microbiology Flashcards
6 main bacterial causes of meningitis (and age groups for some)
streptococcus pneumoniae
neisseria meningitidis
heamophilus influenzae (infants - but vaccine)
listeria (neonates and elderly)
group B streptococcus -agalacticae (neonates)
e.coli (neonates)
but the age allocations are not strict
what does streptococcus pneumoniae look like in microscope
gram + diplococci
what is streptococcus pneumoniae like on blood agar
alpha hemolytic (partially hemolytic – green)
what is the relation between streptococcus pneumoniae and optochin discs
step. pneu is optochin sensitive
what does neisseria meningitidis look like in microscope
gram - diplococci
gram - diplococci =
neisseria meningitidis
gram + diplococci =
streptococcus pneumoniae
gram - cocci-bacillus
haemophilus influenzae
what does haemophilus influenzae look like in microscop
gram - cocci-bacillus
e. coli in microscope
gram negative bacilli
litseria in microscope
gram + bacilli
haemophilus influenzae on blood and choc agar?
doesnt grow on blood but does on choc (it is fussy and choc gives it better stoof)
can both bacteria and virus causes meningitis
yes
can both baceria and virus cause encephalitis
no. only virus
list 3 viruses that causes meningitis
mumps
enterovirus
herpes simplex virus
polio
echo
list 3 viruses that cause encephalitis
herpes simplex virus = most common
varicella zoster = 2nd most common
parvovirus HIV mumps measles CMV EBV
CSF is used for meningitis (/ encephalitis) investigation as this is a CNS infection. how is this obtained? what is the macroscopic appearance? then what?
lumbar puncture
should be gin-clear. cloudy = white blood cells and already –> memingitis!
then cultured + gram film
what are the treatments for meningitis
main= antibiotic from cephlasporin group (from beta lactan group) – cefotaxime or ceftriaxone
also - amoxicllin (a penicillin ) for listeria
they can both cross the blood brain barrier
what are the signs in CSF analysis (not microscope) of bacterial infection
neutrophils
raised protein and low glucose (due to bacteria and neutrophils)
meningitis triad of symptoms
photophobia
neck stiffness
headache
what other non-antibiotic treatment is given with meningitis
anti inflammatories – corticosteroids (dexamethosone) and NSAIDs. these dampen immune system so decrease risk of nerve damage
also analgesia
also fluids
blood agar hemolysis
when would this be useful to identify bacteria?
alpha hemolysis - partial hemolysis, - not fully transparant, green/grey (due to hydrogen peroxide produced by bacteria)
beta hemolysis - full hemolysis (rbc burst open) - transparent/ clear
non hemolytic
this is useful to distinguish gram + cocci chains (all catalase negative. all streptococci)
lancefield test
how is it done
what does it distinguish between
colonies in water + some antibody coated latex beads from a kit
between B hemolytic bacteria in streptococci group (gram + clusters - = all catalase negative)
two types of neisseria and their effect
gonococcal –> urethritis
meningococcus –> meningitis
neisseria in blood and choc agar
blood- no haemolysis
choc - grows!
what clinical feature in addition to meningitis symptoms points to meisseria meningitidis as a cause
peticheal rash
should you perform a lumbar puncture with neisseria meningitis
no. no need - rash + present in blood cultures is enough to diagnose. plus it is dangerous (something to do with coagulation)
what should you do with a diagnosis of neisseria meningitidis
treatment = cefotaxime or ceftriaxone (3rd generation cephlasporin group)
notify public health england
appearnace of lymphocytes and neutrophils in gram stain microscope
lymphocytes = purple cells neutrophils = pink
route of transmittion for group B strep (agalactiae) and e.coli
mothers birth canal –> baby skin
X+ V discs ?
if a clearing around them- this means the bacteria have munched the nutrient that has spilled out of the discs
how to apply gram stain
heat fixate bacteria apply crystal violet iodine treatment remove stain counterstain
blue/purple colour gram stain
gram +
red/pink colour gram stain
gram -
coagulase test
done how
used when
different results
meaning
colonies in tube with saline and rabbit plasma
used to differentiate gram + cocci that are clusters (aka staphylococcus, aka catalase +)
positivie = yes coagulase produced by bacteria. clumping like precipitate looks like. if tilted doesnt move like normal liquid
– staph aureus
negative = no coagulase produced
no clumping. tilts as normal. may be more yellow
– staph epidermidis
– staph saprophiticus
staphylococcys vs streptococcus
both are gram + cocci
staphylococcus = clusters streptococcus = chains
staph = catalase + strep= catalase -
staphylococcus under microscop
gram + cocci clusters
streptococci under microscope
gram + cocci chains
catalase test
done how
results
hydrogen peroxidase + colonies.
