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ECOLOGY: ON THE DECLINE OF THE BLUE CRAB

The following points are made by R.F. Lee and M.E. Frischer (American Scientist 2004 92:548):

1) The blue crab's participation in various appetizing recipes supports an important fishery along the Atlantic and Gulf coasts of the US, where tens of millions of crabs are harvested annually. In recent years, however, the commercial crab industry on the East Coast has suffered a significant decline. Blue crab landings along coastal Georgia, for example, dropped well below the 45-year average of 3.9 million kilograms to about 816,000 kilos in 2002. The effect of this dramatic crash has been catastrophic. Fishermen whose families have caught blue crabs for generations are going bankrupt, and the cost of crabs for consumers has soared.

2) The ecological and economic impacts have motivated several investigations into the cause of the decline. There are hints that weather-related changes may be responsible. There is also evidence that a parasitic disease in blue crabs has become both more prevalent and more severe. Our group has been studying these events along the coast of southeastern Georgia, a region that has been hit especially hard, to see whether the two phenomena might be related. These investigations contribute to understanding the conditions that led to the outbreak of disease in the blue crab population.

3) Blue crabs on the East Coast appear to be suffering from a parasitic infection of a dinoflagellate called Hematodinium perezi. This parasite was first reported in 1931 in crabs collected along the French coast. Hematodinium is related to two other toxic dinoflagellates: Gymnodinium brevis, which causes the red-tide algal blooms, and the fish-killing Phiesteria piscicida. In the past few decades, outbreaks of Hematodinium have reduced populations in a number of commercially important crab fisheries throughout the globe, including Alaska, Newfoundland, Scotland and France.

4) Hematodinium is a noxious pathogen that proliferates in the crab's blood, the hemolymph. As it grows inside the crab, the parasite consumes the hemolymph cells and the primary hemolymph protein, hemocyanin. This protein transports oxygen in crustaceans in much the same way that hemoglobin performs this task in vertebrates. Crabs suffering from a heavy infection of Hematodinium are lethargic and eventually die from suffocation for lack of oxygen.

5) The blue crab appears to be particularly susceptible to infection by this dinoflagellate. Part of the reason may be the defense mechanisms that blue crabs use to protect themselves against infections. Crustaceans lack the specialized immune system of vertebrates and instead depend on non-specific blood cells called hemocytes. These cells encapsulate parasites in nodules, which are then processed for elimination. This mechanism seems to be most effective in cold conditions when parasites such as Hematodinium are less metabolically active, and, indeed, winter crabs are generally free of the dinoflagellate. However, during a heavy infection, the hemocytes are overwhelmed by the prolific reproduction of the parasite, and the crab succumbs to the disease. The apparent inadequacy of the blue crab's defense mechanism is not the complete story, however. Other crabs, including the closely related lesser blue crab (Callinectes similis), do not appear to be susceptible to Hematodinium infection at all. So there must be something unique about the interaction between Hematodinium and the blue crab.[1-5]

References (abridged):

1. Field, R. H., C. J. Chapman, A. C. Taylor, D. M. Neil and K. Vickerman. 1992. Infection of the Norway lobster Nephropos norvegicus on the west coast of Scotland. Diseases of Aquatic Organisms 13:1-15

2. Gruebl, T., M. E. Frischer, M. Sheppard, M. Neumann, A. N. Maurer and R. F. Lee. 2002. Development of an 18S rRNA gene-targeted PCR-based diagnostic for the blue crab parasite Hematodinium sp. Diseases of Aquatic Organisms 49:61-70

3. Harvell, C. D., et al. 1999. Emerging marine diseases--climate links and anthropogenic factors. Science 285:1505-1510

4. Johansson, M. S., and K. Soderhall. 1989. Crustacean immunity in crustaceans and the proPO system. Parasitology Today 5:171-176

5. Le Moullac, G., and P. Haffner. 2000. Environmental factors affecting immune responses in Crustacea. Aquaculture 191:121-131

American Scientist http://www.americanscientist.org

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ON THE EVOLUTION OF DINOFLAGELLATES

