meningitis/brain abscesses Flashcards
Describe the pathogenesis of meningitis
Portal of entry
Bacteria enter Via haematogenous spread
a)From nasopharynx (through bony defect or head injury – colonization of nasopharynx, invasion of epithelium and into blood vessels;; further dissemination. Head injury- post traumatic meningitis is rare but is typically a/w skull fracture and CSF leak
b)From Focal infection (sinutsitis/mastoiditis)
c)From direct implantation (Trauma including facial, spinal cranial etc or neurosurgery or other neuro procedures)
Following entry– bacteria replicate in subarachanoid space and cause inflam of meninges
(pathogenesis cont’d) What are the host factors that increase susceptibility to meningitis?
- No spleen – Splenectomy/congenitally absent/functional asplenia
– Increased risk of severe infection with encapsulated bacteria
– H. influenzae type b, S. pneumoniae, N. meningitidis - Diabetes mellitus and alcoholism
- S. pneumoniae - Altered cell-mediated immunity
– e.g. immunosuppressive therapy
– Listeria monocytogenes, Cryptococcus neoformans - Fracture or bony defect of the skull
– Recurrent S. pneumoniae - Inherited defects in the late complement components
– Recurrent invasive N. meningitidis infection - Pregnant women
– Increased risk of invasive disease including meningitis
if Listeria monocytogenes is acquired
Describe the causes of meningitis (non viral causes)
Dependent on age and geographical location
All ages: N. meningitidis, Strep pneumo , M tuberculosis, H. Influenzae type b
Neonate: Listeria Mono , Group B strep , E coli and other GNBs
Elderly: Strep pneumo
Pregnancy : Listeria mono
Immunocompromised: Listeria and Crytococcus neoformans
HIV: Cryptococcus neoformans
Describe the clinical presentation of bacterial meningitis
children/ infants
- refusing to eat food and vomitting
- fever, cold hands and feet
- Also fretful, crying, moaning, stiff neck, convulsions, pale blotchy skin, drowsy, sloppy, unresponsive
older adults
- fever and headache most common
- photophobia, neck stiffness, vomitting, cold hands and feet
Classical signs of meningism
Kernig’s sign- inability to straighten the hamstrings flexed at 90 degrees
Brudzinski’s neck sign- flexion of knees and hip when neck flexes
opisthotonus- spasm of the muscles causing backward arching of the head, neck, and spine
Nuchal rigidity (inability to flex neck upward) w rash in meningococcal meningitis w septicaemia others a/w meningococcal septicaemia include purpuric non blanching rash, petechial rash and gangrene of toes due to small blood vessel damage
Discuss the complications of bacterial meningitis
Neurological
• Hearing loss (common; 15- 30%)
• Subdural abscess
• Cranial nerve palsies
• Intellectual problems
• Hydrocephalus & raised intracranial pressure
Outside the CNS
• Dissemination & its consequences, e.g.,
meningococcal bloodstream infection & shock
Diagnosis of meningitis
clinical assessment is the mainstay of diagnosis
lab testing simply confirms the clinical suspicion
Typically for bacteria- microscopy, culture and PCR
specimens; blood and CSF via lumbar puncture(LP)
firstly observe macroscopic appearance of CSF from LP - turbid = bacterial (usually water clear and colourless)
c/i lumbar puncture if signs of increased intracranial pressure/ coagulopathy aka bleeding risk
microscopy on CSF - WCC count, differential WCC, Gram stain
Culture on CSF ( inoculated on blood and choc agar plates), Blood culture
PCR on CSF and blood
What are the CSF characteristics in bacterial vs viral vs TB
Bacterial- very elevated protein low blood glucose Raised PMN;s microscopy, culture, PCR
Viral elevated protein normal blood glucose raised lymphocytes PCR only
TB elevated protein low blood glucose raised lymphocytes TB culture and PCR
Which organisms can PCR be used for?
Bacteria :
(think of those that are a/w absent spleen i.e encapsulated bacteria)
H. influenzae type b, strep pneumo, n meningitidis
Group B strep in neonates
Viral
VZV, herpes 1 &2, enteroviruses
Why is a blood culture necessary?
