advanced micro Flashcards
what 5 parts of a patients social history could be relevant to ascertain the causative organism of an infection?
- travel
- occupation
- hobbies
- animal contact
- sexual history
at what temperature is someone deemed to have a definite fever?
38 degrees (or above)
FBC blood test: what types of blood cells are raised in:
- bacterial infection?
- viral infection?
bacterial = neutrophils
viral = lymphocytes
what colour does:
- gram positive stain?
- gram negative stain?
gram positive = purple
gram negative = pink/red
“stuff that’s red is bad”
what is the difference between an antibiotic and an antibacterial agent?
antibiotic
- chemical PRODUCTS OF MICROBES that inhibit/kill bacteria
antibacterial agent
- ANY chemical that inhibits/kills bacteria (irregardless of source)
nb often used interchangably in practise
what does minimum inhibitory concentration (MIC) or minimum bactericidal/fungicidal concentration (MBC/MFC) mean?
what does it mean if there is a low MIC?
MIC = minimum conc of antimicrobial agent at which visible growth is inhibited
MBC/MFC = minimum conc of antimicrobial agent at which most organisms are killed
a low MIC (or MBC/MFC) means that the bacteria (or fungi) is killed by a very small amount of antimicrobials - ie it’s sensitive
what type of cell mechanics tend to be targetted in:
- bacteriostatic antibiotics?
- bacteriocidal antibiotics?
bacteriostatic
- eg protein synthesis inhibitors
bacteriocidal
- eg attack cell wall or membrane
nb in vivo little difference, mainly terms used in lab
in terms of antimicrobial interactions, define the following terms:
- synergism?
- antagonism?
- indifference?
synergism
- activity of 2 antimicrobials given together is greater than the sum of their activity if given seperately
antagonism
- one agent diminishes the activity of the other
indifference
- activity unaffected by the addition of another agent
what is the component of the fungal cell wall which a lot of anti-fungals target?
what is another component of the fungal cell wall?
beta-1,3-glucan
chitin - antifungals don’t currently target this
what classes of antimicrobials are cell wall synthesis inhibitors:
- in bacteria? 2
- in fungi? 1
antibacterial agents:
- B-lactams
- glycopeptides
antifungal agents:
- echinocandins
what is an anti-tuberculous agent which targets the cell wall of TB?
cycloserine
“need lots of cycles of treatment to treat drug-resistant TB”
in terms of drug delivery, what does parenterally mean?
injection or infusion
- eg IM, IV, subcutaneous
(ie NOT orally)
how do B-lactam antibiotics kill bacteria?
interfere with function of ‘penicilin binding proteins’
- these are transpeptidase enzymes involved in peptidoglycan cross-linking
what three types of drug name suffixes or prefixes indicate that an antibiotic is a B-lactam antibiotic?
why is this important to know in clinical practise?
what are the 2 main exceptions to this?
suffixes:
= -cillin (penicillins)
= -penem (carbapenems)
prefixes:
= cef- (cephalosporins)
people with ‘penicilin allergies’ are allergic to ALL B-lactam antibiotics
other B-lactams:
- aztreonam (a monobactam)
- co-amoxiclav (combination of an antibiotic and an acid)
name 4 different types of penicillins (with at least one example for each)
penicillins
- benzylpenicillin
- phenoxymethylpenicillin
broad spectrum penicillins
- amoxicillin
- pivemecillinam
penicillinase-resistant penicillin:
- flucloxacillin
beta lactam-betalactamase inhibitor combinations
- amoxicillin-clavulanic acid (aka co-amoxiclav
- piperacillin-tazobactam
name 3 different classes of B-lactam antibiotics (with at least one example for each) which AREN’T penicillins!
monobactam
- aztreonam
cephalosporins
- cephalexin
- cefuroxime
- cefotaxime
- ceftriaxone
- ceftazidime
carbapenems
- ertapenem
- imipenem
- meropenem
what enzymes do penicillin-resistant bacteria produce?
what is their mechanism of action?
B-lactamase enzymes
enzyme hydrolyses, thus inactivating, B-lactams
what does BLBLI stand for?
name 2
why are they used?
what problems can they cause? 2
B-lactam/B-lactamase inhibitor combinations
amocixillin-clavulanate
- aka augmentin
- aka co-amoxiclav
piperacillin-tazobactam
- aka tazocin
increases the spectrum of antibiotics by deactivating B-lactamases produced by the bacteria
- very broad spectrum (predispose to C. diff infection)
- names don’t have -illin/cef- so importance of penicillin allergy may be missed
what is another class of antibacterial agents (bar B-lactams) which targets bacterial cell walls?
give 2 examples.
when are they used?
glycopeptides
- vancomycin
- teicoplanin
- penicillin resistance
- penicillin allergy
name a class of antifungals which target fungal cell walls.
give at least one example (what is the suffix?)
what is the mode of action?
echinocandins
- anidulafungin
- caspofungin
- micafungin
-fungin suffix
inhibition of B-1,3-glucan synthase
nb very good as few side effects
name 5 classes of anti-bacterial agents which work by targetting protein synthesis
give at least one example for each
aminoglycosides
- gentamicin
- amikacin
Macrolides
- erythromycin
- clarithromycin (fewer side effects than erythromycin)
- azithromycin
lincosamide
- clindamycin
tetracyclines
- tetracycline
- doxycycline
- tigecycline (more broad, active against gram -ve)
oxazolidionones
- linezolid (used against MRSA + nasty infects but lots of side effects)
(nb also fusidic acid)
nb macrolides and aminoglycosides are ones used most in practise
name 2 antiobiotics which are DNA synthesis inhibitors
mehanism of action:
- both agents inhibit folate synthesis (act at different steps in pathway)
trimethoprim
sulfonamides
name a combination treatment of an anti-fungal and an anti-biotic which are normally given together as an antibacterial agent but is also effective a type of fungal pneumonia seen in immunosuppressed patients
co-trimoxazole
trimethoprim-sulfamethoazole
name a class of antibiotics which are DNA synthesis inhibitors - give 2 examples (suffix?)
mechanism of action:
- inhibit remodelling of DNA during DNA replication
quinolones
- nb most in clinical use are actually fluoroquinolones (incl egs below)
- ciprofloxacin
- levofloxacin
-oxacin suffix
name an anti-biotic which is a RNA synthesis inhibitor
what infection is it predominately used against?
rifampicin
cornerstone of anti-tuberulous chemotherapy
- ie used against TB
name a class of antibacterial agents which target bacterial cell MEMBRANES
give 2 examples
(gram -ve or +ve?)
cyclic lipopeptides
- colistin (gram -ve)
- daptomycin (gram +ve)
nb these are old but having to use them more + more due to anti-biotic resistance
name 1 class of antifungal agents which target fungal cell MEMBRANES - and 2 other different antifungals (that target cell membranes)
what specific component of fungal cell membranes do these drugs target?
azoles
- clotrimazole
- fluconazole
terbinafine
nyacin
target: ergosterol
nb ergosterol is only in fungal cell membranes, not human cell membranes!
metronidazole:
- how it targets bacteria?
