278 



PI^SMODIUM, HAEMOPROTEUS AND LEUCOCYTOZOON 



Plasmodium . The sporozoites are 5 to 

 10(1 long, slender, with one end rounded 

 and the other pointed. They break out of 

 the oocysts and pass to the salivary 

 glands, where they accumulate. Viable 

 sporozoites can be found for at least 18 

 days after infective feeding. 



Pathogenesis : L. simondi is mark- 

 edly pathogenic for ducks and geese. The 

 heaviest losses occur among young birds. 

 O'Roke (1934) reported mortalities of 

 35%, 57% and 85% among young ducks in 3 

 different years in Michigan, but noted that 

 the death rate among adults was very low. 

 Knuth and Magdeburg (1922) and Stephan 

 (1922) described serious outbreaks in 

 young geese in Germany. According to 

 Chernin (1952b), about 68%. of the deaths 

 in ducklings occur 11 to 19 days after ex- 

 posure. 



Briggs (1960) found that Muscovy 

 ducklings were more resistant to L. 

 simondi infections than white Pekin duck- 

 lings under conditions of natural exposure 

 in Michigan. Altho both became readily 

 infected, the mortality and number of sex- 

 ual forms in the blood were much lower 

 among the Muscovies than the white Pekins. 

 In addition, deaths were delayed in the 

 Muscovies. 



The outstanding feature of an outbreak 

 of leucocytozoonosis is the suddenness of 

 its onset. A flock of ducklings may appear 

 normal in the morning, may become ill in 

 the afternoon, and may be dead by the next 

 morning. Acutely affected ducklings are 

 listless and do not eat. Their breathing 

 is rapid and labored due to obstruction of 

 the lung capillaries with schizonts. They 

 may go thru a short period of nervous ex- 

 citement just before death. Adult birds 

 are more chronically affected. They are 

 thin and listless, and the disease develops 

 more slowly in them. If they die at all, it 

 is seldom in less than 4 days after the 

 appearance of signs. Ducklings which have 

 recovered often fail to grow normally. Re- 

 covered birds, as mentioned above, re- 

 main carriers. 



The principal lesions of leucocyto- 

 zoonosis are splenomegaly and liver hy- 



pertrophy and degeneration. Anemia and 

 leucocytosis are present, and the blood 

 clots poorly. Cowan (1957) described the 

 tissue reactions of infected ducks against 

 the megaloschizonts. These include des- 

 truction by phagocytes and inflammatory 

 cells, necrosis and possibly encapsulation. 



Diagnosis : Leucocytozoonosis can be 

 diagnosed by finding and identifying the 

 gametocytes in stained blood smears or the 

 schizonts in tissue sections. 



Treatment : No effective treatment is 

 known. Fallis (1948) found that quinacrine, 

 sulfamerazine and chlorguanide were in- 

 effective. 



Prevention and Control : Prevention 

 depends upon blackfly control--ordinarily 

 a difficult task--or on raising ducks and 

 geese under conditions which prevent them 

 from being bitten by blackflies. In black- 

 fly areas this means raising them in 

 screened quarters. Blackflies pass readily 

 thru ordinary, 16 mesh per inch window 

 screening, and 32 to 36 mesh screen is 

 needed to keep them out. Since this type 

 of screening is expensive, a good grade of 

 cheesecloth has been recommended for a 

 single season's use. 



This disease can be avoided entirely 

 by raising ducks and geese in regions 

 where blackflies do not occur in significant 

 numbers. Since wild ducks and geese are 

 reservoirs of infection for domestic birds, 

 the latter should not be raised close to 

 places where wild waterfowl congregate. 



LEUCOCYTOZOON SMITHI 

 LAVERAN AND LUCET, 1905 



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). 



