Flashcards in Infections in the CNS Deck (85):
infection/inflammation of the meninges
infection/inflammation of the brain substance
inflammation/infection of the spinal cord
what is the classical triad of meningitis?
> neck stiffness
> altered mental status
what are the clinical features of meningitis?
> short history of progressive headache
> petechial skin rash (non-blanching)
> cranial nerve palsy
> focal neurological deficit
what is the differential diagnosis for meningitis?
> infective: bacterial, viral and fungal
> inflammatory: sarcoidosis
> drug induced: NSAIDs, IVIG
> malignant: metastatic, haematological
what are the bacterial causes of meningitis?
> Neisseria meningitidis : meningococcus
> streptococcus pneumonia : pneumococcus
what are the viral causes of meningitis?
what are the clinical features of encephalitis?
> flu like prodrome
> progressive headache with associated fever
> progressive cerebral dysfunction
> focal symptoms/signs
what is the difference between viral encephalitis and bacterial meningitis?
viral encephalitis is generally slower and cerebral dysfunction is a more prominent feature
what is the differential diagnosis for encephalitis?
> infective: viral
> inflammatory: limbic encephalitis
> metabolic: hepatic, uraemic, hyperglycaemic
> malignant: metastatic, paraneoplastic
> post ictal
what are the two antibodies involved in autoimmune encephalitis?
> anti-VGKC (voltage gated potassium channel)
> anti-NMDA receptor
describe the clinical features of Anti-VGKC encephalitis
> frequent seizures
> amnesia (not able to retain new memories)
> altered mental state
describe the clinical features of anti-NMDA receptor
> flue like prodrome
> prominent psychiatric features
> altered mental state and seizures
> progressing to a movement disorder and coma
what investigations would you carry out for meningitis?
> blood cultures
> lumbar puncture
> there is no need to image if there are no contraindications to lumbar puncture
what investigations would you carry out for encephalitis?
> blood cultures
> CT (+/- MRI)
> lumbar puncture
what are the contraindications for a lumbar puncture?
> focal symptoms or signs suggesting a focal brain mass
> reduced conscious level suggesting raised intracranial pressure
> in the immunocompromised you should image first as some features can be lost
what CSF findings would you find in bacterial meningitis?
> increased opening pressure
> high neutrophillic cell count
>reduced glucose (as bacteria consume glucose)
> high protein
describe the CSF findings in viral meningitis and encephalitis
> normal/increased opening pressure
> high mainly lymphocytic cell count
> normal glucose
> slightly increased protein
what is the commonest cause on encephalitis in Europe?
herpes simplex encephalitis
what is the lab diagnosis for herpes simplex encephalitis?
PCR of CSF for viral DNA
how do you treat herpes simplex encephalitis?
aciclovir in clinical suspicion
where does the herpes simplex virus remain latent?
in the trigeminal ganglion or sacral ganglion
how are enterovirses spread?
by the faecal-oral route
what can cause non-paralytic meningitis?
do enteroviruses causes gastroenteritis?
how are arbovirus encephalitides transmitted?
by vector (mosquito or tick) from non-human host
give some examples of arbovirus encephalitides?
> west nile virus
> st louis encephalitis
> western equine encephalitis
> Japanese b encephalitis
define a brain abscess
localised area of pus within the brain
what is a subdural empyema?
thin layer of pus between the dura and arachnoid membrane over the surface of the brain
what are the clinical features of brain abscesses and empyema?
> focal symptoms and signs (depressed conscious level)
> meningism (particularly in empyema)
> features of the underlying source
name some causes of brain abscesses and empyema
> penetrating head injury
> spread form adjacent infection (dental, sinusitis, otitis media)
> blood borne infection
> neurosurgical procedure
how would you diagnose a brain abscess and empyema?
> imaging: CT or MRI
> investigate source
> blood cultures
> biopsy (drainage of pus)
what streptococci group are often present in brain abscesses?
penicillin sensitive strep-milleri group (strep. anginosus, strep intermedius, strep constellatus)
in a brain abscess is there more likely to be one organism present of a mixture of organisms present?
a mixture of organisms
how would you manage a brain abscess?
> surgical drainage if possible
> high dose antibiotics (culture and sensitivity tests on aspirate provide useful guide)
what antibiotics could you give to cover strep infection in a brain abscess?
what treatment would you give for an anaerobic brain abscess?
name HIV indicator illnesses
> cerebral toxoplasmosis
> aseptic meningitis/encephalitis
> primary cerebral lymphoma
> cerebral abscess
> cryptococcal meningitis
> space occupying lesion of unknown cause
what brain infections could you see in HIV patients with low CD4 counts?
> Cryptococcus neoformans
> toxoplasma gondii
> progressive multifocal leukoencephalopathy
> HIV encephalopathy
what tests could you carry out to differentiate the causative organisms in HIV low CD4 count brain infections?
