Tyzzeria Perniciosa

Host: Domestic Pekin duck.

Location: Thruout the small intestine, but especially in the upper half.

Geographic Distribution: North America.

Prevalence: Uncommon. This species has been reported from domestic ducks only by Allen (1936) on Long Island. However, its relationship to T. alleni, which Chakravarty and Basu (1946) described from the cotton teal (Cheniscus coromandelianus) in India, to Tyzzeria sp. which Farr (1952) reported from the black duck (Anas rubripes), to T. anseris reported by Farr (1959) from the lesser scaup duck (Nyroca affinis) in Michigan, and to T. anseris from domestic and wild geese and the whistling swan (see Hanson, Levine and Ivens, 1957) remains to be determined.

Morphology: The oocysts are ellipsoidal, 10 to 13 by 9 to 11 u. The oocyst wall is thick, colorless, composed of an outer thin, transparent layer and an inner thicker layer. A micropyle is absent. The sporozoites are curved, with one end rounder and broader than the other, about 10 u long and 3.5 u wide at the larger end. The oocyst residuum is large, usually spherical. The sporulation time is 1 day.

Life Cycle: According to Allen (1936), the endogenous stages are found in the mucosal and submucosal cells. There are at least 3 asexual generations. The first generation schizonts are relatively small, about 12 by 8 u, and contain relatively few, small merozoites. The later schizonts measure about 15 to 16 by 14 to 15 u and contain more and larger merozoites than the first generation ones. Schizogony continues long after the formation of gametes.

The first microgametocytes appear 2 days after infection. They measure about 7.5 by 6 u and produce a large number of tiny microgametes. The macrogametes are somewhat irregular in shape. Oocysts first appear in the feces 6 days after infection.

Pathogenesis: According to Allen (1936), T. perniciosa is highly pathogenic for ducklings. All of 7 experimentally infected, week-old ducklings died.

Affected birds stop eating, lose weight, become weak and cry continuously as if in distress. At necropsy, inflammation and hemorrhagic areas were found thruout the small intestine and especially in its upper half. The intestinal wall was thickened, and round, white spots were visible thru its serosal surface. In severe cases the lumen was filled with blood and often contained a cheesy exudate. The intestinal epithelium sloughed off in long pieces, sometimes forming a tube which could easily be lifted out.