Reactions against the Megaloschizonts of Leucocytozoon Simondi Mathis and Leger in Ducks

Cowan, A. B.

doi:10.1093/infdis/100.1.82

Cited by 15 publications

(9 citation statements)

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“…Neither clinical signs such as lethargy, loss of appetite, and diarrhea, which commonly accompany L. simondi infections 2n ducks (Fallis et al 1974), nor pathological manifestations such as hypertrophy of the liver and spleen (O'Roke 1930;Desser 1967), inflammatory and necrotic foci in the liver, lung, brain, and other organs (Cowan 1957;Desser 1967), and hemosiderosis of the liver and spleen (Newberne 1957) were observed in the geese in this study.…”

Section: Pathogenesiscontrasting

confidence: 56%

The development and pathogenesis of Leucocytozoon simondi in Canada and domestic geese in Algonquin Park, Ontario

Desser¹,

Ryckman²

1976

Can. J. Zool.

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1976. The development and pathogenesis of Leucocytozoon simondi in Canada and domestic geese in Algonquin Park, Ontario. Can. J. Zool. 54: 634-643.The development of Le~icocytozoon simondi was studied in naturally and experimentally infected Branta canadensis maxima, Branta canadensis interior, and Anser domesticus. The number of mature round gametocytes in the peripheral blood of the Canada geese increased between days 9 and 15 post exposure (PE) and decreased rapidly thereafter. Mean peak parasitemias recorded on day 13 PE were (per 1000 red blood cells (RBC)): 8 gametocytes in B.c. maxima, 16 gametocytes in B.c. interior, and 17 gametocytes in A . domesticus. About 3 weeks PE, gametocytes disappeared from the peripheral circulation and were not observed again during the autumn, winter, and spring in birds kept in the laboratory.Haematocrit determinations in the Canada geese revealed a low fluctuating anemia during the primary infection which subsided by day 21 PE. A more severe anemia was recorded in A . domesricus with a mean low packed RBC value of about 18% on day 11 PE. Immature and mature hepatic schizonts were observed in the Canada and domestic geese between days 3 and 8 PE.Neither megaloschizonts nor elongate gametocytes were seen. Clinical signs, pathology, and mortality commonly associated with L. simondi infection in ducks were not observed. Hypotheses are advanced to explain reports of severe pathogenesis associated with L. simondi infections in Canadageese in other localities. DESSER, S. S., et A . K. RYCKMAN. 1976. The development and pathogenesis of Leucocytozoon simondi in Canada and domestic geese in Algonquin Park, Ontario. Can. J. Zool. 54: 634643. On a itudi6 le diveloppernent de Leucocyro~oon simondi chezdes Branfa r u n o d~m i s maxima. des Brantcr runadensis inrerior et des Anser dorn~sricus infectts naturellement et expirimentalement, t e nornbre de garnet~cytes sonds i maturiti dans le sang piriphtrique des bernaches canadiennes subit me augmentation des jours 9-15 aprks I'infection (PE) pour ensuite diminuer rapidement. Les parasitimies maximales moyennes le 13ejour aprts I'infection son1 : 8 gamct~ytes par 11)00 globules roupcs chez B.c. maxima, iS gamitocytes par 1000 glohules rouges chez B.r. inrerior et 17 gamitocyfes par lOOn glohule~ rouges chez A. d o m~s r i c~w . Environ 3 sernaines apr.2~ I'infect~on. les ~amitocytes ont quittl la circulat~on piriphkrique et ne reapparaissent ni I'automne. ni a I'hiver. ni au printemps. chez Ies uiseoux gardis en fahoratoire. L'hirna~writc des h a c h e s met en evidence une animie subissant peu defluctuations durant la phase primaire de I'infection et disparaissant entiirement avant le Z l e jour apres I'infection.Chez A. donrrsric~rs. I'anemie est plus grdve. la v~l e u r moyenne minimale de I'hkrnatocrite Ctant d'environ 18%. le onzieme jour nprts I'infection. On observe des schizontes Mpatiques immatures ct d'autres i maturitt chez la krnache et chez I'oie domestique entre le? jours ?-8 aprks I'infection. Par cmrre. on n'a vu ni me~losc...

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Section: Pathogenesiscontrasting

confidence: 56%

The development and pathogenesis of Leucocytozoon simondi in Canada and domestic geese in Algonquin Park, Ontario

Desser¹,

Ryckman²

1976

Can. J. Zool.

