Dendromonocotyle species (Monogenea: Monocotylidae) are the only monocotylids to parasitize the skin of chondrichthyan hosts. Currently 11 species are recorded from the skin of ray species in the Dasyatidae, Myliobatidae and Urolophidae. There have been increasing reports of Dendromonocotyle outbreaks on rays kept in public aquaria. This paper provides a broad review of Dendromonocotyle that should assist taxonomists and aquarists with species identification and help decisions on potential control methods for Dendromonocotyle infections. The taxonomy and host-specificity of Dendromonocotyle are discussed and a key to current species is provided. We summarise what little is known about the biology of Dendromonocotyle including egg embryonation and hatching, feeding, camouflage and reproduction. The efficacy of freshwater baths, chemical treatments and biological control measures such as the use of cleaner fish for Dendromonocotyle is also discussed. We demonstrate that effective control of Dendromonocotyle on captive rays is hampered by the lack of basic biological data on the life cycle of the parasites. A case history is provided outlining the success of a public aquarium (Underwater World, Mooloolaba, Queensland, Australia) in managing D. pipinna infections on captive Taeniura meyeni without chemical intervention simply by taking measures to reduce host stress.

Most Monogenea are recorded from the skin, fins and gills of teleost fish and only about 200 valid monogenean species in seven families (Acanthocotylidae, Amphibdellidae, Capsalidae, Hexabothriidae, Loimoidae, Microbothriidae, Monocotylidae) are known from various sites on chondrichthyans (Whittington and Chisholm 2003). In our experience, the infection intensity of monogeneans on wild sharks and rays is generally low. However, when elasmobranchs are kept in captivity, monogenean intensities can increase significantly due to their direct life cycle. In extreme cases, monogeneans can cause lesions at their attachment site which may result in the death of the elasmobranch either indirectly (via secondary infections) or directly (eg Poynton et al. 1997, Bullard et al. 2001).