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. 2nd Virginia Eastern Shore Natural Resources Symposium, The Eastern Shore Institute, Exmore, VA. TESI Publication #4: 23-29.)


Hematodinium in hemolymph

Schizogony of plasmodium.
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).


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


Initial reference

Major tissue


Relation to Mortality

1. Viruses


Reolike virus, RLV

Chincoteague Bay, VA, Chesapeake Bay, MD

Johnson & Bodammer, 1975

hemopoetic tissue, nerve cells, hemocytes, epithelial cells


Injection caused mortality in 3 days!

Rhabdolike virus A, RhVA

Atlantic, Gulf of Mexico

Jahromi, 1977

nerve cells, endothelial cells, hemocytes, connective tissues


Found with RLV, unknown, stress-related mortality

Picornalike virus, Chesapeake Bay Virus, CBV

Tangier Sound

Johnson, 1983

Nerve cells, epithelial cells including gills


2 weeks - 2 months

Herpeslike virus, HLV

Chincoteague Bay, VA; Assawoman Bay, DE

Johnson, 1976



High prevalence, 1-2 months till mortality

2. Bacteria


Vibrio parahemolyticus

Chesapeake Bay

Krantz et al., 1969



High mortality in short term shedding facilities

Other bacteria

Chesapeake Bay

Colwell et al., 1975



High prevalence

3. Fungi


Lagenidium callinectes


Couch, 1942; Rogers-Talbert, 1948

Eggs, larvae


High prevalence, 25-50% of the sponge

4. Protozoa


Ameson michaelis

Atlantic, Gulf of Mexico

Sprague, 1970

Muscle tissue


Highly pathogenic, not assoc. with outbreaks

Paramoeba perniciosa

Mid Atlantic states

Sprague et al., 1969

Connective tissues, hemolymph


High prevalence, late spring, and winter, 30 days after injection

Hematodinium perezi

Atlantic, NE Gulf of Mexico

Newman & Johnson, 1975



High prevalence, juveniles up to 100%

5. Helminths (worms)


Microphallus and pepper-spot disease

Atlantic, Gulf of Mexico

Overstreet, 1978; Couch, 1974

Connective tissues


No mortality

Carcinonemertes carcinophila

Atlantic, Gulf of Mexico

Humes, 1942



High prevalence, 5-25% of the sponge



Colwell, R.R., T.C. Wicks, & H.S. Tubiash. 1975. A comparative study of the bacterial flora of the hemolymph of Callinectes sapidus. Mar. Fish. Rev. 37 (5-6) 29-33.

Couch, J.N. 1942. A new fungus on crab eggs. J. Elisha Mitchell Sci. Soc. 58: 158-162.

Couch, J.A. 1974. Pathological effects of Urosporidium (Haplosporida) infection in microphallid metacercariae. J. Invertebr. Pathol. 23: 389-396.

Couch, J.A. 1983. Diseases caused by protozoa, pp 79-111. In: The Biology of the Crustacea, Vol. 6, Pathobiology, (Ed. A.J. Provenzano, Jr.) Academic Press, New York, NY.

Field, R.H., C.J. Chapman, A.C. Taylor, D.M. Neil, & K. Vickerman. 1992. Infection of the Norway lobster Nephrops norvegicus by a Hematodinium-like species of dinoflagellate on the west coast of Scotland. Dis. Aquat. Org. 13: 1-15.

Humes, A.G. 1942. The morphology, taxonomy, and bionomics of the nemertean genus Carcinonemertes. Ill. Biol. Monogr. 18: 1-105.

Jahromi, S.S. 1977. Occurrence of Rhabdovirus-like particles in the blue crab, Callinectes sapidus. J. Gen. Virol. 36: 485-494.

Johnson, P.T., & J.E. Bodammer, 1975. A disease of the blue crab, Callinectes sapidus, of possible viral etiology. J. Invertebr. Pathol. 26: 141-143.

Johnson, P.T. 1976. A herpeslike virus from the blue crab, Callinectes sapidus. J. Invertebr. Pathol. 27: 419-420.

Johnson, P.T. 1983 Diseases caused by viruses, rickettsia, bacteria and fungi, pp 2-78. In: The Biology of the Crustacea, Vol. 6, Pathobiology, (Ed. A.J. Provenzano, Jr.) Academic Press, New York, NY.

Johnson, P.T. 1986. Parasites of benthic amphipods: dinoflagellates (Duboscquodinida: Syndinidae). Fish. Bull. 84: 605-614.

Krantz, G.E., R.R. Colwell, & E. Lovelace. 1969. Vibrio parahemolyticus from the blue crab Callinectes sapidus in Chesapeake Bay. Science 164: 1286-1287.

Kuris, A.M., & K.D. Lafferty. 1992. Modelling crustacean fisheries: Affects of parasites on management strategies. Can. J. Fish. aquat. Sci. 49: 327-336.

