The final step in vitamin C synthesis is catalysed by L-gulonolactone oxidase. The gene encoding it is inactivated in guinea pigs, in haplorhine primates including humans, in most bats and in some passerine birds, in each case by separate mutations. The convergence is why guinea pigs became the standard scurvy model and why the vitamin was first isolated with their help.
A guinea pig on a deficient diet shows the same disease process as a scorbutic sailor: failure of collagen cross-linking, leading to swollen joints, poor wound healing, bleeding gums and lethargy, developing over a few weeks. Commercial pellets are vitamin-C fortified, but ascorbic acid degrades in storage and in water, so fresh vegetable sources remain the reliable route.
The name is doubly misleading. The animal is a caviid rodent from the Andes, not a pig, and it did not come from Guinea; the etymology is unsettled, with proposals ranging from the Guiana coast to a corruption of a trade route name. Its own species name, porcellus, means little pig, so the confusion is embedded in the taxonomy.