Tags: Vidarabine

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Neurotoxicity secondary to aciclovir is rare and is associated with high plasma concentrations, such as result from impaired renal function. Although the risk is greatest with intravenous administration, neurotoxicity has previously been noted with oral use. Symptoms of neurotoxicity, which usually appear within the first 24-72 hours of administration, include tremor, myoclonus, confusion, lethargy, agitation, hallucinations, dysarthria, asterixis, ataxia, hemiparesthesia, and seizures.

Central Nervous System Infections

Central nervous system infections include a wide variety of clinical conditions and etiologies: meningitis, meningoencephalitis, encephalitis, brain and meningeal abscesses, and shunt infections. The focus of this chapter is meningitis. N. meningitidis meningitis is the leading cuase of bacterial meningitis in children and young adults in the United States.

Antimicrobial therapy: general principles

A wide variety of antimicrobial agents is available to treat established infections caused by bacteria, fungi, viruses, or parasites. This section will cover the general principles of antimicrobial therapy and will also include illustrative clinical problems to emphasize proper decision-making in using antimicrobials.

Toxicity of Antimicrobial Therapy

The mechanisms associated with common adverse reactions to antimicrobials include dose-related toxicity that occurs in a certain fraction of patients when a critical plasma concentration or total dose is exceeded, and toxicity that is unpredictable and mediated through allergic or idiosyncratic mechanisms. For example, certain classes of drugs such as the aminoglycosides are associated with dose-related toxicity.

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Ketoconazole is administered orally. To ensure absorption in patients with achlorhydria, it has been recommended that each 200 mg of ketoconazole be dissolved in 4 mL of 0.2N hydrochloric acid solution or taken with 200 mL of 0.1N hydrochloric acid.

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Acyclovir is active against herpes simplex virus type 1 and type 2 and against varicella-zoster virus. This activity requires intracellular conversion of aciclovir by viral thymidine kinase to the monophosphate with subsequent conversion by cellular enzymes to the diphosphate and the active triphosphate.