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Infections with Leucocytozoon spp are most often subclinical but can occasionally be clinical and even fatal. Mortality may approach 100% in susceptible species and varies greatly with species and strain of parasite, host species, degree of exposure, and other factors. Acute outbreaks of leucocytozoonosis have been reported in chickens (Asia, Africa), turkeys (North America), waterfowl (North America, Europe), and a number of free-living and captive avian species throughout the world. Species in domestic birds include L simondi in waterfowl; L smithi in turkeys; and L caulleryi, L sabrazesi, L andrewsi, and L schoutedeni in chickens. L caulleryi can be highly pathogenic, causing a lethal hemorrhagic disease of chickens in southeast Asia. L simondi causes mortality in ducks and geese. Numerous Leucocytozoon spp infect nondomestic birds (eg, blood smears from raptors often contain gametocytes). Clinical disease and mortality result from anemia caused by antierythrocytic factors produced by the parasite, high numbers of the large gametocytes blocking pulmonary capillaries, or parasites invading the endothelium of vessels in vital tissues (brain, heart, etc) where they form megalomeronts that occlude vessels and result in multifocal necrosis.
Parasitemia often increases dramatically in late April and early May (called spring rise), just before arthropod vectors, black flies (Simulium spp), or biting midges (Culicoides spp) increase. Ducks that have recovered from infection with L simondi relapse when light cycles are manipulated to increase egg production. Increased levels of prolactin have been suggested as a possible cause.
Acute disease is seen more often in the young when they have high parasitemia and when black flies or biting midges are most abundant. Subacute or chronic disease is seen in the young outside fly season and in older birds at any season; parasitemia is usually low. Recovered birds remain carriers and serve as a reservoir for young, susceptible birds.
Clinical Findings, Lesions, and Diagnosis
Acutely affected birds are listless and have anemia, leukocytosis, tachypnea, anorexia, diarrhea with green droppings, and often CNS signs. Egg production is impaired in laying chickens infected with L caulleryi. Signs are evident ~1 wk after infection and coincide with the onset of parasitemia. Visibly affected birds die after 7–10 days or may recover with sequelae of poor growth and egg production. Hemorrhages, splenomegaly, and hepatomegaly are seen. Grossly visible white dots in affected organs are megalomeronts.
In thin blood smears, gametocytes may be seen along the edges and tail of the smear. Leucocytozoon is identified by large gametocytes that lack pigment and distort the host cell (RBC or WBC), making it no longer identifiable. Shape of gametocytes varies—some are elongated with long tapering extremities, while others are round. Serology may detect prior infection.
Treatment and Control
Treatment usually is not effective. Preventive medication using pyrimethamine (1 ppm) and sulfadimethoxine (10 ppm) combined in the feed controls L caulleryi; clopidol (0.0125–0.025%) controls L smithi. Measures to control invertebrate vectors are helpful. Humoral immunity resulting from vaccination will protect against L caulleryi infection. Treatments with quinacrine hydrochloride or trimethoprim/sulfamethoxazole solution have been used in raptors; the parasitemia is reduced but the infection is not cleared.
Last full review/revision March 2012 by Arnaud J. Van Wettere, DVM, MS, DACVP
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