Unit 6 Case 1: Meningitis Flashcards
key diagnostic symptoms of meningitis
focal neurological signs
abnormal eye movement
fever
facial palsy
nuchal rigidity
photophobia
altered mental state
balance problems/hearing impairment
headaches
other symptoms of meningitis
coma
delirium
irritability
confusion
vomiting
nausea
risk factors for meningitis
close contact exposures e.g. military barracks and college dorms
incomplete vaccinations
immunosuppression
children younger than 5 and adults over 65
alcohol use disorder
symptoms of meningitis in newborns
high fever
constant crying
sleepy/irritable/ hard to wake from sleep
inactive/sluggish
poor feeding
vomiting
not waking to eat
bulging fontanelle
physical examinations done to investigate meningitis
glass test, non blanching rash
brudzinskis sign
kernels sign
nuchal rigidity
eye exam
ear exam
kernels and brudzinksis sign
blood test to investigate meningitis
FBC to compare to CSf results
antibody test to detect a potential cause
blood cultures if suspected septicaemia
lumbar puncture
l3/4/5
spinal cord ends l1/2
take sample of CSF
may cause: headaches, lower back pain and swelling at the site of needle insertion
normal CSF results
clear and colourless
0-5 micro litres of WBC no neutrophils mainly lymphocytes
0-10mm3 RBC
1% serum conc of protein
60% plasma glucose conc
10-20cm H2O opening pressure
CSF results for meningitis
CT scan
view any fluid changes in the brain
gram stating
negative in up to 60% cases of bacterial meningitis, prior to antibiotics
predominance of lymphocytes doesn’t exclude bacterial meningitis
neutrophils may predominate in viral meningitis ever after first 24 hours
if CSF is abnormal treat for bacterial meningitis
gram negative, pink staining diplococci, meningococci
different meningitis vaccines
MenB
6 in 1
pneumococcal
Hib/MenC
MMR
MenACWY
men B vaccine
present in 90% of paediatric cases
vaccinated at 8 and 16 weeks then again at 1 year
side effects: pain, localised swelling, D&V
give preventative paracetamol post vax
contains: 3 proteins that are present on MenB surface and 1 membrane of the MenB strain
6 in 1 vaccine
protects against: diphtheria, tetanus, whooping cough, hepB, polio, haemophiliac influenza B
given at 8,12,16 weeks
side effects: localised pain, fever, vomiting
not administered: neuro condition or allergy to the drug
contains: Hib/MenC
given booster at 1 year
pneumococcal vaccine
streptococcus pneumoniae bacteria
given to: babies, risk children, adults and aged 65+
PCV, conjugate= under 2s
PPV, polysaccharide= over 2s
13 strain protection
not live
side effects: localised pain, fever, allergic reaction
Hib/MenC vaccine
inactivated Hib
contains: capsular polysaccharide form Hib cultures, conjugated with protein
given in combination with other vaccines
tetanus toxid proteins often in children, increase inmmunogeneticity
side effects: localised pain, fever, decreased appetite
MMR vaccine
relevant as meningitis can be a complication of one of these conditions
measles mumps and rubella
MenACWY vaccine
teenagers and freshers under 25
protects against meningococcal and groups A C W135 and Y
contains: polypeptide coating found on the surface of each bacteria
not administered when: bleeding condition, fever, pregnant or breastfeeding
which drug is administered if suspected meningitis
benzylpenicillin
benzylpenicillin
aka penicillin G
beta-lactam antibiotic
treats gram positive streptococci and staphylococci
gram negative= meningococcal
prescribed
pharmacology of benzylpenicillin
interferes with bacterial cell wall synthesis causing bacterial cell death
inhibits transpeptidases, essential to cross-link peptidoglycan chains
cell wall weakens
bacteria became vulnerable to osmotic pressure
leads to bacterial cell death
physiology of benzylpenicillin
bacteria can no longer reproduce
clears infection
prevents spread
clinical benzylpenicillin
given as an IV drug
most common side effects of benzylpenicillin
nausea
diarrhoea
headaches
abdominal pain
rare side effects of benzylpenicillin
allergic reactions
seizures
neurological problems
GI disturbances
long term impact of meningitis
kidney problems
hearing loss, either partial or total so given hearing test a few weeks later
epilepsy
memory and concentration difficulties
coordination, movement and balance issues
learning difficulties and behavioural problems
vision loss
loss of limbs, amputation
bone and joint problems
physical consequences of meningitis
fatigue
not being able to return to normal life immediately
disturbed sleep
bedwetting
fear of doctors or hospitals
personality changes: aggression, anxiety mood swings
depression
isolation
low self-esteem
impact of communicable diseases
disease spreading: guilt, shame and embarrassment
isolation
stigma
sick pay, SSP: £99.35 for up to 28 weeks, single parents may struggle
family/ relationships: sick parent can’t care for the child so may need family support
function of the meningeal layers of the brain
supportive framework for vasculature
act with CSF to protect CNS from mechanical damage
what are the meningeal layers
dura mater
arachnoid mater
pia mater
dura mater
outermost layer
between skull and vertebral column
thick, tough and inextensible
2 layers: periostea and meningeal and between are dural venous sinuses
vasculature: middle meningeal artery and vein
innervation: trigeminal nerve
4 dural reflections
what are dural venous sinuses
responsible for venous drainage of cranium and empty into the internal jugular veins
arachnoid mater
middle layer
avascular, no innervation
underneath is the subarachnoid space
