Avian haemoparasites are known to exert negative pressures on theirhosts causing considerable pathology and mortalities. The present study reports on the prevalence of haemoprotozoa and microfilaria in various species of wild birds and domestic poultry in Selangor, Malaysia, and contributes to the database on the occurrence of thesepathogens among avifauna in the country. Giemsa-stained thin blood smears were screened from 728 birds representing five avian orders, namely Galliformes, Anseriformes, Phoenicopteriformes, Pelecaniformes and Gruiformes. The most common haemoparasite was Plasmodium, with a prevalence of 8.0%. The aquatic/wetland species of birds (Anseriformes and Gruiformes) were the most common hosts for this pathogen with high infection rates (31.8% – 50.0%). The prevalence of Plasmodium in domestic poultry was moderate (2.7%). Leucocytozoon sabrazesi and L. caulleryi were confined to the Galliformes with relatively low average infection rates of 0.7% and 0.5%, respectively. Haemoproteus was detected for the first time in domestic poultry and Red Jungle fowls in the country, with anaverage prevalence of 0.8%. Trypanosomes and microfilaria were only present in the village chickens and Red Jungle fowls, with high microfilaraemia rates (19.0%) in the latter. The current compilation will contribute to our understanding on avianhaemoparasite transmission in the country.

Histopathological changes were studied in Swiss albino mice (N:36)which were challenged with the South Indian local strain of Trypanosoma evansi. Each animal was infected with 5×105 trypanosomes intraperitoneally. The animals were examined daily for development of clinical signs and infection status by wet blood-films made from the tail veins. The infected mice were dull and depressed from two days post-infection (DPI) onwards. Systematic post-mortem examination of the infected mice was performed and pathological changes were recorded. The different tissue samples were collected in 10% formalin and were used to study the histopathological changes. Postmortem examination from 3-4 DPI (the maximum period of observation) revealed splenomegaly, hepatomegaly, marked congestion of lungs, presence of fl uid in peritoneal cavity. Histopathologically, heart muscles showed hyaline degenerative changes and haemorrhages. Liver parenchyma revealed congestion of central vein and sinusoids, binucleated hepatocytes and fatty change of hepatic cells. Thickening of interstitial space with mononuclear infiltration, areas of collapse, areas of emphysema, edema and dilated and congested blood vessels were the histopathological changes noticed in the lungs of the infected mice. In the spleen, giant cells aggregation, hyperplasia, thickening of capsule and trabecule were the changes indicating irreversible degeneration. The affected kidney showed inter-tubular hemorrhages in the cortex, medullary hemorrhages, congested glomerulus, atrophied glomerulus, desquamated tubular epithelium and disruption of renal tubules at some places.