catalase + looks like white, foamy, bubbles of Oxygen
– staphylococcus
catalse - looks like clear flat liquid droplet
– streptococcus
what are the possible bacteria of alpha hemolytic blood agar observation
how would you distinguish them?
- strep viridans (think endocarditis)
- streptococci pneumoniae (think meningitis, and pneumonia)
distinguish them with an optochin disc. strep viridans is not sensitive. strep pneumoniae is
macconkey agar
distinguishes gram - rods
lactose fermenting = red- pink
– e.coli, klebsiela
non-lactose fermenting = yellow/white (normal colour)
– shigella, salmonella, pseudomonas, proteus
CLED agar
normally blue
can distinguishes gram - rods:
lactose fermenting- yellow
– ecoli, klebsiella
lactose non fermenting- blue (normal colour)
– shigella, salmonella, pseudomonas, proteus
grows UTI pathogens well
doesn’t let proteus swarm
sp and spp meaning
sp= species singular spp = species plural
where are the sterile sites of the body? name 5
1 blood 2 CSF 3 pleural fluid 4 joints 5 lower resp tract 6 urinary tract 7 peritoneal cavity
where are the areas in the body naturally colonised by bacteria? name 3
1 mouth 2 skin 3 vagina 4 urethra 5 large intestines
what colour is CCDA agar
black
chocolate agar
brown
allows organisms to grow that dont grow easily on blood agar because they are fussy
XLD agar colour
- good for?
bright red/pink/orange
v selecitve
good for shigella, salmonella
optochin disc
whether bacteria are sensitive to optochin
yes= strep pneumoniae
is blood agar selective
no. many can grow here
name two examples of enteroviruses
rhinovirus
echovirus
name 3 examples of respiratory viruses
1 influenza 2 coronavirus 3 rhinovirus 4 measles 5 mumps 6 rubella 7 parvovirus
viral vs bacteria swab
viral swab = green
then PCRed
bacterial swab = charcoal
then cultured
what test is used to identify viruses
PCR
- specific primers detect
when is PCR available to view
next day
PCR pros and cons
fast
sensitive
identifies specific viral cause
expensive
blood film time
get results in hours
glandular fever treatment
supportive
avoid contact sport for 6w+ to avoid splenic rupture
ELISA test
viral antibody binds to enzyme in assay (grid thing)
clotted (yellow top) serum sample to serology?
looks for evidence of past/ present infection and immunity (eg rubella, HIV, HBV)
neonate with rubella IgG
adult with CMV igG
traveller rabies immunoglobulin
passive antibody but not infected
protective antibody from prior infection
passive antibody from injection
HIV tests
3
antibody
antigen
HIV RNA
why do you need to retest a HIV test
if reported negative : repeat after 4 w (could be early stage so not detectable yet/ test error/ mic up)
if reported positive: repeat straight away (2xpos = pos, 1 pos and 1 neg = do a third test)
which antibiotics can you give if someone is allergic to penicillin
clindamycin
erythromycin
vancomycin
name an antibiotic that is good for MRSA
vancomycin
a glycopeptide
c diff down microscope
gram + rods
c diff
aquired when
symptoms
squired after antibiotic use - replace gut flora
old patients, hospitals
collitis
symptoms -
diarrhea
E.coli related diseases
UTIs inc pyelonephritis etc
Gastroenteritis
meningitis
bloody diarhea, abdom cramps
staph aureus related diseases
osteomyelitis
septic arthritis
UTI
do helicobacter pylori have flagellae?
yes
which layer of the stomach do helicobacter pylori live in?
pathophysiology
mucin layer.