- what other type of organism does it target?
targets DNA replication
protazoa
give 4 examples of groups of bacteria which have innate resistance to specific antibacterial agents
nb remember this is what DOESN’T work!
gram-negatives:
- glycopeptides (vancomycin, teicoplanin)
- daptomycin
gram-positives:
- aztreonam
- colistin
anaerobes:
- aminoglycosides (amikacin, gentamicin)
streptococci:
- aminoglycosides (amikacin, gentamicin)
name two methods by which bacteria can acquire genes, which encode an antibiotic resistance mechanism.
- new mutation
- horizontal transfer (genetic exchange between bacteria, via plasmids)
name the 5 possible types of resistance mechanisms (can be innate or acquired)
- absent target
- decreased permeability
- target modification
- enzymatic degradation
- drug efflux
what is the most common acquired resistance mechanism found in anti-fungal-resistant candida?
drug efflux
what mechanism is present in MRSA which results it being resistant to many antibiotics?
which antibiotics is it resistant to?
target modification
- altered penicillin-binding protein (encoded by MecA) does not bind B-lactams
resistant to ALL B-lactams!
what is the most common mechanism of resistance to B-lactams?
enzymatic degradation
- bacteria produce penicillinases (inactivate penicillin etc)
what does ESBL stand for? what are they?
extended-spectrum B-lactamases
enzymes produced by B-lactam resistant bacteria which inactivate penicillins AND cephalosporins
what does VRE stand for?
what method of resistance is found in these organisms?
vancomycin resistant enterococci
target modification
- mutation results in reduction of binding to vancomycin 1000-fold
what does minimum inhibitory concentration (MIC) mean?
the lowest concentration of an antimicrobial drug (antibiotics/antifungals/etc) that will inhibit the visible growth of a microorganism after overnight incubation
which types of viruses tend not to have lipid envelopes?
ones that replicate in the gut
eg:
- adenoviruses
- enteroviruses
what type of DNA/RNA to acute/chronic viruses tend to have?
give at least 4 examples of each
acute - RNA
- influenza
- measles
- mumps
- hep A
chronic - DNA
- latent with/without recurrences:
- herpes simplex
- varicella zoster
- cytomegalovirus
- persistent:
- HIV
- HTLV
- hep B
- hep C
rashes:
- difference between vesicular and non-vesicular rash?
- examples of 5 viruses which cause non-vesicular rashes?
- examples of 3 viruses which cause vesicular rashes?
vesicular just means vesicles are present
non-vesicular rashes:
- measles
- rubella
- parvovirus
- adenovirus
- HHV6 (human herpes virus 6)
vesicular rashes:
- chicken pox (HHV3)
- herpes simplex (HHV1/2)
- enteroviruses
name 6 viruses which can cause respiratory infections
- influenza A/B
- respiratory syncitial virus
- parainfluenza virus
- human metapneumovirus
- rhinovirus
- coronavirus (incl SARS)
name 5 viruses which can cause gastroenteritis
- rotavirus
- norovirus
- astrovirus
- sapovirus
- adenovirus (group F)
name 5 viruses which can cause encephalitis/meningitis
- HSV (reactivation)
- enteroviruses
- rabies
- japanese encephalitis virus
- nipah virus
when would you use antivirals for acute infections in general population? 4
- primary HSV + herpes simplex encephalitis
- chickenpox in adolescents + adults
- shingles in eye
- elderly (shingles, influenza)
nb 99% of people with viral infections won’t need antivirals
nb many viruses don’t actually damage the host cell, it’s the immune response to the virus which causes the damage
what is AZT (azidothymidine)?
what’s it used for?
a nucleoside reverse transcriptase inhibitor (NRTI)
- inhibits reverse transcriptase (used by retroviruses to transform RNA -> DNA)
used against the reterovirus HIV
- inhibits its replication
what are the two types of NRTIs used to treat HIV?
give 2 examples of each
NRTI = nucleoside reverse transcriptase inhibitor
pyrimidine analogues:
- zidovudine (thymidine analogue)
- lamivudine (cytosine analogue)
purine analogues:
- abacavir
- tenofovir
which NRTIs are effective against hep B?
- lamividine
- tenofovir
name 2 herpes virus polymerase inhibitors.
give 2 strains of herpes virus which each is effective against
aciclovir
- herpes simplex
- varicella zoster
ganciclovir
- cytomegalovirus
- HHV6 (human herpes virus 6)
(- as well as HSV + VZV)
nb MUST KNOW THESE!
name an antiviral used to treat hep C
how does it work?
sofosbuvir
hep C RNA polymerase nucleotide inhibitor
“people with hep C tend to be sat on their SOFAS taking drugs”
apart from NRTIs, what is another type of anti-viral drug used to treat HIV?
give 2 examples
non-nucleotide reverse transcriptase inhibitors (NNRTIs)
(work the same as NRTIs but structure is not based on nucleotides)
- efavirenz
- nevirapine
what is another type of antiviral which is used to treat both HIV and hep C?
give some examples
protease inhibitors (PI)
HIV
- atazanavir
- darunavir
- ritonavir
Hep C
- paritaprevir
- grazoprevir
what does HAART stand for?
what’s it used to treat?
what does it consist of?
highly active antiretroviral therapy
HIV
- started when CD4 count falls
- aims to switch off virus replication
- taken lifelong
- 2 NRTIs + NNRTI
- 2 NRTIs + boosted PI
nb now problems with toxicity
what are exogenous interferons used to treat? 6
- some leukaemias
- AIDS related Kaposi’s sarcoma
- chronic hep B
- chronic hep C
- MS
- genital warts (caused by HPV)
what are two anti-virals used in the treatment of influenza?
what is the mechanism?
osteltamivir
- “TAMI flu”
zanamavir
- both are neuramididase inhibitors
what is the antiviral used for the treatment of RSV, hep C and hep E?
ribavirin
when would you deliberately use bacteriocidial antibacterial agents (as opposed to bacteriostatic)?
if the patient had a compromised immune system
- as bacteriostatic drugs require endogenous immmune system to ‘finish off the job’
what is the difference between:
- sepsis?
