Infections of the Nervous System Flashcards
Clinical features of encephalitis
Flu-like symptoms for 4-10 days Fever and progressive headache Progressive cerebral dysfunction - confusion, abnormal behaviour, memory disturbance, depressed conscious level Seizures Focal signs
Differential diagnoses for encephalitis
Infective e.g. viral Inflammatory e.g. limbic encephalitis Metabolic e.g. uraemic Malignancy e.g. metastases Migraine Post-ictal
Antibodies present in autoimmune encephalitis
Anti-VGKC and anti-NMDA receptor antibodies
Features of Anti-VGKC autoimmune encephalitis
Frequent seizures
Amnesia
Altered mental state
Features of Anti-NMDA receptor autoimmune encephalitis
Flu-like prodrome Prominent psychiatric features Altered mental state Seizures Progression to movement disorder and coma
How is encephalitis caused by HSV (herpes simplex virus) diagnosed?
Lab diagnosis by PCR of CSF for viral DNA
Treatment of encephalitis caused by HSV
Acyclovir on strong clinical suspicion
Morbidity/mortality rate of encephalitis caused by HSV
over 70% mortality and high morbidity if untreated
Where does the HSV lie latent after primary infection and what does this mean there is a risk of?
Lies latent in trigeminal or sacral ganglion after primary infection, risk of reactivation
Investigation of encephalitis
Blood cultures
Imaging - CT, MRI
LP
EEG
Encephalitis treatment
Acyclovir
What is a brain abscess?
Localised area of pus within the brain which causes high-pressure symptoms
When would a fever be present in brain abscess?
If there was systemic infection
Clinical features of brain abscess
Fever Headache Seizures Dysphasia Hemiparesis Papilloedema False localising signs Depressed conscious level Meningism Features of underlying source of infection e.g. poor dentition
Differential diagnoses for brain abscess
Any focal lesion, most commonly a tumour
Subdural haematoma
Causes of brain abscess
Penetrating head injury
Spread from adjacent infection e.g. dental, sinusitis
Blood borne infection e.g. bacterial endocarditis
Neurosurgical procedure
Brain abscess investigation
MRI, CT
Investigate source
Blood cultures
Biopsy
What is the risk of a biopsy of a brain abscess?
Drainage of pus and removal of needle puts patient at risk of spread of infection
Infective organisms in brain abscess
Streptococci - 70%, especially streptococcus Milleri group
Anaerobes
Treatment of brain abscess
Surgical drainage if possible
Penicillin or ceftriaxone to cover strep infection
Metrondiazole for anaerobe infection
What is meningitis?
Inflammation/infection of the meninges
Clinical features of meningitis
Fever, neck stiffness, altered mental status Short history of progressive headache May be associated with fever and meningism Cerebral dysfunction Cranial nerve palsy Seizures Focal neurological deficits Petechial skin rash
Differential diagnoses of meningitis
Infective - bacterial, viral or fungal
Inflammatory - sarcoidosis
Drug induces - NSAIDs, IVIG
Malignant - metastatic, haematological
Causes of meningitis
Bacterial
Viral (enteroviruses)
Bacterial organisms that cause meningitis
Neisseria meningitidis
Streptococcus pneumoniae
Investigation of meningitis
Blood cultures
Lumbar puncture
Opening pressure in LP of bacterial meningitis
Increased
Opening pressure in LP of viral meningitis and encephalitis
Normal or increased
Cell count in LP of bacterial menignitis
High, mainly neutrophils
Cell count in LP of viral meningitis
High, mainly lymphocytes
Glucose in LP of bacterial meningitis
Reduced
Glucose in LP of viral meningitis
Normal
Protein in LP of bacterial meningitis
High
Protein in LP of viral meningitis
Slightly increased
HIV indicator illnesses in the brain
Cerebral toxoplasmosis Aseptic meningitis/encephalitis Primary cerebral lymphoma Cerebral abscess Cryptococcal meningitis Space occupying lesion of unknown cause Dementia Leukoencephalopathy
Brain infections in HIV patients with low CD4 counts
Cryptococcur neoformans Toxoplasma gondii Progressive multifocal Leukoencephalopathy Cytomegalovirus HIV encephalopathy
How are cryptococcal infections established?
Following inhalation of airborne organisms into the lungs
How do most cases of cryptococcal infections present?
With meningoencephalitis
Most patients will have defects in immune function
Spirochaete infections in the CNS
Lyme disease
Syphilis
Leptospirosis
Causative organism of Lyme disease
Borrelia burgdorferi
How is Lyme disease transmitted
Vector borne via ticks
What parts of the body are affected by Lyme disease?