they then damage the gastric cells below –> ulceration
what do neisseria gonnorhea look like down microscope in discharge/smear
gram - diplococci within cytoplasm of polymorphs
proteus effect on agar
swarms agar, tide marks
eg blood agar, MacConkey
but not CLED
- so CLED is good for urine microorganisms
lower UTI vs upper UTI symptoms
lower- dysuria, frequency, urgency
upper - loin pain,fever, rigors, haematuria
causes of UTI
KEEPPSS Klebsiella e coli enterococci proteus pseudomonas staph epideermis staph saprophyticus
what is looked at in microscopy for UTIs (whats the sample)
mid stream urine (this avoids contamination from perineum / vagina)
what does MSU stand for
mid stream urine
what does pure growth mean?
only 1 bacteria growing there
lactose fermenting vs non lactose fermintnig gram - bacilli
lactose fermenting
- e.coli
- klebsiella
non-lactose fermenting
- shigella
- salmonella
- proteus
- psuedomonas
how might pseudomonas be differentiated from non-lactose fermenting gram - rods
pseudomonas is oxidase +ve
what does CSU stand for? what is important to note about it
catheter sample urine
can not perform dipstick urinalysis / microscopy. on catheter bag
because urinary catheter bag may produce inflam response with no infection present
what happens if epithelial cells are found in the microscopy of a urine sample
poorly taken sample. it is contaminated. needs to be repeated. can not be analysed
what is the point of using a CLED plate with a LUTS patient
- promotes growth of urinary tract pathogens
- differentaites between lactose and non-lactose fermenting bacteria
- doesnt let proteus swarm
why is urine analysed at antenatal visits
looking for blood/protein
screening for pre-eclampsia
and for asymptomatic bacteriuria (Ascending UTI–> pyelonephritis –> miscarriage)
what does multiple bacteria growing on agar suggest in respect to UTIs?
mixed culture suggests contamination (from vagina/perineum)
may not be a correct MSU sample
what is the most common site for soft tissue skin infection/
lower leg
abscesses signs
few
tender
deep skin infection signs/symptoms
erythema
marked pain
causes of soft tissue infection
group A beta hemoltic streptococcus (s.pyogenes)
staphylococcus aureus
atypical causes seen in needle drug users/ immunocomprimised
types of soft tissue infection
- erysipelas = where
- cellulitis = where
erysipelas – intradermal
cellulitis – sub-cut
both same bacterial causes
is skin soft tissue infection more commonly caused by local breach of body defences (…eg?) or blood stream spread?
local breach
- ulcer
- eczema
- insect bite
- athletes foot
sampling for soft tissue infection
- blood culture
- pus from abscess if poss
- swab skin at site of entry if skin breached (eg athletes foot)
impetigo
- presentation
- affects who
- itchy, red, growing lesion which is weeping/ crusty
- infants/kids
what antibiotics can most gram + be treated with
flucoxycillin
what antibiotic can most gram - be treated with
cefotaxime (A cephlasporin)
would staph and strep grow better on aerobic or anaerobic blood agar
both - aerobic
anaerobic= peptostreptococcus
what antibiotc is used to treat group a lancefield strep (strep pyogenes)
pencillin
empirical antimicrobials=?
initial antibiotics regimen given within 24h of admission. started just after sample specimens are collected
what does MRSA stand for
what is it resistant to
methicillin resistant staph aureus
this is resistant to flucloxicillin
how is MRSA carriage identified
swab –> chromogenic MRSA plate
if resistant to cefoxitin, then = MRSA
encephalitis symtpoms
fever lethargy, fatigue decreased conciousness, drowsy maybe fits associated with meningitis (= meningo-encephalitis)
pnuemonia features
plueritic chest pain
rusty/green sputum coughed up
cough
breathless ness
asympotmatic pneumonia if these symptoms predominate:
myalgia
arthralgia
headache
signs:
fever
consolidation (dullness to percussion, bronchial breathing)
most common cause of pneumonia =
Strep pneumoniae
pulmonary TB causes
mycobacterium tuberculosis and mycobacteium bovis
infective endocarditis diagnosis
modified duke criteria
definite IE = 2 major crieria, OR 1 major and 3 minor, OR 5 minor
MAJOR
- positive blood culture with typical IE microorganisms
- new partial dehiscence (wound seperation) of prosthetic valve
- new valvular regurgitation
MINOR
- predisposing factor (cardiac lesion, recreational drug inj)
- fever >38
- embolic evidence (arterial emboli, pulmonary infarcts, janeway lesion, conjuntival haemorrhage)
- immunological problems (glomerulonephritis, osler’s nodes, roth’s spots)
- rheumatoid factor
- microbiological evidence (positive blood culture (but not major criteria) or serological evidence of infection )
if something is resistant to cefoxitin, what is it resistant to also?