- severe sepsis?
- septic shock?
sepsis
= presence (probably/definite) of infection with systemic manifestations of infection
severe sepsis
= sepsis-induced tissue hypoperfusion or organ dysfunction
septic shock
= sepsis-induced hypotension, persisting despite adequate fluid resuscitation
what does SIRS stand for?
what can it be due to?
what are the most common/obvious acute clinical signs? 3
systemic inflammatory response syndrome
- may be due to an infection but can also be autoimmune etc
- low BP
- high RR
- altered mental state
what is seen as a more specific biochemical marker for systemic bacterial infection than CRP?
procalcitonin
- doesn’t react to viral/fungal malignancy
nb CRP has a 24hr time lag
what happens to platelet levels in infection?
- platelets can go UP in chronic inflammation
- but can go down in severe acute infection (DIC)
what is the ‘sepsis 6’?
BUFALO
B - take Blood cultures U - measure Urine output F - give IV Fluid A - give broad-spectrum Antibiotics L - measure serum Lactabe + Hb O - give high-flow Oxygen
take 3 things:
- blood cultures
- lactate/Hb
- urine
give 3 things:
- fluid
- antibiotic
- oxygen
nb start antibiotics within ONE hour of severe sepsis/septic shock
why are nitrites present on urine dipstick test if infection is present?
nitrAtes are excreted by kidney normally, some bacteria will reduce them to nitrItes -> nitrites in urine
- so useful test, but not: not all bacteria do this!!
what are the 3 main groups of bacterial flora in the gut?
what is the likelihood of each causing a UTI?
what is a group of bacteria of skin flora which can, rarely, cause UTIs?
gram negative bacilli
- almost always (mainly e coli)
anaerobes
- very rarely
- if see, suspect something like fistula
enterococci
- can see, but uncommon
from skin flora
= staphylococci
what type of staphylococcus if commonly the cause cystitis in younger women?
staph saprophyticus
what is urine likely to look like macroscopically if there is a UTI?
cloudy
nb ‘smelly’ urine does not necessarily mean an infection, more to do with what you’ve eaten
which 3 antibiotics are most likely to result in C. diff infection?
- ciprofloxacin (a fluoroquinolone)
- cefuroxime (a cephalosporin)
- co-amoxiclav
what is the treatment time for an uncomplicated UTI?
3 days of Abx
what factors should influence your choice of antibiotics:
- related to Abx? 6
- related to the patient? 6
Abx related:
- spectrum
- bacteriostatic/cidal
- tissue penetration
- does it need to be monitored?
- side-effects
- route of administration
patient related:
- severity of illness
- site of infection
- immunosuppresed?
- co-morbidities
- co-medications
- allergies
what sort of empirical Abx should be given in:
- local infection?
- sepsis?
local infection
- ‘educated guess’, treat for most likely pathogen
sepsis
- give broad spectrum antibiotics
what broad types of cocci are:
- gram positive? 3
- gram negative? 2
gram positive:
- staphylocci
- streptococci
- enterococci
gram negative:
- meningococci
- gonococci (cause of gonorrhoea)
how are streptococci classified?
alpha haemolytic strep
- eg pneumococci
beta haemolytic streptococcus
- further categorised into group A, B, C or… etc strep
what type of organisms are seen as part of normal skin flora?
staphylococci
- coagulase negative staph (v unlikely to cause infection, only in immunosuppressed patients or something like central lines)
- staph aureus
streptococci
- alpha haemolytic
- beta haemolytic
what type of organisms commonly cause skin + soft tissue infections (SSTIs)?
staph aureus
- MSSA (methicilling sensitive…)
- MRSA
beta haemolytic strep
- group A strep
- strep pyogenes
what sort of normal colonising flora are seen in the:
- mouth/URT? 2
- nasopharynx? 5
mouth/URT:
- streptococci
- anaerobes
(also: gram -ve cocci, candida, staphylococci)
nasopharynx:
- strep pneumoniae
- haemophilus influenzae (gram -ve cocci)
- moraxella catarrhalis (gram -ve cocci)
- other gram negative cocci
- staph aureus
nb majority of URTI are caused by viruses
common causes of sore throat/tonsillitis:
- viral? 2
- bacterial? 2
viral:
- epstein barr virus
- rhinovirus
( and others)
bacteria:
- group A strep
- anaerobes
common causes of sinusitis:
- acute? 2
- chronic? 1
acute sinusitis:
- strep pneumoniae
- haemophilus influenzae
chronic:
- anaerobes
what are the common causes of pneumonia:
- bacterial CAP? 3
- bacterial HAP? 2
- atypical bacteria? 3
- viral? 2
bacterial CAP:
- STREP PNEUMO
- haemophillus influenzae (GNC)
- moraxella catarrhalis (GNC)
bacterial HAP:
- gram -ve bacilli
- staph aureus
(+ ones that cause CAP)
atypical bacteria:
- mycoplasma
- chlamydia
- legionella
viruses:
- influenza
- respiratory syncitial virus
nb virus can causes pneumonia by themselves but commonly just damage the mucosa -> secondary bacterial infection
what is a common cause of ventilator-associated pneumonia?
pseudomonas (a gram negative bacillus)
what are the two commonest causes of encephalitis?
herpes simplex viruses
enteroviruses
nb encephalitis almost always viral
common bacterial causes of meningitis:
- in all ages? 3
- neonates? 3
- immunosuppressed? 2
- post-neuro op? 1
in all ages:
- neisseria meningitis
- strep pneumoniae
- haemophilus influenzae
neonates:
- group B strep
- gram neg bacilli
- listeria
immunosuppressed:
- gram neg bacilli
- listeria
post neuro op
- + skin organisms (eg staph)
what type of bacteria tend to cause cerebral abscesses? why?
normally occur secondary to a local infection so tend to be caused by resp tract flora
what are the three main types of blood stream infections?
what are they often caused by?
