Understanding how griseofulvin works helps explain why treatment takes time and why certain administration requirements are so important. This unique antifungal medication has a specific mechanism that makes it particularly effective against fungal infections of the skin, hair, and nails.
Griseofulvin works in a fascinating way that's quite different from antibiotics that fight bacteria. This antifungal medication specifically targets the fungi that cause infections of the skin, hair, and nails - called dermatophytes. Think of these fungi like tiny invaders that feed on keratin, the protein that makes up your child's hair, skin, and nails. Griseofulvin acts like a molecular 'stop sign' that prevents these fungi from multiplying. When the fungus tries to divide and spread, griseofulvin interferes with its internal machinery, specifically the tiny tubes (called microtubules) that the fungus needs to separate its genetic material during cell division. Without working microtubules, the fungus gets stuck and can't reproduce. What makes griseofulvin special is that it doesn't just float around in the bloodstream - it specifically concentrates in the areas where these fungi like to grow: the skin, hair, and nails. As your child's body produces new skin cells, hair, and nails, the griseofulvin gets built right into these new tissues, making them resistant to fungal infection. This is why treatment takes so long - you're essentially waiting for all the infected tissue to grow out and be replaced by new, protected tissue. For a scalp infection, this means waiting for new hair to grow (about 1/4 inch per month), while nail infections take even longer because nails grow so slowly. The medicine only works on actively growing fungi, which is why it's called 'fungistatic' rather than 'fungicidal' - it stops growth rather than killing the fungus outright. This is also why it's so important to take the medicine with fatty food, as the fat helps the medicine get absorbed into the body where it can do its protective work.
protein - inhibitor
Prevents microtubule assembly essential for fungal mitosis
Pediatric Note: No effect on human tubulin at therapeutic doses
cellular_structure - disruption
Arrests fungal cell division at metaphase
Pediatric Note: Explains fungistatic rather than fungicidal action
structural_protein - deposition
Concentrates drug where dermatophytes grow
Pediatric Note: Protects new hair and nail growth in children
Inhibition of fungal mitosis through microtubule disruption
Griseofulvin absorbed with dietary fat, enters bloodstream
Drug deposits in keratin precursor cells in skin, hair follicles, nail matrix
Active dermatophytes take up griseofulvin from infected keratin
Griseofulvin binds to fungal tubulin, preventing microtubule polymerization
Fungal cells cannot complete mitosis, growth stops
Infected keratin gradually replaced by protected new growth
Bioavailability
25-70% (highly variable, fat-dependent)
Time to Peak
4-8 hours post-dose
Food Effect
Not specified
Route
Oral only
Fat increases absorption from ~30% to ~90%
Ultramicrosize has 1.5x better bioavailability
Absorption variability major cause of treatment failure
Not specified
Pediatric: Children may metabolize faster than adults
Half-life
9-24 hours (average ~20 hours)
Primary Route
Fecal (>70%), renal (<30%)
Griseofulvin's keratin affinity means it concentrates exactly where dermatophytes grow, providing targeted therapy
The drug only works on actively dividing fungi, explaining why clinical cure lags behind mycological cure
Treatment duration is determined by tissue growth rates, not arbitrary timelines - track new growth
Rising resistance in T. tonsurans may explain increasing treatment failures in tinea capitis