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Flashcards in W4 - Infections of the CNS Deck (19):

How do bacteria find their way to the meninges?

Direct spread - Nearby infective focus (paranasal sinusitis, osteomyelitis, otitis media), open skull fracture

Haematogenous (blood borne) - Septicaemia, septic emboli (bacterial endocarditis, bronchestasis, TB)

Iatrogenic - Post lumbar puncture, neurosurgery etc


Write notes on pachymeningitis.

Definition: Inflammation of the dura mater.
- Relatively uncommon compared to leptomeningitis
- Spread: Usually direct spread from from: Mastoiditis, Otitis media, skull fracture
- Main pathogens: G-Bacilli, a/B haemolytic streptococci (from paranasal sinuses), mixed organisms (compound fractures)

Abscess formation above and below the dural layer of meninges can cause:
Epidural abscess:
- Abscess forms between dura and bones of skull or vertebral column --> suppuration
- Types: Spinal epidural abscess (SEA), intracranial epidural abscess (IEA)
Subdural abscess:
- Suppuration occurring within the subdural space (potential space)
- Complications include: Infection and thrombosis of subdural arteries and veins, CNS infarction


Name two (2) bacteria which are known to cause acute bacterial meningitis.

Streptococcus pneumonia
Neisseria meningiitidis
Haemophilus influenza
Liseria monocytogenes
Streptococcus agalactiae (group B)
Escherichia coli
Staphylococcus aureus 


Discuss the pathogenesis of acute meningococcal meningitis.

1. Organism resides in nasal cavities, oral cavity and throat of asymptomatic carriers
2. Direct spread via droplet inhalation (eg sneezing) and saliva (eg mouth kissing, sharing drink bottles, sharing cooking utensils etc)
3. Host infected (+/- URTI Ssx) and haematogenous spread
4. Bacteria reaches meminges and suppuration ensues


Discuss the clinical manifestations of meningococcal meningitis.

- Headache (severe)
- Fever (High, >39 deg)
- Neck stiffness and pain (meningeal irritation)
- Vomiting
+/- any of the following:
- Brudzinski's sign (forced neck flexion causes reflex hip flexion)
- Kernig's sign (90 deg of hip & knee flexion --> painful knee extension)

Acute Ssx:
Confusion, photophobia, drowsiness and lethargy, fits, high temp, joint pains, neck stiffness, rash, violent/severe HA

Babies and infants:
Fever (hands and feet cold), Refusing feeds or vomiting, High pitched moaning/crying, dislike of being handles, neck retraction with arching of back, blank and staring expression, lethargic and difficult to wake, pale blotchy complexion


How is acute bacterial meningitis diagnosed? How is is treated?

Diagnosed based on the clinical picture (symptoms, and Kernig's and Brudzinski's sign) and a lumbar puncture (including heparin binding levels)

Lumbar puncture:
- Patients with early bacterial meningitis may not have CSF pleocytosis
- Heparin binding protein is a new biomarker (may assist with early identification of bacterial meningitis in adults), pus, blood, bacteria
- HBP levels >20ng/mL should prompt empirical therapy while awaiting results of CSF culture and immunoassays



List four (4) complications of acute bacterial meningitis.

- Disseminated Intravascular Coagulation (DIC) --> skin rash
- Obstructive hydrocephalus - Due to blockage of CSF from 4th ventricle from fibrous tissue and exudate --> CSF backflow
- Cerebral infarction
- Cerebral or subdural abscess
- Epilepsy
- Waterhouse-Eriderchsen syndrome
- Chronic meningitis
Septicaemia - septic (haemorrhagic) rash), conjunctival haemorrhage, tissue necrosis


Discuss the epidemiology of acute viral meningitis.

