Some Parasitic Diseases of Blue Crab

Some Parasitic Diseases Of the Blue Crab

This is in need of some updating and will soon be supplanted with a more rigorous and thorough review. (Shields, J.D. 1997. The potential effects of outbreaks of parasitic diseases on the blue crab fishery of Virginia. 2^nd Virginia Eastern Shore Natural Resources Symposium, The Eastern Shore Institute, Exmore, VA. TESI Publication #4: 23-29.)


Hematodinium in Hemolymph		Vermiform plasmodium of Hematodinium perezi. This stage is diagnostic. The plasmodia are also motile. The cells in the background are hemocytes.		Schizogony of plasmodium. The plasmodia divide via budding to produce more plasmodia, and via schizogony to produce trophonts. The mass of cells in the center of the field represents the schizont.

Introduction and Summary of Disease Agents

Some Parasitic Diseases Of the Blue Crab

Several disease agents have occurred in outbreaks or epizootics in blue crabs from Maryland and Virginia (Table 1). In general, the outbreaks are localized to specific bays or regions, but widespread epizootics are known to occur, especially along the seaside locations of the Eastern Shore. In most cases the causative agents were virtually unknown until the occurrence of the epizootics (e.g., Sprague & Beckett, 1966, Johnson, 1976; Couch, 1983). In fact, we know little about the conditions that lead to the epizootics.

While eight viruses have been reported from blue crabs (Johnson, 1983), four are known pathogens documented in epizootics from Chesapeake Bay or Chincoteague Bay. The pathogenic viruses typically live in hemocytes, or epithelial cells, and are associated with significant mortalities during outbreaks. Infected crabs are lethargic, susceptible to stress-induced mortality (e.g., capture, and handling), and often show signs of tremors or paralysis, or even blindness (CBV) (Table 1). Transmission experiments with the viral agents were undertaken via injection of virus-laden tissues. The reolike virus (RLV) may have an extremely short, and acute patent period; infection experiments resulted in mortalities in just 3 days (Johnson & Bodammer, 1975)! The other pathogenic viruses had patent periods ranging from 2 weeks to 2 months. Transmission in nature has not been examined, but the short duration of infection for RLV indicates that it could represent a significant problem to the soft-shell crab industry during epizootics.

Vibrio bacteria are ubiquitous in the marine environment, and several invertebrates are infected by or passively transport the disease agents. Vibrio parahemolyticus has been documented in outbreaks in shedding facilities for soft-shell crab where it can be a significant source of mortality. The bacterial pathogen invades the hemolymph through abrasions in the cuticle of the crab, and multiplies in the nutrient-rich environment of the crab’s blood. Few studies have addressed transmission, or prevalence of the Vibrio bacteria in blue crabs, yet the disease may have an effect on the lucrative soft-shell industry.

Two egg parasites can be found in the high salinity waters of the region. The fungus Lagenidium callinectes can assimilate large numbers of crab eggs in infected clutches. In some cases, most of the egg clutch can be destroyed by the fungus. It is widespread and can tolerate moderately low salinities (Rogers-Talbert, 1948). The nemertean worm Carcinonemertes carcinophila can ingest relatively large numbers of eggs during development. On other crab species, epizootics of nemertean worms have virtually wiped out an entire year’s broodstock (Shields et al., 1991; Kuris et al., 1991), and can impact significantly on a fishery. For the blue crab, the freshwater influence of the estuarine environment may limit the spread of the worm and curtail potential outbreaks in the region (as for C. mitsukurii, Shields & Wood, 1993). In addition, while both egg predators can occur in relatively high prevalences in the region, their overall effect may be limited by the high fecundity of their host.

Two parasites can affect the general quality of the meat of the blue crab. The microsporan Ameson michaelis causes severe muscle lysis that results in a condition known as "cotton crab." Crab meat infected with the microsporan is cottony in texture, and poorly flavored. The parasite can be transmitted via cannibalism; and since as much as 25% of a blue crab’s diet is other blue crabs, it is surprising that the parasite is only found at low prevalences (<1%, Shields, pers. obs.). Pepper spot disease is the other condition that affects the quality of crab meat. It is an unusual condition brought about by a hyperparasitic protozoan, Urosporidium crescens, that infects the trematode Microphallus bassodactylus. Pepper spot occurs when the trematode cysts are attacked by the protozoan; the cysts become blackened or melanized. Crabs are not affected by the disease but it can affect the aesthetics of the meat. Pepper spot is common on the Eastern Shore (>30% of crabs from some locations). It appears be related to high salinities.

