Final stuff lecture 21-30 Flashcards
igA
-main role - external body surfaces, surface protection of gut, resp and genitourinary tracts
Cytotoxic T cell action
-3 ways of action
- perforin and enzymes
- hydrolytic enzymes
- cytokins for apoptosis
Viridian streptococci - lab test
Same as strep pneumonia - except
has resistant to optochin sensitivity
3 things that can cause endocardititis
- viridans streptococci - MAinly this!! - peniclin + gentamicin
- staph aureus - flucoxacillin + gentamicin
- enterococcus facalis - amoxycillin + gentamicin
Differences between viral, bacterial or protozoa cause of gastroenteritis
Bacteiral - 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
How to diagnose which microbe with gastroenteritis
- Sheeps blood agar - grows most organism (apart from listeria)
- MAC - e.coli - ferment lactose - goes pink, salmonella, shigella - do not and goes yellow
- XLD - salmonella and shigella grow
what are the main ones in food?
salmonella, campylobacter
Salmonella lab test
Gram negative, oxidase negative
-MAC plate - non fermenter - goes yellow
-can grow on XLD agar
Risk factors for pneumonia
age less than 2, over 56
chronic lung disease
smoking
immune dysfunction
- problem with lung innate immune system
- people are unable to clear the infection
Streptococcus pneumonia
- where it colonises
- virulence factors
colonises nasopharynx, increase colonisation in winter
Capsule - causes disease
-prevents neutrophil recognition and phagocytosis
-prevents compliment opsonisation
Pili - help to colonise and bind to human cells
-when gets into lungs, it produces a toxin (pneumolysin) and this damages neutrophils and epithelial cells
others
- 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
treatment - pencillin IV, macrolides
lab test - same as strept pyogenes but alpha haemolysis
4 clinical features found with pneuomonia
- Increased resp rate
- crackles when listening to lungs
- fever/ chills
- can see on xray - puss in lungs
- fatigue
5 features of the innate immune system of resp tract that prevent healthy people developing pneumonia
- ciliated epithelium - removes pathogens from large airways
- Mucuous - traps the bacteria, or dust ect. and then can cough it back up so doesnt get into lungs
- Lysozyme - has enzymes in it which will kill bacteria
- Macrophages in lung - phagocytose material and can get inflammation ocuring
- Pamps can be recognised by dendritic cells and then can go on to warn immune system
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
How to diagnose
Listen to the lungs - chest expansion for pneumonia decreased, sacs filled with pus, and also can hear crackles
- if examine someone good enough do not need a chest Xray
- sputum culture
- blood culture
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
peritonitis signs and symptoms
Fever increased heart rate Increase resp rate nausea and vomiting diffuse abdominal pain that may become localised rebound tenderness abdominal wall rigidity
increase blood leukocytes
fluid accumulation, inflammation
What are the main bacteria when there is peritonitis
- what lab tests
- how to treat?
Bacteriodetes fragilis (anerobic)
E.coli (mac agar - ferments lactose - pink colonies)
Enterococcus
Metronidazole - b. fragilis
ampicillin - enterococous
How body responds to Live attenutated vaccines vs innactivated vaccines
Live virus vaccine - cytotoxic t cells, antibodies
- while viruses or bacteria - (influenza, pertussus)
- Protein based vaccines (toxoids - tetanus) - T cell dependent
- Polysacharide based vaccines - t cell independent (s. pneuomniae vaccine)
- Recombinant vaccines (hep B
passive immunity with tetanus who is most likely to get disease
- will nuetralise the toxins, no tprotected agaisnt another attack
- children - no passive immunity from mother
Bordetella pertussis - whooping cough
- gram negative bacillis
- vaccine preventable
- highest mortality in first year of life
- highly contagious, household spread
- is spread by aerosol droplets and is very infectious
- catarrhal phase- 1 to 2 weeks - runny nose, conjunctival injection, malaise
- Paroxysmal phase - short expiratory burst of rapid coughs, then inspiratory gasp and high pitched whoop
- convalescent phase - weeks- months
Complications
-can get secondary bacterial infections such as pneumonia
Treatment - antibiotics are useful, erythromycin can shorten the corse of illness and also make you less infective later on
vaccine - Now we use an acellular vaccine
- consists of a number of virulence factors
- very effective, however need 3 donese and then 2 booster doeses (hard to get people to come back and get booster doses)
-however can get it when you are adults later on
Measles
- highly infectious
- red dots, also can have rash on their inner lip
- conjunctivities, fever, rash
- can get secondary infections quite commonly
- Need two doses
MMR - 15 months, 4 years
viral agents that can cause meningitis
-herpes simplex, enterovirus
conjugate vacine example
HiB - haemophilus influezna type b
- polyscharide added to a carrier protein
- taken up by b cells
- carrier protein digests antigen, presents to t helper lcels
- convertsa t cell independt carb antigen to a t cell depeneidn
- good immunogeniciity in those less than 2
- good production of memory cells
- given at 6 weeks, 3 months, 5 mothsn , 15 months
- mostly eradicated disease
Meninigicocal vaccine
also is a recombinant vaccine
what does t17 do?