The following points are made by C.W. Morden and A.R. Sherwood (Proc. Nat. Acad. Sci. 2002 99: 11558):

1) It is well established that chloroplasts in green and red algae are derived from a primary endosymbiotic event between a cyanobacterium and a eukaryotic organism 1 billion years ago (1,2). Although these two groups account for many of the world's photosynthetic species, most other major taxonomic groups of photosynthetic organisms (stramenopiles -- including diatoms, phaeophytes, chrysophytesand haptophytes) have plastids derived from a photosynthetic eukaryote implying a secondary endosymbiosis (1,2). Still other groups, such as the dinoflagellates, have more complicated associations believed to be derived from tertiary endosymbioses involving the engulfment of a secondary endosymbiont. Each endosymbiotic event has characteristic structural changes associated with it, the most notable of which is the addition of two membranes surrounding the plastid (the inner representing the cell membrane of the engulfed organism and the outer representing the phagocytosis vacuole membrane) (2). Dinoflagellates, although believed to be tertiary endosymbionts, have only 3 membranes surrounding their plastids (1,2), suggesting that the acquisition of too many membranes may be functionally unstable and can cause some to be lost.

2) Dinoflagellates are fascinating organisms that have intrigued researchers for many years. They are most well known for toxic blooms associated with red tides and symbiotic relationships with corals (zooxanthellae) (2). They contain an astounding array of unique features that has been the impetus for continued evolutionary studies. One is their close phylogenetic link with apicomplexans, organisms that are best known for causing some of our most deadly infectious diseases (3,4). Another is the diverse array of light harvesting pigments within the group. Peridinin is a xanthophyll found exclusively in dinoflagellates and, together with chl-a (ubiquitous among photosynthetic organisms), makes up the light harvesting complex found in most species. Dinoflagellates with other combinations of plastid pigments are also known, including chl-b (also in green algae), fucoxanthin, chl-c1 and -c2 (also in stramenopiles and haptophytes) and chl-c1 and phycobilins (also in cryptophytes), and are believed to be the products of further endosymbioses with species from those groups (5). Yoon et al (Proc. Nat. Acad. Sci. 2002 99:11724) provide new evidence that implicates dinoflagellate plastids containing fucoxanthin and chl-c1 and -c2 (derived from a haptophyte ancestor) as being ancestral to those with peridinin. This new paradigm in the relationship of these species forces us to rethink many aspects of dinoflagellate evolution.

3) In many respects, the findings by Yoon et al (2002) allow a more parsimonious view of dinoflagellate evolution. Previously long-held theories suggested that primitive dinoflagellates were heterotrophic and the addition of a peridinin-containing plastid occurred relatively recently, which was borne out by the fact that approximately 50% of dinoflagellate species are heterotrophic (1) and that many photosynthetic dinoflagellates have retained heterotrophic behavior. However, recent studies have demonstrated that photosynthetic dinoflagellates are clearly ancestral, and that heterotrophy has been independently derived numerous times within the group. Fucoxanthin and chl-c1 and -c2 are the predominant form of light harvesting pigments among stramenopiles and haptophytes. With the finding that haptophytes are the sister group to dinoflagellates in phylogenetic analyses and that dinoflagellates with fucoxanthin and chl-c1 and -c2 are apparently ancestral to the peridinin-containing species, there is no need to hypothesize an independent origin of these pigments nor a later endosymbiosis of a haptophyte in dinoflagellates.

References (abridged):

1. Van Den Hoek, C. , Mann, D. G. & Jahns, H. M. (1995) Algae: An Introduction of Phycology (Cambridge Univ. Press, Cambridge, U.K.).

