Tutorial 03: Meningitis and Septicaemia

The meninges are three layers of connective tissue covering the brain and spinal cord: the dura mater (tough outer layer), the arachnoid mater (middle layer), and the pia mater (delicate inner layer adherent to the brain surface). The subarachnoid space between the arachnoid and pia contains cerebrospinal fluid (CSF), which cushions the brain and maintains the ionic environment of neurons.

Meningitis is inflammation of the leptomeninges (arachnoid and pia) and subarachnoid space. It is a medical emergency. Clinical presentation is driven by two mechanisms: raised intracranial pressure (headache, vomiting, papilloedema, altered consciousness) and meningeal irritation — meningism (neck stiffness/nuchal rigidity, photophobia, Kernig's sign — inability to extend the knee with hip flexed). A petechial or purpuric rash suggests meningococcal disease.

Acute pyogenic (bacterial) meningitis is usually caused by Neisseria meningitidis (serogroups B, C; most common in adolescents and young adults), Streptococcus pneumoniae (most common overall in adults; highest mortality), Haemophilus influenzae type b (now rare due to vaccination), and Listeria monocytogenes (elderly, immunocompromised, neonates). CSF findings: turbid (cloudy), neutrophilia (>1000 cells/µL), very high protein, low glucose (bacteria consume glucose; CSF:blood glucose ratio <0.6). Macroscopically: the brain surface is covered with purulent exudate (pus), concentrated at the base of the brain; meningeal vessels are congested; brain is oedematous.

Aseptic (viral) meningitis is the most common form overall. Enteroviruses (Echovirus, Coxsackievirus) are responsible for the majority. CSF: clear, lymphocytosis, mildly elevated protein, normal glucose. Self-limiting; no specific treatment except supportive care.

Tuberculous meningitis is a severe complication of miliary TB or primary bacteraemia. Granulomatous inflammation involves the base of the brain, causing cranial nerve palsies (CN II, III, IV, VI most commonly), hydrocephalus (CSF outflow obstruction), and vasculitis with cerebral infarction. CSF: lymphocytosis, very high protein, low glucose, AFB on ZN stain (low sensitivity) or PCR.

Complications of bacterial meningitis (if treatment is delayed): cerebral oedema → transtentorial herniation, hydrocephalus (adhesions blocking CSF flow), cortical vein thrombosis, cerebral infarction (vasculitis), cranial nerve palsies, deafness (labyrinthitis), and cognitive impairment.

Meningococcal septicaemia (Neisseria meningitidis bacteraemia) causes rapid systemic deterioration. Endotoxin release activates complement, monocytes, and endothelium → cytokine storm → systemic inflammatory response → disseminated intravascular coagulation (DIC). The petechial/purpuric rash reflects micro-emboli of meningococcal septic thrombi in dermal capillaries. Waterhouse-Friderichsen syndrome is bilateral adrenal cortical haemorrhage from DIC and direct bacterial adrenal invasion, causing acute adrenal insufficiency; it is characteristically associated with N. meningitidis septicaemia and is usually fatal without treatment. DIC causes consumption coagulopathy (prolonged PT/APTT, low fibrinogen, thrombocytopenia, elevated D-dimers), leading to paradoxical bleeding alongside microvascular thrombosis and multi-organ failure.