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This chapter deals exclusively with the pharmacologic properties of the agents used to treat infections due to parasites. Specific treatment recommendations for the parasitic diseases of humans are listed in the chapters on those diseases. Information on these agents′ major toxicities, spectrum of activity, and safety for use during pregnancy and lactation is presented in Chap. 208. Many of the agents discussed herein are approved by the U.S. Food and Drug Administration (FDA) but are considered investigational for the treatment of certain infections (see Table 208-1). Drugs marked in the text with an asterisk (*) are available only through the Centers for Disease Control and Prevention (CDC) Drug Service (telephone: 404-639-3670 or 404-639-2888; Drugs marked with a dagger (†) are available only through their manufacturers; contact information for these manufacturers may be available from the CDC.


Like all benzimidazoles, albendazole acts by selectively binding to free β-tubulin in nematodes, inhibiting the polymerization of tubulin and the microtubule-dependent uptake of glucose. Irreversible damage occurs in gastrointestinal (GI) cells of the nematodes, resulting in starvation, death, and expulsion by the host. While highly injurious to nematodes, this fundamental disruption of cellular metabolism also offers treatment for a wide range of parasitic diseases.

Albendazole is poorly absorbed from the GI tract. Administration with a fatty meal increases its absorption by two- to sixfold. Poor absorption may be advantageous for the treatment of intestinal helminths, but successful treatment of tissue helminth infections (e.g., hydatid disease and neurocysticercosis) requires that a sufficient amount of active drug reach the site of infection. The metabolite albendazole sulfoxide is responsible for the drug′s therapeutic effect outside the gut lumen. Albendazole sulfoxide crosses the blood-brain barrier, reaching a level significantly higher than that achieved in plasma. The high concentrations of albendazole sulfoxide attained in cerebrospinal fluid (CSF) probably explain the efficacy of albendazole in the treatment of neurocysticercosis.

Albendazole is extensively metabolized in the liver, but there are few data regarding the drug′s use in patients with hepatic disease. Single-dose albendazole therapy in humans is largely without side effects (overall frequency, ≤1%). More prolonged courses (e.g., as administered for cystic and alveolar echinococcal disease) have been associated with liver function abnormalities and bone marrow toxicity. Thus, when prolonged use is anticipated, the drug should be administered in treatment cycles of 28 days interrupted by 14 days off therapy. Prolonged therapy with full-dose albendazole (800 mg/d) should be approached cautiously in patients also receiving drugs with known effects on the cytochrome P450 system.


Amodiaquine has been widely used in the treatment of malaria for >40 years. Like chloroquine (the other major 4-aminoquinoline), amodiaquine is now of limited use because of the spread of resistance. Amodiaquine interferes with hemozoin formation through complexation with heme. Although rapidly absorbed, amodiaquine behaves as a prodrug after oral administration, with the principal plasma metabolite monodesethylamodiaquine as ...

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