- More common than bacterial meningitis, incidence figures hard to come by, but most sources state it is relatively common
- Affects >450 people/year in Australia
- All ages involved, but viral meningitis mainly disease of children and young adults (90% <30, 70% <20)
- Peak incidence = late summer (mainly due to enteroviruses
- Differences exist in the ratio female:male and depends on type of virus involved (eg mumps male: female = 2-3:1)
- 85-95% of all cases of viral meningitis caused by enteroviruses
- Less common causes: Herpes simplex viruses (1&2), varicella-zoster virus, cytomegalovirus, Epstein-Barr virus


Describe the clinical presentation of acute viral meningitis

Acute onset of:
- Headache (severe pre-orbital/frontal, exacerbated by coughing, moving, +/- photophobia)
- Fever (high - 38-40 deg)
- Ssx of meningeal irritation (listlessness, malaise and vomiting, neck pain and stiffness, positive Brudzinski's and Kernig's signs)
Clinical examination may provide clues as to identity of causative virus.


Describe the typical "acute viral meningitis" headache.

A severe throbbing, frontal/retro-orbital headache exacerbated by coughing, moving, +/- photophobia. May be describes as "worst they've ever had".


Define the term "meningeal irritation". What are the main clinical manifestations?

Irritation of the meninges by bacterial, viral or external lesions.

Key manifestations:
- Neck stiffness (nuchal rigidity) on flexion
- Headache (severe pre-orbital/frontal, exacerbated by coughing, moving, +/- photophobia)
- Spine stiffness
- Positive Brudzinski's sign
- Positive Kernig's sign


List and describe the main clinical tests used to detect meningeal irritation. By which mechanisms are these manifestations caused?

Brudzinski’s sign – Pt supine on bed, practitioner rapidly flexes neck. A positive test will see instantaneous reflex flexion at the hip and knee – a reaction to decrease the tension on the meninges.

Kernig’s sign – Pt supine with knee and hip both flexed at 90 degrees. Pt is unable to completely extend the leg when the thigh is flexed on the abdomen. Pt can usually extend the leg completely when the leg is not flexed on the abdomen.

Mechanism: Inflammation of meninges will cause irritation when put under tension. These positions increase meningeal tension (and thus, cause irritation).


Discuss the diagnosis of acute viral meningitis.

CSF examination of Lumbar puncture:
- Pressure: Raised
- Turgid or cloudy appearance (due to presence of pus)
- Elevated neutrophils and proteins
- Normal glucose levels (very low in bacterial meningitis as bacteria use glucose as fuel)
- Negative gram stain and acid-fast bacilli strain (not a bacterial infection)
- Positive viral culture

Typical menigitis Ssx
Clinical findings may also present clues as to identity of virus (parotiditis may implicate mumps virus, skin rash may implicate cox-sackie/echo virus)


Discuss the treatment and prognosis of acute viral meningitis.

Generally very good. In most cases, condition is benign and self-limiting (usually complete resolution in 7-10 days).
May suspect encephalitis if seizures, sensory changes or focal neural Ssx present.

Treatment: Antibiotics, rest and hydration


Discuss the pathogenesis of cerebral abscess.

Usually occurs as a complication of other disease (bronchiectasis, frontal sinusitis, trauma, otitis media).
1. Microbes invade CNS tissue, leading to liquefactive necrosis
2. Formation of pus filled cavity
3. Fibrogliosis occurs, forming a hard capsule around the pus
4. Inflammatory oedema to surrounding area


Describe the cerebral abscess

An area of suppurative inflammation in the brain substance that may be caused by: Staph Aureus, bacteroides, nocardia.
Consists of a pus-filled cavity surrounded by a fibrogliotic wall (full of astrocytes and fibroblasts) that is usually surrounded by inflammatory oedema.


Discuss the clinical manifestations of the cerebral abscess.

A combination of:
- Space occupying lesions (SOLs) causing usual Ssx of raised ICP (HA, vomiting, papilloedema, focal neuro Ssx)
- Infection Ssx - Fever, malaise, weight loss etc
- Ssx of primary infection (otitis media, suppurative lung disease etc)

If left untreated enlargement may occur, exacerbating Ssx (especially those associated with raised ICP)


How is cerebral abscess diagnosed?

- Cerebral abscess is diagnosed via clinical manifestations and CT/MRI
- Lx puncture is not generally used due to risk of herniation (raised ICP is a clinical features of cerebral abscess). However, if obtained, CSF would have normal parameters except for a mild increase in neutrophils and lymphocytes.


How is cerebral abscess treated?

- Surgical evaluation
- Antibiotics
- Able to be drained (invasive)
- Mortality rate with treatment is 5-10%