The parasitic nematode Haemonchus contortus lacks molybdenum cofactor synthesis, leading to sulphite sensitivity and lethality in vitro.
Sulphite oxidase has an essential role in detoxifying environmental and endogenously generated sulphite into sulphate and requires the molybdenum cofactor (Moco) to function. Until recently it was believed that the synthesis pathway for Moco was so important for survival that it was conserved in all multicellular animals. Here we report the use of comparative genomics to identify the absence of the first enzyme involved in Moco synthesis in Haemonchus contortus, a highly pathogenic and economically important helminth of livestock that, similar to many parasitic nematode species, has proved difficult to maintain in vitro. We show that Moco deficiency in Haemonchus leads to a high sensitivity to environmental sulphite and limits the ability to maintain the early parasitic larval stages in vitro. Analogous losses in Moco synthesis in other recently sequenced nematode species are also identified. These findings may lead to improved culture methods for parasitic nematodes and to novel approaches for their control.