methicillin
sabaraud’s agar (SAB)
promotes griwth of non bacterial pathogens eg fungus
what type of organism is candida
fungus
are enterococcus species streptococcus?
yes
where do enteric infections refer to?
intestines
name 3 symptoms of enteric infection
1 stomach ache 2 diarrhae (can be sever/fatal) 3 vomitting 4 fever 5 abdominal cramps
c. diff diarrhea treatment
stop the causative antibiotic if still taking.
+ vancomycin / metronidazole
what does metrondiazole antibiotic treat
anaerobic bacteroides (+c.diff)
what is an API strip
series of biochemical reaction that determine the bacteria based on metabolic and enzymatic qualities
name 3 microorganism causes of ascending cholangitis due to impacted gall stone
1 klebsiella pneumoniae 2 e coli 3 enterobacter 4 enterococcus 5 anaerobes
is bacterial or viral meningitis more serious
bacterial
viral is benign and selflimiting
commensal
organism colonises part of body but is not disease causing
virulence
degree of ability to cause disease (eg toxins and how good it is at colonising)
- spores
- name their virulence factor
- store DNA
- resistant to destruction (eg heat, chemicals)
ziehl neelson stain detects what
mycobacteria
good for when gram stain doesn’t work
in to out describe bacteria structure
circular double stranded DNA membrane(S) cell wall capsule flagella
not all have each thing though
gram + /- membranes
gram + = 1 membrane (large peptidoglycan)
gram - = outer and inner membrane – with lipoprotein and small peptidoglycan in between. lipopolysacharide attached to outside
gram +/- peptidoglycan
gram + = large peptidoglycan component (on outside cos only 1 membrane)
gram - = small, in between 2 membranes
gram +/- lipopolysaccharide
gram + = no
gram - = yes. attached to outer membrane. this is the endotoxin
gram +/ - endo and exotoxin
compare features of endo/exotoxins
ENDOTOXIN
- only gram - : the lipid A of the lipopolysaccharide on the outer membrane
- non specific
- stable in hear
- weak antigenicity (response in immune system)
- cannot convert to toxoid
EXOTOXIN
- gram + and - : protein secreted
- specific
- unstable in heat
- strong antigenicity
- can concert to toxoid
how to bacteria swap genetic info (horizontally)
plasmid . these replicate autonomously and pass between bacteria (=transformation) picked up naked from enviroment eg after rupture
bacterial conjugation = cell-cell contact via pilus - plasmid exchanged here (=conjugation)
phage ( virus) infects and replicates bacteria, giving it new gene (=transduction)
what is transforamtion
when plasmids pass from one bacteria to another, picked up naked from environment eg after rupture
new genetic material introduced (horizontal gene transfer)
how is staph aureus spread
touch and aerosols
how can you distinguish staph aureus and staph epidermis on blood agar
staph aureus - golden colonies
staph epid - white colonies
where is strep pneumoniae commensal?
