L34. Bacterial meningitis Flashcards
Define meningitis and list signs of clinical presentation
Inflammation of the subarachnoid space which extends onto the pia mater, surface of the brain.
Earlier: presentation of cold.
Late symptoms
- Septic shock: Fever, tachycardia, Increased ICP,
- Stiff neck: spasm to protect,
- reduced consciousness/brain changes: photophobia
- small pink blanchable Rash–> petechial rash (for N. meningitidis)
What are the main causes of meningitis and give an example
Virus: normally benign.
eg. enteroviruses, herpes simplex V2: recurrent meningitis
Bacteria: rapidly deadly
eg. N meningitidis, Strep pneumoniae
Fungi: rare, cryptococcus neoformans
Protozoa: rare ingestion of worm eggs/larvae not in NZ
Other causes are drugs, trauma, neurosurgery, cancer
What is the time course of the bacterial meningitis
- Illness preceded by nasopharyngeal colonisation - 10-20% of YA
- Bacterial enter blood stream –> sub arachnoid space
- CSF contains bacteria, WBC, Immunoglobulins and cell debris.
How is meningitis diagnosed - what tests
- Clinical suspicion - need to exclude meningococcal disease.
2) Lumbar puncture-> CSF culture: gram stain - if negative consider N. mengitidis - Detect bacterial DNA by pcr - hours, high sensitivity
- Blood culture: meningococcus
- Throat swab: carriage of meningococcus/penumococcus
- Kernigs sign: lifting the legs slowly causes cauda equina to pull, making headache and backache worse
- Neck is stiff can’t be folded, if you hold the head by the occipit
What are the differentiating signs of bacterial and viral meningitis in CSF
Both will have elevated protein (more in bac) - Look at RBC: WBC in case of sub arach haem
In viral meningitis:
- glucose: normal
- WBC are T and B lymphocytes
- Cells are lymphocyte
- No gram stain or culturable
In bacterial meningitis:
- glucose decreased
- WBC Increased neutrophils, phagocytes
- gram stain is + a 1/3 of the time and culture is mostly positive
How does PCR work
- Add primers of a short DNA sequence to a sample - heat to 94 C to displace strands
- Reduce heat x C to allow primers to anneal
- Increase heat to 72 C to allow DNA polymerase to elongate the complimentary strand
- Heat to displace strands and repeat 20-40 times
- Visualise - a fluorescent tag is added to the primers then the amount of amplified DNA can be visualised during the reaction
How does N. meningitidis avoid the immune system (4)
- sugar capsule expresses LPS which is same as human blood group antigen
- Expresses capsules which prevent formation of complement MAC and opsonisation
- It binds human Factor H to down regulate complement
- releases blebs of LPS that stimulates immune system -TLR4 (on macrophages) as a decoy for complement
How does Neissera mengitidis (meningococcal) progress to life threatening
- Increased LPS in the blood stream and bacterial load is high, neutrophils release their DNA (NET) into small bv.
- DNA is sticky and traps bacteria, RBC and platelets. Contains enzymes which help to breakdown bacteria
- This can clog small vessels leading to reduced flow and oxygenation
- Shock : reduced perfusion to organs
How is bacterial meningitis managed compared to viral
- Goal is maintain organ function and resolve cause of infection as mortality is high
Bacterial
- Resuscitate: ABC- place an IV line in
- Give antibiotics: Ceftriaxone if very unwell - Take blood cultures when IV line sited
- Transfer to hospital: precautions for spread…
- Investigations: Lumbar puncture; CSF
- Pain relief, fluids, IV antibiotics
Viral : benign
- Reassurance, analgesia
- usually recover at home
What precautions are taken with bacterial meningitis to prevent spread to contacts - which bacteria
- Droplet precautions: staff and patients wear mask to prevent droplets of potential meningococcus spreading
- Prophylaxis to contacts: siblings, household, staff on airway management to remove carriage/colonisation of Meningococcus –> not so much pneumococcal.
- Rifampicin x 2 doses over a day
- Ciprofloxacin
What IV antibiotics + other medication recommended to treat bacterial meningitis.
Why other medication are given –> their effect on a specific meningitis bacteria.
- Dexamethasone 10mg IV –> potent corticosteroid given before/same time of antibiotics to dampen innate immune response to dying bacteria (LPS, peptidoglycans released). Reduces mortality for Strep pneumoniae, TB, no harm done in others.
- Ceftriaxone 2g IV: achieves moderate conc in CSF, broad spectrum of activity. Used instead of penicillin because no n. meningitidis strains resistant.
- Vancomycin IV (dose calculated according to weight + renal function). This is to kill any strains of strep pneumoniae which are resistant (poor cephalosporin binding)
Describe the mechanism of action of cephalosporins (derived from Acremonium mould) and what are the specialties of 1-4 generations. (5 in total) + example
Mech: B-lactam ring which inhibits transpeptidase
- Cefazolin IV: 2nd line for skin infections, pneumonia gram +
- Cefuroxime: Gut infections eg peritonitis
- Ceftriaxone: pneumonia, UTI, GIT infections:
1–>3 There is improving activity gram (-) bacteria, but worse gram (+) activity
- Cefepime, Cefpirome: restored Gram + activity: fumigating agent with broad gm + or - activity in leukaemic febrile neutropenia
Why are cephalosporins generally second line treatment to penicillins
Penicillins have a narrower spectrum than cephalosporins so preferred as C can kill E.coli and other gut flora therefore increasing chance of complications with C. difficile diarrhoea, resistant bacteria colonisation. vit k deficiency etc.
Which cephalosporin treats P. aeruginosa and which generation is it. What do 5th generation cephalosporins do
Ceftazidime (3). This is generally in hospital acquired infections.
5th generations : Ceftaroline (not in NZ) has activity against MRSA –> can bind to the changed transpeptidase enzyme. It is good to treat sepsis or bacteremia, but generally Vancomycin used instead.