- infective endocarditis (native/prosthetic)
- intracardiac device infections
- graft infections
- staphylococci
- streptococci
what are the four antibiotics/types of antibiotics which are most likely to result in c diff infections?
- clindamycin
- co-amoxiclav
- cephalosporins
- fluoroquinolones (-floxacin)
Penicillin G + V
- their other names?
- routes of administration?
- act well against? 1
- act okay against? 2
- not great against? 1
- destroyed by B-lactamases?
Penicillin G
- benzylpenicillin - “ben pen”
- IV/IM
penicillin V
- phenoxymethylpenicillin
- oral
good for:
- streptococci
okay for:
- many anaerobes
- some GNC
bad for:
- staphylocci (as often produced b-lactamases)
yes, destroyed by b-lactamases
flucloxacillin:
- route?
- act well against? 2
- act okay against? 2
- don’t work for? 1
- destroyed by b-lactamases?
oral/IV
good for:
- streptococci
- staphylcocci
okay for:
- many anaerobes
- some GNC
don’t work for:
- MRSA
NOT destroyed by b-lactamases
amoxicillin:
- route?
- act well against? 3
- not great against? 1
- destroyed by b-lactamases?
oral/IV
good for:
- streptococci
- enterococci
- some GNB
not good for:
- staphylococci
yes, destroyed by b-lactamases
co-amoxiclav:
- constituents?
- act well against? 5
- don’t work for? 2
- amoxicillin
- clavulanic acid (inhibits b-lactamases)
good for:
- streptococci
- staphylococci
- most enterococci
- many GNB
- many anaerobes
don’t work for:
- extended spectrum b-lactamase (EBSL) producers
- MRSA
tazocin:
- constituents?
- act well against? 7
- don’t work for? 2
- problem with it? 1
- piperacillin
- tazobactam (inhibits b-lactamases)
good for:
- staphylococci
- most streptococci
- most enterococci
- anaerobes
- PSEUDOMONAS
- GNC
- GNB
doesn’t work for:
- ESBL producers
- MRSA
doesn’t cross blood brain barrier!
nb not much stuff is active against pseudomonas!
macrolides:
- examples? 3
- effective against? 3
- not great against? 1
- erythromycin (lots of GI side effects)
- clarithromycin (fewer GI side effects)
- azithromycin (broader, also covers gram -ve stuff)
good for:
- atypical organisms (chlamydia, gonorrhoea, mycoplasma, legionella)
- staphylococci
- streptococci
not good for:
- gram negatives
glycopeptides:
- examples? 2
- route?
- good for? 3
- don’t work for? 1
- vancomycin
- teicoplanin
IV
- except oral vancomycin, not absorbed but works in gut, used for c diff
good for: - staphylococci - streptococci - enterococci basically gram positive stuff
don’t work for:
- gram negative (intrinsic resistance)
clindamycin:
- route?
- good for? 3
- problems with? 2
- good things about it? 2
oral/IV
good for: - staphylococci - streptococci - some anaerobes basically gram positive
problems:
- variable acquired resistance (do sensitivity test)
- associated with c diff
good things:
- anti-toxin action
- good tissue penetration (good for SSTIs)
ciprofloxacin:
- class?
- route?
- good for? 4
- poor for? 2
- problem? 1
- good things? 2
fluoroquinolones
oral/IV
good for:
- gram negatives
- pseudomonas
- staphylococci
- atypicals
poor for:
- streptococci
- anaerobes
problem:
- associated with c diff
good things:
- good absorption/tissue penetration
- intracellular activity
nb aka early fluoroquinolones
levofloxacin:
- class?
- route?
- good for? 3
- poor for? 2
- problem? 1
- good things? 2
fluoroquinolones
oral/IV
good for:
- gram positive
- streptococci
- atypicals
nb ‘respiratory FQ’ - tend to be used for pneumonias
poor for:
- gram negatives
- pseudomonas
problem:
- associated with c diff
good things:
- good absorption/tissue penetration
- intracellular activity
aminoglycosides
- examples? 2
- route?
- good for? 2
- don’t work for? 2
- problems? 2
- erythromycin (only one that’s really used!)
- amikacin
IV/IM/(topically)
good for:
- gram -ve bacilli (incl pseudomonas)
- staphylococci
don’t work for:
- streptococci
- anaerobes
problems:
- need monitoring
- nephrotoxic + ototoxic
metronidazole:
- route?
- used for? 3
- side effects? 3
IV/oral
good for:
- anaerobes (bacteria)
- protozoa (eg malaria)
- some helminths
side effects:
- can’t have with alcohol
- GI upset
- neurotoxicity
what does necrotising fasciitis tend to be caused by? 2
- group A strep
or:
- mixed infection (in people who are immunosuppressed or have comorbidities)
what antibiotics are used to treat MRSA? 4
- doxycycline
- clarithromycin
- clindamycin
- trimethoprim/co-trimoazole
what is the empirical treatment for CAP?
co-amoxiclav
+clarithromycin if very unwell
what are the two different types of immune response (relevant to vaccines)? and which Ig is predominately found in each?
primary immune response:
- develops in weeks following first exposure to an antigen
- slow and weak
- mainly IgM
- “I’m ill”
secondary immune response
- reactivated when body encounters antigen again
- fast and strong
- mainly IgG
- “I’m Gone”
vaccinations which induce active immunity:
- live vaccines? 4
- inactivated organisms? 3
- componenets of organisms? 2
- inactivated toxins? 2
live vaccines:
- MMR
- BCG
- yellow fever
- varicella zoster (chicken pox/shingles)
inactivated organisms:
- pertussis (whooping cough)
- typhoid
- polio
components of organisms:
- influenza
- pneumococcal
inactivated toxins:
- diptheria
- tetanus
nb the more ‘live’ the vaccine the stronger and longer-lasting the immunity
- but contraindicated in immunosuppressed
vaccines which give passive immunity:
- HNIG - what is it?
