Trichosporon Infections Medication

Updated: Jan 16, 2015
  • Author: Ryan C Maves, MD, FACP, FCCP, FIDSA; Chief Editor: Mark R Wallace, MD, FACP, FIDSA  more...
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Medication

Medication Summary

The goals of pharmacotherapy are to eradicate the infection, to reduce morbidity, and to prevent complications. In general, empiric monotherapy should be avoided without specific testing of fungal sensitivity to available drugs.

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Antifungal Agent, Systemic

Amphotericin B (Amphocin, Fungizone)

Amphoteric polyene antifungal with activity against many fungal pathogens. Administered in solution only and is well known for a variety of toxic side effects. May be injected intrathecally or into a joint space, or it may be used as an irrigant, although it is usually administered IV. Dose should be adjusted for the indication. For trichosporonosis, high doses are required. Lipid formulations of amphotericin B (see below) are generally preferred, however.

Amphotericin B, liposomal (AmBisome)

Lipid formulations of amphotericin B that deliver higher concentrations of the drug, with a theoretical increase in therapeutic potential and decreased nephrotoxicity. Produced from a strain of Streptomyces nodosus. Antifungal activity of amphotericin B results from its ability to insert itself into fungal cytoplasmic membrane at sites that contain ergosterol or other sterols. Aggregates of amphotericin B accumulate at sterol sites, resulting in an increase in cytoplasmic membrane permeability to monovalent ions (eg, potassium, sodium).

At low concentrations, the main effect is increased intracellular loss of potassium, resulting in reversible fungistatic activity; however, at higher concentrations, pores of 40-105 nm in cytoplasmic membrane are produced, leading to large losses of ions and other molecules. A second effect of amphotericin B is its ability to cause auto-oxidation of the cytoplasmic membrane and release of lethal free radicals. Main fungicidal activity of amphotericin B may reside in ability to cause auto-oxidation of cell membranes.

Voriconazole (Vfend)

A triazole antifungal agent that inhibits fungal cytochrome P450-mediated 14 alpha-lanosterol demethylation, which is essential in fungal ergosterol biosynthesis. Commonly used in the treatment of aspergillosis, invasive candidiasis, and neutropenic fever. Has excellent MICs against Trichosporon species and has occasionally been effective as monotherapy.

Posaconazole (Noxafil)

Triazole antifungal agent. Blocks ergosterol synthesis by inhibiting the enzyme lanosterol 14-alpha-demethylase and sterol precursor accumulation. This action results in cell membrane disruption. Available as oral susp (200 mg/5 mL). Indicated for prophylaxis of invasive Aspergillus and Candida infections in patients at high risk because of severe immunosuppression.

Fluconazole (Diflucan)

Triazole derivative with high enteral bioavailability used for Candida infections and infections with endemic mycoses. Also useful for Trichosporon infections. Dose depends on the indication. For trichosporonosis, the dose should be the maximum dosage.

Flucytosine (Ancobon)

Pyrimidine analog available enterally or IV for use against a variety of fungal pathogens but is not generally used as monotherapy owing to emergence of resistance during therapy. Well absorbed orally but should be administered IV to critically ill patients.

Caspofungin (Cancidas)

Routinely used to treat refractory invasive aspergillosis and invasive candidiasis. First of a new class of antifungal drugs (glucan synthesis inhibitors). Inhibits synthesis of beta-(1,3)-D-glucan, an essential component of fungal cell wall.

Micafungin (Mycamine)

Member of new class of antifungal agents, echinocandins, that inhibit cell wall synthesis. Inhibits synthesis of 1,3-beta-D-glucan, an essential fungal cell wall component not present in mammalian cells.

Approved indications include (1) prophylaxis of candidal infections in patients undergoing hematopoietic stem cell transplantation and (2) treatment of esophageal candidiasis.

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