in oro pharynx
where is viridans streptococci
often oral
also deep organ absesses (brain, liver, lung)
endocarditis
name 3 bacterial causes of endocarditis
staph aureus enterococci strep viridans strep pneumoniae pseudomonas
corynebacterium
- appearance under microscope
- an/aerobic
- produced
- treatment
- prevention
gram + rods
aerobic
produces toxins that inhibit protein synthesis
treatment : anti-toxin, erythromycin
prevention: toxoid vaccination (inactive toxin)
do gram negative have a capsule
yes
proteobacteria
2 types
gram + or -
gram -
enterobacteria and non-enterobacterial proteobacteria
e coli
where is commensal
what feature
name 3 things it causes
commensal in gut
peritrichous flagella (=all over surface)
UTIs, wound infection, gastroenteritis, Travellers diarrhea
shigellosis =
cause
symptoms
toxin
shigella caused disease
severe bloody diarrhea, >30/day inc pain and cramping, fever
low infective dose
toxin = shiga toxin. binds to receptors and stops translation and protein synthesis, killing the cell
salmonellosis =
route
toxins
effect
salmonella enterica causes it
ingest contaminated food/water
no toxins
diarrhea (fluid+electroylte loss) and tissue injury
salmonella species
salmonella enterica = causes salmonellosis
salmonella bongori = rare
what are ETEC and EHEC
forms of e.coli
additional genes make them more pathogenic
ETEC causes travellers diarrhea
vibriocholera virulence factor
1 flagellum
pilli
toxin
cholera route of transmission
symptoms
treatment
undercooked shellfish
drinking contaminated drinking water
diarhea voluminous (litres of lost fluid + electrolyte –> hypovolemic shock)
ORS oral rehydration salts
obligates=
eg
cannot be cultured on a medium, only in humans
eg chlamydiae
fungi cell wall=
fungi membrane=
chitin
contains ergosterol rather than cholesterol
yeast vs mould
yeast = single celled. divide by budding mould = multicellular. hyphae and spores
when is fungi life threatening
immunocomprimised, post surgical
lots cannot grow in humans and most that do are mild
fungi treatment (theoretical)
inhibit RNA/DNA synthesis
attack membrane (contains ergosterol rather than cholesterol)
– put pores in
– inhibit ergosterol synthesis
target cell wall (humans have no cell walls)
fungi detection in blood/fluids/tissues
blood cultures are undersensitive
fluid/tissues is better
how do viruses replicate
intracellular - requires host:
- attaches to cell receptor
- enters cell and uncoats – sheds virion
- does transcription using host cell materials and machinery to create proteins, genome, enzymes etc
- virion assembled in host cell
- bursts out/ budding/ exocytosis
are viruses DNA or RNA
can be either
this is surrounded by protein coat +/- membrane
which are bigger viruses or bacteria
bacteria
do viruses have cell wall
do viruses have membrane
do viruses have organelles
no
sometimes
no
how do viruses cause disease
1 direct destruction of host cells - (lysis)
2 damage through cell proliferation (continuous expression of oncogenes –> dys/nepplasia–>cancer)
3 modification of host cell (eg flattens epithelial cells and villi atrophy so decrease absorption area in the small intestine)
4 ‘over-reactivity’ of immune system
5 evasion of host cells inc immune cells
- lies latent and can reactivate
- spreads cell-cell –doesn’t need to leave and re-enter
- antigenic variability
- prevents host cell apoptosis as needs it to live
- downregulation of host defence proteins
- prevents MHC displaying of antigens
protozoa
classes
based on
classification based on how they move
- amoeboids (temporary protrusions = pseudopodia)
- ciliates (have cilia)
- sporozoa (non-motile)
- flagellates (flagella)
amoeboids transmission
faecal-oral (unsanitary food/water)
African trypanosomiasis
aka
vector
microorganisms
symptoms
sleeping sickness
tsetse fly
flagellate (protozoa)
systemic infection (fever, fatigue etc) + CNS involvement (drowsy, personality change)
american trypanosomiasis
aka
vector
microorganisms
Chagas disease
triatome bug
flagellate (protozoa)
systemic infection (fever, headache etc) + cardiac, megaoesophagus and megacolon + eye swell
examples of flagellate (protozoa)
american trypanosomiasis african trypanosomiasis leishmaniasis giardia lambia trichomoniasis
malaria types
microorganism
plasmodium falciparum (most common and most severe) p malariae p ovale p vivax p knowlesi
protozoa
malaria epidemiology
sub-S Africa
North of S America
S Asia
rare in UK
malaria risk factors