- specific? 5
specific:
- tetanus
- botulism
- hep B
- rabies
- varicella zoster
nb passive immunity is much shorter lived than active
what is the ‘susceptible population’? 3
people who are at risk of infection from an infectious person:
- has not encountered/been vaccinated against it
- unable to mount an immune response
- vaccination is contraindicated
define term: decontamination
the destruction/removal of micro organisms from a surface/object
define term: sterilisation
complete killing (or removal) of ALL types of micro-organisms
define term: disinfection
removal or destruction of sufficient numbers of potentially harmful micro-organisms to make an item safe to use
nb almost always chemical
sterilisation methods? 4
heat
- moist (eg autoclave)
- dry (eg oven)
chemical
- gas
- liquid
filtration
ionising radiation
define term: antisepsis
removal/destruction of sufficient numbers of potentially harmful micro-organisms on damaged skin/living tissues
ie disinfectant applied to living tissues
nb requires a disinfectant with minimal toxicity
what type of decontamination should be used on items/devices that:
- will enter sterile body areas or break the skin?
- will contact mucous membranes or that will be contaminated with bodily fluids?
- thatonly contact intact skin (no bodily fluids)?
sterile body areas/break skin:
- sterilise
mucous membranes/bodily fluids:
- disinfect
intact skin:
- clean
how are these things decontaminated:
- reusable surgical instruments?
- flexible endoscopes?
- syringe needle?
- central venous catheter (CVC) insertion site?
reusable surgical instruments:
- sterilisation by autoclave (moist heat)
flexible endoscopes:
- ‘high level’ disinfection via chemicals
syringe needle:
- sterilised by gamma irradiation before use (disposal after use)
CVC insertion site:
- antisepsis via chemicals (2% chlorhexidine in 70% isopropyl alcohol)
when should you do a HIV test? 2
- acute medical admission
- new GP registration
nb leeds is an area of high prevalence
lumbar puncture for meningitis:
- normal findings?
- viral findings?
- bacterial findings?
- fungal or TB findings?
categories are:
- opening pressure
- appearance of CSF
- WBC count
- WBC differentiation
- protein (g/L)
- glucose (CSF:blood ratio)
normal:
- opening pressure: 5-20
- clear CSF
- WBC count <3
- 0.2-0.5g/L protein
- 0.6 glucose (CSF:blood)
viral:
- opening pressure: normal/slight increase
- clear CSF
- WBC count medium
- mainly lymphocytes
- low/normal protein
- high glucose
bacterial:
- opening pressure: high
- turbid CSF
- WBC count high
- mainly polymorphs
- high protein
- low glucose (bacteria eat it all!)
fungal/TB:
- opening pressure: variable
- variable CSF
- variable WBC count
- mainly lymphocytes
- low/normal protein
- low glucose (fungus/TB eats sugar)
basically:
- viral: clear, lymphocytes, high glucose
- bacterial: turbid, polymorphs, high protein, low glucose, high opening pressure
- fungal/TB: lymphocytes, low glucose
“living organisms (ie not viruses) eat sugar!”
other tests (bar LP) done for meningitis? 8
- blood cultures
- blood for bacterial PCR
- FBC
- CRP
- clotting
- U+Es
- LFTs
- blood glucose
encephalitis:
- normal cause?
- diagnostic test?
viral (norm herpes)
lumbar puncture
- CSF requesting viral PCR specifically
brain abscess:
- diagnostic tests? 2
- don’t do?
local sampling
- pus, from surgical biopsy/drainage
- – gram, culture, sensitivity
blood cultures
don’t do: LP!
- high risk due to increased ICP
- rarely positive anyway
nb normally spread from local source mof infection, eg ear or sinuses
diagnosis of:
- acute otitis media?
- acute otitis externa?
otitis media:
- clinical diagnosis
- send pus if ear drum perforated
otitis externa:
- ear swab to determine cause
- do sensitivity testing on this
nb for both, beware of colonising bacteria, hard to interpret, often get false positive
what is the diagnostic test for influenza?
who is this given to? 2
viral PCR from nose/throat swabs
- those who may require treatment (ie antivirals)
- those at risk of transmitting (eg in hosp/prisons/etc)
what diagnostic interventions are required for pneumonia with:
- a low CURB65 score? 1
- a mod/severe CURB65 score? 3
low CURB65:
- CRP
mod/severe CURB65:
- sputum
- blood cultures
- stypical screen
what is involved in an ‘atypical screen’? 2
- test urine for legionella antigen
- nose/throat swab for mycoplasma PCR
(- may include serum)
what is the diagnostic tests for:
- exposure to TB? 2
- symptomatic pulmonary TB?
exposure:
- mantoux
- IGRA (interferon G releasing assay)
nb both of these rely on intact immune system
pulmonary symtpms:
- 3 sputum samples
- microscopy + culture (for 8 weeks)
less common causes of respiratory infection:
- who would you test?
- diagnostic tests? 3
- type of sample needed?
consider in immunosuppressed
- on chemo
- post-transplant
- HIV
- on steroids
- diabetes
- CKD
- viral (eg RSV, CMV) = viral PCR
- fungal (eg aspergillus) = culture, aspergillus antigen
- pnemocystis - pneumocyctis PCR
deep respiratory sample (lavage)
h pylori infection:
- 4 diagnostic tests?
- best one?
h pylori antiBODY test
- doesn’t distinguish active from past infection
h pylori stool antiGEN test
- BEST ONE!!
urea breath test
- expensive (but gold standard for test of cure)
biopsy urease test
- invasive
nb with all of these should stop PPIs before testing!
liver abscess
- 3 main causes?
- diagnostic tests? 5
- pyogenic (bacteria)
- hydatid parasite
- amoebic
history to guide aetiology - imaging (USS/CT)
- pus (if safe to drain)
- blood cultures (+ normal blood tests)
- hydatid serology
- stool for parasitic eggs
diagnostic blood test for endocarditis?
blood cultures
- 3 should be taken, each at different time of day
(as bacterial loads in blood vary throughout day so may get false negative if only test once)
what imaging techniques should be used for suspected endocarditis?
echocardiography (2 types:)
trans-thoracic echo (TTE)
- less invasive but more sensitive
trans-oesophageal echo (TOE)
- more invasive but more sensitive
- should always do in suspected prosthetic valve endocarditis
how is viral hepatitis diagnosed?
serology +/- PCR
nb serology comprises antigen + antibody detection
clostridium botulinum
- what does it cause?
- what sort of toxin does it produce?
a rare cause of food poisoning
an exotoxin
what is the difference between an endotoxin and an exotoxin?
Exotoxins are usually heat labile proteins secreted by certain species of bacteria which diffuse into the surrounding medium.
