LIFE HISTORY OF LEUCOCYTOZOON SIMONDI MATHIS AND LEGER IN NATURAL AND EXPERIMENTAL INFECTIONS AND BLOOD CHANGES PRODUCED IN THE AVIAN HOST

Abstract

Ducks exposed outdoors in Algonquin Park during the summer became infected with Leucocytozoon simondi and many of them died from the infection in June and July when black flies were abundant. The minimum prepatent period was five and a half days. Young parasites were observed in erythrocytes and lymphocytes; mature gametocytes, as shown by exflagellation of microgametocytes, occurred in round and elongated host cells. Asexual development was observed in the spleen, liver, heart, brain, lung, lymphoid tissue, and pancreas. The schizonts were large and contained, at maturity, more than a million merozoites about 1 μ in diameter. Sexual development of the parasites within two species of black flies was completed in three days at summer temperature. Ookinetes were present in the stomach of black flies about four to six hours after the flies had ingested blood containing gametocytes. Developing oocysts were found free among the stomach contents of flies 40–48 hr. after the blood meal. Sporozoites were observed between 60–70 hr. after the flies had ingested gametocytes. Artificial infections were produced in ducks following the injection of macerated black flies that had fed two and one-half to seven days previously on infected ducks. The resulting infections were less severe than those that resulted from natural infections, although the pattern was similar and a minimum prepatent period of eight days was observed. The asexual cycle was completed in fewer than six days although some asynchronicity was apparent. Artificial infections were produced following the injections of blood, spleen, liver, lung, and bone marrow that were taken from ducks at various intervals following their exposure to natural infection. The minimum prepatent period in these infections was eight days and low parasitemias were produced. Gametocytes survived for at least one week in peripheral blood. Ducks developed some resistance following repeated infections but single infections did not protect ducks that were exposed to infection six weeks later. Heavy infections developed in ducks that were splenectomized. The leucocytosis and anemia associated with infections were measured and recorded.

Leucocytozoonosis

“…Anemia is the most important clinical sign (Maley and Desser 1977) and packed cell volumes may be only 20% of normal (Fallis et al 1951). Other signs are anorexia, lethargy, labored breathing, and diarrhea (Wobeser 1997).…”

“…Domestic ducks exposed to a single infection and not challenged until 6 weeks later are not resistant to reinfection (Fallis et al 1951). However, ducks exposed to primary infections of L. simondi and then repeatedly exposed to infected vectors over a 3-week period have persistently lower parasitemias than do uninfected control ducks that are exposed to infected vectors at the same time (Fallis et al 1951). Fallis et al (1974) referred to this as a state of premunition.…”

Prevalence of haemosporidians in a Neotropical endemic bird area

“…This is probably a reflection of the ecological constraints of Leucocytozoon, which is transmitted by blackflies (Fallis et al 1951). The larvae of these vectors require streams with constant current rates (Zahar 1951), which are common in mountainous areas such as the SNSM.…”

Island and Taxon Effects in Parasitism and Resistance of Lesser Antillean Birds

“…The positive relationship between WBC levels and the intensity of haemoproteid infection recalls hematological changes that accompany infection with other avian hematozoa, such as Leucocytozoon spp. (Fallis et al 1951, 1956, Desser et al 1968. Even after factoring out the presence/absence or intensity of Haemoproteus infection, species effects on levels of blood leukocytes remained significant (Tables 6 and 7).…”

“…demonstrated that the sampling program was large enough to discern statistically significant host-parasite combinations. Moreover, blood leukocyte counts, which indicate an individual host's response to its parasite load (Fallis et al 1951, Desser et al 1968, show that both deterministic and historical factors shap e host-parasite associations. Finally, we suggest a framework for gauging the relative importance of these factors based on island biogeographic analysis.…”