Opportunistic Nervous System Infections

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As with other organ systems, the spectrum of opportunistic infections of the nervous system results from the intrinsic vulnerabilities of the tissue (fertile soil) and the pattern of immunosuppression, in this case circumscribed impairment of T-cell/macrophage defenses. The patient’s long-term history of exposure to particular organisms is also important because most of the opportunistic infections result from reactivation of latent infections rather than from new encounters with pathogens. An important implication of the pre-eminence of reactivated infection relates to serologic testing, which is most useful for assessing prior exposure to an organism and hence susceptibility to clinically important reactivation, but not for defining active infection. For example, patients with cerebral toxoplasmosis nearly always exhibit antecedent positive Toxoplasma gondii blood serology, and therefore a negative serum lgG antibody titer militates against this diagnosis.

On the other hand, these serum antibody titers most often do not rise before or during the course of disease, and therefore a fourfold increase cannot be relied upon to establish disease activity. Moreover, as long as immunosuppression persists and therapy still cannot eliminate latent infection, suppressive antibiotic therapy must be maintained for the remainder of the patient’s life. Prophylaxis also influences vulnerability to some infections and therefore their diagnostic probability. Thus, whether or not a patient is taking trimethoprim-sulfamethoxazole affects the likelihood of cerebral toxoplasmosis.

The reason for the intrinsic vulnerability of the nervous system to certain infections (e.g., T. gondii) and not others (e.g., Pneumocystis carinii) in many cases remains uncertain. However, in some instances susceptibility relates to the capacity of local cells to support intracellular replication. Thus, the virus causing progressive multi-focal leukoencephalopathy (PML), JC virus, causes a productive and lytic infection of oligodendrocytes and hence leads to spreading infection and demyelination as the processes of these myelin-producing cells disappear. In the case of HIV-1, productive infection appears to involve monocyte-derived macrophages and local microglial cells.

The circumscribed nature of the immunologic defect in AIDS determines the range of opportunistic infections, which therefore differs somewhat from that of other immunosuppressed states. For example, AIDS patients are particularly susceptible to cerebral toxoplasmosis but, unlike patients with organ transplants, are much less likely to develop cerebral Candida or Aspergillus infections. For this reason, AIDS patients present a unique set of disease probabilities.

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