Leucocytozoon Smithi

Disease: Leucocytozoonosis.

Hosts: Domestic and wild turkeys.

Location: The gametocytes are in the leucocytes. Schizogony occurs in the liver.

Geographic Distribution: North America, Europe (France, Germany, Crimea).

Prevalence: This species is common in northern and southeastern United States, along the Gulf Coast and Pacific Coast and in Canada in mountainous or hilly areas wherever cold, rapid streams permit suitable blackfly vectors to breed. It was first seen by Smith (1895) in eastern United States, and has been encountered in North Dakota, Minnesota, Nebraska, Wisconsin, Illinois, Virginia, South Carolina, Georgia, Alabama, Florida, Pennsylvania, Missouri, Texas, California, Ontario and Manitoba (Volkmar, 1929; Skidmore, 1932; Johnson, 1942, 1945; Johnson et al., 1938; Hinshaw and McNeil, 1943; Banks, 1943; Stoddard, Humlin and Cooperrider, 1952; Travis, Goodwin and Gambrell, 1939; Mosby and Handley, 1943; Wehr and Coburn, 1943; Kozicky, 1948; West and Starr, 1940; Atchley, 1951; Bierer, 1950; Simpson Anthony and Young, 1956; Savage and Isa, 1945; Fallis, Pearson and Bennett, 1954).

Travis, Goodwin and Gambrell (1939) found it in 81% of 357 adult domesticated turkeys in Georgia, Florida, Alabama and South Carolina. Mosby and Handley (1943) found it in 40% of 268 captivity-reared wild turkeys, wild turkeys and domestic turkeys in Virginia. Kozicky (1948) found it in 21% of 92 captivity-reared and all of 5 native wild turkeys in Pennsylvania. Atchley (1951) found it in all of 10 domestic turkeys in South Carolina.

Morphology: The mature macrogametes and microgametocytes are rounded at first but later become elongate, averaging 20 to 22 u in length. Their host cells are elongate, averaging 45 by 14 u, with pale cytoplasmic "horns" extending out beyond the enclosed parasite. The host cell is elongate, forming a long, thin, dark band along one side of the parasite; often it is split to form a band on each side of the parasite. The cytoplasm of the macrogametes is rather dark blue and the nucleus compact and red when stained with a Romanowsky stain. The cytoplasm of the microgametocytes is very pale blue and the nucleus diffuse and pale pink.

Life Cycle: The life cycle of L. smithi is similar to that of L. simondi, but is not known in nearly so much detail. The prepatent period is about 9 days. Newberne (1955) and Richey and Ware (1955) described hepatic schizonts in the liver parenchyma of infected turkeys. According to Newberne, they measure 10 to 20 by 7 to 14 u, with a mean of 13.5 by 10.5 u. The earliest stage he saw contained round and crescent-shaped, basophilic cytomeres. These developed into masses of deeply staining merozoites which completely filled the host cell cytoplasm. Megaloschizonts have not been seen.

The vectors of L. smithi are various species of blackflies (Simulium). Skidmore (1932) found that S. occidentale transmitted it in Nebraska, Johnson et al. (1938) found S. nigroparvum to be the vector in Virginia, and Richey and Ware (1955) showed that S. slossonae could transmit it in South Carolina. The stages in the blackflies are similar to those of L. simondi.

Pathogenesis: L. smithi is markedly pathogenic for turkeys, and extremely heavy losses have been reported. Savage and Isa (1945) described an outbreak in Manitoba in which more than 3000 out of 8000 birds died in 2 months. Not more than 10% of the birds which became ill recovered. Stoddard, Humlin and Cooperrider (1952) described an outbreak in Georgia in which 75% of 1600 5-month-old turkeys died within a week. Adult birds are less seriously affected than poults, and the disease runs a slower course in them, but even they may die.

Affected poults fail to eat, appear droopy and tend to sit. They move with difficulty when disturbed; in the later stages there may be incoordination, and the birds may suddenly fall over, gasp, become comatose and die. If the birds do not die within 2 or 3 days after signs of disease appear, they recover.

Recovered birds continue to carry parasites in their blood. Some may show no serious after-effects, but others develop a chronic type of the disease. They never regain their vigor, and the males pay little attention to the females and rarely strut. They often have moist tracheal rales, and cough and repeatedly try to clear their throats when disturbed. They may die suddenly under stress caused by undue excitement or handling.

The spleen and liver of affected birds are enlarged, and the duodenum is more or less inflamed. This enteritis may sometimes extend thruout the small intestine. The birds are anemic and emaciated, their flesh is flabby, and their muscles may be brownish. There are no gross lesions in adult carriers, but the liver may occasionally be icteric, enlarged and cirrhotic. Newberne (1955) saw no local tissue reaction around the hepatic schizonts, but noted hepatic hemosiderosis and lymphocytic infiltration. According to Johnson et al. (1938), death is due to obstruction of the circulatory system by large numbers of parasites.

Diagnosis, Treatment, Prevention and Control: Same as for L. simondi.