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.

References for this article may be found here

Introduction
Marine ectoparasites are a source of considerable losses both within the food and ornamental fish markets. Once established within a system, infections may become chronic, with periodic blooms of disease sweeping the system. Costly and wasteful for fish farmers, these infections can be heartbreaking for marine aquarium owners as they watch their pets succumb to these virulent pathogens. This series of articles will cover the general infection cycle of some parasites with an emphasis on the dinoflagellate Amyloodinium ocellatum, the cause of marine velvet disease. Pathogenesis, immunology, and current treatments will be covered, as will considerations for fish farms and options available to develop vaccination strategies to prevent these diseases.
As the world’s population continues to grow, so does the demand for fish, both as a food, as well as for entertainment as inhabitants of aquariums. Increasingly polluted and overharvested, natural waters will be hard pressed to meet demand. In response, emphasis on intensive aquaculture has been growing rapidly. Intensive aquaculture allows for the maximal production of aquatic organisms per unit of rearing volume by closely controlling the physical and biological parameters of the system. But, with increased density comes increased potential for rapid spread of disease within the system. A small stressor may decrease immunity in a fish such that it predisposes it to lethal infection by pathogens (13). Similarly, a minor failure in a contamination control system could spell disaster in a system running at the limits of its capacity. Traditional methods of controlling pathogens in such system have relied on chemotherapeutics and are becoming rapidly antiquated or impractical as antibiotics are being more tightly controlled and are often ineffective with the emergence of resistant strains. Other old-standby treatments such as formalin and copper sulfate, while effective, are being disallowed in the culture of food fishes due to potential adverse effects on human health. As such, newer methods are necessary. Vaccination against disease would be an ideal strategy, relying on the fishes’ own immune system to maintain health and productivity while decreasing reliance on chemotherapeutics and complex contamination control systems.
Of key importance in maintaining fish health is control of ectoparasitic pathogens. While viral and bacterial pathogens are at the forefront of human medical research, in aquaculture, they are often considered secondary diseases. Instead, it is the ectoparasites that are of primary concern. No current marine pathogens cause the massive morbidity and mortality associated with these diseases (3). Infections can spread rapidly throughout a facility, often causing massive loss of livestock within 24 hours of an outbreak occurring. Among the most virulent of these is the dinoflagellate Amyloodinium ocellatum, a highly infective parasite that when in the trophont stage attaches to the gills, fins and body of infected fishes (3). Effective treatments exist for this parasite, but the outcome is often poor due to the massive damage that can occur in the fish before signs of the disease are visible. A vaccine to prevent disease from occurring, or to limit the virulence of the organism would be highly desirable.