The complex host-parasite relationship in cysti-cercosis is still poorly understood. Some patients present a remarkable tolerance to the parasite, which can live in the brain for long periods without inducing a noticeable immune reaction (Pitella, 1997); in others, the immune response is unable to destroy the parasite, but is an important cause of damage to the surrounding tissue; in still other patients, the immune response is intense, leading to rapid destruction of the larva. The reasons for this variable response between individuals are not yet understood. Some HLA antigens have been weakly associated either to increased resistance (HLA DQw2) or susceptibility (HLA A28) to infection. It has also been shown that the parenchymal inflammatory response is more intense in females than in males; however, the reasons for these differences have not been explained (Monteiro et al., 1993; Rangel et al., 1987; Del Brutto et al., 1988).
The sequence of events corresponding to the stage of the parasite in the brain begins when the hexacanth embryo (oncosphere) is passively carried by the systemic circulation to the brain parenchyma, where it differentiates into a larva 1-1.5 cm in diameter within 2 months. Different events will follow, depending on the immune response of the host to the newly established parasite (Figure 23.10) (Pitella, 1997):
1. If immune tolerance develops, the cyst can remain in the tissue for several years (up to 12 years have been documented by neuro-imaging studies). In most of these cases, the cysts will continue to grow undisturbed; some may develop into cysts 10-15 cm in diameter years after infection (Figure 23.11). In many other cases, although the cysts grew undisturbed for long periods, the sudden appearance of a host immune reaction will induce an intense inflammation around the cyst, an event which seems to trigger death of the cysticercus. When the size of the cyst exceeds 2 cm in diameter, most of them lose the scolex due to a degenerative process that nevertheless allows the tegumentary membranes of the cysticercus to continue proliferating. The membranes can produce a giant cyst containing up to 50 ml fluid without an identifiable scolex in its interior.
2. Within 2 months of implantation, the cysti-cercus will acquire its typical morphological features of a 1 cm diameter cyst filled with a clear fluid and containing the scolex and neck, with the characteristic features of the cestode, a worm-like body with a head composed by four suckers and a double crown of hooks. If the immune response is strong enough to induce death of the parasite, it will undergo hyaline degeneration of the cystic fluid, followed, a few weeks later, by macrophage infiltration and the formation of a granulo-matous lesion, which in turn will either disappear without evident damage to the surrounding tissue or remain as a permanent granuloma, composed mostly of fibrotic scar tissue. Over 2-7 years this granuloma will
Fig. 23.12 Computed tomography, showing a parenchymal brain calcification, the most conspicuous sequel of neurocysticercosis and a frequent cause of epilepsy in endemic areas gradually calcify, becoming a permanent calcification which is easily observed in a simple X-ray study of the skull (Figure 23.12).
3. The two patterns described above in the natural history of brain parenchyma cysticer-cosis represent opposite pictures that depend on either immune tolerance or a hyperimmune response of the host (Estanol et al., 1986). However, in many patients the immune response is mild and chronic, not enough to destroy the parasite but sufficient to induce damage in neighboring tissues, such as vasculitis, fibrosis and astrogliosis. The parasites may remain for long periods in this stage. Thus, by imaging studies, many patients are found to have degenerating cysts that remain unchanged and surrounded by a thick capsule of fibrous tissue secondary to chronic peri-lesional inflammation. An intriguing feature of NC is the frequent finding of various parenchymal lesions in different stages, i.e. live cysticerci without signs of surrounding inflammation, hyaline cysts, granulomas and calcifications. This combination of lesions indicates either that the intensity of the local immune response varies from one site to another in the same host or that the cysticerci were the result of different infections (see Figure 23.10). Both possibilities appear feasible.
When cysticerci are lodged in cavities, such as the ventricular system or the vitreous cavity of the eye, the cysticercus may remain viable, floating within the fluid for long periods. In the case of ventricular cysticercosis, the parasite may lodge in the third or fourth ventricle and occlude the cerebrospinal fluid (CSF) circulation causing subacute hydrocephalus. Meningeal cysticercosis is the most severe form of the disease (Lobato et al., 1981; Estanol et al., 1983). When cysticerci infect the arachnoid membrane, the inflammatory response is intense, and may last for several years and be a persistent source of tissue damage, which, in contrast with parenchymal cysticercosis, is not restricted to the infection site. The CSF circulation disseminates the inflammatory cells and cytokines throughout the central nervous system, causing cerebritis, vasculitis (Del Brutto, 1992), fibrous entrapment of cranial nerves and fibrotic obstruction of CSF absorption at the arachnoid villi, which in turn will induce chronic hydroce-phalus in most patients (Sotelo and Marin, 1987). The intense inflammation of the meninges and its dissemination by the CSF circulation are the source of severe neurological damage, evidenced as brain infarctions, amaurosis, diplopia, other cranial nerve dysfunctions, intracraneal hypertension and dementia. In meningeal cysticercosis, the inflammatory response of the host is the source of most of the pathological features.
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