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“…Much of the pathology resulting from heavy infections with Leucocytozoon has been attributed to tissue damage caused by the inflammatory response to the megaloschizonts (Cowan 1957;Akiba 1960;Desser 1967;Atkinson et al 1986). Schizonts, apparently not of the megaloschizont series, were seen in our study in only a few autopsied or necropsied sparrows; none were seen inducing any tissue reaction.…”

Section: Discussionmentioning

confidence: 99%

“…Peirce (1984) reported on a sick, emaciated dove (Turtur chalcosphilos) infected with L. marchouxi and Haemoproteus columbae. The pathological process in anserine infections with L. simondi has been linked to developing megaloschizonts in the spleen, liver, lungs, heart, and brain (Cowan 1957;Newberne 1957;Desser 1967;Desser and Fallis 1967). Khan and Fallis (1970) explained the considerably lower pathogenicity of other species, such as L. fringillinarum, L. dubreuilli and L. berestneffi, by the absence of megaloschizonts in the course of their development.…”

Section: Introductionmentioning

confidence: 99%

Leucocytozoonosis in the Israeli sparrow, Passer domesticus biblicus Hartert 1904

Gill

Paperna

2005

Parasitol Res

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Among the 91 house sparrows (Passer domesticus biblicus Hartert, 1904) examined and caught in the Jordan valley, Israel, 79% were found to be infected with Leucocytozoon fringillinarum Woodcock 1910. In the coastal plain of Israel (South of Tel Aviv), Leucocytozoon infection was found in only 3 out of 43 examined sparrows. In the birds examined, Leucocytozoon gametocytes were present, often in large numbers, in the circulating blood of the visceral organs, whereas they were only sporadic or even absent in the peripheral blood. Gametocytes were seen in the brain capillaries in only a few birds. Only one of the heavily infected sparrows was anemic. Leucocytozoon merozoites were present in the liver and kidneys in only a few infected birds. Merogonic infections did not induce any severe pathological changes, while the gametocyte congestion caused dilation of the blood vessels and sinuses. Tissue damage by the gametocyte parasitemia was most evident in the liver and kidneys. Leucocyte infiltration developed alongside the affected vessels; diffuse necrosis developed in the infiltrated areas. In the kidneys, many tubules were degenerated. Leucocytozoon gametocyte infection in sparrows is unique in that it appears to be confined, for most of its duration, to the visceral circulation, resulting in clinical consequences. Geographically, it is confined to habitats presumably supporting vectors.

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“…Classification of the parasite as a sporozoan is reasonable, although further subclassification is difficult because no description of an organism with the same histologic features was found in the literature. Leucocytozoon simondi causes disease in ducks and L. smithi causes disease in turkeys [3,8,9,18]. An aberrant form of leucocytozoon infection has been noted in parakeets [2,25].…”

Section: Discussionmentioning

confidence: 99%

“…Renal schizonts were reported in birds infected with L. dubreuili or L. fringillinarum [12]. Asexual multiplication of L. simondi takes place in the vertebrate host and sexual reproduction occurs in certain species of blackflies (Simulium) [3]. The number of gametocytes varies in the blood of ducks.…”

Section: Discussionmentioning

confidence: 99%

An Epizootic among Knots (Calidris canutus) in Florida I. Disease Syndrome, Histology and Transmission Studies

et al. 1977

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About 150 knots found sick or dead had distention of serosal blood vessels, and small, raised hemorrhagic foci on the serosal surface of the jejunum and ileum. The principal finding was endaortitis with large intimal multinucleated cysts that contained a protozoan parasite within a cytoplasmic vacuole. There was endarteritis of mesenteric arteries and muscular arteries of the external layers of the intestinal tract. Single or multiple schizont-like stages containing zoites were in the wall of the small intestine and close to affected muscular arteries. The more usual intestinal lesion was an aneurysm of the inflamed muscular artery. It was concluded that endarteritis led to colonic infarction. Schizonts in medullary renal tubular cells were smaller than stages in the intestine. There was necrosis of epithelial cells of themedullary collecting ducts and inflammatory and regenerative changes. Schizonts and zoites were free in collecting ducts and ureters.

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Reactions against the Megaloschizonts of Leucocytozoon Simondi Mathis and Leger in Ducks

Cited by 15 publications

References 0 publications

The development and pathogenesis of Leucocytozoon simondi in Canada and domestic geese in Algonquin Park, Ontario

The development and pathogenesis of Leucocytozoon simondi in Canada and domestic geese in Algonquin Park, Ontario

Leucocytozoonosis in the Israeli sparrow, Passer domesticus biblicus Hartert 1904

An Epizootic among Knots (Calidris canutus) in Florida I. Disease Syndrome, Histology and Transmission Studies

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