Kuris, A.M., S.F. Blau, A.J. Paul, J.D. Shields, & D.E. Wickham. 1991. Infestation by brood symbionts and their impact on egg mortality in the red king crab, Paralithodes camtschatica, in Alaska: Geographic and temporal variation. Can. J. Fish. aqu. Sci. 48: 559-568.

Latrouite, D., Y. Morizur, P. Noël, D. Chagot, & G. Wilhelm. 1988. Mortalité du tourteau Cancer pagurus provoquée par le dinoflagelle parasite: Hematodinium sp. Coun. Meet. int. Counc. Explor. Sea C. M. ICES/K:32.

MacLean, S.A., & C.L. Ruddell. 1978. Three new crustacean hosts for the parasitic dinoflagellate Hematodinium perezi (Dinoflagellata: Syndinidae). J. Parasitol. 64: 158-160.

Messick, 1994

Meyers, T.R., T.M. Koeneman, C. Botelho, & S. Short. 1987. Bitter crab disease: a fatal dinoflagellate infection and marketing problem for Alaskan Tanner crabs Chionoecetes bairdi. Dis. aquat. Org. 3: 195-216.

Newman, M.W., & C.A. Johnson. 1975. A disease of blue crabs (Callinectes sapidus) caused by a parasitic dinoflagellate, Hematodinium sp. J. Parasitol. 61: 554-557.

Newman, M.W., & G.W. Ward, Jr., 1973. An epizootic of blue crabs, Callinectes sapidus, caused by Paramoeba perniciosa. J. Invert. Pathol. 22: 329-334.

Overstreet, R.M. 1978. Marine maladies? Worms, germs, and other symbionts from the Northern Gulf of Mexico. MASGP-78-021, Mississippi-Alabama Sea Grant Consortium, Ocean Springs, Miss.

Ragan, J.G., & B.A. Matherne. 1974. Studies of Loxothylacus texanus. In: R.L. Amborski, M.A. Hood, & R.R. Miller (eds.), Proceedings of the 1974 Gulf Coast Regional Symposium on diseases of aquatic animals, pp. 185-203. Louisiana State Univ. Sea Grant Publ. # 74-05.

Rogers-Talbert, R. 1948. The fungus Lagenidium callinectes Couch (1942) on eggs of the blue crab in Chesapeake Bay. Biol. Bull. 94: 214-228.

Shields, J.D., D.E. Wickham, & A.M. Kuris. 1989. Carcinonemertes regicides n. sp. (Nemertea), a symbiotic egg predator on the red king crab, Paralithodes camtschatica, from Alaska. Can. J. Zool. 67: 923-930.

Shields, J.D., D.E. Wickham, S.F. Blau, & A.M. Kuris. 1990. Some implications of egg mortality caused by symbiotic nemerteans for data acquisition and management strategies of the red king crab. Proc. Int. Symp. King & Tanner Crabs, Nov., 1989. Anchorage, Alaska, pp. 397-402.

Shields, J.D. 1992. The parasites and symbionts of the crab Portunus pelagicus from Moreton Bay, eastern Australia. J. Crustacean Biol. 12: 94-100.

Shields, J. D. 1994. The parasitic dinoflagellates of marine crustaceans. Ann. Rev. Fish Diseases 4: 241-271.

Shields, J.D., & F.E.I. Wood. 1993. The impact of parasites on the reproduction and fecundity of the blue sand crab Portunus pelagicus from Moreton Bay, Australia. Mar. Ecol. Prog. Ser. 92: 159-170.

Sloan, N.A. 1984. Incidence and effects of parasitism by the rhizocephalan barnacle, Briarosaccus callosus Boschma, in the golden king crab, Lithodes aequispina Benedict, from deep fjords in northern British Columbia, Canada. J. Exp. Mar. Biol. Ecol. 84: 111-131.

Sloan, N.A. 1985. Life history characteristics of fjord-dwelling golden king crabs Lithodes aequispina. Mar. Ecol. Prog. Ser. 22: 219-228.

Sprague, V. & R,K, Beckett, 1966. A disease of blue crabs (Callinectes sapidus) in Maryland and Virginia. J. Invert. Pathol. 8: 287-289.

Sprague, V., R.L. Beckett, and T.K. Sawyer. 1969. A new species of Paramoeba (Amoebida, Paramoebidae) parasitic in the crab Callinectes sapidus. J. Invert. Pathol. 14: 167-174.

Sprague, V. 1970. Some protozoan parasites and hyperparasites in marine decapod Crustacea. In A symposium on diseases of fishes and shellfishes, S. F. Snieszko, S.F. (ed.). American Fish. Soc. Spec. Publ. #5, Washington, D.C., pp. 416-429

Walker, G. 1974. The occurrence, distrubtion and attachement of the pedunculate barnacle Octolasmis mulleri (Coker) on the gills of crabs, particularly the blue crab, Callinectes sapidus Rathbun. Biol. Bull. 147: 678-689.