Vaccines/Infectious disease Flashcards
ACTIVE AND PASSIVE IMMUNISATION
i) what is the main difference between active and passive vacc?
ii) what type of immunisation utilises horse serum? what disease can this lead to? explain
iii) what can repeat admin of horse antiserum cause?
i) active - organism mounts an immune response
passive - provide the organism with prefabricated immune response eg antibody concentrate
ii) horse serum - passive
- anti-abs in patient form complexes with horse Ig > immune complex disease
iii) repeat admin of horse anti serum > severe anaphylactic shock
LIVE VACCINES
i) what are they aka?
ii) which group of people may they cause disease in?
iii) what length of protection do they often provide?
iv) give three examples
i) aka attenuated vaccines
ii) weakened version of disease but not killed so can cause disease in immunocompromised people
iii) often provide lifelong protection
iv) eg BCG, shingles, MMR
INACTIVATED VACCINES
i) what do they contain?
ii) can they replicate in the body?
iii) are they still recognised by the immune system?
iv) what level of immune response do they often produce? what is therefore needed?
v) give three examples
i) contain agents that have been destroyed by chemicals/heat
ii) cannot replicate in the body
iii) are still recognised by the immune system
iv) produce weaker imm response therefore require more doses eg boosters
v) influenza, pertussis, poliomyelitis
COMMON PASSIVE VACCINATIONS
i) give three examples of serums that can be given post exposure
ii) when is Hep A hyperimmune serum given?
iii) what situation may VZV hyperimmune globulin be given in?
i) Hep B, tetanus, rabies hyperimmune serum
ii) give hep a HIS as exposure prophylaxis
iii) give VZVUF as prophylaxis for babies born to mothers who develop varicella in a 1wk before brefore or after delivery
ROUTINE CHILDHOOD IMMUNISATIONS
i) at how many weeks do vaccinations start?
start at week 8
COVID 19 VACCINE DEVELOPMENT
i) antibodies to which two parts of the sars cov 2 virus appear to correlate with protection?
ii) which two cell surface proteins does the spike protein bind to?
iii) why is a antibody cocktail used to interfere with this binding?
i) antibodies to the spike and nucleocapsid can correlate with protection
ii) spike protein binds to ACE-2 and Nrp-1 on the cell surface of cells
iii) taking an antibody cocktail from recovered patients can competitively bind to receptors to stop the spike protein binding
- using only one antibody to block binding causes spike proteins to mutate but giving lots of non competitive antibodies together can prevent novel spike mutants
B CELLS AND ANTIBODIES
i) when may antibodies recognising the spike protein be given?
ii) what did treatment with REGN-COV2 result in in relation to viral load?
iii) how may B cells block entry of sars cov2 to a cell?
i) Abs to the spike protein can be given to individuals with COVID19 to avoid serious disease courses
ii) tx with REGN-COV3 results in stat sig reduction in time weight average daily change from baseline in viral load
iii) B cells can bind to spike glycoprotein to stop it entering cells
RNA VACCINES
i) what do RNA vaccines use to achieve the production of relevant proteins in host cells?
ii) what is the structure of the molecule to allow stability? (what is at each end and what is found in the middle?)
iii) give three advantages of mRNA vaccines
i) use mRNA to produce proteins of a pathogen in host cells - do not interefere with host genes
ii) 5’ cap, poly A tail and 5’/3’ UTR and open reading frame in between
iii) adv - no pathogen particles, non infections
- good efficacy - reliable immune response and well tolerated
- can be produce more rapidly - good in emerging outbreaks
COMMON VACCINES AND COVID 19
i) what can exposure to vaccines/infections change in relation to genes? what does this mean for the cells?
ii) name two vaccines that may improve first line innate immunity to covid
iii) infection with which pathogen may improve resistance to covid?
i) exposure can change epigenetic regulation and cells can be more able to respond to another challenge for some time after
ii) TB and flu vaccines
iii) infection wih common cold coronavirus strains can improve resistance to COVID19
TRAINED IMMUNITY VS VACCINATION
i) what is trained immunity?
ii) name two things that can induce trained immunity
i) trained imminitty is epigeneic reprogramming of innate immune cells to figh infection
ii) epigenetic programme can be changed by infections/ vaccination
HERD IMMUNITY
i) what is it?
ii) what is R0?
i) herd immunity is where an infection is no longer effectively transmittted across a population because too many individuals are immune
ii) R0 - how many other people typically get infected by 1 case
UNDESIRABLE EFFECTS OF VACCINES
i) what part of the vaccine may side effects be attributed to?
