Lecture 21 - 25 overview Flashcards
IGM
IgG
igA
igE
- blood borne infectiosn (bacteria) . primary response, effective agglutinator
- good at viral infections, child has high levels of this - given from mother crosses placenta, can enhance pahgocytosis
- main role - external body surfaces, surface protection of gut, resp and genitourinary tracts
- important in parastiic infections and allergins, bind storngly to mast cells
Skin graft rejection
-what happens with primary graft vs secondary graft
First graph - taken from a different person, has been sewn into place
- if it is not compatable with recepipietn then will look like big blood dot thats dead- dies due to immune response due to T cell mediated recognising the antigen and responding
- Second graft - from same donor to same recipient where graft doesnt vascularise very wel, and is rejected quickly - will be more immediate as memory cells will be there and will be mostly antibody mediated
Cytotoxic T cell action
-3 ways of action
- perforin and enzymes
- hydrolytic enzymes
- cytokins for apoptosis
B cell maturity
- have a heavy chain - V,D,J these are reanranged into many different combinations to make alot of different antigen sensitivities
- then have 2 light chains - these can be choped and form differnt forms of antibodies e.g igg vs igm
-bone marrow - igM is the antibody receptor type, however when it gets tests agaisnt slef antigen then will make igD and be a mature b cell
Main bacteria causing infective endocarditis , main treatment
Viridans streptococci - in mouth
-aplha haemolysis
IV Pencillin for one month
what are the main valves affected?
aortic and mitral
why does this occur to some people?
- generally occurs to people with an abnormal heart valve - usually mitral or aortic could be due to rheumatic fever, or genetic
- leads to rough surface, and then can get platelets and firbin attatchign to the damaged valvular epithelium which form vegetations
- organsims living in the mouth can get out when chewing on food and get into capilaries and get into blood
- neutrophils usually kill them
- howver these types of bacteria can easily stikc onto platelets and firbin and some can stick onto heart valve with the fibrin platelet clot
- also could be due to staph in nose and this can also stick to the heart valves
- infected vegetation enlarges and sheds infected emboli and leads to vavlular destruction
Rhematic fever vs endocarditis
Endocardi)s -get bloods viridans streptococci + others mouth commensals infec)on of valves vegeta)ons on valves treatment with IV penicillin for one month prophylaxis with oral penicillin when dental work
Rheuma)c Fever
-take throat swab
Streptococcus pyogenes only pharyngi)s
immunologic damage to valves nodules on valves
treatment with oral penicillin for 10 days
prophylaxis with IM penicillin for many years
Rhematic fever vs endocarditis
Endocarditis -get bloods viridans streptococci + others mouth commensals infec)on of valves vegeta)ons on valves treatment with IV penicillin for one month prophylaxis with oral penicillin when dental work
Rheuma)c Fever
-take throat swab
Streptococcus pyogenes only pharyngi)s
immunologic damage to valves nodules on valves
treatment with oral penicillin for 10 days
prophylaxis with IM penicillin for many years
Differences between viral, bacterial or protozoa cause of gastroenteritis
Bacterial - may get blood in stool if the bacteria gets into the intestine
- Colonisation of intestines and the production of toxins
- clostridium difficle
- escherichia coli
- vibrio cholerae
- Colonisation of intestines invasion of intestinal tissue (may see blood in stool)
- campylobacter jejuni
- salmonella
- escherichia coli
- toxin produced in food and ingested, no infection - food poisoning (generally short lived, symptoms cleared within 1-2 days)
- staphylococcus aureus
- clostridium perfringens
Viral (rota virus, norovirus) - watery dihorrhea
Protozoa - can last for 4-6 weeks
Bacteria diagnostic tests
1 stool culture - want to confirm the carrier
-grow on sheep blood agar, macconkey agar with lactose, macconkey agar with sorbitol ect.
treatment
- Most important - replace fluid, sugar and salt
- easily digestable food
- anti-motility drugs - can be bad if the toxins and bugs are trapped
antibiotics - not usually required, may have small effect on severity and duration of symptoms, however may reduce the numbers shed
- is used for C. difficlie
- salmonella/campylobacter if patient progresses to or risks of systemic infectin
35 year old moriori man - wroks as chef - 3 days abdominal cramping and diarrhoea
- tramping, bbq food, fresh spirng water, giardia, chicken ect.
- potato salade - has eggs and mayonaise in it
What could the causative agents be? how would we tets thest
WHat is first treatmetn
DO we give anitbiotics
WHen are they allowed to go back to work?
