|
|
|
|
|
|
|
| Acute purulent meningitis | ||
| Etiology •Purulent meningitis is due most often to hematogenous spread of bacteria to the leptomeninges. •It can also be seen after head trauma as skull fracture through the sinuses. •Local infections such as mastoiditis may also lead to meningitis. •The most comman bacteria causing meningitis in neonates are streptococcus and E. Coli. In young children and adults Hemophilus influenzae, is common and in adults meningiococcus and pneumococcus are common. | ||
| Pathogenesis •Bacteria extend through the wall of blood vessels into the subarachnoid space followed more slowly by neutrophils as the blood brain barrier breaks down. •The combination of bacteria and neutrophils in the subarachnoid space irritates the underlying cerebral cortex causing edema and increased intracranial pressure. •If the meningitis is not treated neutrophils are followed by lymphocytes and macrophages which with the bacteria, cause irritation and degeneration of cranial nerves, production of intimal fibrosis in arteries and fibrosis of the leptomeninges which can lead to cortical infarcts and blockage of the foramina of Lushcka and Magendie with hydrocephalus., | ||
| Epidemiology •Neonates are the most susceptible to meningitis followed by the elderly, debilitated individuals and those on chemotherapy. •AIDS patients do not often get bacterial meningitis as their neutrophils are competent and normal in number. | ||
| General Gross Description •The brain in purulent meningitis has an opacity of the leptomeninges by neutophils and bacteria. This is seen over the convexity and the base. •The brain is also usually swollen. •Examples: | ||
| General Microscopic Description •In acute purulent meningitis, the subarachnoid space is filled with neutrophils and bacteria with increasing numbers of macrophages and lymphocytes over time. •The underlying brain is usually protected by the pia so that there is no intracerebral inflammation, however, the cortex and white matter will show spongy change or vacuolization due to edema. •Infants more often show bacteria and neutrophils invading the underlying parenchyma. •Examples: | ||
| Clinical Correlation •Patients with acute purulent meningitis usually have headache, stiff neck, lethargy which can proceed to coma and neutrophils, bacteria and increased protein and decreased glucose in their CSF. When the meningitis is not treated rapidly and correctly the patient may die or develop neurological defecits such as loss of hearing from infiltration of the 8th nerve, hydrocephalus, paraplegia or mental retardation. | ||
| References • Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 1315-1316. • Poirer J et.al. Manual of basic neuropathology. Philadelphia: Saunders, 1990, pp.103-105. Please be patient during transfer. Medline will open in a new window. To return, close the Medline Window Acute purulent meningitis
| Synopsis by: Dr ML Grunnet (TX1110M40000)[500]
| |
|
|
|
|
|
|