Travel to or residency in areas with malarial risk
Poor
young/old
pregnant
malaria liver stage
Infected mosquito takes a blood meal and injects SPOROZOITES (infected form of plasmodium)
Sporozoites travel to the liver and infect LIVER CELLS
Liver cells mature into SCHIZONTS
Schizonts grow and RUPTURE, releasing MEROZOITES into the blood
what is the dormant stage and which forms of malaria have it
In p.vivax and p.ovale there is an additional dormant stage here where HYPNOZOITES can persist in the liver, allowing relapses
blood stage malaria cycle
Merozoites enter circulation and infect RBC (from liver stage)
Rbc mature into TROPHOZOITES, which mature into SCHIZONTS
Schizonts grow and RUPTURE, releasing more merozoites into blood
Continued cycle, infecting more rbc
Immature trophozoites also go on to differentiate into sexual stage GAMETOCYTES
Gametocytes mature and are picked up by the next mosquito that bites you in their BLOOD MEAL (infecting the mosquito)
malaria vector
infected female anopheles mosquito
vector stage malaria cycle
Mosquito takes in blood meal and ingests gametocytes
Gametocytes mature from MICRO –> MACROGAMETOCYTES
MALE AND FEMALE macrogametocytes FUSE to form an OOCYTE
Oocyte grows and ruptures, releasing SPOROZOITES
Sporozoites travel to SALIVARY GLAND - here they will be passed on when the mosquito takes a blood meal
which is the most severe form of malaria and why
Plasmodium falciparum
1) Rapid replication
2) Cytoadherence
Infected rbc show surface proteins that cause adherence between rbc and endothelial walls
3) Rosetting
Big blobs or rbc - including non-infecting ones
Allows SEQUESTRATION - they hide from the body’s immune system in rosettes, surrounded by non-infected rbc so infiltrate organs
Vascular occlusion → bleeding, leaky vessels
is it the liver, blood or vector stage that is responsible for malarial symptoms
blood stage
malarial symptoms and why
merozoites→ trophozoites → schizonts → rbc rupture so this causes waste products and toxic factors as the infected cells lyse. Macrophages and other mediators release inflammatory cytokines in response.
Chills (fever) Rigors Cough Headache Muscle ache (myalgia) Fatigue Nausea, vom , diar Flu-like symptoms
Haemolysis rises big time - to break down infected rbc. This, along with cell lysis of infected cells causes
Anaemia (tired, sob)
Jaundice (pre-hepatic accumulation)
Haemoglobinuria (rbc products in kidney → dark urine)
Severe : hypovolemia, fits, impaired consciousness
signs of malaria
Fever
Splenomegaly
Hepatomegaly
Severe: fits, hypovolemia
diagnosis of malaria
Blood film- smear
–Thick blood film
Count parasitic rbc (dark dots)
% parasitemia in rbc indicates severity - 2%+ is severe
–Thin blood film
Determine which type/ strain of malaria
Repeat to ensure no false results form gamete stage of cycle
malaria treatment
uncomplicated = oral quinine (others)
complicated (has complications) = IV artesunate
(if not possible, IVE quinine and doxycycline)
Primaquine eliminates dormant hypnozoites (p.vivax, p.ovale)
Artemesmin = for uncomplicated, mixed infection type malaria
treat symptoms
malarial complications x4
Cerebral malaria:
- Vascular occlusion
- Hypoglycaemia
- Leak causes rise in intracranial pressure (ICP)
- Coma, Drowsy, Seizures
Renal failure
- Vascular occulsion
- BP drop
- Dehydration
- Overwork
- Proteinuria, fatigue, haematuria
ARDS = acute respiratory distress syndrome
- Vascular occlusion
- Increased vascular permeability
- Oedema, anaemia, breathless ness, hypoxic
Shock
- Sepsis
- Increase in vasc permeability
- Bleeding
- Inflammation
- anaemia
primary vs opportunistic pathogen
primary pathogen can cause disease in a proportion of exposed individuals irrespective of immunological status. opportunistic only causes disease if immunocompromised
how does IgA fight against viruses and bacteria
cells are coated with IgA
blocks attachment binding to host cell
how do antibodies fight against viruses and bacteria
osponisation - attach to pathogen so they are more easily phagocytosed
how does IgM fight against viruses
agglutinates viruses together in clumps so they are trapped
igM is a large molecule- many attached
how do complements fight against viruses and bacteria
osponisation and cell lysis
how do antibiotics work
+ example of each
inhibit cell wall synthesis
- beta lactans inc penicillin and cephalosporins (target peptidoglycan layer so work best on gram +)
impair nucleic acid synthesis
- rifampacin
