Antifungal drugs save lives by treating dangerous fungal infections, just like antibacterial drugs (antibiotics) are used to treat bacterial infections. Unfortunately, germs like bacteria and fungi can develop the ability to defeat the drugs designed to kill them. That means the germs are not killed and continue to grow. When this occurs with fungi that no longer respond to antifungal drugs, it is called antifungal resistance. This is especially a concern for patients with invasive infections like those caused by the fungus , a yeast, which can cause serious health problems, including disability and death. More information is needed about the risk antifungal resistance poses on human health and how many people are sickened by drug-resistant fungal infections each year. CDC and its partners are working to: infections (those that are resistant to both fluconazole and an echinocandin) have very few remaining treatment options. The primary treatment option is Amphotericin B, a drug that can be toxic for patients who are already very sick. Fluconazole is a first-generation triazole antifungal medication. It differs from earlier azole antifungals (such as ketoconazole) in that its structure contains a triazole ring instead of an imidazole ring. While the imidazole antifungals are mainly used topically, fluconazole and certain other triazole antifungals are preferred when systemic treatment is required because of their improved safety and predictable absorption when administered orally. Fluconazole's spectrum of activity includes most Candida species (but not Candida krusei or Candida glabrata), Cryptococcus neoformans, some dimorphic fungi, and dermatophytes, among others. Common uses include: Fungal resistance to drugs in the azole class tends to occur gradually over the course of prolonged drug therapy, resulting in clinical failure in immunocompromised patients (e.g., patients with advanced HIV receiving treatment for thrush or esophageal Candida infection). albicans, resistance occurs by way of mutations in the ERG11 gene, which codes for 14α-demethylase. These mutations prevent the azole drug from binding, while still allowing binding of the enzyme's natural substrate, lanosterol. glabrata is increasing the rate of efflux of the azole drug from the cell, by both ATP-binding cassette and major facilitator superfamily transporters. Development of resistance to one azole in this way will confer resistance to all drugs in the class. Other gene mutations are also known to contribute to development of resistance.
ABSTRACT - We a case of chronic Aspergillus sp. meningitis in a healthy 43-year-old woman successfully treated with fluconazole given orally 300 ms/day. Oral fluconazole recommended as preferred therapy; IV dosing recommended as alternative therapy for infants and children of all ages. -If neonate creatinine level is greater than 1.2 mg/dL for 3 consecutive doses, the dosing interval for the higher dose may be extended to 12 mg/kg every 48 hours until serum creatinine level is less than 1.2 mg/dL.