arachnoid granulations
leptomeninges
subarachnoid space
contains CSF
cerebral arteries and veins
function of the arachnoid granulations
allow CSF to re-enter circulation via dural sinuses
pia mater
inner layer
under the subarachnoid space
very thin
follows contours of the brain
highly vascularised: blood vessels to neural tissue
leptomeninges
what are the 4 dural reflections
falx cerebri
tentorium cerebelli
falx cerebelli
diaphragmatic sellae
falx cerebri
projects down to separate right and left cerebral hemispheres
tentorium cerebelli
separates occipital lobes from cerebellum
falx cerebelli
separates right and left cerebellar hemispheres
diaphragmatic sellae
covers hypophysical fossa of the sphenoid bone
3 meningeal spaces
epidural
subdural
subarachnoid
describe the epidural space
between superficial layer of dura mater and bone of skull
describe the subdural space
between dura mater and arachnoid mater
describe the subarachnoid space
between arachnoid and Pia mater
contains CSF and major blood vessels
provides expansions, cisterns
subarachnoid spaces of cranium and vertebral column are continuous with each other
creates closed route for CSF circulation
what is CSF
cerebrospinal fluid
clear and colourless
located in the subarachnoid space and central canal of the spinal cord
produced by choroid plexus
500ml produced daily
150ml in body at a given time
choroid plexus
invagination of Pia mater to ventricles of brain
covers 2 lateral ventricles, roof of 3rd and 4th ventricles
forms selectively permeable BBB, controls movement of water and solutes into the CSF
structures in the BBB superficial to deep
choroid ependymal cells and their tight junctions
pia mater
endothelial cells of capillaries
basal membrane of endothelial capillary cells
route of CSf circulation
lateral ventricle
3rd ventricle
4th ventricle
through 2 lateral foramina of Luschka and medial foramen of Magendie
subarachnoid space and/or central canal of spinal cord
arachnoid villi (small protrusions of arachnoid mater)
drain to superior sagittal venous sinus to venous sinus
functions of CSF
protection
homeostasis
clearing waste
clinical diagnosis
buoyancy
protection as a function of CSF
acts as a shock absorber
prevents damage caused by brain hitting the cranium
homeostasis as a function of CSF
regulates distribution of metabolites that surround the brain
clearing waste as a function of CSF
waste products created by brain cells are excreted into CSF which then drains to blood stream
clinical diagnosis as a function of CSF
lumbar punctures to obtain samples from subarachnoid space
causes of meningitis
viral
bacterial
fungal
parasitic
amoebic
non-infectious
meningitis most common in
babies, E coli
young children
teens
adults, N.men
epidemiology of meningitis
N meniningitidis has 12 subtypes
transmitted via droplets, must pass the submucosal layer
incubation period is 4 days
10% population carries in bac of throat with no infection
notifiable disease
neisseria meningitidis as a pathogen
gram negative, capsulated, diplococcus
type 4 plus involved in mucosal colonisation (host adhesion)
capsule helps to avoid phagocytes
major toxin: lipo-oligosaccharide (LOS) endotoxin found inside pathogen and released when pathogen is degraded
3 methods of neisseria meningitidis to enter the CSF once in the bloodstream
paracellular
leukocyte-facilitated/ trojan horse
transcellular
paracellular neisseria meningitidis
bind to the endothelial cells
deplete tight junctions (zona occludens) between endothelial cells in the BBB
creates signalling pathways, allows pathogens to travel through gaps in cells
leukocyte facilitated neisseria meningitidis
once phagocytose in bloodstream they’re not degraded due to capsules
due to depletion of tight junctions by bacterial cells
they canc squeeze between gaps in the BBB
transcellular neisseria meningitidis
pilus mediated adhesion induces formation of micro-villi like structures
triggers bacterial internalisation
pill-induced signalling= reorganisation of actin cytoskeleton= formation of membrane protrusions= engulfing bacterial pathogens
travel intracellular vacuoles
then exocytosed to CSF by transcytosis
describe NMEC as a pathogen
gram negative
K1 capsule
rod shaped
mechanism of action NMEC
protected form host immune response by K1 capsule
can prevent fusion of lysosomes and lysosomal degradation of bacteria once engulfed by phagocytes
bacteria across BBB into the CSF
attachment: type 1 pili bind to CD48 and ompA (outer membrane protein A)
CNF1 binds to 67LR (67kDa laminin receptor) as well as type 1 pili and IbeA inducing rearrangement of actin cytoskeleton in target cells for transcytosis across BBB
mechanism of action of bacterial meningitis
pro-inflammatory cytokines secreted in response to pathogens in the CSF
MMP’s from pathogens and tissues can degrade tight junctions and increase endothelial permeability, changes CSF composition
altered cerebral blood flow due to thrombosis asa result fo clotting around pathogens and damaged blood vessels induced by DAMPs can cause schema and decreased perfusion pressure of blocked vessels
may result in increased inter cranial pressure and cerebral edema
proteolytic enzymes and reactive oxygen species: released from granulocytes causes damage to endothelial cells aswell as neural damage and increased BBB permeability
toxins and endotoxins: released by Bacteria when degraded can also cause tissue damage
ischemia
lack of oxygen to tissue
decreased perfusion pressure
less pressure required for substances to leave blood vessels
