Mechanism of Antimicrobial Action of Albendazole
Albendazole exerts its antiparasitic effect by binding to β-tubulin in parasites, inhibiting microtubule polymerization, which disrupts glucose uptake and ultimately causes parasite death through ATP depletion. 1
Molecular Mechanism
Albendazole binds specifically to the colchicine-sensitive site of β-tubulin, preventing polymerization into microtubules. 1
The resulting decrease in microtubules within intestinal cells of parasites impairs their absorptive function, particularly blocking glucose uptake by both adult and larval forms. 1
This glucose deprivation depletes glycogen stores and prevents adequate ATP production, leading to parasite death. 1
The drug exhibits ovicidal, larvicidal, and vermicidal effects through this mechanism. 2
Spectrum of Activity
Albendazole demonstrates broad-spectrum antiparasitic activity against multiple organism types:
Nematodes (Roundworms)
Highly effective against intestinal nematodes including Ascaris, hookworm, Trichuris, Strongyloides, and Enterobius. 3, 2
Also active against tissue nematodes causing visceral larva migrans, trichinellosis, and various other tissue infections. 3, 2
Cestodes (Tapeworms)
Active against larval forms of Echinococcus granulosus (hydatid disease) and Taenia solium (neurocysticercosis). 1
Effective for both intestinal tapeworm infections and tissue cestode infections like cysticercosis and echinococcosis. 2
Other Parasites
Used for filarial infections (lymphatic filariasis, onchocerciasis) alone or combined with other agents. 2
Has been utilized for certain trematode and protozoan infections including giardiasis and microsporidiosis, though these are less established indications. 2
Resistance Mechanism
Parasitic resistance develops through amino acid changes in β-tubulin protein, reducing drug binding affinity. 1
Emerging resistance has been documented in hookworms, Trichuris trichiura, possibly Ascaris lumbricoides, Wuchereria bancrofti, and Giardia species. 2
Pharmacological Considerations
Albendazole is rapidly converted in the liver to albendazole sulfoxide, the primary active metabolite responsible for antiparasitic effects. 1
Oral bioavailability increases up to 5-fold when administered with fatty meals (approximately 40 grams fat content), significantly enhancing therapeutic efficacy. 1
The drug achieves widespread tissue distribution, including CSF penetration, making it effective for tissue parasites like neurocysticercosis. 3