House sparrows (Passer domesticus biblicus Hartert, 1904) caught in the Jordan valley, the coastal plain, and the desert region in Southern Israel were found massively infected with extraintestinal proliferative stages of Isospora, previously named Atoxoplasma. Infection coincided with Isospora spp. infections in the digestive tract. Prevalence of infection reached 70% among sparrows of all three regions; however, only in the Jordan valley did the severity of the sparrows compromised their survival. Healthy appearing captured birds showed symptoms of "going light" syndrome -- diarrhea, emaciation, and death. Birds succumbed within 48 h to 15 days after confinement to cages. Merozoites accumulated predominantly in the spleen but were rarely found in the peripheral blood. The parasite stages in the visceral leukocytes propagated by merogony and yielded single large waiting-stage merozoites. Visceral infections resulted in multifocal necrosis. Proliferative visceral Isospora infection (atoxoplasmosis) is one of the more severe causes of mortality among captive birds, free-ranging birds appear to coexist with the infection but succumb under capture stress.

We describe and discuss species of Plasmodium with four nuclei arranged in doublets or forming a maltese cross and loose, residual cytoplasm, described from Passer hispaniolensis in Algeria. The following species are described: Plasmodium rouxi from Alauda arvensis, from France Plasmodium mohammedi sp. nov. from Passer domesticus biblicus and Plasmodium pachysomum sp. nov. from Anthus campestris, from Israel, Plasmodium pfefferi sp. nov. from Pica pica and Plasmodium sergentorum sp. nov. from Alauda arvensis and Pica pica from France and Plasmodium stellatum sp. nov. from Muscicapa striata from Israel. All species vary in the spatial position of their four nuclei and the presence or absence of refractile, blue-staining globules. All of the described species differ from P. vaughani Novy et Mac Neal, 1904 and its siblings (example: P. vaughani merulae Corradetti et Scanga, 1973) in their number of merozoites (always four versus four to eight in the latter) and their spatial arrangement in the schizont.

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.

Parasitol Res (2005) 96:373-377 In the online PDF and the print version, Figs. 5-8 are duplicates of Figs. 1-4. The correct Figs. 5-8 are given here.The online version of the original article can be found at http:// dx.