2. Graham, L. E. & Wilcox, L. W. (2000) Algae (Prentice-Hall, Englewood Cliffs, NJ).

3. McFadden, G. I. , Reith, M. E. , Munholland, J. & Lang-Unnasch, N. (1996) Nature (London) 381, 482.

4. Fast, N. M. , Kinninger, J. C. , Roos, D. S. & Keeling, P. J. (2001) Mol. Biol. Evol. 18, 418-426.

5. Wilcox, L. W. & Wedemeyer, G. J. (1984) J. Phycol. 20, 236-242.

Proc. Nat. Acad. Sci. http://www.pnas.org

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ECOLOGY: ON EMERGING DISEASES IN WILDLIFE

The following points are made by Adam G. Jones (Current Biology 2004 14:R842):

1) Emerging diseases seemed to enter the nightmares of mainstream culture with the ebola and hantavirus scares of the 1990s. Since then, emerging diseases have become a major health concern in human populations, with such diseases as severe acute respiratory syndrome (SARS), avian influenza, and West Nile virus disease sickening and frightening people around the globe.

2) Most people do not realize that emerging diseases are also a problem for wildlife and may be a major threat to endangered species [1]. In the last decade, there has been an increase in the number of cases of a wide spectrum of diseases in populations of diverse species of plants and animals [1,2]. Emerging diseases in wildlife are important for the obvious reason that they can cause population declines in the susceptible species. But these diseases in wildlife are important from a human health standpoint too, because many of the emerging diseases in humans have been linked to wildlife species that serve as reservoirs of the pathogen. Furthermore, the study of emerging diseases in wildlife may well provide general insights that help us to understand the dynamics of emerging diseases in human populations.

3) Herbst et al.[3] investigated the cause of the recent outbreak of marine turtle fibropapillomatosis by examining the evolution of the virus that causes the disease. This disease affects mainly the green sea turtle, but cases have also been documented in loggerhead, olive ridley, and now Kemp's ridley sea turtles. The fibrous growths typical of fibropapillomatosis were first described in 1938 and reports of the disease were relatively rare until after 1980 [4]. Now, fibropapillomatosis occurs around the globe and in one recent sample from the Hawaiian Islands more than 90% of green turtles showed symptoms of the illness [4].

4) From the standpoint of a wildlife enthusiast, fibropapillomatosis is a heinous disease, marring the usually noble appearance of the beloved sea turtles. The growths associated with the disease occur mainly on the soft skin of the turtle, but they can appear internally as well. The growths can be so large that they interfere with normal mobility, vision, feeding and organ function. In addition to these gross mechanical effects, the disease appears to result in suppression of the immune system and a susceptibility to bacteremia [5]. Consequently, death is the ultimate outcome for many of the turtles affected by the disease.

5) All the current evidence suggests that marine turtle fibropapillomatosis is caused by a herpesvirus that has been shown to be associated with the growths (although definitive experiments involving cultured virus particles have not yet been possible). But why does the virus causes so much harm now compared to 50 years ago? Two non-exclusive hypotheses can explain the sudden increase in frequency of fibropapillomatosis (and most other emerging diseases in wildlife for that matter). One possibility is that a change in the environment caused the host species to become extremely susceptible to a previously harmless strain of virus, for example, as a consequence of immune suppression, a new vector and so on. The other possibility is that the disease is caused by a virulent mutant form of a previously harmless virus.

References (abridged):

1. Daszak, P., Cunningham, A.A. and Hyatt, A.D. (2001). Anthropogenic environmental change and the emergence of infectious diseases in wildlife. Acta Tropica 78, 103-116

2. Harvell, C.D., Kim, K., Burkholder, J.M., Colwell, R.R., Epstein, P.R., Grimes, D.J., Hofmann, E.E., Lipp, E.K., Osterhaus, A.D.M.E. and Overstreet, R.M. et al. (1999). Emerging marine diseases - Climate links and anthropogenic factors. Science 285, 1505-1510

3. Herbst, L., Ene, A., Su, M., DeSalle, R. and Lenz, J. (2004). Worldwide outbreaks of a transmissible, life-threatening tumor in endangered marine turtles are not due to recent herpesvirus mutations. Curr. Biol. 14, R697-R699

4. Herbst, L. (1994). Fibropapillomatosis of marine turtles. Annu. Rev. Fish Dis. 4, 389-425

5. Work, T.M., Balazs, G.H., Wolcott, M. and Morris, R. (2003). Bacteraemia in free-ranging Hawaiian green turtles Chelonia mydas with fibropapillomatosis. Dis. Aquat. Org. 53, 41-46

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