A/w Sepsis workup
as septic patients w meningitis usually a/w bacteraemia
organisms may fail to grow from CSF but also from blood
Blood is also sent for PCR if there is no CSF sample available
Example of diagnosis of crytococcal meningitis
Suspect it - HIV pt w low CD4 count
Antigen detection in blood/ CSF
CSF culture
CSF microscopy- India ink stain
Discuss the management of meningitis
PRE-HOSPITAL ADMISSION
• Meningitis is a medical emergency – immediate
referral to hospital
• “Red flag” symptoms and signs of invasive
meningococcal disease
– Confusion/leg pain/photophobia/rash/neck stiffness or
pain
• All GPs and advanced paramedics should carry
benzylpenicillin or ceftriaxone/cefotaxime and
administer it without delay in patients with a fever
+ petechial/purpuric rash
IN HOSPITAL - THE BASICS…
• IV antibiotics- START SMART ; IV and agents that cross blood brain barrier
• IV steroids
• More than just antibiotic treatment – the patient is
often critically ill
- Fluid replacement
- Fluid restriction - may be necessary with increased
intra-cranial pressure
- Correction of coagulation abnormalities
- Ventilation & ICU care may be required
- Treatment of organ failure
- Seizure precautions and treatment (if necessary),
along with airway protection (if warranted)
Antibiotics empiric tx
Infants<3 months
amoxicillin, ceftriaxone/cefotaxime, gentamicin
- Listeria is covered by amoxicillin and gentamicin
-E coli covered by gentamicin and 3rd gen cephalosporin
-Group B strep covered by 3rd gen cephalosporin
Adults and Infants>3 months
ceftriaxone/cefotaxime and vancomycin
H influenzae, Strep pneumo and N meningitidis covered by 3rd gen cephalosporin
vancomycin in case of penicillin / 3rd gen cephalosporin resistance strep pneumo
Elderly/immunocompromised
same as for infants>3 months + amoxicillin to cover listeria
In regards to steroids ; should be given prior to or at same time of first dose of steroids
• In Hib meningitis, steroids reduce overall mortality &
incidence of deafness
• In adults with pneumococcal meningitis there may be
a reduced mortality rate with steroids
• No information on steroids in meningococcal
meningitis
• In tuberculous meningitis, steroids are used - reduce
fibrosis & risk of secondary hydrocephalus
“THEN FOCUS”
• Rationalise empiric therapy to targeted therapy
when the organism is identified and
susceptibilities are known
• Narrow-spectrum if possible e.g., high-dose IV
benzylpenicillin for susceptible N. meningitidis
or Str. pneumoniae
Prevention and epidemiology
Vaccination
available for N meningitidis, H. influenzae, Strep pneumo
Prevention of invasive meningococcal infection w vaccination
-population level ; against locally preventable serotypes
-at risk groups ; those at risk due to underlying conditions (against all serotype) and close contacts of case (against specific serotype)
PROPHYLACTIC ANTIBIOTICS FOR PREVENTION OF BACTERIAL MENINGITIS
ARE INDICATED IN SOME SITUATIONS
• Hyposplenism/Absent spleen/
Post-splenectomy
– Risk of infection with encapsulated organisms
– Long-term prophylaxis with daily oral penicillin reduces the
risk of invasive infection with Str. pneumoniae
• Close contacts of a patient with
– Meningococcal meningitis (and/or other invasive
meningococcal disease)
– HiB meningitis (and/or other invasive Hib disease) in some
cases
Prophylaxis is NOT indicated for contacts of pneumococcal
meningitis (and/or other invasive pneumococcal disease)
PREVENTION OF EXPOSURE TO AN INFECTED PATIENT
Droplet precautions (in addition to standard
precautions)
• Patient placement: ≥1m from other patients (single
room ideally) for first 24 hours of antibiotics
• Surgical mask when droplet exposure is likely i.e.
within 1m of patient, suctioning, intubation, autopsy
etc.
What is the pathogenesis of cerebral abscesses
Secondary to a focus elsewhere
• Contiguous: sinusitis/otitis media/severe dental
infections
• Haematogenous spread e.g., secondary to S.aureus
bloodstream infection (especially L sided endocarditis)
Trauma
• Penetrating head wound
• Fractured skull
• Post-operative surgical sepsis
Microbial causes of cerebral abscess
• May be polymicrobial e.g., streptococci & anaerobes (nasopharyngeal/oral flora)
• Streptococci (35%) e.g Strep milleri group
• Staphylococci (20%), including occasionally
MRSA
• Aerobic Gram negative bacilli (23%) e.g., E.
coli
• Anaerobes (14%) e.g., Bacteroides spp.
Toxoplasma gondii, e.g., poorly controlled HIV infection
Aspergillosis, single organ or disseminated in
immunosuppressed patient, e.g., severe & prolonged
neutropenia
Clinical presentation of cerebral abscess
• Signs of raised intracranial pressure
– Headache
– Seizures
– Nausea & vomiting
– Altered mental status
• Signs of infection e.g. high temperature
• Signs & symptoms of underlying condition
(e.g., sinusitis)
• Difficult to diagnose: clinically- broad
differential including tumour, bleed,
meningitis/ encephalitis
