CNS Infections Flashcards
Meningitis, Encephalitis, Tetanus, Rabies
What is meningitis? Presentation? Causes?
(1. ) It is acute infection of the meninges.
(2. ) Presents with a combination of pyrexia + meningism (headache, photobia, neck stiffness)
(3. ) It is a medical emergency as it can lead to hearing loss, seizures, brain damage, death.
Causes
(4.) Meningitis can arise due to infective or non-infective causes (paraneoplastic, lyme’s, drug SE, AI)
Viral Meningitis: What is it? Aetiology (4)? Ix?
- Most common cause of meningitis h/e usually benign and self-limiting
- HSV, VSV, Enterovirus, Mumps
- LP & CSF culture: lymphocytes, high protein, normal glucose
Name 6 bacterial causes of Meningitis and what ages we’d expect to see them in?
(1. ) Neisseria Meningitis = all ages
(2. ) Strep.pneumoniae = all ages
(3. ) Listeria = neonates, elderly, IMC, diabetics, alcoholics, pregnant women
(4. ) Group B strep = neonates
(5. ) HiB = children
(6. ) E.coli = neonates
Note: M.tuberculosis, syphilis can also cause meningitis
What bacteria is Neisseria Meningitidis? and what can it cause?
(1. ) Gram negative diplococci
- Carriage: 5-11% adults, 25% teenagers
(2. ) N.Meningitidis in CSF = Meningitis
(3. ) N.Meningitidis in blood: Meningococcal Septicaemia (sepsis)
(4. ) Sx of sepsis: Non-blanching purpuric rash, necrosis, high mortality
Pathophysiology of meningitis?
(1. ) Infection gets into the CNS by three ways:
(a. ) Direct spread from infection e.g. sinusitis
(b. ) Direct inoculation e.g. surgery, trauma
(c. ) Blood (most common) i.e. bacteraemia
(2. ) Pathogens cross BBB + are isolated from immune system so can replicate.
(3. ) Body tries to fight infection which makes blood vessels become leaky and inc pressure.
(4. ) WBC, cytokines etc enter brain - which account for the changes seen in CSF
(5. ) Severe meningitis:
- brain parenchyma is invaded by inflammatory process
- leads to widespread cortical swelling and destruction
- Causing permanent neurological damage
Presentation of Meningitis (5)
(1. ) Fever
(2. ) Meningism: Headache, Neck stiffness, photophobia, kernig’s + brudzinski sign
(3. ) N+V
(4. ) Irritability
(5. ) Signs of cerebral dysfunction i.e. severe disease:
- confusion, delirium, sleepiness, coma
Presentation of Meningococcal sepsis
- Meningitis Sx
- Rash
- Shock
- Intravascular coagulation
- Renal failure
- Gangrene
- Arthritis
- Pericarditis
What is Kernig’s sign and Brudzinski’s sign?
Signs of meningism
Kernig’s sign
- Resistance to extension of the leg while the hip is flexed
- whilst extending pt’s leg they flinch/may be in pain
Brudzinski’s sign
- Flexion of the hips and knees in response to neck flexion
- raising the head you’ll see a sudden flexion of hip and knee
Mx of bacterial meningitis
It is a medical emergency (5% mortality), when suspected start tx immediately
(1.) Primary care: IM/ IV benzylpenicillin and ADMIT PT
On arrival of hospital
(2. ) Assess GCS (low score = poor prognosis)
(3. ) Blood cultures
(4. ) Broad spectrum Abx: Ceftriaxone or cefotaxime (1st line). Consider: penicillin allergies, IMC (risk of listeria), recent travel (risk of penicillin resistance)
(5. ) Steroids - IV dexamethasone
All cases of meningitis are notifiable to PH
- Identify close contacts as there is a risk of them developing it
- Abx prophylaxis (ciprofloxacin, rifampicin) will reduce risk and prevent onward transmission
Ix (after Mx of acute meningitis)
(1. ) Lumbar puncture
- To confirm Dx of meningitis
- CI = abnormal clotting, petechial rash, raised ICP
(2. ) CT Scan
- Performed before LP if brain herniation is suspected e.g. lesions, elevated ICP.
