Feeding Injury to the Orange Caused by the Citrus Rust Mite, Phyllocoptruta oleivora (Prostigmata: Eriophyoidea)1

Abstract

The citrus rust mite, Phyllocoptruta oleivora (Ashmead), appeared to probe randomly at the fruit surface, usually showing no preference for feeding sites. Probing was generally initiated by anchoring the idiosoma to the fruit surface with the anal sucker and arching the body. Searching time and insertion time were relatively short, averaging 11.3±7.4 s and 26.0±20.0 s, respectively. Feeding terminated with a jerking withdrawal of the mouthparts and an abrupt ascending of the rostrum. According to scan electron micrographs, the chelicerae were retained between the palpal segments, emerging at the base of a short truncate rostrum during feeding. A pair of protractile stylets were observed as attachments to the chelicerae. Length of the extended chelicerae (ca. 7 μm) restricted feeding to the epidermal cell layer. Active feeding by high populations (50–200 mites/cm2) of the mite during summer and fall on the surface of different varieties of orange caused a significant increase in ethylene (C2H4) emission at the time visible injury (russet) first appeared on fruit surfaces. Ethylene production by injured cells also stimulated premature degreening in the fall. Fruit surface discoloration (russet) was associated with the formation of lignin and probable oxidation of some substances of the cytoplasm within epidermal cells. In July and August, a wound periderm was formed 16–21 days after russeting first appeared on fruit surfaces. Concurrently, lipids accumulated in the wound periderm cell walls. Injury to fruit after growth termination did not lead to wound periderm formation in late November. Photomicrographs of fruit cuticles showed one or more mite punctures per epidermal cell in and around injured areas. Lignin formation and subsequent epidermal cell mortality appeared to be triggered by a high puncture frequency per cell, which is probably relative to mite population density.