title: Neospora caninum and Toxoplasma gondii: relationship between hepatic lesions, cytological and biochemical analysis of the cavitary liquid during the acute phase of the diseases in experimental models.
abstract: The objective of this study was to evaluate the pathogenesis of ascites in mice infected with Toxoplasma gondii and gerbils infected with Neospora caninum during the acute phase disease. For that, 12 gerbils [Experiment I: not infected/control (n=6) and infected (n=6)] and 12 mice [Experiment II: control (n=6) and infected (n=6)] were used. Infected gerbils and mice showed marked ascites on days 5-7 post-infection (PI), while the not-infected animals had not ascites. Peritoneal liquid was collected from the all mice with uninfected animals receiving 1.5mL of saline solution into their abdominal cavity, allowing the recovery of cavity liquid. As a result, it was possible to observe differences in physics, chemistry and cytological analysis of the fluid cavity of animals infected with N. caninum and T. gondii, when they were compared with uninfected animals, as well as between animals experimentally infected. Additionally both, N. caninum and T gondii, caused an increase in the levels of nitric oxide (NOx-nitrate/nitrite), protein oxidation (AOPP) and lipid peroxidation (TBARS), while serum total protein and albumin were reduced in infected gerbils and mice. Gerbils infected with N. caninum showed multiple large cells with multilobulated nucleus, lytic necrosis and abundant amount of eosinophilic cytoplasm into the hepatic parenchyma. By the other hand, mice infected with T. gondii developed myriad foci of lytic necrosis combined with tachyzoites and cysts containing bradyzoites in liver. Both experimental models for N. caninum and T. gondii showed inflammatory foci and tachyzoites the peritoneum, which could be a major cause of ascites. Toxoplasmosis and neosporosis were able to cause clinical signs in experimental models with similar alterations in peritoneal fluid; however the toxoplasmosis histological changes were much more evident. Therefore, the pathogenesis of ascites appears to be directly related to liver damage, which strongly suggests alteration in the normal production of proteins as observed in this study, along with peritonitis.
authors.affiliation: Program of Postgraduate in Biochemical Toxicology, Universidade Federal de Santa Maria, Brazil.
authors.forename: Nathieli B
authors.initials: NB
authors.lastname: Bottari
authors.affiliation: Department of Small Animals, Universidade Federal de Santa Maria, Brazil.
authors.forename: Alexandre A
authors.initials: AA
authors.lastname: Tonin
authors.affiliation: Department of Pathology, Universidade Federal de Santa Maria, Brazil.
authors.forename: Rafael
authors.initials: R
authors.lastname: Fighera
authors.affiliation: Department of Pathology, Universidade Federal de Santa Maria, Brazil.
authors.forename: Mariana M
authors.initials: MM
authors.lastname: Flores
authors.affiliation: Department of Small Animals, Universidade Federal de Santa Maria, Brazil.
authors.forename: Raqueli T
authors.initials: RT
authors.lastname: França
authors.affiliation: Department of Preventive Medicine Veterinary, Universidade Federal de Santa Maria, Brazil.
authors.forename: Giovana
authors.initials: G
authors.lastname: Camillo
authors.affiliation: Department of Preventive Medicine Veterinary, Universidade Federal de Santa Maria, Brazil.
authors.forename: Gustavo
authors.initials: G
authors.lastname: Toscan
authors.affiliation: Department of Preventive Medicine Veterinary, Universidade Federal de Santa Maria, Brazil.
authors.forename: Fernanda S F
authors.initials: FS
authors.lastname: Vogel
authors.affiliation: Department of Clinical and Toxicological Analysis, Universidade Federal de Santa Maria, Brazil.
authors.forename: Manuela B
authors.initials: MB
authors.lastname: Sangoi
authors.affiliation: Department of Clinical and Toxicological Analysis, Universidade Federal de Santa Maria, Brazil.
authors.forename: Guilherme V
authors.initials: GV
authors.lastname: Bochi
authors.affiliation: Department of Clinical and Toxicological Analysis, Universidade Federal de Santa Maria, Brazil.
authors.forename: Rafael N
authors.initials: RN
authors.lastname: Moresco
authors.affiliation: Department of Small Animals, Universidade Federal de Santa Maria, Brazil.
authors.forename: Sonia T A
authors.initials: ST
authors.lastname: Lopes
authors.affiliation: Program of Postgraduate in Biochemical Toxicology, Universidade Federal de Santa Maria, Brazil; Department of Animal Science, Universidade do Estado de Santa Catarina, Brazil. Electronic address: aleksandro_ss@yahoo.com.br.
authors.forename: Aleksandro S
authors.initials: AS
authors.lastname: Da Silva
mesh_terms: D000009:Abdominal Muscles / Q000473:pathology; D000208:Acute Disease; D062107:Advanced Oxidation Protein Products / Q000032:analysis; D000418:Albumins / Q000032:analysis; D000818:Animals; D001202:Ascitic Fluid / Q000737:chemistry* / Q000166:cytology*; D003048:Coccidiosis / Q000473:pathology*; D004195:Disease Models, Animal; D005849:Gerbillinae; D008099:Liver / Q000469:parasitology / Q000473:pathology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D018688:Neospora; D009569:Nitric Oxide / Q000032:analysis; D010537:Peritoneum / Q000473:pathology; D011506:Proteins / Q000032:analysis; D013154:Spleen / Q000473:pathology; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D014122:Toxoplasma; D014123:Toxoplasmosis / Q000378:metabolism / Q000473:pathology*
chemical_list: D062107:Advanced Oxidation Protein Products; D000418:Albumins; D011506:Proteins; D017392:Thiobarbituric Acid Reactive Substances; D009569:Nitric Oxide
keywords: Gerbils; Liver damage; Mice; Neosporosis; Peritoneal fluid; Toxoplasmosis