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Hematodinium Sp crustacean Protozoa Hematodinium sp. - Bitter Crab Disease of Tanner Crabs I. Causative Agent and Disease IV. Transmission Bitter crab disease is caused by a Although the natural route of trans- parasitic dinoflagellate,Hematodinium mission has not been established, there sp. belonging to the protozoan phylum are likely to be several modes in which Alveolata, subphylum Dinoflagellida, the parasite is transmitted horizontally order Syndinida and family Syndiniceae. via: stages of the parasite in seawater A major feature of classification for di- that enter breaks in the cuticle during noflagellates is the biflagellated grooved mating and molting; cannibalism or dinospore stage. Obligate Hematodinium feeding on detritis containing resting parasites have been described from spores; sexual transmission via semi- several species of crustaceans, certain nal fluids of parasitized male crabs and fishes and cephalopods. In crustaceans possibly through a reservoir host such as the type species is H. perezi parasitizing bottom dwelling amphipods. The para- the European shore crab. All Hema- site and disease have been transmitted in todinium described from crustaceans the laboratory by injection of hemo- parasitize the hemolymph causing lymph containing vegetative trophonts systemic disease and mortality affecting and dinospore stages. Life history stages at least 26 species of crustacean hosts in include: trophonts which are single cells Europe, Australia and North America and have slow division; larger plasmo- including many commercially important dia with multiple nuclei; pre-spores crab species and 13 species of benthic with multiple nuclei and rapid division amphipods. followed by sporulation of biflagellated spores with a single nucleus. Spores II. Host Species are of two types, a large macrospore The bitter crab Hematodinium is and a small microspore, generally with reported from Tanner and snow crabs (C. only one spore type occurring per host. bairdi, C. opilio) in southeast Alaska, the Spores may possibly have a dissemina- Gulf of Alaska and the eastern and west- tory or resting stage function rather than ern Bering Sea; from deep water Tanner transmission. Laboratory studies suggest crabs (C. tanneri) in British Columbia, that the life cycle of the parasite occurs Canada and from snow crabs in Atlantic over a 15 to 18 month period. Infestation Canada. likely occurs from the trophont stage during the spring molting period from III. Clinical Signs mid-March to May. Crabs dying in the Parasitized crabs are lethargic and die summer and fall following sporulation when handled, have an exaggerated red were likely parasitized in the spring color of the carapace, flaccid chalky tex- of the previous year. After sporulation tured meat and white opaque hemolymph in the fall the prevalence of parasitism caused by the myriad numbers of dinofla- becomes almost undetectable (eclipse) gellates. The cooked meats of parasitized until the new infestations of the previous crabs have an astringent aspirin aftertaste spring build to detectable levels that can and are unmarketable, hence the “bitter be observed the following late winter and crab” name of the disease. early spring. 84 85 crustacean Protozoa V. Diagnosis lowed by a reduction or eclipse until late Diagnosis is based on typical clinical winter and early spring. Peak mortality signs with the occurrence of myriad occurs in August through September due numbers of dinoflagellate stages (usually to sporulation. Chronic mortality occurs non-motile trophonts) in wet mounts or in weakened hosts from secondary infec- stained smears of hemolymph. Trophonts tions by other pathogens. Options for are 15.4 X 20.7 µm, have an indistinct control of bitter crab disease in southeast nuclear profile and foamy cytoplasm Alaska include: harvest Tanner crabs with droplets exuding from the surface from October through November during pellicle in a stained hemolymph smear. the eclipse period of the disease when A key diagnostic feature visible in many crab meats may be less full but of accept- trophonts is the dinokaryon nuclear able quality (requires no culling of para- division producing condensed V-shaped sitized crabs); grossly parasitized crabs pairs of chromosomes. Nonmotile should be properly disposed of (landfill; plasmodia are similar in appearance but incinerated; ground and cooked or chlo- larger and multinucleated. Prespores are rinated) rather than released; discourage similar to plasmodia but each nucleus culling through education programs to has a distinct lobed nuclear outline. Mac- recognize the disease and follow proper rospores are oval 15.2 X 11.4 µm having disposal; provide an economic incentive slow motility and a beaked protrusion by developing alternative use products on one end. The nucleus is longer than for harvested parasitized crabs (surimi, it is wide with a distinct outline. The chitin products, etc.). microspore is elliptical and smaller at 12.0 X 4.4 µm and has rapid motility VII. Human Health Significance with a refractile body at the posterior There are no zoonotic human health end and 2 flagella more often visible on concerns regarding bitter crab disease in stained smears. The microspore develops Tanner crabs. However, parasitized crabs an obvious bent corkscrew shape within have an unpalatable flavor and undesir- 6 days after sporulation. Histologi- able meat texture. cal examination demonstrates parasite stages within hemal sinuses throughout the tissues of the crab host. PCR primers are available for certain Hematodinium sp. parasitizing commercial crab species. VI. Prognosis for Host Virtually 100% mortality occurs in Tanner crabs naturally parasitized by Hematodinium sp. when maintained in the laboratory. A similar mortality of parasitized crabs is assumed to occur in wild Tanner crab populations. Signifi- cantly higher prevalences of bitter crab disease occur in new shell crabs and crabs less than 60 mm carapace width. There is a seasonal prevalence/intensity peaking in July through October fol- 84 85 crustacean Protozoa Hematodinium sp. - Bitter Crab Disease of Tanner Crabs Exaggerated reddening of the crab carapace (bottom) typical of bitter crab disease White viscera with milky hemolymph (arrow) 86 87 crustacean Protozoa Vegetative stages in a hemolymph smear SEM showing droplet exuding from pel- with irregular nuclear profile and droplets licle of vegetative stage (arrow) exuding from pellicle Twisted microspores with flagella visible in SEM showing the smooth surface of a phase contrast microscopy microspore and two flagella 86 87 crustacean Protozoa Hematodinium sp. - Bitter Crab Disease of Tanner Crabs Wet mount of beaked macrospores Beaked macrospore (SEM) showing warty surface and one of the two flagella Histological section showing vegetative Histological section showing typical stages (arrow) inside spermatophore dinokaryon nuclear division (arrow) 88 89 crustacean Protozoa Possible Hematodinium Life Cycle Possible Transmission By: Damaged cuticle during molt Insemination from parasitized male Cannibalism ' Trophont ---------- Slow Reproduction 15 - 18 months ' Vegetative Plasmodia Stages ' Pre-Spore ---------- Rapid Reproduction Sporulation 10 - 14 days ' Dinospore ---------- Crab Mortality 24 - 48 hours Microspore Tanner Crabs Macrospore Disseminatory resting Amphipods - reservoir hosts? stages transmitted to detritus feeders? 88 89.
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