells (CD8) recognise peptide presented by MHC class I molecules B cells = B cell receptor (BCR): membrane bound antibodies -recognises macromolecules & small chemicals
What are the effector functions of the different antibodies?
IgG = Fc-dependent phagocytosis, complement activation, neonatal immunity & toxin/virus neutralisation
IgE = immunity against helminths, mast cell degranulation (allergies)
IgA = mucosal immunity
IgM (only one where production is T helper independent) = complement activation
List which interleukins stimulate which T-helper cell
(all secreted by naïve CD4+ T cells)
IL-12 -> Th1 = CD8+ T cells: differentiation, macrophages: recruitment & activation, B cells: IgG or IgA production
IL-4 -> Th2 -> B cells: IgE production, eosinophils: killing of pathogens, mast cells: allergies
IL-1/IL-6 -> Th17 -> neutrophils: recruitment & activation
IL-10 -> Treg -> tolerance & immune suppression
What is the difference between cell mediated immunity and humoral immunity?
Cell mediated immunity = defence against intracellular & extracellular pathogens
-done by Th1 response
Humoral immunity = defence against extracellular pathogens
-done by Th2 & Th17 response
Describe the pathogenesis of infections at a surface
1) Adherence to host cells or prosthetic surface
2) Biofilm formation
3) Invasion and multiplication
4) Host response
5) Pyogenic
6) Granulomatous
Explain a ‘biofilm’ and the implications for an infection on a surface
Biofilms comprise of microbial communities that are attached to surfaces and encased in an extracellular matrix of microbial origin
Protect the bacteria by preventing bacterial phagocytosis, antibodies & complement recognition/binding of receptors
How do you treat patients with biofilm infections?
Sterilize tissue & reduce bioburden on tissue
Can do this via antibacterial drugs & removing prosthetic material with surgery
Challenges: poor antibacterial perforation into biofilm & dangers/difficulties of surgical procedures
What are common biofilm infections?
Prosthetic valve endocarditis
Cardiac pacing wire endocarditis
Prosthetic joint infections
Describe endocarditis infection & its clinical symptoms
Formation of vegetation that binds to valves or mural endocardium (abhorrent flow predisposes to a collection of fibrin, platelets & scant inflammatory cells) = BIOFILM
Clinical features: fever, heart murmur, other cardiac complications & embolic features (Janeway lesions, splinter haemorrhages)
Duke criteria used for diagnosing endocarditis
Describe the management of infected surfaces
Sterilisation is key to prevent biofilm formation
Efficacy of antimicrobials to treat biofilms is limited
List the five steps to produce a biofilm
1) Bacteria adopt a spore-like state under starvation/limited nutrients availability
2) Once they encounter an environment suitable for growth they go from a ‘swimming’ state to a ‘sticking’ state & attach to the chosen surface
3) Bacteria start to multiple, forming colonies & adhering to each other
4) Matrix allows for diffusion of nutrients between bacteria + allows for transmission of molecular signals between cells -> allows behaviour of the entire biofilm to be regulated
5) Under certain circumstances, bacteria can detach from their matrix & invade other structures
What are 4 key principles required in the process of biofilm formation?
1) Quorum sensing – modulation of gene expression in response to changes in cell population density
2) Release of a signal (autoinducer) – when a quorum (critical number of bacteria required) has been reached
3) Receptor for the signal – on the bacteria to carry out the process
4) Switching mechanism – alter gene expression to carry out the process
