Which statement best describes how echinocandins cause fungal cell death and a typical clinical route of administration?

Echinocandins inhibit squalene epoxidase, causing accumulation of toxic squalene and inhibition of ergosterol formation; they are usually delivered by inhalation for pulmonary fungal infections.

Echinocandins bind ergosterol in the membrane creating pores and causing leakage of cytosolic contents; they are given topically as creams for mucocutaneous infections.

Echinocandins noncompetitively inhibit (1,3)-beta-D-glucan synthase, reducing beta-glucan synthesis, weakening the cell wall and leading to osmotic instability and lysis; they are typically administered intravenously for serious infections.

Echinocandins intercalate into fungal DNA and block replication, which indirectly reduces cell wall synthesis enzymes; they are available as oral tablets used primarily for outpatient superficial infections.