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INFECTIONS OF THE CENTRAL NERVOUS SYSTEM. Meningitis Encephalitis Brain abscess. MENINGITIS. A medical emergency!. Clinical features that suggest the diagnosis of acute meningitis. Headache Irritable Neck stiffness Photophobia Fever Vomiting Varying levels of consciousness Rash. - PowerPoint PPT Presentation
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Clinical features that suggest the diagnosis of acute meningitis
Headache Irritable Neck stiffness Photophobia Fever Vomiting Varying levels of consciousness Rash
Groups in which clinical features are not so specific
Neonates (first few weeks of life) Elderly Immunosuppressed
BACTERIAL
Incidence:
Primary meningitis: spread via the bloodstream
Secondary meningitis:Ears, sinuses, trauma,
Surgery
Main pathogens:Neisseria meningitidis
Strept. Pneumoniae
Haemophilus influenzae
N meningitidis (meningococcus) and meningococcal meningitis
The most common cause of acute bacterial meningitis
Most cases in children and young adults Gram negative diplococcus 3 main serological types A, B. C Person to person transmission Reservoir nasopharynx (2-25% carriage) Respiratory droplet spread Incubation period 1-3 days
Most cases are sporadic Close family contacts of cases at risk Outbreaks may occur in eg, schools Group B serotype traditionally most
frequent cause Group C serotype has become
increasingly common Epidemics occur in eg, Africa, South
America
CLINICAL FEATURES
May be sore throat Progression from headache, drowsiness, signs
of meningitis Haemorrhagic skin rash (non-blanching) Sepsis complicated by intravascular coagulation,
shock, acute renal failure Bleeding into organs may occur eg, adrenal
gland causing Waterhouse Friderichsen syndrome
Gangrene of peripheral limbs
TREATMENT OF ACUTE BACTERIAL MENINGITIS KEYPOINTS:
Once the diagnosis is clinically suspected don’t delay treatment
If the causative agent is not clear eg, no rash, give ceftriaxone or cefotaxime
This provides cover of the 3 main causes until a microbiological diagnosis is made
If meningococcal meningitis confirmed then a change to high doses of benzylpenicillin can be considered
Chloramphenicol can be an alternative if allergy to beta lactams
MICROBIOLOGICAL DIAGNOSIS
If possible collect Cerebrospinal fluid (may not be, if raised intracranial pressure)
Blood culture, both before antibiotic therapy
Sample from petechial skin lesion may yield meningococcus
CSF subjected to cell count, gram stain of deposit, and culture on chocolate agar in CO2 atmosphere
CSF Abnormalities in Meningitis
Condition Appearance Cells/cu mm Gram Protein Glucose
Normal Clear, colourless
0-5 lymphocytes
Bacterial Cloudy, turbid
100-2000 polymorphs
Orgs High Low
‘Aseptic’ (viral)
Clear, slightly cloudy
10-500 lymphocytes
Normal Normal
TB Clear, slightly cloudy
10-500 lymphocytes
High Low
Cryptococcal Clear 10-200 lymphocytes
Normal, slightly elevated
Normal, slightly reduced
Additional lab investigations
Latex agglutination test on CSF to detect meningo polysaccharide antigen
PCR to amplify bacterial DNA in blood (EDTA sample) or CSF which may be positive even after start of antibiotics
Save serum sample for antibody tests with a subsequent “convalescent” sample
Set up antibiotic sensitivities to penicillin, cephalosporins, ampicillin, chloramphenicol and others
Some features of meningococcal isolate
Gram: gram negative cocci some within neutrophils (intracellular)
Grows within 24-48 hours best on chocolate agar in CO2
Will agglutinate with group specific antisera eg, B, C
Caution needed in lab as making suspensions can be a hazard to the lab worker (may acquire pathogen)
MENINGOCOCCAL MENINGITIS
Notifiable to public health authorities Close contacts in home, school/university,
nursery should be given antibiotic prophylaxis Rifampicin X 2 days (ciprofloxacin is used but
not licensed) Hospital contacts only need prophylaxis if
contact with secretions, eg, mouth to mouth resuscitation
Vaccine against group C now widely in use and for overseas travellers group A vaccine may be indicated
Pneumococcal meningitis
Strep pneumoniae is the cause, a capsulate gram positive coccus
Highest incidence in those at extremes of age, infants <3yrs and elderly
Alcoholism, debilitation, malnutrition, hyposplenism
May spread from middle ear or sinus infection
Or following trauma causing basal skull #
Pneumococcal meningitis: clinical features
Acute onset with rapid development of loss of consciousness
Skin rash not a feature May be a history of ear infection,
splenectomy Bacteraemia a feature Higher mortality than other causes High incidence of complications in
survivors
Microbiological investigations
CSF and blood cultures should be taken Gram stain of CSF deposit shows gram
positive cocci in short chains Culture on blood and choc agar in CO2
gives alpha haemolytic (green) colonies with “draughtsmen”
Direct sensitivities for penicillin, cefotaxime, ceftriaxone, ampicillin
Treatment
High doses of penicillin eg, 1.2g (2mill units) 2 hourly
Note some strains have reduced susceptibility to penicillin, and some are resistant!