Endotoxins are heat stable lipopolysaccharide-protein complexes which form structural components of cell wall of Gram Negative Bacteria and liberated only on cell lysis or death of bacteria.
ie exotoxins is stuff the bacteria actively produce and secrete, endotoxins are molecules in bacterial cell wall which is released when that cell lyses
what is the name given to an organism which, when present, almost invariably causes disease?
primary pathogen
which structures on the surface of bacteria facilitate bacterial adhesion?
fimbrae
give 4 examples of common gram positive cocci species
- staph aureus
- staph epidermis
- strep pneumoniae
- strep pyogenes
give 4 examples of gram positive rods (genuses)
- clostridium (eg c diff)
- bacillus
- corynebacteria (eg c diptheria + c bovis)
- listeria (eg L monocytogenes)
give 2 examples of gram negative cocci species
neisseria meningitides
neisseria gonorrhoea
give 7 examples of gram negative rod genuses
- escerichia (eg e coli)
- pseudomonas
- salmonella
- shigella (causes dysentry)
- kleibsiella (eg k pneumoniae)
- proteus (eg p vulgaris)
- haemophilus (eg haemophilus influenzae)
what antibiotic should you use to treat MRSA?
vancomycin
or any other glycopeptide
out of the 3 main classes of B-lactams which are most and least broad spectrum?
penicillins = least
cephalosporins = middle
carbapenems = most broad spectrum
give an example of a macrolide
what do these types of antibiotics target in bacteria?
- erythromycin
- azithromycin
- clarithromycin
protein synthesis
give an example of an aminoglycoside
what do these antibiotics target in clinical practise?
gentamycin
protein synthesis
what is the first line treatment for anerobic bacteria?
metronidazole
what antibiotic is first line for treatment of c diff infection?
metronidazole
nb c diff is an anaerobe
what is (often) the first line treatment for UTIs?
what class is it?
what part of the bacteria does it target?
ciprofloxacin
fluoroquinolones
DNA replication
which of these antibiotics ONLY work on gram negative or gram positive bacteria:
- penicillin?
- gentamicin?
- vancomycin?
penicillin
= gram positive only
(nb amoxicillin + other broad spectrum penicillin derivatives have broader cover)
gentamicin
= gram negative only
vancomycin
= gram positive only (eg MRSA)
which type of antibiotic can bacteria become resistant to, by the use of an efflux pump?
quinolones
name a common:
- broad-spectrum penicillin?
- penicillinase-resistant penicillin?
broad-spectrum penicillin
= amoxicillin
penicillinase-resistant penicillin
= flucloxacillin
(nb this is still resistant against MRSA)
what is the first line treatment for:
- mild typical pneumonia?
- serious typical pneumonia?
what criteria do you use to tell the difference between the two?
mild typical pneumonia
- amoxicillin
serious typical pneumonia
- co-amoxiclav AND clarithromycin
CURB-65 score
(confusion, urea, RR, BP, age >65)
what is the most common cause of community acquired pneumonia?
what type of bacteria is it?
strep pneumoniae
gram positive diplococci
which bacteria often causes pneumoniae in people who are recovering from influenza virus?
staph aureus
which bacteria tend to cause hospital acquired pneumonia?
kleibsiella pneumoniae and other gram negatives
also MRSA
signs/symptoms of:
- lower UTI? 2
- upper UTI? 4
lower UTI:
- dysuria
- frequency
upper UTI: - fever - loin pain - tachycardia - low BP (+ lower UTI symptoms)
name 2 antibiotics which are often used to treat lower UTIs
- trimethoprim
- amoxicillin
nb just give orally
what is often the first line treatment for upper UTIs?
IV cefuroxime
what is the most common cause of lower UTIs?
e coli
meningitis:
- most common cause in children/young adults?
- most common cause in elderly?
what type of bacteria are these)
children/young adults:
- neisseria meningitides (gram neg diplococci)
elderly:
- strep pneumoniae (gram pos diplococci)
what would the first line treatment be in a young adult with suspected meningitis?
IV ceftriaxone
what is the difference between meningitis and meningococcal septicaemia?
meningitis
= CNS only
meningococcal septicaemia = CNS + blood stream infection - non-blanching rash - low BP - tachycardia
what is SIRS?
criteria? 4
difference between that and sepsis?
systemic inflammatory response syndrome
2 of the following:
- temp >38
- pulse >90
- RR >20
- WBC >12
sepsis = SIRS AND a suspected focus of infection
ie SIRS is just saying that there is a systemic immune response but this doesn’t mean it necessarily has an infective cause
- eg could be a PE
what is septic shock?
sepsis AND a low BP (<90/60)
ie body isn’t coping
what does buffalo stand for?
blood cultures
- take 2 sets
urine output
- catheterise to measure
fluids
- 500ml IV saline over 15 mins
antibiotics
- as per suspected infection, go broad
- norm tazocin (piperacillin tazobactam)
lactate
- do ABG for lactate + pH
oxygen
- 15L/min via reservoir face mask
cellulitis:
- what is it?
- normal causative organism?
skin + soft tissue infection
caused by gram positive cocci
almost always:
- staph aureus
- strep pyogenes
necrotising fasciitis:
- what is it?
- normal causative organism?
- treatment? 2
a SEVERE skin + soft tissue infection
a polymicrobial mix
- usually involving strep pyogenes
- debridement
- broad spectrum Abx (eg meropenem + clindamycin)
nb strep pyogenes is NOT normal skin flora
what main group of antibiotics is the safest to use in pregnancy?
what is another drug that is safe in pregnancy?
ALL beta lactams are safe in pregnancy
also erythromycin
“erythromycin may cause GI problems but you probably already have morning sickness in pregnancy so not gunna make things any worse”
nb CAN’T use clarithromycin though!!
which main 3 antibiotics should you avoid in pregnancy?
what effects do they have if taken?
quinolones (eg ciprofloxacin)
- damage to cartilage of foetus
trimethoprim
- is a folic acid antagonist (want folic acid in pregnancy to prevent neural tube defects)
tetracyclins
- deposits + stains bones/teeth of babies
what is antimicrobial stewardship?
what are the 4 goals of it?
an organisational or healthcare-system-wide approach to promoting and monitoring judicious use of antimicrobials to preserve their future effectiveness
- improve patient outcomes
- improve patient safety (eg c diff)
- reduce resistance
- reduce healthcare costs
when reviewing a patient who is on IV antibiotics, what are the 5 possible continuing management plans?