ii) what did one in 55,000 people develop after having the swine flu vaccine?
i) adjuvants eg mineral salts, TLR agoniss
ii) post swine flu vaccine > narcolepsy
SUMMARY
i) what two things does vaccination aim to achieve? (direct and indirect protection)
ii) name two groups of people that live vaccines shouldnt be given in?
iii) what type of preparations can achieve passive immunisation? give two diseases this may be used in
iv) what does the success of a vaccine ultimately depend on?
v) name a role that adjuvants play in vaccines
i) aims to achieve individual protection (direct) and herd immunity (indirect)
ii) dont give live vaccines to HIV positive or advanced immunodeficiemcy
iii) passive imm with hyperimmunoglobulin eg tetanus anti toxin, hep B antibody
iv) vaccine success depends on the recipients ability to mount an immune resoonse
v) adjuvants can reinfornce the effect of vaccines so less antigen is needed
CELLULITIS
i) what is it? what are the two most common causative organisms? name three other organisms that can cause it?
ii) how is it characterised? (3) what is dx usually based on? when may a swab/aspiration cultures be done?
iii) name four investigations to be sent for patients that are acutely unwell? what should be taken if pt needs admission?
iv) what is first line tx if admin and severe? what severity classification can be used?
v) name five indications for admin
i) Cellulitis is an acute spreading infection of the skin with visually indistinct borders that principally involves the dermis and subcutaneous tissue
- most common causative bacteria are Streptococcus pyogenes and Staphylococcus aureus, but infection can be caused by Streptococcus pneumoniae, Haemophilus influenzae, gram-negative bacilli, and anaerobes
ii) it is characterised by redness, swelling, heat, and tenderness, and commonly occurs in an extremity
- based on history and examination only, although consider swab and aspiration cultures if cellulitis is associated with a break in the skin
iii) FBC, ESR (elevated), CRP (elevated), UE, blood culture (if pt needs admin)
iv) IV abx - start with fluclox or clarithromycin if allergic
- review after 48hrs and may be able to oral switch
- Eron classification (if class II or more > admit)
v) admin if > Signs of systemic illness, such as Confusion, Tachycardia, Tachypnoea, Hypotension, Suspected sepsis, Spreading cellulitis not responding to oral medication. Limb-threatening infection due to vascular compromise. Necrotising fasciitis, Orbital cellulitis
BACTERIAL MENINGITIS
i) what is it? what causes cerebral oedema, increased ICP? what are the three classifications and causative organisms of each?
ii) name five common symptoms? name three RF
iii) how quickly should blood cultures be done? what test can allow idenitification of bacteria?
iv) what may be seen on blood glucose? FBC? UE? VBG? LFT?
v) how quickly should LP be done? what type of meningitis does high lactate in CSF indicate?
vi) name seven contraindications to LP
i) Bacteria > CNS by haematogenous spread (the most common route) or by direct extension from a contiguous site
- bacteria multiply quickly once they have entered the SA space
- induc of inflammatory mediators, which in turn enhance the influx of leukocytes into the cerebrospinal fluid > inflammatory cascade leads to cerebral oedema and increased intracranial pressure, which contribute to neurological damage and even death
- Pneumococcal meningitis - Streptococcus pneumoniae
- meningococcal meningitis - Neisseria meningitidis, and
- Hib meningitis - Haemophilus influenzae type b (Hib)
ii) headache, neck stiffness, fever, altered mental state, vomiting, confusion, photophobia, seizure
- RF - older age, crowding (bacterial tranmission), close comntactt, immunocompromise eg HIV, malignancy, asplenia, cochlear implant, sickle cell
iii) within an hour into admin
- serum pneumococcal and meningococcal PCR
iv) pts with bac meningitis often have metabolic disturbance
- hyper or hypogly
- FBC > leucocytosis, anaemia, thrombocytopenia
- UE - acidosis, hypokal, hypocalc, hypomag (low sodium may indiovcte TB)
- VBG > high lactate if in shock
- LFT - raised
v) do LP within an hour of admin
- see elevated protein
- high lactate suggests bacterial rather than viral
vi) Thrombocytopenia, Lateness (delay in antibiotic adminm, Pressure (signs of raised ICP), Unstable (Cardio + resp systems), Coagulation disorder, Infection at LP site, Neurology (focal neurological signs)