- Indications: >60y, IMC, Hx of CNS disease, Seizures <1w, GCS <14, Focal neurological signs or seizures, Papilledema, Atypical Hx
CSF Analysis: identifying causative organism
CSF: protein and glucose levels
- ALL = high protein
- Bacterial, TB = Low glucose
- Viral = normal glucose
CSF: appearance
- Bacterial = cloudy due to neutrophils
- Viral = Clear
- TB = fibrin web
What is encephalitis?
Inflammation of the brain
Aetiology of encephalitis?
(1. ) Usually viral: HSV, VZV
(2. ) Other: Mosquito or tick-borne, Rabies, West Nile, Japanese encephalitis outbreaks
(3. ) Non-infective causes
- Post infection
- Autoimmune
- Paraneoplastic
Pathophysiology of encephalitis?
- Infection provokes an inflammatory response that involves the cortex, white matter, basal ganglia, brainstem
- Distribution of lesions varies with the type of virus e.g. HSV, the temporal lobes are usually affected.
- Inclusion bodies may be present in neurons and glial cells & infiltration of polymorphonuclear cells in the perivascular space.
Presentation of encephalitis? (6)
(1. ) Acute or sub-acute onset (hours to days) of: headache, Fever, Flu-like Sx
(2. ) Focal neurological signs: aphasia or hemiplegia, visual field defects
(3. ) Altered GCS e.g. confusion
(4. ) Seizures
(5. ) Memory loss
(6. ) +/- meningism (e.g. neck stiffness, photophobia etc but usually absent)
Ix of encephalitis? (3)
(1.) MRI - detect lesions/abnormalities e.g. in temporal lobes
- **(2.) LP for culture + viral PCR
- Once imaging has excluded mass lesion
- CSF = lymphocytes, elevated protein, normal glucose
- Viral PCR = causative organism
(3.) HIV TEST
Tx and Mx of encephalitis? (4)
(1. ) IV Aciclovir if HSV or VZV
- given 3 times daily for 2-3w
(2.) Mostly supportive
(3. ) Some pt develop residual epilepsy or cognitive impairment. Consider:
- Anti-epileptic tx
- Dexamethasone if RICP
(4.) Neuro-rehabilitation
What is Rabies? Aetiology? Inoculation?
- Human rabies is rare h/e it is fatal.
- Caused by rhabdovirus that travels along nerves, infects CNS tissues and salivary glands of various mammals
- Inoculation is achieved through skin through saliva via bites, licks of rabid animal (dogs, bats, cats etc)
- Incubation period varies from 2w to years
Clinical features of Rabies?
(1.) At onset i.e. bite, there may be: paraesthesia, fever
(2. ) Once reaches CNS:
- furious or paralytic presentation
- delusions, hallucinations
- spitting, biting mania
- Anxious
(3. ) Once symptomatic
- It can be fatal within 10w of Sx onset
Mx of Rabies? (3)
(1. ) Cannot be treated, most pt die in a few weeks
(2. ) Palliative care, Sedatives: diazepam, IV nutrition, fluids
(3. ) Prophylaxis is key
- Pre-exposure prophylaxis (vaccination)
- Post-exposure prophylaxis
Pathophysiology of Tetanus?
(1. ) Causes by clostridium tetani spores (found in soil) e.g. stepping on a nail, dirty wound
(2. ) Perfect environment = anaerobic and warm
(3. ) Produces neurotoxins
- Tetanolysin (tissue destruction)
- Tetanospasmin (clinical tetanus): inhibits GABA axon transmission -> inc muscle contraction -> spasms
Clinical features of tetanus
Generalised tetanus/Tetanic Triad
- Locked jaw
- Risus Sardonicus Grin caused by facial muscle spasm
- Opisthotonos: Arch of back, persistent spasm of back muscles
- Toxin can also affect the ANS, causing HTN, tachycardia, arrhythmia,
Localised tetanus
- Persistent spasm localised around area of injury
- Unopposed flexion of fingers
- Spasm of forearm
Dx of tetanus
Spatula test: touch posterior pharyngeal wall
- Positive = involuntary contraction of jaw
- Negative = normal gag reflex
Tx & Mx of tetanus (4)
(1.) Prevention: Triple DPT vaccine (diphtheria, tetanus, pertussis)
(2. ) Supportive Tx for spasms and fevers
- Muscle relaxants
- Paracetamol
(3. ) Immunoglobulins/Antitoxic: TIG, Binds to tetanospasmin and mop up toxins
(4. ) Metronidazole: Clear up residual bacterial