Multi-system involvement Skin Rheumatological Neurological/neuropsychiatric Cardiac Opthalmological
Consequence of untreated Lyme disease
80% will develop disseminated disease
Describe stage 1 Lyme disease
Early localised infection 1-30 days
Expanding rash at site of tick bite - erythema migrans
Flu-like symptoms (50%) - fatigue, myalgia, arthralgia, headache, fever, chills, neck stiffness
Treatment of stage 1 Lyme disease
doxycycline
Describe stage 2 Lyme disease
Early disseminated infection (weeks-months)
One or more organ systems become involved - haematological or lymphatic spread
Musculoskeletal and neurological involvement most common
Possible presentations of neurological involvement in Lyme disease
Meningo-encephalitis Cranial neuropathy Painful radiculopathy Plexopathy Diffuse or focal mononeuritis multiplex Mononeuropathy Myelitis
Describe stage 3 Lyme disease
Chronic infection months - years, occurring after a period of latency
Musculoskeletal and neurological involvement most common
Neurological involvement - subacute encephalopathy, encephalomyelitis
Investigation of Lyme disease
Serological tests CSF lymphocytosis PCR of CSF MRI brain/spine if CNS involvement Nerve conduction studies/EMG if PNS involvement
Lyme disease treatment
Prolonged antibiotic treatment IV, 3 weeks-1 month
IV ceftriaxone
Oral doxycyclin
Treatment of neurosyphilis
High dose penicillin
Aetiologies of Creutzfeldt-Jakob disease (CJD)
Sporadic
New variant
Familial
Acquired
Clinical features of sporadic CJD
Rapidly progressive dementia Insidious onset, usually over 60s Behavioural abnormalities Myoclonus Global neurological decline Motor abnormalities Cortical blindness Seizures
Sporadic CJD differential diagnoses
Alzheimer's disease with myoclonus Subacute sclerosing panencephalitis CNS vasculitis Non-convulsive status Toxic/metabolic encephalopathies
Sporadic CJD prognosis
Rapid progression
Death, often within 6 months
Features of new variant CJD
Younger onset (< 40)
Linked to bovine spongiform encephalopathy in cattle - eating infected material
Early behavioural changes more prominent
Longer course, around 13 months
Investigation of CJD
MRI - Pulvinar sign present in variant CJD, often no specific signs in sporadic CJD
EEG - generalised periodic complexes typical, often normal/non-specific in early stages
CSF - normal or raised protein
Cause of poliomyelitis
Polioviruses type 1, 2 and 3 (enteroviruses)
What percentage of poliomyelitis will result in paralytic disease?
1%, 99% are asymptomatic
Features of poliomyelitis
Infects anterior horn cells of lower motor neurones
Asymmetric, flaccid paralysis, especially of the legs
No sensory features
Transmission of rabies
By bite or salivary contamination of an open lesion
Features of rabies
Virus enters peripheral nerves and migrates to CNS
Paraesthesiae at the site of the original lesion
Ascending paralysis and encephalitis
Diagnosis of rabies encephalitis
Culture
Detection
Serology
Treatment of rabies encephalitis
Condition has 100% mortality, sedation and intensive care
Main sources of rabies encephalitis
Dogs and bats
How is rabies pre-exposure prevention carried out?
Active immunisation with killed vaccine
Rabies post-exposure treatment
Wash wound
Give active rabies immunisation
Give human rabies immunoglobulin if high risk
Organism causing tetanus
Clostridium tetani
Anaerobic gram-positive bacillus, spore forming
Clinical features of tetanus
Rigidity and spasm
Treatment of tetanus
Immunisation combined with other antigens
Penicillin and immunoglobulin for high risk wounds/patients
Infective organism causing botulism
Clostridium botulinum
Anaerobic sporre producing gram positive bacillus
How does clostridium botulinum work?
Neurotoxin, binds irreversibly to the presynaptic membranes of peripheral neuromuscular and autonomic nerve junctions
Toxin binding block ACh release
Modes of infection of clostridium botulinum
Infantile
Food-borne
Wound
Clinical presentation of botulism
Incubation period 4-14 days Descending symmetrical flaccid paralysis Pure motor Respiratory failure Autonomic dysfunction
Botulism diagnosis
Nerve conduction studies
Mouse neutralisation bioassay for toxin in blood
Culture for debrided wound
Botulism treatment
Anti-toxin
Penicillin/metronidazole
Radical wound debridement