46 March 2009 by slightly different genetic mechanisms, and some animals have less variable antibodies than humans. But, in essence, the antibody-based immune system is very similar among all vertebrates. The same is not true of invertebrates, including key aquaculture species, such as, shrimp, oysters and mussels. Antibodies have never been identified in these animals (Flajnik and Du Pasquier 2004, Litman et al. 2005). Most importantly, antibody-like genes cannot be found in the complete genome sequences that are now available for a variety of invertebrates. All of the DNA in sea urchins, sea squirts, worms, flies and bees have now been decoded and thorough gene databases have been constructed. Other comprehensive, albeit incomplete, gene databases are available for a many other invertebrates, including oysters and shrimp. Antibodies have not been found in any of these genetic resources. So, it seems clear that invertebrates do not have antibodies, or even genes that are similar enough to antibodies to operate in the same way (Flajnik and Du Pasquier 2004). But this doesn’t mean that invertebrates are defenseless. In every animal, no matter how simple, there must be mechanisms to fight infection or they would not survive. Infection is inevitable because all animals provide a nutrient rich, stable environment that can promote the growth of infectious microorganisms and parasites. Therefore, it is essential to have immune systems that fight infection. The universality of disease is borne out in many invertebrate aquaculture industries where disease outbreaks represent the greatest challenges to sustained production. To combat the threat of infection, invertebrates have many of the same mechanisms that are used by vertebrates to kill infectious agents. Each individual has a variety of these so-called effector systems to cope with highly diverse types of pathogens that need to be killed in different ways. Despite the diversity of effector systems Fig. 1. High magnification image of a Sydney rock oyster blood cell that has engulfed a protozoan parasite. Fig. 2. The defensive enzyme, phenoloxidase, inside an oyster blood cell. Fig. 3. Oyster blood cells forming a capsule around a fungal hypha. that have evolved in most animals, there are a surprising number of common processes. Many of these processes are undertaken by specialized blood cells (more strictly called hemocytes or coelomocyte in invertebrates). Perhaps the most common cellular defense system is phagocytosis - the ability of defensive blood cells to engulf microorganisms, such as bacteria and fungi. A high magnification, ultraviolet image of a Sydney rock oyster blood cell (hemocyte) that has engulfed by phagocytosis one of the protozoan parasites that causes fatal QX disease (Marteilia sydneyi) is shown in Figure 1. Once pathogens have been engulfed by phagocytosis they can be killed by specialized processes within the cell. The smaller bright dots inside the oyster blood cell shown in Figure 1 are membrane bound granules packed full of defensive molecules, including the enzyme phenoloxidase. The contents of these granules are used to kill parasites once they have been engulfed. In oysters phenoloxidase is one of the most important of these sub-cellular killing processes. Phenoloxidase produces the pigment, melanin - the same pigment responsible for the coloration of human skin. In many animals, particularly crustaceans and molluscs, pigmentation seems to be just one function of phenoloxidase. Its other, perhaps more important job, is to kill microorganisms and parasites. Many by-products of melanin production are toxic to bacteria, fungi and protozoan parasites, and melanin itself is directly involved in microbial killing. Our research group is particularly interested in phenoloxidase because of its role in preventing the infection of Sydney rock oysters by M. sydneyi, the causative agent of QX disease (Bezemer et al. 2006, Butt et al. 2006). QX is a crippling parasitic disease. Outbreaks can sweep through farms killing up to 95 percent of the oysters within a few months. The disease is so severe that production has been abandoned in a number of prime oyster farming areas on Australia’s east coast. Our work suggests that phagocytosis, followed by phenoloxidasemediated killing, is an effective defense that normally keeps M. sydneyi infections under control. Figure 2 shows another high magnification image of a rock oyster hemocyte that has engulfed an M. sydneyi parasite. In that
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