Read the passage below. Use the information in the passage and your own knowledge to answer the questions that follow.
At the beginning of the 21st century, the rapid emergence of the multidrug-resistant yeast Candida auris has posed a severe global health threat. This eukaryotic pathogen causes invasive infections in hospitalised patients, particularly targeting immunocompromised individuals. Standard treatments rely on classes of antifungals called echinocandins, which target the synthesis of glucan in the fungal cell wall.
Echinocandin therapy is highly selective because human cells lack cell walls, leaving the patient's cells unharmed. However, Candida auris strains can develop resistance. One mechanism of resistance involves a mutation in the FKS1 gene, which alters the glucan synthase enzyme so the antifungal can no longer bind. Another mechanism is the upregulation of efflux pumps, which actively pump the antifungal drug out of the cell.
When echinocandins successfully bind to susceptible fungi, they inhibit cell wall synthesis, causing the cell wall to become structurally weak. Eventually, the osmotic pressure within the fungal cell causes it to swell and lyse (burst), destroying the pathogen and allowing the host's immune cells to clear the cellular debris.
State what is meant by the term pathogen.
Name the kingdom of organisms to which Candida auris belongs.
Suggest why antifungal drugs administered to patients must be purified to remove bacterial toxins and contaminants.
Based on the passage, why are echinocandins chosen over non-selective drugs to treat these infections?
Suggest the name of a digestive enzyme that breaks down the structural carbohydrate chitin found in fungal cell walls.
Describe how the body's white blood cells, specifically phagocytes, destroy fungal pathogens.
Use your knowledge of natural selection to explain how a population of Candida auris can become resistant to echinocandins.