Two highly pathogenic protozoans are known to cause signficiant mortalities to blue crabs. Gray crab disease is caused by an amoeba, Paramoeba perniciosa, that invades the connective tissues, and hemolymph of crabs. As the common name implies, the ventral surfaces of infected crabs turn gray in color. As in other systemic infections, the hemocytes of heavily infected crabs are virtually replaced by the trophic stage of the parasite. Crabs become lethargic and eventually die, or die from stress-related handling. The disease and related crab mortalities appear centered around the small coastal bays of the mid Atlantic states. In spring, mortalities in shedding facilities have been related to this disease (Newman & Ward, 1973; Couch, 1983). Winter mortalities of crabs have also been associated with high prevalences of the amoeba. Transmission of the disease remains unknown but we can speculate that lethargic crabs would fall easy prey to their voracious brethren, and thus, effect transmission. Alternatively, the amoeba could invade crabs in the winter while their hosts are buried in the bottom, especially if infected hosts are dying at this time.

Hematodinium perezi is an unusual parasitic dinoflagellate that also occurs in outbreaks. It lives in the hemolymph of crabs and rapidly proliferates (Shields & Squyars, 2000). Outbreaks of H. perezi have been reported from the high salinity waters of the lower Chesapeake Bay, coastal bays in Maryland and Virginia, Georgia, and Florida (Newman and Johnson, 1975; Couch, 1983; Messick, 1994). During epizootics, crab mortality can reach 50% in set pots, and 75% in shedding facilities on the Eastern Shore. One outbreak showed a prevalence of 100% in juvenile crabs and up to 70% in mature crabs (Messick, 1994). Infections are generally terminal with crabs dying metabolic exhaustion and stress-related handling (Shields et al., in review). Evidence indicates that temperature and salinity play a key role in the epizootics of the dinoflagellate (Messick & Shields, in prep.). The disease is most prevalent in the fall (Messick, 1994; Messick & Shields, in prep.).

Hematodinium perezi or related species has been identified from a wide range of host species from many geographic regions. On the eastern seaboard of the USA, the parasite infects the American blue crab, the rock crabs, Cancer irroratus, C. borealis, and the lady crab, Ovalipes ocellatus (Maclean & Ruddell, 1978). Related parasites have also been reported from amphipods (Johnson, 1986). Other species of Hematodinium have caused considerable losses to several other important crab fisheries, i.e, Tanner crab, the Norway lobster, and the European rock crab (Meyers et al., 1987; Latrouite et al., 1988; Field et al., 1992; and others).

Epizootiology

Recent outbreaks of egg predatory nemerteans, rhizocephalan castrators, and dinoflagellates on crabs and lobsters have seriously affected or even devastated host populations in California, British Columbia, Alaska and Scotland. The causative agents were virtually unknown until the occurrence of the epizootics (e.g., Shields et al., 1989; Meyers et al. 1987). In Alaskan waters, environmental factors such as hydrographic conditions and seasonal increases in water temperature (i.e., fjords with shallow sills) appear to have contributed to the epizootics (Sloan, 1984; Sloan, 1985; Kuris et al., 1991), and models suggest that closed populations of hosts may be more seriously affected by parasites than open populations (Kuris & Lafferty, 1992). Circumstantial evidence points to the apparent reduction in water mixing/flushing in the isolated fjords as the primary factor affecting host recruitment and prevalence of diseases (Sloan, 1984; 1985; Kuris et al., 1991).

The Delmarva Peninsula with its shallow lagoons and backwaters may be an ideal region for the growth and spread of parasitic diseases in the blue crab. I have speculated that the region possesses a triad of conditions that are required for an epizootics of pathogenic diseases (Shields, 1994). The conditions are (1) relatively closed crab populations (i.e., those with little immigration and emigration of juveniles and adults), (2) relatively high salinities with, in some cases, little water exchange between the open ocean and backwaters (i.e., narrow channels with shallow sills and barrier islands/bars), and (3) stressful conditions for the crab populations (heat and salinity stress, seasonal hypoxia, seasonal fishing and predation pressure). Many of the pathogenic agents appear limited to salinities above 15 o/oo and thus may only be of significance to the crab fisheries located in the small coastal bays of the mid Atlantic.