Need to review to find a potential underlying risk factor
Polyvalent vaccine for risk groups eg, before splenectomy
Haemophilus influenzae meningitis
Gram negative coccobacillus, capsulated strains (type b used predominate)
Peak incidence 2 years old, range 3 months to 5 years
Incidence has declined greatly since the successful introduction of Hib vaccine
More insidious onset, no rash, lower mortality Diagnostic approach as for other causes Treament with cefotaxime or ceftriaxone
Other bacterial causes of meningitis in adults and children
Post trauma or surgeryStaph aureus, streps, anaerobes, coliforms, Pseudomonas
ImmunocompromisedListeria monocytogenes
OthersM tuberculosis, Leptospira, Borrelia burgdorferi
Tuberculous meningitis Higher incidence in immigrant populations who come
from countries with a higher incidence of TB Insidious onset High frequency of complications, cranial nerve palsies Delayed diagnosis makes complications more likely CSF shows predominantly lymphocytic response but
polymorphs also present High protein, low/absent sugar Treat: probably with 3 agents eg, isoniazid, rifampicin,
pyrazinamide Note occasional reports of MDR TB
CSF Abnormalities in Meningitis
Condition Appearance Cells/cu mm Gram Protein Glucose
Normal Clear, colourless
0-5 lymphocytes
Bacterial Cloudy, turbid
100-2000 polymorphs
Orgs High Low
‘Aseptic’ (viral)
Clear, slightly cloudy
10-500 lymphocytes
Normal Normal
TB Clear, slightly cloudy
10-500 lymphocytes
High Low
Cryptococcal Clear 10-200 lymphocytes
Normal, slightly elevated
Normal, slightly reduced
NEONATAL MENINGITIS Group B streptococcus (S agalactiae) and Esch coli are
the principal causes Travel via the bloodstream but direct infection may occur Premature rupture of membranes, pre-term delivery
(“VLBW”) are risk factors May complicate maternal infection High morbidity and mortality Clinical features can be non-specific Early onset Group B infection more common than late
onset disease Other causes: Listeria, Staph, Salmonella, other GNB Treat: Cephalosporin, or penicillin + aminoglycoside
VIRAL MENINGITIS
Primarily affects children and young adults Milder signs and symptoms May start as respiratory or intestinal
infection then viraemia CSF shows raised lymphocyte count (50-
200/cu mm); protein and sugar usually normal
Full recovery expected
Causes of viral meningitis
Enteroviruses: Echo, coxsackie A ,B, polio Paramyxovirus: mumps Herpes simplex, VZV Adenoviruses Other: arboviruses, lymphocytic
choriomeningitis, HIV
Diagnosis: viral meningitis
Examination of CSF Storage at -700C of CSF for subsequent
virus isolation Additionally throat swab, stool, paired sera
CSF Abnormalities in Meningitis
Condition Appearance Cells/cu mm Gram Protein Glucose
Normal Clear, colourless
0-5 lymphocytes
Bacterial Cloudy, turbid
100-2000 polymorphs
Orgs High Low
‘Aseptic’ (viral)
Clear, slightly cloudy
10-500 lymphocytes
Normal Normal
TB Clear, slightly cloudy
10-500 lymphocytes
High Low
Cryptococcal Clear 10-200 lymphocytes
Normal, slightly elevated
Normal, slightly reduced
Fungal meningitis
Cryptococcus neoformans is main cause HIV and immunosuppressed pts at risk Insidious onset of headache, fever, neck
stiffness Diagnosis made on CSF examination Shows raised lymphocyte count, protein,
