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The aim of the study was to diagnose Sarcocystis sp. infections in cattle and to detect coinfections by Toxoplasma gondii and/or Neospora caninum. Blood, diaphragm, esophagus, and myocardium from 90 beef cattle from Argentina were collected. Histopathological, immunohistochemical, polymerase chain reaction assays, and direct microscopical examination were carried out. Sarcocysts from myocardium were measured and counted. Indirect fluorescent antibody test (IFAT) for the three protozoans was performed. Sarcocystis cruzi sarcocysts were found in 100% of myocardium samples. Sarcocysts per gram ranged from 8 to 380 with higher values found in adult cattle (p < 0.001). T. gondii and N. caninum were not detected by immunohistochemistry. T. gondii DNA was found in myocardium of 2/20 seropositive animals, while N. caninum DNA was not found. Antibodies against S. cruzi were detected in all samples, those against N. caninum in 73% and against T. gondii in 91% of the samples (IFAT titer > or =25). It is concluded that serology by IFAT is a suitable method to diagnose these protozoan infections due to its specific IgG detection; therefore, IFAT may be a useful tool to evaluate the impact of each protozoan infection in coinfected animals.

A case of eosinophilic myositis (EM) in an 8-year-old beef cow was investigated. The animal originated from a herd in which a high incidence of the disease had been observed in slaughtered adult females over a period of 2 years. Histologically, the lesions in the muscles were characterized as granulomas with a central core of degenerate eosinophils and remnants of necrotic muscle fibres, surrounded by a rim of epithelioid cells and fibrous tissue with an infiltrate consisting predominantly of eosinophils radiating outwards. Degenerate sarcocysts with a thick (7-9 microm) wall were present in the suppurative centre of most lesions. Intact sarcocysts with similar morphology were present in adjacent muscle fibres but without an associated inflammatory reaction. By transmission electron microscopy the sarcocysts were identified as Sarcocystis hominis, based on the morphology of villar protrusions of the sarcocyst wall, which were broad-based and cylindrical, with a blunt distal end, and contained numerous long microfilaments. Circumstantial evidence indicated a human source of infection, human faecal material having been spread on the pasture grazed by the cattle. The findings supported a causal relationship between S. hominis infection and EM in cattle.

The effects of experimental infection of calves with Sarcocystis cruzi on the blood coagulation cascade were investigated. Calves were inoculated orally with 1 x 10(5) sporocysts (group S1, n = 6) or with 5 x 10(5) sporocysts of S. cruzi (group S2, n = 3). A group of eight calves served as non-infected controls (group C). The animals were bled once during the first 4 weeks of infection and twice a week thereafter until day 40 p.i. The following parameters were measured: activated partial thromboplastin time, prothrombin time, thrombin time, reptilase time, thrombin coagulase time, factors XII, XI, X, IX, VIII:C, VII, V, prekallikrein, fibrinogen, alpha 2-antiplasmin, antithrombin III, alpha 1-antitrypsin, alpha 2-macroglobulin, haematocrit, haemoglobin, numbers of erythrocytes and thrombocytes. The infected calves developed acute sarcocystiosis from 25 (S1) or 29 (S2) days p.i. onwards. During the acute disease, antiproteases tended to elevated values and thrombocyte counts were generally reduced. In group S1 prolonged prothrombin time and reduced activities of factors VII or V were found. In group S2 accelerated prothrombin time and activated partial thromboplastin time, as well as elevated factor X activities, were recorded even before the onset of clinical disease at 19 days p.i. While prothrombin time returned to normal levels thereafter, activated partial thromboplastin time remained short. Activities of factor V, factor VII and factor X were significantly reduced in group S2 at the onset of acute sarcocystiosis, and one of the three calves died at 29 days p.i. The other parameters were not significantly affected by either dose of infection. No evidence for a classical disseminated intravascular coagulation syndrome could be found; however, it was demonstrated that S. cruzi alters plasma coagulation in a dose-dependent way.

A multistage protozoan parasitic disease was used as a cachexia model to study the effects of daily administration of bovine growth hormone (GH) on endocrine and body composition changes of young calves from the onset of the acute phase response (APR). Male calves averaging 127.5 +/- 2.0 kg body weight were assigned to control, ad libitum fed, noninfected (C); ad libitum fed, infected (250,000 oocysts Sarcocystis cruzi, per os, I); noninfected, pair-fed (PF) to matched I-treatment calves and these respective same treatments in calves injected daily with GH (USDA-bGH-B1), 12.5 mg/calf/day, im) designated as CGH, IGH and PFGH. GH injections were initiated on Day 20 postinfection (PI), 3 to 4 d before the onset of clinical signs of APR, and continued to Day 56 PI, at which time animals were euthanized for tissue collections. Abrupt increases in rectal temperature commensurate with up to 70% reduction in voluntary feed intake were observed in I and IGH beginning 23-25 d PI. For the trial period between Days 20 and 56 PI, average daily carcass protein gains were 123, 52, 109, 124, 48, and 67 g/d and average daily carcass fat gains were 85, 11, 43, 71, -23, and 29 g/d for C, I, PF, CGH, IGH, and PFGH, respectively. Effects of GH were significant for fat accretion and plasma urea depression. Rectus femoris was highly refractory to catabolic effects of infection while psoas major was significantly catabolized during infection. Plasma concentrations of insulin-like growth factor-I (IGF-I) increased significantly in all GH-treated calves between Day 20 and 23 PI. Plasma IGF-I declined well below Day 20 values in all infected calves from the onset of the APR through the end of the study. The decrease in plasma IGF-I concentrations in I and IG was highly correlated with the magnitude of the fever response. Hepatic mRNA for GH receptor and IGF-I was decreased in infected calves. Hepatic microsomal membrane binding of 125I-GH did not differ between groups. The data suggest that effects of GH and parasitism on tissue metabolism during disease may vary among different specific tissue pools. The data demonstrate that daily GH administration in young calves does not prevent lean tissue losses and may accelerate fat depletion associated with cachectic parasitism. Furthermore, the onset of APR overrode the capacity for GH to maintain elevated plasma concentrations of IGF-I, an effect not readily explained through changes of GH-receptor binding.

Extensive brain pathology attributed to Sarcocystis is described in a heifer and a 2- to 4-month-old calf. These appear to be the first recorded cases of naturally occurring acute sarcocystosis in cattle in sub-Saharan Africa. The heifer became recumbent and had convulsions before dying, while clinical signs in the calf included loss of body mass, diarrhoea, nervousness and opisthotonus. Disseminated haemorrhages were noted in the brains of both animals at necropsy. Microscopically, the grey and white matter contained multiple areas of necrosis associated with haemorrhage, fibrinoid vasculitis, perivascular cuffing and gliosis. A multifocal meningitis was also present. First-generation Sarcocystis schizonts were evident in, or adjacent to endothelial cells of several arterioles and small arteries. The association of first- (as opposed to second-) generation schizogony with overt and fatal bovine sarcocystosis, has not previously been reported.

A case of generalized eosinophilic myositis with sarcosporidiosis in a Finnish cow is reported. The whole carcass was condemned because of massive changes in skeletal muscles. Cat or man are the final hosts of Sarcocystis bovifelis or Sarcocystis hominis. The aetiology of eosinophilic myositis remains open and so does the question whether sarcosporidiosis has something to do with it.