- continue on IV
- OPAT (IV at home, out-patient antibiotic therapy)
- change antibiotic
- stop antibiotic
- IV to oral switch
what are the three different types of antibiotic therapy, describe when they are used?
empiric therapy:
- based on:
- – likely pathogen based on clinical history + exam
- – local antimicrobial policies
- likely to be relatively broad spectrum
targeted therapy:
- based on:
- – predicted susceptibility of organism found in culture
- – local antimicrobial policies
- likely to be more narrow spectrum
susceptibility-guided therapy:
- based on:
- – antimicrobial susceptibility testing results (ie on an agar plate)
- as narrow spectrum as possible
what is the 90-60 rule?
the range of correlations between susceptibility and outcome in studies of bacterial infections
infections due to susceptible isolates respond to therapy about 90% of the time
infections due to resistant isolates respond to therapy about 60% of the time
if you give someone an antibiotic for an infection, they are much more likely to be resistant to that same antibiotic if you try to give it to them next time they have an infection.
how long does this resistance hang around for?
up to a year
so must always check what antibiotics patients have been prescribed in the past, if possible, when deciding what to prescribe them now
what two classes of antibiotics often have synergistic effects when used together?
B-lactams and aminoglycosides (ie gentamicin)
1 + 1 = 3
eg in streptococcal endocrditis
what two antibiotics have an antagonistic effect when used together?
sodium fusidate and flucloxacillin
nb sodium fusidate is rarely used now
first line antibiotic used to treat staph aureus infection (not MRSA)?
flucloxacillin
first line antibiotic used to treat strep pyogenes infection?
benzylpenicillin
first line antibiotic used to treat gram-negative infections?
who should this use be cautioned in?
cephalosporins
caution in elderly (due to c diff)
first line treatment for gram positive bacteria (incl MRSA)?
vancomycin
an glycopeptide
what is the last line treatment for most conditions?
meropenem
a carbopenem
nb doesn’t work for MRSA
what is the last option for multi-resistant gram-negatives?
side effect?
colistin
very nephrotoxic so rarely used
which class of antibiotics has very good availability in the CSF?
which 2 classes of antibiotics have very poor availability in CSF?
very good availability:
- B-lactams
very poor availability:
- aminoglycosides (gentamicin)
- glycopeptides (vancomycin)
which two classes of antibiotics have very good availability in urine? (ie good to treat UTIs)
which class of antibiotics has very poor availability in urine?
very good availability:
- trimethoprim
- B-lactams
very poor availability:
- macrolides (erythromycin, clarithromycin, azithromycin)
what are the 2 main different types of pharmacodynamic considerations to take into account when deciding dosages of antibiotics to give?
how does this effect the dose and time between doses that you administer?
give an example of each
antibiotics which are CONCENTRATION dependent:
- main determinant of bacterial killing is the factor by which cioncentration exceed MIC
- administered at high doses but with long gaps between doses
- eg aminoglycosides (gentamicin)
antibiotics which are TIME dependent:
- main determinant of bacterial killing is the amount of time for which antibiotic concentration exceeds MIC
- administered slightly lower doses but very frequently to keep above MIC
- eg B-lactams
what 3 main reasons are there for prescribing more than one antibiotic for an infection?
to increase efficacy
- synergistic combination (eg B-lactam + gentamicin)
to provide adequately broad spectrum
- singl agent may not cover all required organisms
- polymicrobial infection
- empiric treatment of sepsis
to reduce resitance
- organism would need to develop resistance to multiple agent simultaneously
- eg antituberculous chemotherapy
what are the reasons why you WOULDN’T prescribe an antibiotic orally? 6
ie would give by IV or another route instead
- sepsis
- deep seated infection (endocarditis, meningitis, osteomyelitis etc)
- patient vomitting
- patient very sick (as reduced perfusion to gut so reduced GI absorption)
- compliance/adherance problems (eg therapy can be given intramuscular)
- prone to GI side effects
nb always try and give antibiotics orally if possible!! better for everyone
- reduces risk of line infections etc and means can leave hosp earlier
what three questions should you ask when taking an allergy history?
- what allergic to?
- what happened?
- how long ago?
who should ceftriaxone NOT be used in?
why?
neonates with jaundice
can displace bilirubin from albumin
which two antibiotics should NOT be used in people with epilepsy?
why?
quinolones/fluroquinolones (ending -floxacin)
imipenem (an IV carbopenem)
can lower seizure threshold
which class of antibiotics are contraindicated in children?
why?
quinolones/fluroquinolones (ending -floxacin)
can cause athropathy
what is a major possible adverse effect of quinolones/fluroquinolones (ending -floxacin)?
can cause tendonitis/tendon rupture
use with caution in elderly
who should tetracyclines not be used in?
why?
children under 12
can stain teeth
which two main classes of antibiotics are at greatest risk of causing nephrotoxicity?
- aminoglycosides (gentamicin)
- glycopeptides (vancomycin)
which 2 antibiotics can cause bone marrow suppression?
- chloramphenicol
- linezolid
which 2 antibiotics can cause cholestatic jaundice?
nb this is indicated by change in LFTs
- co-amoxiclav
- flucloxacillin
which antibiotic has an increased risk of leading to myopathy/rhabdomyolysis?
daptomycin
why should you ALWAYS treat bacteruria in pregnancy?
as it’s linked with premature birth
what drug do macrolides (ery,clary,azithromycin) and metronidazole interact with?
what is the effect?
warfarin
increase anticoagulant effect of warfarin
as these Abx are enzyme inhibitors
what drug does clarithromycin interact with?
what is the effect?
simvastatin
increase the risk of myopathy
which 2 types of antibiotics can antacids + calcium reduce the absorption of?
- tetracyclines
- quinolones
which antibiotic should you not consuem alcohol while on?
metronidazole
which antibiotic has no bioavailability when given orally?
gentamicin
always given IV (or IM/topically?)
how should you prescribe antibiotics to an obese person (as opposed to a patient with a normal BMI)?
may need larger doses (see guidlines)
which infections typically need long courses of IV therapy? 7
- osteomyelitis
- liver abscess
- meningitis
- bacteraemia/sepsis
- endocarditis
- CF
- infections in immunocompromised
consult relavent guidlines for these!
how long should Abx typically be prescribed for UTIs in:
- women?
- men?
women = 3 days
men = 7 days
how long should antibiotics typically be prescribed for in upper resp tract infections?