mucosal immunity and promote inflammatory processes
interferons
Interferons - induce transient antiviral state, activate NK activity, upregulate HLA expression (improves cytotoxic T cell killing)
what happens to b and t cells when we get increased or decreased igG or igM
- can also depend on levles of igG and igM - high levels of igM can promote B cells, weather high conc of igG tend to diminish b cells
- igM - want to make more to respond, and when have lots of igG have more memory cells so dont need to make as many
Nervous system interacting with Immune system
have autonomic nervous system interacting with the endocrine system and immune system
- get increase body temp, slow wave sleep, promote illness behaviours
- IL-1 acts on vagus nerve branches and has neurotransmitter activity
Nervous system interacting with Immune system
have autonomic nervous system interacting with the endocrine system and immune system
- get increase body temp, slow wave sleep, promote illness behaviours
- IL-1 acts on vagus nerve branches and has neurotransmitter activity
- there are sympathetic autonomic nerves inside lymph nodes going into secondary lymphoid organs
- are in strong influence of T cells
- norepinephrine communicates with T cells
severe combined immunodeficiency
- produces defects in both antibody and cellular immunity
- causes -genetic
- widespread effects on immune system
-both low b and t cells
hyper igM syndrome
- high levels of igM antibodies but low igG and igA
- this is because all lymphocytes initially make igM
- then they switch, but this requires a signal from helper T lymphocytes
- this occurs when CD40 molecule on the B cell binds its ligand on the T cell
- patients can have a mutation in the CD40 ligand molecule so cant make the switch
selective igA deficiencey
lack igA - this is important in mucous membranes lining mouth, airways ect.
Complement deficiency syndrome
-get infections with certain bacteria such as - neisseria meningitidis, niserria gonorrhoeae
Clinical presentations of immunodeficiency
type of infection can give a a hint at what immune defect there is.
Extracellular bacteria (e.g streptococci) - igM and igG antibodies, complement, phagocytes
Intraceulluar bacteria (TB) - t cells, macrophages
Viruses (measles) - t cells, igG and igA antivoides, complement, interferon
Parasits - ascaris - t cells, igE, eosinophils, mast cells
Fungi (candidia) - t cells, iga, neutrophils
when do you suspect immunodeficiency?
-when a patient has recurrent bacterial infections, or infections with unusual organisms
secondary immunodeficinceyc - suspected if patietn is takign steroid, or cytotoxic drugs for other disorders, with known major disease
-lifestyle risk factors for HIV
WHAT ANTIBODIES DO !!
IGM - blood and lymphatics, effective agglutinator, complement activator, important against blood borne spread infections e.g bacteria
igG - antitoxic antibody, effective barrier against virus infections, protects child when born, bound to phagocytic cells
igA - mucous membranes, fungal infections, gut, respt tract ect.
igD - on outside of antibody, foudn on surface of antigen senstivie naive B cells
igE - trace amounts in blood, binds to mast cells, important for parasitic and allergic reactions
Campylobacter and salmonella
- gram negative
- oxidase positive
- have a helical shape or curved, not a straight rod - yes
- growth on hba, no growth on MAC -
- urease est - negative
salmonella - oxidase negative, growth on lactose fermantion on MAC plate - negative
