Final answer:
The patient developed a hemolytic anemia due to a mutation in the Hexose monophosphate shunt pathway. This mutation provides protection against malaria in individuals living in countries where the disease is endemic.
Step-by-step explanation:
The patient rapidly developed a hemolytic anemia due to a mostly silent mutation in the Hexose monophosphate shunt pathway.
The Hexose monophosphate shunt pathway, also known as the pentose phosphate pathway, plays a critical role in protecting red blood cells from oxidative damage. A mutation in the glucose 6-phosphate dehydrogenase (G6PD) gene, which is involved in this pathway, can lead to hemolytic anemia when exposed to certain medications, including primaquine.
Individuals with this mutation are less prone to malaria infection, which historically was a widespread deadly disease among humans. This provides a selective advantage to individuals with the mutation when living in countries where malaria is endemic.