impair protein synthesis
- 30S part of ribosome - tetracyclines
- 50S part of ribosome - macrolides (clarithromycin, erythromycin)
impair folate synthesis
- sulphonamides
bacteriostatic antibiotics
bactericidal antibiotics
prevent growth of bacteria (and kill most)
- prevent protein synthesis (and so toxin production), metabolism or DNA production
kill majority of bacteria (more)
- inhibit cell synthesis
antibiotics MIC and MBC
MIC = minimum inhibitory concentration (minimum concentration of antibiotic that inhibits growth)
MBC = minimum bactericidal concentration (minimum concentration of antibiotic that kills)
two qualities of antibiotics
concentration dependant – low MIC - low conc of antibiotic needed. then dose size needs to be above this MIC
time dependant – time antibiotic stays bound to site = long (give doses regularly enough to keep amount above MIC)
how do bacteria resist antibiotics
antibiotic target on bacteria changed by the bacteria (mutations, covering it)
bacteria destroy/inactivate antibiotics (beta lactamase enzyme breaks down beta lactam antibiotics)
bacteria prevent antibiotic access to it (change porin size/number/selectivity)
remove antibiotic (active pump in bacteria removes antibiotic from bacteria)
how do bacteria become resistant
some are intrinsically, naturally resistant (=all strains are resistant)
most = acquired . either by spontaneous gene mutation or horizontal gene transfer from another bacteria
conjugation
plasmids exchanged by pilus –>new genetic material introduced (horizontal gene transfer)
transduction
new gene inserted by phages (viruses) –> new genetic material introduced (horizontal gene transfer)
what are macrolides (clarithromycin, erythromycin) / lincosamides (clindamycin) good for
penicllin allergy
why are beta lactams better for gram + than gram -
inhibit cell wall synthesis by targetting peptidoglycan layer gram + have big peptidoglycan layer but gram - is small (between inner and outer membrane)
mycobacteria=
gram stain?
example
type of bacteria
they cannot be identified with gram stain due to high molecular weight lipids on cell wall (neither gram +/-). they are identified with ziehl neelson stain.
acid fast bacilli
eg TB
mycobacteria qualities
- an/aerobic
- mobility
- spore formation?
- cell wall?
- phagocytosis
- speed of growth and implications of this
- immune response
- aerobic
- nonmotile
- no spore formation
- cell wall present - has high molecular weight lipids on it. this helps it survive in the environment and against phagocytosis (survives inside macrophage
- slow growing – so slow onset in disease, slow to grow in cultures and slow to respond to treatment
- granulomas (with mycobacteria inside)
high risk of TB
infant elderly malnutrition intense exposure immunosuppression
tb pathogen
mycobacterium tuberculosis
primary vs latent TB
primary = inhaled to lungs. goes into lymph nodes. cell-mediated immune response (intrinsic)
latent = not unwell. but cell mediated immune response from T cells remains inc skin test positive still
HIV stages
1 acute primary infection
- 2-4w after exposure
- abrupt non specific symptoms
- transient immunosuppression as HIV causes CD4 count to drop before rising slowly (as HIV replicates in CD4 (Th) cells
2 i) asymptomatic phase / clinically latent
- long
- -progressive loss of immunity
-
- still infectious despite no symptoms
3 AIDS
- opportunistic infections
- CD4<200
HIV replication
replicates in CD4 ( Th )
this causes CD4 count to fall, before gradually rising again (transient immunosuppression)
what is normal CD4 count and what is it in AIDS
what is considered a late HIV diagnosis
normal = 500-1500
AIDS = less than 200
late diagnosis is when HIV found and CD4<350
how is HIV monitored
CD4 count (cell count per microlitre) HIV viral load (RNA copies per microlitre)
extension of progression, prognosis, and response to treatment
HIV symptoms
abrupt onset of non specific symptoms fever rash lethargy depression weight loss
PGL =
persistant generalised lymphadenopathy
enlarged lymph nodes at at least 2 non contigous sites
seen in clinally latent/asymptomatic stage of HIV
what infections might flare up with HIV, name 3
oral candida shingles (in 2+ dermatomes) thrombocytopenia toxoplasmosis (ring enhancing lesions in brain) pneumonia herpes
HIV treatment/ prevention
TREATMENT
ART antiretroviral therapy
target diff points in HIV life cycle
once viral load is undetectable, it is untransmittable!
