The correlation of TNF alpha levels with acute phase proteins in acute Toxoplasma gondii infection in mice.

Acute Toxoplasma gondii infections can influence the liver as well as other organs. Many cytokines and proteins play a role in the acute response against infection. Tumor necrosis factor alpha (TNF alpha) is a cytokine that plays a key function in stimulating hepatocytes to produce acute phase proteins. In this study, we investigated TNF alpha levels associated with the levels of macroglobulin, haptoglobin, hemopexin, C-reactive protein (CRP), albumin, serum amyloid alpha protein (SAA), and clusterin, which are acute phase proteins, in serum of mice with T. gondii infection. In the experiment, a total of 24 mice were used; 6 mice constituted the control group and 18 mice were infected with the RH strain. On the 2nd, 4th, and 6th days following the infection, 6 animals were euthanized, and their serums were collected. Compared to the control group, we observed a statistically significant decrease in albumin concentration in the group with T. gondii infection on the 6th day. Also, this group displayed a statistically significant, gradual increase in clusterin levels on the 2nd and 6th days, C-reactive protein levels on the 4th day, haptoglobin levels on the 2nd and 4th days, hemopexin levels on the 2nd day, serum amyloid A levels on the 2nd, 4th, and 6th days, and TNF-α levels on the 2nd, 4th, and 6th days (p < 0.05). TNF-α was strongly positively correlated with CRP, SAA, and clusterin, moderately positively correlated with hemopexin, and strongly negatively correlated with albumin. The increase in CRP, SAA, clusterin, and hemopexin levels on the 2nd day after infection, in parallel with the increase in TNF-α levels, indicates that these proteins can be considered as major acute phase proteins in acute T. gondii infection in mice. The data obtained here may be helpful for the diagnosis of T. gondii infection and for monitoring treatments.

Increased expressions of ADAMTS-13 and apoptosis contribute to neuropathology during Toxoplasma gondii encephalitis in mice.

Toxoplasma gondii (T. gondii) is a protozoan parasite with the potential of causing severe encephalitis among immunocompromised humans and animals. Our previous study showed that T. gondii induces high nitric oxide (NO) production, high glial activation (GFAP) and neurofilament expressions, leading to severe neurodegeneration in toxoplasma encephalitis (TE) in the central nervous system (CNS). The aim of this experimental study was to investigate ADAMTS-13 expression and apoptosis in CNS and to identify whether they have any correlation with toxoplasmosis neuropathology and neurodegeneration. Mice were infected with ME49 strain T. gondii and the levels of ADAMTS-13, caspase 3, caspase 8, caspase 9, TNFR1 and Bcl-xL expressions were examined in brain tissues by immunohistochemistry, during the development and establishment of chronic infections at 10, 30 and 60 days post-infection. Results of the study revealed that the levels of ADAMTS-13 (P < 0.005), caspase 3 (P < 0.05), caspase 8 (P < 0.05), caspase 9 (P < 0.005) and TNFR1 (P < 0.05) expressions in the brain markedly increased while Bcl-xL expression decreased (P < 0.005). The most prominent finding from our study was that 10, 30 and 60 days post-infection ADAMTS-13 increased significantly and this may play an important role in the regulation and protection of the blood-brain barrier integrity and CNS microenvironment in TE. These results also suggest that T. gondii-mediated apoptosis might play a pivotal role and a different type of role in the mechanism of neurodegeneration and neuropathology in the process of TE. Furthermore, expression of ADAMTS-13 might give an idea of the progress and is critical for diagnosis of this disease. To the best of the authors' knowledge, this is the first report on ADAMTS-13 expression in the CNS of T. gondii-infected mice.

Paracetamol-induced nephrotoxicity and oxidative stress in rats: the protective role of Nigella sativa.

Context Nigella sativa L. (Ranunculaceae) (NS) is traditionally used to treat many conditions such as inflammation. Objective This study evaluates the effects of NS seeds ethanol extract in paracetamol-induced acute nephrotoxicity in rats. Materials and methods Forty-eight female Wistar Albino rats were divided into eight groups: I = sham; II = sham + 1000 mg/kg NS; III = sham + 140 mg/kg (N-acetyl cysteine) NAC; IV = 2 g/kg paracetamol; V = 2 g/kg paracetamol + 140 mg/kg NAC; VI, VII and VIII = 2 g/kg paracetamol + 250, 500 and 1000 mg/kg NS, respectively. Paracetamol administration (oral) was carried out 1 h after NS and NAC administrations (oral), and all animals were sacrificed 24 h later. Results Paracetamol administration significantly increased serum urea (88.05 U/L) and creatinine (0.80 U/L) when compared with the sham group (49.80 and 0.31 U/L, respectively). However, serum urea level was reduced to 65.60, 56.00 and 54.18 U/L, with 250, 500 and 1000 mg/kg doses of the extract, respectively. Also, serum creatinine level was reduced to 0.64, 0.57 and 0.52 U/L with 250, 500 and 1000 mg/kg doses of the extract, respectively. NS administration increased superoxide dismutase and glutathione, and decreased malondialdehyde levels in the kidneys. Kidney histopathological examinations showed that NS administration antagonized paracetamol-induced kidney pathological damage. Discussion and conclusions The results suggest NS has a significant nephroprotective activity on paracetamol-induced nephrotoxicity. It may be suggested that the antiinflammatory and antioxidant effects of NS ethanolic extract originated from different compounds of its black seeds.

