L28: Fever and headache Flashcards
How does meningitis get into the brain?
- Infection gets in through the bloodstream or frontal sinus via cribriform plate
- CSF circulates in SA space
- Infection settles in the SA space which is sterile so there is no competition
- Innate immune system not overly active
- Inflammation of SA space extends onto surface of brain
Meningitis = increase in WBCs in CSF within subarachnoid space (+cell debris, inflammatory proteins, bacteria)
Causes of meningitis
- Virus
- Bacteria
- Fungi
- Protozoa
- Others (common - drugs, trauma, neurosurgery, cancer)
Viral meningitis
- Common, mostly benign
- Spontaneously improves
- Influenza (mainly A), enteroviruses, HSV2
Bacterial meningitis
- Common, serious, medical emergency
- N. meningitidis, S. pneumoniae
- Rarer = Listeria monocytogenes (generally older patients), M. tuberculosis
- Illness preceded with nasopharyngeal colonisation
- 10-20% of young adults colonised with N. meningitidis
- Bacteria enter SA space via bloodstream or directly (e.g. sinus surgery) and propagate
Fungal meningitis
- Rare
- Usually only in AIDS
- Cryptococcus neoformans
Protozoal meningitis
- Angiostrongylus cantonensis (not in NZ)
- Rare, accidental ingestion of worms eggs or larvae
- No effective treatment, usually self-limiting
Signs and symptoms of meningitis
Inflammation of meninges: headache, photophobia, neck stiffness, drowsiness
Systemic inflammatory response = fever, drowsiness, septic shock, rash (Neisserian meningitidis)
Diagnosis of meningitis
- Clinical suspicion
- Symptoms vague early in illness, signs of meningitis appear late
- Kernigs sign (lift legs up - worsens headache/neck pain)
Samples: CSF, blood culture, throat swab, blood to detect bacterial DNA by PCR
Lumbar puncture
- Needle between L4/5 spinous processes (spinal cord ends at T12)
- Fluid drawn from subarachnoid space
- Main indication: predominantly neutrophils is bacterial meningitis, predominantly lymphocytes in viral meningitis
CSF in meningitis
Bacterial:
- Decreased glucose
- Increased protein
- Increased white cells (mainly neutrophils)
- Gram stain +/- and culture ++/-
Viral:
- Normal glucose
- Increased or normal protein
- Increased white cells (mainly lymphocytes)
- No gram stain or culture
PCR testing
- Tests for nucleic acid
- Primers with complimentary sequences on it (specific to pathogen)
- Amplifies it
- Does not require live bacteria
Uses: in serious illness (e.g. meningitis) or when pathogens cannot be cultivated early
(e.g. URTI viruses) or to improve diagnostic yield (e.g. urethritis - chlamydia or gonorrhoea)
If there is no characteristic rash…
- All efforts to find aetiology especially to exclude meningococcal disease
If CSF gram stain negative: - Streptococcus pneumoniae antigen test CSF
- CSF PCR
- Blood PCR - meningococcus
- Throat swab (carriage of meningcoccus or pneumococcus)
Meningococcal meningitis epidemiology
= Neisserian meningitidis
- Characteristic rash: petechial, non-blanching (sign of vasculitis)
- Cases most often in winter and overlap with rise and fall of influenza (often misdiagnosed)
- Most commonly very young Maori and Pacific children (household overcrowding)
- Mortality rate ~7%
Pathogenic mechanisms of meningococcal meningitis
- Expert at avoiding complement cascade
- Gram negative cocci (thin peptidoglycan layer in cell wall)
- Terminal components of cascade form membrane attack complex (protein drill, enter cell wall, bacteria explode) = one of main defences against germs such as N. meningitidis
- Features that stop it being destroyed by complement e.g. pili, factor H
- Bacteria produces lipopolysaccharides to release in bloodstream (stimulates bloodstream causing shock, multi-organ failure), avoids complement fixation
Neutrophil extracellular traps
- When bacterial load very high -> neutrophils commit suicide releasing their DNA into capillaries
- DNA form net in capillary, trapping circulating bacteria and immune cells
- In doing so, reduces blood flow to organs = shock
Septic shock presentation
Reduced blood pressure, tachycardia, reduced perfusion of organs (skin grey/clammy, aches/pains, reduced urine output, breathing increased, drowsy, confused, fever)
Management of bacterial meningitis
- IV antibiotics (penicillin)
- Resuscitate
- Take blood cultures when IV line inserted
- Transfer to hospital
- Investigations
- Pain relief, fluids, IV antibiotics
- Drop precautions (1-2 weeks)
- In meningococcus: prophylactic antibiotics to contacts
Management of viral meningitis
Reassurance, analgesia, usually recover at home
Management of shock
Maintain organ perfusion = IV fluids, oxygen
Resolve cause = antibiotics, surgery
High mortality so early recognition essential
Role of cephalosporins
- Derived from mould acremonium
- Beta lactam ring same as penicillin
- Interferes with transpeptidase enzyme and cell wall loses structure
- Widely used, effective, well-tolerated
- Can use ceftriaxone to treat bacterial meningitis (broad spectrum)
Generations of cephalosporins
- Cefazolin, cephalexin - skin infections, pneumonia
- Cefuroxime, cefaclor - surgery, gut infections
- Ceftriaxone, ceftazidime - pneumonia, UTI, GI infection
- Cefempime, cefpirome - febrile neutropenia, ICU
- Ceftaroline - MRSA
(1-3 have increased activity against gram neg bacilli but decreasing against gram pos)
