Fungal infection may be classified into

1- Systemic fungal infections (Systemic mycosis

•Drug used: Amphotericin B, flucytosine, Azoles
2- Superficial fungal infections
A- Mucocutaneous fungal infections (candidiasis, moniliasis
•Drug used: Topical: azoles, nystatin, amphotericin
Oral: azoles
B- Dermatophytic fungal infections (Dermatophytosis
•Drug used: Topical: azoles, terbinafine, tolnaftate, ciclopirox
olamine,undecylenic acid, butenafine, quiniodochlor.
Oral: Azoles, griseofulvin, terbinafine.
 Ultrafine crystalline preparations are absorbed. Distributed to infected
keratinized tissue. Partially metabolized in liver & slowly excreted in urine &
faeces
 Mechanism of action:It is an oral fungistatic agent, binds to microtubules
and prevents spindle formation and mitosis in fungi also binds filament
proteins such as keratin. It accumulates in the infected, newly synthesized,
keratin-containing tissue. Protects skin from new infection.
 Uses: Orally in superficial mycosis (dermatophytosis) e.g.
ringworm of skin, hair & nail & athlete's foot. Not effective
against Candida albicans or systemic mycosis
 Side effects: Headache, GIT disturbance, hepatotoxicity,
teratogenicity, estrogen like effects, leucopenia, agranulocytosis
and photosensitivity.
 Contraindicatios: acute intermittent porphyria, and in
pregnancy
 
Kinetics:
 Poor oral absorption,

poor CSF penetration,

crosses placenta.
Eliminated mainly
through biliary route.
 Mechanism of action: ↑ fungal cell membrane
permeability through binding to ergosterol of cell
membrane leading to loss of intracellular
constituents.
 Uses: IV infusion (Systemic fungal infection),
intrathecal (Fungal meningitis), eye drops
(Fungal corneal ulcer), cream (Cutaneous
candidiasis) and orally (intestinal candidiasis)
Side effects:
Fever and chills (can be prevented

by steroids and antipyretics),

Nephrotoxicity (potentiated by
sodium depletion), Hypotension,
hypokalemia, Thrombophlebitis,
anemia, convulsion and arrhythmia
Drug interaction: Nephrotoxicity is
potentiated by aminoglycosides and
cyclosporin, Amphotericin ↑toxicity
of digitalis
 It is synthetic pyrimidine analogue related to 5-
flourouracil.
 Kinetics: absorbed orally, distributed allover
the body, pass BBB & 80% excreted
unchanged in urine so its dose reduce in renal
failure.
 Mechanism of action: It is transported into
fungal cell by permease enzyme. Then
converted to 5-flourouracil and subsequently to
5- fluorodeoxyuridylic acid, which is an inhibitor
of pyrimidine and nucleic acid synthesis.
 Uses: It used in combination with amphotericin
B for treatment of systemic fungal infection or
alone for treatment of chromoblatomycosis.
 Side effect: blood dyscriasis, GIT disturbance,
hepatic toxicity and alopecia.
 Mechanism of action: similar to amphotericin B
 Uses: Too toxic for systemic administration. Used
in candidiasis of skin, mucous membranes and
intestinal tract.
Mechanism of action: Act by binding to cytochrome P- 450
enzyme (lanosterol 14-demethylase) responsible for the
demethylation of lanosterol to ergosterol. Reduced fungal membrane
ergosterol concentrations result in damaged, leaky cell membrane.
A- Ketoconazole
Uses:Systemic & superficial fungal infection. Topically for
treatment of dandruff.
Side effect: Inhibit adrenal & gonadal (androgen) hormone
synthesis leading to Gynecomastia, loss of libido and
azospermia in males. GIT upset, hepatotoxicity
B- Fluconazole ,Itraconazole
Similar to ketoconazole, but lacks its endocrine side effects.
Orally for pharyngeal & vaginal candidiasis & various tinea
infections.
C- Clotrimazole ,Miconazole :Used topically for local fungal
infection.