Further prevention
water - giardia
Food - eggs, mayonaise - salmonella
chicekn - salmonella, campylobacter
How to test - stool sample, grow on agar
-XLD aga 0 salmonella
Mackonkey agar w lactose - samonella, shigella grow (only shigella will not turn it a differnt colour) , sheeps blood agar
Antibiotics - usually not, only has a small effect on duration and severity, hwoever may reduce the spread
Back to work - only when faces are clear
Prevention - hand hygeine, sanitisaiton, cooking hygeine
-further advice for next tramp
How does pneumonia cause infection (how does it get into lungs, what are main causes)
risk factors
Bacteria get in through upper airways through nose and mouth - breathing
-nasty infection, and person unable to clear it with immune system
age less than 2, over 56
chronic lung disease
smoking
immune dysfunction
-problem with lung innate immune system
Virulence factors of streptococcus pnuemonia
- alpha haemolytic (partially haemolyses RBCs)
- colonises nasopharynx
- prevalence of colonisaiton increases in winter
Capsule - causes disease
- prevents neutrophil recognition and phagocytosis
- prevents compliment opsonisation
Also has ..
-when gets into lungs, it produces a toxin (pneumolysin) and this damages neutrophils and epithelial cells
-choline binding protein on the outside which binds immunoglobulin on epithelial cells and allows entrance into cells
-Pneumococcal surface protein A helping it bind to epithelial cells and prevents opsonisation
Pili - help to colonise and bind to human cells
Pspc - prevents activation of complement cascade
how to test people with pneumonia
Listen to lungs - Listen to the lungs - chest expansion for pnemonia decreased, sacs filled with pus, and also can hear crakles
-if examine someone good enough do not need a chest Xray
Chest xray is first test Sputum culture Nasopharyngeal swab blood cultures urine ICT Serology CT chest bronchoscopy
treatment
- In an otherwise healthy person with pneumonia, can give antibiotics and dont really need to do many of the other tests
- However if they are very unwell, maybe on ventilator - need to do other tests to find out what the cause is so we can treat it better
Antibiotic treatment necessary
- reduces duration of illness and reduces risk of death
- penicillin resistance increasing
- also give IV
- can get over this by increasing the dose of penicilin
are differences for mild, moderate and very sick people - look at page 175
Hyper IgM syndrome
-Inability to switch from igm class to other classes
-linked to co stimulator CD40 and CD40 ligand and usually is due to a mutation in CD40 ligand gene to stop it working
(need this to swtich form Igm to igg)
How does our body respond to different types of infections
Microbial factors
- e.g differnt types of organisms will make differnt responses
- also degree of exposure - where it is exposed ect.
- virulence
- route of entry
Host factors
- integrity of innate barriers
- adaptive immune system
- HLA, Ig and TCR genes
- previous exposure
- other infections
Response to PAMPs
Local inflammation
- vascular permeability changes
- phagocyte recruitment
- acute phase protein induction
- local temp change
- -> leads to phagocytosis, complement activation
alternative pathway complement activation
-becomes activated form PAMPs this also activates a pathway to activate C3 converatse
How to treat bacterial infections
Antibodies and complement
- prevent adherence or reduce mobility
- enhance bacterial destruction (complement)
- enhance phagocytosis (opsonisation)
Avoid antibody effects of bacteria
- capsule resists opsonisation
- intracellular growth
mucosal immunity
In mucous can have igA and igE antibodies
- these serve as a blocking thing and stops bacterial adherence
- often in resp tissues there are mast cells and these have a high affinity for igE, so are often coated in igE material and antigen/pathogen that associate with these lead to degranulation and releasing molecules that affect blood vessel permeability and are chemotactic for neutrophils and other cells
- this stops things going in, and also helps the recruitment of non specific mediators through mast cell degranulation
NK cells
They have FC receptor (for above slide)
-also have 2 other receptors
Killer activating receptor -
Killer inhibiting receptor -
- these allow them to interact with cells in our body that might have changed their expression of HLA
- sometimes virally infected cells will downgrade their HLA receptors, to avoid getting recognised by cells of immune sytems - this is called natural killing activity
Dealing with viral infections
- First thing made is interferon (released by virally infected cells to signal to other cells to induce as state to become less able to be infected by viruses)
- these up regulate NK activity
- also then get cytotoxic T cells - to kill these cells infected with viruses
- then we have the antibodies developing later on and these can prevent re infection and viruses from spreading from cell to cel
