Chronic bacterial infections and neurosarcoidosis
TUBERCULOSIS
MACROSCOPIC APPEARANCES
Tuberculous meningitis is characterized by a gelatinous subarachnoid exudate. This may appear slightly nodular and is usually thickest in the sylvian fissures, over the base of the brain (Fig. 16.1a), and around the spinal cord. Sectioning of the brain usually reveals a similar exudate within the choroid plexus and lining the ventricles. Tubercles may be visible in the meninges, usually adjacent to sulcal veins, and in the ventricular lining (Fig. 16.1b). Small superficial tuberculomas are quite common (Fig. 16.2) and may be associated with an overlying meningeal exudate. Large tuberculomas occasionally occur, but are rare in patients with meningitis.
16.1 Tuberculous meningitis.(a) Thick pale yellow exudate over base of brain, particularly around the optic chiasm. (b) Nodular thickening of the lining of the lateral ventricles.
The ventricles are often moderately dilated, owing to the development of obstructive or communicating hydrocephalus. There may be infarcts.
MICROSCOPIC APPEARANCES
The meningeal and ventricular exudate contains lymphocytes, macrophages, and sparse plasma cells, admixed with necrotic material and fibrin (Fig. 16.3a). There may be accumulations of epithelioid cells and fibroblasts, multinucleated giant cells, and well-defined tuberculous granulomas (Figs 16.2, 16.3, 16.4) with central caseous necrosis.
16.3 Histology of tuberculous meningitis.(a) There is a meningeal exudate of macrophages, lymphocytes, plasma cells, and fibrin. The superficial cortex (at left) is densely gliotic. (b) Meningeal artery surrounded by lymphocytes, macrophages, and an occasional multinucleated giant cell. There is mild endarteritis, with proliferation of subintimal fibroblasts.
16.4 Part of a caseating meningeal granuloma in tuberculous meningitis.There is a characteristic infiltrate of lymphocytes, epithelioid macrophages, and Langhans’-type multinucleated giant cells.
16.5 Tuberculous meningitis in an immunosuppressed patient.(a) Inflammation in the leptomeninges of a patient with AIDS. Note the absence of a typical granulomatous tissue reaction. (b) Numerous acid-fast bacilli in AIDS-associated tuberculous meningitis.
The inflammation extends into the subpial and periventricular brain tissue, which shows reactive astrocytosis (Fig. 16.3a) and microglial proliferation. This may be associated with degeneration of white matter adjacent to the ventricles and in the spinal cord.
The inflammatory cells tend to infiltrate through the adventitia, into the media and even the intima, of blood vessels within the exudate (Figs 16.3b, 16.6). Thrombosis occurs in some blood vessels. In others, the inflammation provokes a subintimal intimal fibroblastic reaction that narrows and can occlude the lumen (Figs 16.3b, 16.7). Infarcts are therefore common (Fig. 16.8), particularly in the superficial cortex and, due to the involvement of perforating branches of the middle cerebral artery, in the basal ganglia.
16.6 Mild tuberculous endarteritis.Extension of granulomatous inflammation through the adventitia and media of a meningeal artery.
16.7 Tuberculous endarteritis.Narrowing of the lumen of an inflamed meningeal artery by accumulation of chronic inflammatory cells and proliferation of intimal connective tissue.
16.8 Acute infarction of superficial brain parenchyma in tuberculous meningitis.Several arteries in the overlying leptomeninges are occluded or severely stenosed by intimal fibroplasias (arrows). The zone of acute infarction is delineated by arrowheads.
Tuberculomas result from the growth of tubercles, which enlarge within the CNS parenchyma or remain encapsulated within the meninges, rather than rupturing into the CSF to cause meningitis (see above), except at a late stage in some cases.
Patients present with a subacute onset of focal neurologic signs and symptoms, often with evidence of raised intracranial pressure. Most have evidence of systemic tuberculosis. Tuberculomas usually respond to antibiotic therapy, although this can, very occasionally, cause central liquefaction and the formation of a tuberculous abscess. Rarely, central liquefaction occurs spontaneously.
MACROSCOPIC APPEARANCES
Tuberculomas appear as solitary encapsulated yellow or gray masses or multinodular aggregates of smaller masses. They are most often cerebral or cerebellar, but can occur anywhere within the neuraxis. The central tissue, though necrotic, has a firm consistency when cut.
MICROSCOPIC APPEARANCES
Histology reveals solitary or confluent tuberculous granulomas with central caseous necrosis surrounded by lymphocytes, epithelioid cells, Langhans’-type multinucleated giant cells, and an outer zone of collagen, fibroblasts, lymphocytes, and macrophages (Fig. 16.9). Older lesions may calcify. The adjacent parenchyma is usually markedly gliotic.
SPINAL EPIDURAL TUBERCULOSIS
This is caused by extension of tuberculous vertebral osteomyelitis into the epidural space. There is usually a history of backache and general malaise over a period of weeks or months. Compromise of the spinal cord (‘Pott’s paraplegia’) is caused by focal compression, which is often exacerbated by local vertebral collapse and kyphosis and, in some cases, spinal infarction. The thoracic cord is most often involved.
MACROSCOPIC APPEARANCES
There is usually extensive destruction, which may be associated with collapse of the affected vertebral bodies and intervertebral discs. This is associated with variable protrusion of gray multinodular granulomatous tissue into the epidural space (Fig. 16.10).
MICROSCOPIC APPEARANCES
The epidural mass shows typical granulomatous tuberculous inflammation with caseation. Changes in the spinal cord reflect a combination of focal compression by epidural inflammatory tissue or vertebral kyphosis, ischemia (see Chapter 9), and secondary long tract degeneration. Compression of the anterior spinal artery may produce a typical ‘watershed’ infarct (see Chapter 9) involving the upper and middle parts of the thoracic cord.

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