5 days
how long should TB be treated on Abx for?
6-9months
longer if drug resistant
name two classes of antibiotics which have narrow therapeutic spectrums?
aminoglycosides (gentamicin)
glycopeptides (vancomycin, teicoplanin)
what 3 different types of surgical procedure would prophylactic antibiotics be indicated for?
- clean surgery involving placement of a prosthesis or implant
- clean contaminated surgery
- contaminated surgery (eg in bowel or abscess)
nb normally just give one dose before surgery, but give more if lng surgery or if lots of blood loss
what is the algorithm of when to switch from IV to oral?
ACED
A - Apyrexial
C - Clinically improving
E - Eating
D - no Deep seated infection
generally speaking, what sort of bacteria tend to cause:
- infections ‘outside’ the body (skin + soft tissue)?
- infections ‘inside’ the body (GI, genitals)?
‘Outside’ (skin, soft tissue)
- gram POSitive
‘inside’ (GI, genitals)
- gram NEGative
“you try and put a positive fact on the outside, even though you are feeling negative on the inside”
which bacteria only tends to cause infections in association with plastics/man made material (eg central line, catheter, prostetic hip)
staph epidermis
is part of normal skin flora
what do coagulase negative and positive staph mean?
give examples?
means how they respond to a coagulase test
staph aureus is coag positive
all other staphs are coag negative (eg s epidermis)
what is alpha and beta haemolytic in reference to? what are the 2 subtypes of one of these?
alpha haemolytic and beta haemolytic are the two main groups of STREPTOCOCCI
beta- haemolytic is then further subcategorised into:
- group A strep
- group B strep
give an example of a group A strep
what 3 conditions can it most commonly cause?
strep pyogenes
- bacterial sore throat
- necrotising fasciitis
- rheumatic fever
what is the commonest cause of bacterial meningitis?
type of bacteria?
strep pneumoniae
a beta-haemolytic strep
nb also most common cause of community acquired pneumonia
what is the most common cause of bacteria; neonatal meningitis?
group b strep
nb this is a sub-type of beta haemolytic strep
what are the possible consequences of contracting a listeria infection:
- early in pregnancy?
- late in pregnancy?
early in preg:
- miscarriage
late in preg:
- baby gets meningitis +/or sepsis
name four anaerobic bacteria and the conditions they can lead to
all clostridium species
c. diff
- Abx associated diarrhoea/colitis
c. perfingens
- gas gangrene
c. tetani
- tetanus
c. botulism
- botulism
what are the difference in effect in tetanus as opposed to botulism
tetanus
- rigid paralysis/lock jaw
botulism
- flaccid paralysis
what is the stain for mycobacterium species?
ziehl-neelsen stain
nb this includes TB + leprosy
what is the treatmetn for TB?
RIPE
R - rifampicin
I - Isoniazid
P - Pyrazinamide
E - Ethambutol
what is the most common cause of endocarditis?
non-prosthetic valves, non IVDU
strep viridans
present in the mouth -> blood stream -> infection
are herpes viruses DNA or RNA viruses?
all double-stranded DNA viruses
nb chronic/reactivating infections tend to be caused by DNA viruses, acute infections tend to be RNA (general rule, not always correct!)
how are these types of herpes viruses transmitted:
- HSV1 + 2?
- VZV?
- EBV?
- CMV?
HSV1 + 2:
- direct contact
- kissing/sleeping with someone with a cold sore/genital herpes
VZV
- respiratory droplets
- “chicken pox parties”
EBV
- saliva + genital secretions
- “kissing disease”
CMV
- saliva + genital secretions
- infected blood/organ donation
- “often occurs post transplant”
what’s the difference being bronchitis and brochiolitis?
who gets which?
bronchitis:
- inflammation of bronchi
- a feature of COPD
bronchiolitis
- inflammation of bronchioles
- kids with RSV
“kids are smaller, as are bronchioles”
who is more likely to develop chronic hepatitis from a hep B infection?
babies
- predominately vertical transmission
if get it congeitally, 90% chance -> chronic
if get it as an adult (eg via blood), 5% chance -> chronic
who does rota virus tend to affect?
children
think of it as norovirus for kids
parvovirus:
- what does it cause?
- symptoms?
- who is it most dangerous in? 2
‘slapped cheek disease’
“if someone is being a PERV the SLAP them round the face”
- fever
- red rash to cheeks
people with high RBC turnover (eg sickle cell)
- can cause transient aplastic crisis
pregnancy:
- if early -> miscarriage
- if late -> hydrops fetalis
what is hydrop fetalis?
severe foetal anemia -> oedema, ascites + heart failure
nb also caused by rhesus incompatibility
enteroviruses:
- examples?
- clinical presentation?
- coxsackie A + B
- enteroviruses
- echoviruses
90% asymptomatic
- or just mild febrile illness (common cold like)
nb these viruses replicate in the gut (hence are called ENTERO viruses) but their clinical effects are on lung, cardiac +/or CNS, do NOT cause GI symptoms!!
- hand, foot + mouth disease in kidss
- meningitis (>50% viral meningitis)
- encephalitis
- other
what antiviral is used for:
- any herpes virus infection?
- CMV infection?
- inflenza? 2
- hep C/RSV?
herpes
= aciclovir (can get cream for cold sores as well)
CMV
= ganciclovir
influenza
= ostelTAMIvir (tami flu)
= zanamavir (“has z in, as does influenza”)
hep C/RSV
= ribovirin
what other, non-antiviral, drug can be used to treat hep B + C?
interferon
triggers immune response from body as well as interfering with viral replication
where can candida albicans infect?
mucous membranes
and also systemically
but NOT skin (dermatophytes do skin)
what is the 1st line antifungals for:
- superficial (eg skin) infection? (topical)
- deep (eg vaginal thrush) infection? (oral)
topical
= clotrimazole
(eg athletes foot + other dermatophytes)
oral
= fluclonazole
(eg vaginal candida infection)
nb fluclonazole is contraindicated in pregnancy
- a big issue as lots of pregnant women get thrush
how would you describe the lesions in impetigo?
what are the ccommon causative organisms? 2
honey-crusted lesions
- staph aureus
- strep pyogenes (group A strep)
what species of schistosoma is responsible for urinary disease?
s. haematobium
“causes HAEM in the urine”
these ones cause liver disease:
- s. masoni
- s intercallatum
- s. japonicum
- s. mekongi