> india ink, cryptococcal antigen
> toxoplasmosis serology
> JC virus PCR
> CMV PCR
> HIV PCR
what do cryptococcal antigens loos like in an indian ink stain?
as a capsule organism in double circles
what spirochaetes infections involve the CNS?
> lyme disease
how is lyme disease transmitted?
vector borne, tick
describe stage one in lyme disease?
> early localised infection
> erythema migrans: characteristic expanding rash at site of tick bite
> 50% flue like symptoms
describe stage 2 lyme disease
> early disseminated infection (weeks-months)
> one or more organ system involvement
> musculoskeletal and neurological involvement
what neurological involvement is there in stage 2 lyme disease if the patient is untreated?
> mononeuritis multiplex
> painful radiculoneuropathy
> cranial neuropathy
describe stage 3 lyme disease
> chronic infection occurring after a period of latency
> musculoskeletal and neurological involvement is the most common
what are the investigations for lyme disease?
> serological tests
> CSF lymphocytosis
> PCR of CSF
> MRI brain/spine
> nerve condition studies
what is the treatment for lyme disease?
> intravenous ceftriaxone
> oral doxycycline
when does tertiary syphilis (neurosyphilis)occur?
years/decades after primary disease
what tests are carried out for neurosyphilis?
> treponema specific antibody test
> non-treponemal specific antibody test
> CSF PCR
how does the CSF change in neurosyphilis?
> CSF lymphocytes increase
> there is evidence of intrathecal antibody production
what is the treatment for neurosyphilis?
high dose penicillin
what causes poliomyelitis?
poliovirus type 1,2 or 3 (enterovirus)
what part of the central nervous system does paralytic poliomyelitis affect?
the anterior horns of the lower motor neurons
describe the paralysis seen in poliomyelitis
> flaccid paralysis
> no sensory features
in the uk what polio types does the vaccine contain?
all three types
rabies is described as neurotropic. what does this mean?
the virus enters the peripheral nerves and migrates to CNS
what is there at the site of the initial lesion in rabies?
what is the affect of rabies infection?
> ascending paralysis
how would you diagnose rabies encephalitis?
> culture (detection or serology)
who is given the rabies pre-exposure prevention?
> bat handlers
> regular handlers of imported animals
> selected travellers to enzootic areas
what is the rabies post exposure treatment?
> wash wound
> active rabies immunisation
> human rabies immunoglobulin (passive immunisation) if high risk
what is the bacteria involved in tetanus infection?
anaerobic gram positive bacillus
describe the pathology of tetanus
toxin acts on the neuro-muscular junction blocking inhibition of motor neurons causing rigidity or spasm
describe the prevention of tetanus
> immunisation (toxoid) combined with other antigens
> penicillin and immunoglobulin for high risk wounds/patients
describe the bacteria involved in botulism
> anaerobic spore producing gram positive bacillus
describe the effect of the neurotoxin in botulism
> binds irreversibly to the presynaptic membranes of peripheral neuromuscular and autonomic nerve junctions
> toxin binding blocks acetylcholine release
what is the recovery form botulism neurotoxin?
sprouting new axons
where is clostridium botulism naturally present?
> aquatic environments
what are the three modes of infection of botulism?
> infantile (intestinal colonisation)
> wound (drug abuse)
what is the clinical presentation of botulism?
> incubation period (4-14 days)
> descending symmetrical flaccid paralysis
> pure motor
> respiratory failure
> autonomic dysfunction
how do you diagnose botulism?
> nerve conducting studies
> mouse neutralisation bioassay for toxin in blood
> culture from debrided wound
what is the treatment for botulism?
> radical would debridement
name a post infective inflammatory syndrome affecting the central nervous system
acute disseminated encephalomyelitis
name a post infective inflammatory syndrome affecting the peripheral nervous system
guillain barre syndrome
what is the aetiology of Creutzfeldt-Jakob disease?
> new variant
> acquired (cadaveric growth hormone, dura matter grafts, blood transfusion)
what should you consider in any rapidly progressing dementia?
what are the clinical features of sporadic CJD?
> insidious onset
> early behavioural abnormalities
> rapidly progressing dementia
> progressing global neurological decline
> motor abnormalities
> cortical blindness
> seizures (sometimes)
what is the differential diagnosis for sporadic CJD?
> Alzheimer's disease my myoclonus
> subacute sclerosing panencephalitis
> CNS vasculitis
> inflammatory encephalopathies
what is the prognosis of sporadic CJD?
> rapid progression
> death within 6 months
what is new variant CJD linked to?
bovine spongiform encephalopathy in cattle
what is the difference in the clinical features of new variant CJD compared to sporadic CJD?
> early behavioural changes are more important
> longer course (average 13 months)