(Sphaeridiotrema globulus)

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Description and Distribution

Verminous Hemorrhagic Ulcerative Enteritis is a disease of waterfowl caused by the trematode (fluke) Sphaeridiotrema globulus. The fluke is spherical in shape, flat, and seed-like, measuring .5 to .8 mm in length and being light pink to red in color. The first reported mortality in wild waterfowl in North America attributed to this parasite occurred in lesser scaup in the Washington D.C. area in 1928.

S. globulus has a cosmopolitan distribution, being reported in wild and domestic waterfowl throughout Europe and North America. This parasite has been reported from Europe with no indication of pathogenicity in the mute swan, old squaw, common merganser, red-breasted merganser, razorbill, greater scaup, tufted duck and northern pintail. In North America it has been reported to cause recurrent die-offs in the lesser scaup, American goldeneye, canvasback, American coot, ruddy duck, whistling swan, mute swan, old squaw, muscovy duck, white-winged scoter, and surf scoter. In Michigan, we have attributed mortality to S. globulus in the old squaw, white-winged scoter, surf scoter, tundra swan, mute swan and trumpeter swan.

Transmission and Development

The development and transmission of S. globulus from one animal to another are quite complex when compared to most parasites. There are a series of asexual reproductive stages, and two intermediate hosts are required before the parasite is infectious to susceptible waterfowl.

An infected bird passes the fluke's eggs in its fecal material into water. Within the egg a miracidium develops and, when fully developed, hatches. The miracidium finds a suitable first intermediate host, a freshwater snail, and penetrates the foot. Species which have been identified as being suitable hosts are Fluminicola virens and Bithynia tentaculata. In the snail the miracidium undergoes structural changes and develops into a sac of germinal cells whose sole purpose is to reproduce (asexually). These cells undergo some structural changes and become a larval stage called rediae. As the rediae mature, within them develops the next larval stage, the cercariae. These are usually found in the viscera of snails, most commonly in the gonads. When fully mature the cercariae leave the rediae by the birth port and escape from the snail through its anal opening. The cercariae vigorously swim to find a second suitable freshwater snail. F. virens, Oxytrema silicula, B. tentaculata, and Goniobasis virginica have been identified as suitable second intermediate hosts. When contact is made with the exposed surface of one of these snails, the cercariae creep along randomly on the foot, head, and mantle. When the edge of the mantle is reached, the cercariae penetrate the columellar muscle between the mantle and the shell and become encysted. A thin-walled cyst develops within 2 hours, and by 5 hours the cercariae are encased in thick-walled cysts and become metacercariae. The metacercariae do not develop any further until the snail is ingested by a suitable definitive host (waterfowl). When this occurs the encysted metacercariae remain in this larval stage until they pass into the intestinal tract. In this location, proper temperature and pH conditions trigger increased activity by the metacercariae. This increased activity and production of enzymes weakens the cyst walls, and the metacercariae are released to finalize their development into adult flukes. When the adult stage is reached the flukes attach to the lining of the posterior portion of the small intestine causing hemorrhages to occur. The fluke feeds on the blood, leading to severe blood loss and anemia in the bird. Eggs are produced following attachment, thus completing the life cycle.

Clinical Signs and Pathology

Clinical signs of a S. globulus infection seen in waterfowl are weakness, limber neck, wing droop, listlessness, lack of fear of humans, anorexia, and blood stained feathers around the vent. The disease can be chronic or acute in nature, as birds can range from very good to poor in their physical condition. Birds often die from shock associated with severe blood loss. As few as 20 flukes can be lethal to the waterfowl host and death generally occurs within 3-8 days following the ingestion of a lethal dose.

Gross pathological changes are usually seen only in the intestinal tract and can occur in both the small and large intestines. The most severe lesions are hemorrhages generally seen in the posterior third of the small intestine and the ceca. The segment of intestine affected is distended and congested with casts of fibrin and clotted blood filling the lumen. The sites of origin of these casts are hemorrhagic ulcers caused by the fluke. The flukes reside in these ulcers and may number from 1 to 22 in each. There may be over 200 flukes present in a single bird's intestinal tract. The flukes are light pink to red in color, measuring 0.5 to 0.8 mm in length, and being spherical, flat, and seed-like in appearance. The flukes adhere to the intestinal mucosa by large acetabula. The only other gross pathological change that may be seen is pale viscera, due to the extreme blood loss.

Microscopic pathological changes seen consist of changes in the muscularis mucosae of the small intestine caused by the adherence of the parasite, and the resulting ulceration. This layer becomes edematous, hyperemic, necrotic, and is infiltrated with lymphocytes and a few eosinophils. Hemorrhage is pronounced in this area as well. A cross section taken through the gut shows the lumen to be filled with a mass composed of desquamated epithelium, fibrin, and blood.

Diagnosis

Diagnosis of birds dying from this parasite can best be done by performing a deep scraping of the intestinal mucosa in the ulcerated area and examining the scraping under a microscope to identify the adult parasite. Further confirmation can be attained by examining the affected segments of intestine microscopically for the parasite.

Treatment and Control

At the present time there is no treatment or means of control for this parasite.

Significance

Mortality attributed to this parasite has been on the increase in waterfowl nationwide and in mute swans in Michigan either due to an increased awareness of the disease or because of an actual spreading of the parasite.

Some of the mortality we have seen in Michigan's waterfowl has occurred during periods of migration, which agrees with what several other authors have seen in various areas of North America. However, the resident, non-migrating mute swans that are present throughout the state have died from this parasite during all times of the year. The parasite may become a population-limiting factor to some mute swan flocks in the future.

No reports of human infection have been reported for this trematode.

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