The role of water temperature, salinity, and other environmental factors in the onset and cycle of crab diseases remains largely unstudied. Several marine parasites and symbionts of portunid crabs are limited by low salinities (e.g., Octolasmis mulleri - Walker, 1974; Loxothylacus texanus - Ragan & Matherne, 1974; Choniosphaera indica and Carcinonemertes mitsukurii - Shields & Wood, 1993) and low temperatures (e.g., Carcinonemertes mitsukurii on P. pelagicus - Shields & Wood, 1993). In addition, host factors like molt stage, size (age), and maturity status contribute significantly to the infestation dynamics of several parasites and symbionts in other portunid crabs (Shields, 1992; Shields, in prep.).

Transmission experiments with many of the disease agents have been partially successful. Most studies rely on artificial methods of infection like injection, or cannibalism, but water-borne transmission via contact and direct invasion of the host are probably the major avenues for many of the disease agents. Cannibalism may be a major route of transmission since crabs are known cannibals; the vegetative stages of the diseases can frequently survive in seawater, or dead flesh for several days; and infected crabs often suffer lethargy and are therefore more susceptible to predation.

In conclusion, epizootics of various pathogens can occur in blue crabs with some regularity. They are frequently associated with high salinity waters, and, in some cases, with water temperature. The hydrography of the Delmarva Peninsula, and other coastal regions of the mid Atlantic may facilitate the spread of the epizootics by retaining infected crabs, and by focusing the infectious agents in the dense populations of hosts.

Table 1. Selected pathogenic agents of the blue crab, Callinectes sapidus, primary source, tissues in which the diseases occur, and the status of the agent in causing epizootics in crabs.

Disease agent	Location	Initial reference	Major tissue	Outbreaks	Relation to Mortality
1. Viruses
Reolike virus, RLV	Chincoteague Bay, VA, Chesapeake Bay, MD	Johnson & Bodammer, 1975	hemopoetic tissue, nerve cells, hemocytes, epithelial cells	Yes	Injection caused mortality in 3 days!
Rhabdolike virus A, RhVA	Atlantic, Gulf of Mexico	Jahromi, 1977	nerve cells, endothelial cells, hemocytes, connective tissues	Unknown	Found with RLV, unknown, stress-related mortality
Picornalike virus, Chesapeake Bay Virus, CBV	Tangier Sound	Johnson, 1983	Nerve cells, epithelial cells including gills	Yes	2 weeks - 2 months
Herpeslike virus, HLV	Chincoteague Bay, VA; Assawoman Bay, DE	Johnson, 1976	Hemocytes	Yes	High prevalence, 1-2 months till mortality
2. Bacteria
Vibrio parahemolyticus	Chesapeake Bay	Krantz et al., 1969	Hemolymph	Yes	High mortality in short term shedding facilities
Other bacteria	Chesapeake Bay	Colwell et al., 1975	Hemolymph	Unknown	High prevalence
3. Fungi
Lagenidium callinectes	Atlantic	Couch, 1942; Rogers-Talbert, 1948	Eggs, larvae	Yes	High prevalence, 25-50% of the sponge
4. Protozoa
Ameson michaelis	Atlantic, Gulf of Mexico	Sprague, 1970	Muscle tissue	No	Highly pathogenic, not assoc. with outbreaks
Paramoeba perniciosa	Mid Atlantic states	Sprague et al., 1969	Connective tissues, hemolymph	Yes	High prevalence, late spring, and winter, 30 days after injection
Hematodinium perezi	Atlantic, NE Gulf of Mexico	Newman & Johnson, 1975	Hemolymph	Yes	High prevalence, juveniles up to 100%
5. Helminths (worms)
Microphallus and pepper-spot disease	Atlantic, Gulf of Mexico	Overstreet, 1978; Couch, 1974	Connective tissues	Yes	No mortality
Carcinonemertes carcinophila	Atlantic, Gulf of Mexico	Humes, 1942	Eggs	Yes	High prevalence, 5-25% of the sponge

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