Antifungal agents Griseofulvin: Obtained from certain penicillium spp. Griseofulvin interact with microtubules and disrupt mitotic - spindle function of the fungal cell (cause shrinkage of fungal hyphae). Amphotericin B: Drived from streptomyces nodosus., belonging to polyenes group. Amphotericin B firmly bind to ergestrol (sterol) in the cell membrane, such binding increase the permeability of the cell with leak essential components as glucose and potassium.
3. Flucytosine (5 flurocytosine): The drug accumulated in fungal cells and converted by cytosine deaminase to 5 fluorouracil, an inhibitor of the thymidylate synthetase (this enzyme is essential for DNA synthesis). 4. Azoles compound: The azole used for systemic mycosis, include ketaconazole, fluconazole and itraconzole. They are orally active agents, and less toxic than Amph. B. Miconazole and clotrimazole which are toxic for systemic administration, are used as topical agents. All antifungal azole act by inhibition of fungal ergestrol biosynthesis which lead to alterations in fungal membrane structure and function.
Echinocandins: Are lipopeptides that work on a compound of fungal cell wall that is not present in mammalian cell. Nystatin: Is a polyene antifungal. Allylamines: Naftifine a topical agent, and the terbinafine an oral agent. The mechanism of action is inhibition of an essential step in fungal ergosterol synthesis. Other topical antifungal agents: Tolnaftate: Its principal use is in tinea pedis,. It is inactive against Candida. Whitfield's ointment: Is a mixture of benzoic and salicylic acid, the usual use for tinea pedis. Sodium thiosulfite for tinea versicolor.
Fungal diseases: Superficial mycosis. Cutaneous mycosis. Subcutaneous mycosis. Endemic (primary systemic) mycosis. Opportunistic mycosis.
Two properties of fungi appear to be very important in the pathogenesis of the disease they caused. Tissue tropism. The ability of many fungi to incite sensitivity especially delayed type sensitivity in the host. Often the sensitivity of the host to fungal antigens account in large part for the pathologic effects produced.
Etiological agent: Malassezia furfur is a lipophilic yeast like species that is a member of the normal flora of human skin. The fungus cause catheter - aquired fungemia in adults, and specially neonates who are receiving intravenous lipid. Epidemiology The distribution of the disease is Worldwide. Malassezia furfur is a member of the normal flora of the skin. The important predisposing factors are poor hygiene and excess sweating, systemic corticosteroid also increase susceptibility to the disease. The fungus has not been found as a free - living saprophyte.
Laboratory Diagnosis Direct examination:
Isolation of M. furfur in culture:A clinical diagnosis can be made in typical cases, and also by the use of wood's light, that the infected lesions show a pale yellow fluorescence under dark condition.
Etiological agent The causative orgarism is Exophiala werneckii. (dematiaceous fungus). Laboratory Diagnosis Direct examination. Direct culture. Treatment Respond to the topical application of fungicidal preparation such as Benzoic acid compound ointments. Topical azole creams such as econazole are also effective.
chlamydospore
hypha
Piedra Infection limited to the hair shafts. Black piedra is caused by piedraia hortae. White piedra is caused by the yeast Trichosporon beigelii. White piedra has a wider geographic distribution than black piedra.
Laboratory Diagnosis Direct examination. The crushed nodules (from black piedra) show numerous asci containing two to eight single - celled fusiform, ascospores. In case of white piedra, the crused nodules show only arthorspores and blastospores, but no asci. Culture. Treatment: By shaving the hair, clipping the hair closely result in cure. The use of a solution of bichloride mercury 1/2000 conc. (for both piedra).