Equine babesiosis is a tick-transmitted hemoprotozoan infection caused by the intraerythrocytic parasites
Babesia equi and B. caballi. The equine infections often become endemic when the infected horses move freely from country to country. Therefore, several non-endemic countries，including Japan, strictly prohibit the entry of infected horses on the basis of their serological status. The ideal diagnostic measures for equine
babesiosis should have sufficiently high sensitivity for the accurate detection of acute and latent infections, high specificity for discrimination from other infections, and high convenience applicable for field use. This is a review of current studies for the development of ideal diagnostic measures for equine babesiosis.
Studies were undertaken to determine the effect of infection with Trypanosoma congolense on the leucocyte and thrombocyte values of six local puppies. The puppies were of mixed sexes and seven weeks old. Although the puppies became parasitaemic 6 to 7 days post infection (PI）, the effect on leucocyte counts were mild as significant leucopenia Characterised by neutropenia ensinopenia, and lymphopenia (P≤0.05) did not occur until the last four weeks of the 8 week observation period. Infection had more effects on thrombocyte counts as thrombocytopenia occured from week one PI. The low impact of infection with T.congolense on the leucocyte values of infected puppies was attributable to trypanotolerance in the local breed of dogs and low antigenicity of the strain of T. congolense used. It was concluded that, ability to resist the development of anaemia may not be the only haematological evidence of trypanitolerance in animals and that further research is needed to determine the true trypanotolerance status of breeds of local dogs in Nigeria and other parts of the West African subregion.
Two species of cryptosporidium infect laboratory mice （Mus musculus) namely C. muris and C. parvum which inhabitant of gastric and intestinal mucosa respectively C. parvum and in rare occasions C. muris are pathogenic for humans particularly in immunocompromised individuals. The animals harbor cryptosporidium organism could be a potential sources of infection for humans and susceptible species.
In the present study to survey the occurrence of cryptosporidium in the laboratory mice, tissue sections stained with Haematoxylin and Eosin and Mepacrine staining methods were carefully examined and the positive specimens were further stained with Modified Ziehl Neelsen technique recommended for identification of cryptosporidial organisms. 100 conventional and BALB/C laboratory mice from six research and educational centers were studied for the presence of cryptosporidium in the gastric and intestinal mucosa. Sixty-three out of hundred (63%)) of animals examined were infected with cryptosporidium organisms:
gastric cyptosporidiosis due to C. muris nine out of hundred (9%), intestinal cryptosporidiosis caused by C.
parvum thirty-four out of hundred (34%) and both cryptosporidiosis of stomach and intestine twenty out of hundred (20%). With the exception of gastric cryptosporidiosis, cryptosporidiosis of intestine is very mild to moderate. It is concluded that a high percentage of laboratory mice harbors cryptosporidium organisms. The infected animals not only could be a source of infection for laboratory animals but also in many instances such the animals may not a suitable one for research purposes.
Var gene is a multicopy family gene and encodes the antigenic protein, Plasmodium falciparum infected-erythrocytes membrane protein-1(PfEMP-1). Here we identified expressed var gene transcripts and their cytoadherent characteristics. Random cloning and sequencing analysis of DBL-alpha domain of var gene transcripts expressed in matured parasites revealed that approximately half of all cDNA clones were derived from a single gene, var-1/ItG. Immunofluorescence assay (IFA) showed that approximately 40% of ItG parasites expressed PfEMP-1 encoded by var-1/ItG-1 (PfEMP-1/ItG-1). Parasitized RBCs (PRBCs) selected for binding to C32 cells (ItG/C32), where the PfEMP-1/ItG-1-positive PRBC population increased to 78%, showed an increased cytoadhesion to C32 cells (241 PRBCs per 300 C32 cells) compared to originally cultured PRBCs (9 PRBCs per 300 C32 cells). To evaluate the contribution of PfEMP-1/ItG-1 in C32 adherence, PfEMP-1/ItG-1-enriched fraction (ItG/8A) was prepared by limiting dilution. In ItG/8A fraction, 83 % of the PRBCs were PfEMP-1/ItG-1 positive and only var-1/ItG was detected in the sequence analysis. PRBCs in ItG/8A fraction also showed higher cytoadhesion to C32 cells (153 PRBCs bound per 300 C32 cells). These results demonstrated that PfEMP-1/ItG-1 is expressed on ItG parasite-infected RBCs and contributes to the cytoadherent phenotype of ItG parasites to C32 cells.