PREVENTION
nonpharmacological - condoms, needles, screen blood products for transfusion, diagnosis, partner notiification etc
PreP: pre-exposure prophylaxis (before sex)
PEP: post- exposure prophylacis (within 72h)
circumsision
STI control (ulcerative STIs have enhanced HIV transmission)
microbicides (vaginal gel, not used much)
does HIV screening exist
yes eg antenatal
venous/salivary
what is a retroviridae
enveloped virus (HIV - outer lipid envelope layer is studded with glycoprotein) RNA is copied into DNA by reverse transcrption then incorporated into the host
hiv
what is a lentivirus
a type of retrovirus with long incubation period
HIV
what is the 90/90/90 target
UN AIDS target
90% of HIV =diagnosed
90% of diagnosed HIV = on ART treatment
90% on ART treatment = viral suppression
by 2020
what is HIV tropic to
to immune cells (esp CD4+ cell, but also macrophages and others)
tropism = where the virus infects and replicates in
if HIV infects immune cells , how does the immune system respond?
made difficult as if macrophage engulfs, it cannot kill and it allows it to meet other immune cells - spread!
there is partial immune response (vigorous but ineffective) for some years
- antibodies neutralise
- CD8 (Tc) kill infected cells
how does HIV affect CD4 cells
depletes :
- by direct cytotoxicity as they are infected and taken over
- decreased production in bone marrow due to HIV (viral reservoir)
varicella zoster virus stages
primary infection = chickenpox dormancy period (lies in dorsal root/ cerebral ganglion) secondary reactivation = shingles
how is chicken pox transmitted
when is it infectious
touching rash (via mucous membranes)
infectious from day 0
not infectious when it has crusted
when is good/bad to get chicken pox
good= child - usually benign bad= pregnant (foetus catches it = foetal varicella syndrome), adult, immunocompromised, smokers
chicken pox diagnosis
swab lesion (pop if needed) send for VZV PCR
chicken pox vs small pox rash distribution
chicken pox =in warmer areas (central)
small pox = more extremeties
foetal varicella syndrome (FVS)
foetus infected in chickenpox pregnancy
usually transient (rarely there are severe defects eg microcephaly, growth retardation, limb hypoplasia, skin /occular scarring)
shingles in year 1 of life
shingles high risk
immunocompromised, elderly
what does shingles look like
skin lesion
blister fluid
v painful
in single dermatome (red flag if multiple)
what does parvovirus look like
rosy cheek
+ reticular mottling
+ risk of anaemia (due to prevention of rbc maturation)
worms categories (helminth categories)
nematodes (round worms)
trematodes (flatworms)
cestodes (tapeworms)
pre-patent period (Worms)
interval between infection and appearance of eggs in the stool
dimorphic fungi=
fungi that exist as both yeasts and moulds, switching between the two depending on the conditions
antigenic drift vs shift
and type of disease prevalence associated
spontaneous mutations – gradually minor changes – epidemics
sudden emergency of new subtype – pandemics
protozoan infection immune response
blood stage = humoral immunity (extrinsic)
tissue stage = cell mediated (intrinsic)
worm replication where?
not in humans, outside body
worm immune response?
poor. insufficient to kill
worms - diagnosis
stool microscopy- look for eggs
or may see macroscopically
antibiotic for strep pneumoniae
amoxicillin
how does an antigen test work
antigen of virus/bacteria added. serum added. antigen will stick to IgM or Ig G if present. enzyme causes colour change
‘atypical’ causes of pneumonia and their treatment
coxiella
chlamidya
legionella
mycoplasma
not susceptible to beta lactams! (amoxicillin) so need macrolide instead - clarithromycin
what do X and V nutrient factors allow to grow
haemophilus influenzae
how can you obtain a sputum sample in someone with dry cough
bronchoalveolar lavage - bronchoscopy passed in, fluid deposited and collected
induced sputum - breathe in saline via a nebuliser ,cough
sabourdad’s agar
- colour of agar
- grows what
pale yellow
fungi (inhibits bacteria) - candida
fungi grows on what agar
sabourdad’s
causes of reactive arthritis
salmonella shigella yersnia chlamidya
warm swollen tender joint = what until proven otherwise
reactive arthritis
which TB treatment interacts with the oral contraceptivepill
Rifampicin
malaria investigations
blood and other cultures not useful
blood FILM
