Control of marine ectoparasites including Amyloodinium ocellatum Part II
References for this article can be found here
Life Cycle and Mechanisms of Pathogenesis
While only distantly related, Amylodinium ocellatum shares a remarkably similar lifestyle and mechanism of pathogenesis with several important protozoan fish pathogens. Taken with care, it appears likely that a vaccination strategy developed for Amyloodinium could be modified to provide the basis for a vaccine in other species of parasites, and conversely, some general themes found in the responses of fish to challenge with these pathogens might be provide insight into effective strategies for Amyloodinium vaccine design. Among these are Cryptocaryon irritans (Saltwater Ich), Icthyopthirius multifilis (Freshwater Ich), and species in the genus Piscinoodinium (Freshwater Velvet)(16).
Infection with Amyloodinium occurs when infective dinospores contact a susceptible fish. In early stages of infection they show a preference for attacking the gill filaments. Upon attachment, they transform into the feeding stage, the trophont. Attached by rhizoids, a root-like structure used both for feeding and attachment, they continue to grow and mature until they reach a size of 80-100 micrometers, occasionally reaching 350 micrometers. At this point, they detach from their host, encyst, and enter the reproductive tomont stage. Within 3-5 days, the cyst hatches releasing up to 256 swarming dinospores, 12-15 micrometers in diameter, ready to begin the infection cycle anew (15). With such high fecundity, and short generation times, a minor infection quickly can become a disastrous epidemic in a closed system.
No specific toxin has been identified in the pathogenesis of Amyloodinium. Instead, it is believed that disease results due to massive damage caused by the invasion of rhizoids into various tissues, particularly the gills, and the associated effects of excreted protozoan digestive enzymes (12). This damage causes difficulty in maintaining proper gill function, resulting in impaired gas exchange and an inability to maintain osmotic balance. Visible signs of infestation include lethargy and faded colors, rapid respiration and lack of appetite, and in severe cases, a general “dusty” appearance as the body becomes covered in trophonts, and dermal tissue is liquefied and consumed. The fishes protective slime layer is also severely damaged, making the fish susceptible to secondary bacterial infections (16). By the time visible signs are evident, significant tissue damage has occurred and death, despite treatment, is likely, underscoring the need for prevention and/or vaccination.