low sugar, capsulate yeasts, antigen Treat with amphotericin B +flucytosine
CSF Abnormalities in Meningitis
Condition Appearance Cells/cu mm Gram Protein Glucose
Normal Clear, colourless
0-5 lymphocytes
Bacterial Cloudy, turbid
100-2000 polymorphs
Orgs High Low
‘Aseptic’ (viral)
Clear, slightly cloudy
10-500 lymphocytes
Normal Normal
TB Clear, slightly cloudy
10-500 lymphocytes
High Low
Cryptococcal Clear 10-200 lymphocytes
Normal, slightly elevated
Normal, slightly reduced
ENCEPHALITIS
Affects children and adults mostly A variety of symptoms and signs Drowsiness, confusion, coma, fits, nerve
palsies, paresis May have sequelae eg, memory loss,
motor impairment, death EEG, brain scan, CSF exam, brain biopsy
may establish diagnosis
Causes of encephalitis
• Sporadic: Herpes simplex, mumps, VZV, EBV rabies
• Epidemic: Togaviruses: equine, louping ill, Japanese B,
enteroviruses
• Post-infectious: Measles, rubella, post-vaccination
• Degenerative: Measles (SSPE), vCJD, JC virus (PML)
Herpes simplex encephalitis
Most common cause of sporadic encephalitis in previously healthy
May be evidence of herpes infecion of skin, mucosae
Causes severe haemorrhagic encephalitis affecting temporal lobe,
Focal signs and epilepsy features High mortality so treatment urgently
needed with aciclovir
Subacute sclerosing panencephalitis (SSPE)
A rare complication of measles infection Usually affects children Intellectual impairment, involuntary
movements High titres of measles antibody Brain biopsy shows measles virus Fatal outcome
Prion diseases
Degenerative disorders Long incubation periods Slow progressive spongiform
encephalopathy Fatal outcome
• Kuru: occurred in New Guinea, diue to cannibalism, eating human brain
• Sporadic Creutzfeldt-Jacob disease (CJD): rare degenerative disease in over 50’s
• Recipients of growth hormone at increased risk, use of surgical instruments contamined with prion protein
• Prions are (Prp) proteins in abnormal configuration resistant to destruction
• Mutations of genes encoding these proteins can be inherited
New variant CJD
In 1980’s emergence of bovine spongiform encephalopathy (BSE)
Could be experimentally transmitted from brains of sheep with scrapie
Similarities between BSE and nvCJD Occurs in young people rapidly fatal Possibly acquired from eating infected beef/ beef
products Diagnosis on brain biopsy (? Tonsillar tissue) No treatment
Brain abscess
Can arise from direct inoculation of infection following trauma, surgery; from spread of infection of ear or sinuses; or haematogenous spread from eg, lungs, heart (endocarditis)
May be non-specific signs, neurological symptoms
Needs urgent investigation by CT/MRI scan Surgical treatment +antibiotics
Causes of brain abscess
Ear: mixed anaerobes, coliforms Sinus: pneumococci, streptococci Trauma/surgery: Staph aureus Chest: strep, staph, pneumococci
Diagnosis and treatment
Examination of pus aspirated from abscess
CSF Blood cultures Surgical drainage a priority Antibiotics chosen with good penetration
of CNS
Guillain-Barre syndrome
Infectious polyneuritis Paraesthesiae, progressive weakness of
limbs, respiratory failure High CSF protein Post infectious Various infections implicated including
Campylobacter, EBV, Mycoplasma Recovery likely to occur with supportive
care