Nitric oxide production increases during Toxoplasma gondii encephalitis in mice.

Toxoplasma gondii is an intracellular parasite with the potential of causing severe encephalitis among immunocompromised human and animals. The aim of this experimental study was to investigate the immunomodulatory and immunopathological role of nitric oxide (NO) in central nervous systems and to identify any correlation between toxoplasmosis neuropathology and investigate the consequences of the cellular responses protect against T. gondii. Mice were infected with ME49 strain T. gondii and levels of endothelial, neuronal and inducible nitric oxide synthase (eNOS, nNOS, iNOS), glial fibrillary acidic protein (GFAP) and neurofilament (NF) were examined in brain tissues by immunohistochemistry, during the development and establishment of a chronic infection at 10 30 and 60 days post infection. Results of the study revealed that the levels of eNOS (p < 0.05), nNOS (p < 0.05), iNOS (p < 0.005), GFAP (p < 0.005) and NF (p < 0.005) were remarkably higher in T. gondii-infected mice than in uninfected control. The most prominent finding from our study was 10 and 30 days after inoculation data indicating that increased levels of NO not only a potential neuroprotective role for immunoregulatory and immunopathological but also might be a molecular trigger of bradyzoite development. Furthermore, this findings were shown that high expressed NO origin was not only inducible nitric oxide synthase but also endothelial and neuronal. We demonstrated that activation of astrocytes and microglia/macrophages is a significant event in toxoplasma encephalitis (TE). The results also clearly indicated that increased levels of NO might contribute to neuropathology related with TE. Furthermore, expression of NF might gives an idea of the progress and critical for diagnostic significance of this disease.

Determination of macrophage types by immunohistochemical methods in the local immune response to liver hydatid cysts in sheep.

Cystic echinococcosis is a zoonotic parasitic disease caused by Echinococcus granulosus. The main hosts in the life cycle of this parasite are dogs and other carnivores; The intermediate hosts are human, sheep, goat, cattle, pig, buffalo, horse and camel. The parasite damages the tissue by forming lesions in the form of fluid-filled cysts in the liver. These lesions are bounded by a layer of local inflammatory cells formed by the host. In the layer formed by this inflammatory response, there are lymphocytes, neutrophils and eosinophil leukocytes, including macrophages. Samples taken from sheep with hydatid cysts in their livers were followed for pathological analysis, and then histopathological and immunohistochemical examinations were performed. After histopathological examinations, the types of macrophages involved in the local immune response against cysts in the liver were determined by immunohistochemical methods using anti-INOS and anti-IL-10 antibodies. INOS and IL-10 immunopositivity were detected in all samples. Statistically, no significant difference was observed between these immunopositivity. This showed that both macrophage types are involved in the local immune response to hydatid cyst, and that Th1 and Th2 immune response stimulation continues together. It was concluded that in future studies that will be planned and experimentally, it will be possible to reveal more clearly how these macrophage types take part in the local immune response.

Expression of serotonin 2A, 2C, 6 and 7 receptor and IL-6 mRNA in experimental toxoplasmic encephalitis in mice.

The neurotropic pathogen Toxoplasma gondii infects about one-third of the human population. Both acute and chronic (latent or life-long) forms of toxoplasmosis are associated with specific neurologic and neuropsychiatric symptoms. In the present study, swiss albino mice were inoculated intraperitoneally with 15-20 tissue cysts of the ME-49 strain of Toxoplasma gondii. The brain samples were collected on the days 10, 20, and 30 for determining the histopathological scores and the number of cysts. Furthermore, a real-time quantitative polymerase chain reaction (RT-PCR) was conducted to find out the gene expression levels of the serotonin 2A receptor (5-HTR2A), serotonin 2C receptor (5-HTR2C), serotonin 6 receptor (5-HTR6), serotonin 7 receptor (5-HTR7), and interleukin-6. The results were compared to the histopathological findings of encephalitic toxoplasmosis. The expression levels were observed to increase for all receptors; however at different time points of infection. This experimental model demonstrates that the expression of serotonin receptors was induced in Toxoplasma gondii infections, displaying unique findings for each of the individual receptors.

Role of stellate cells in hepatic echinococcosis in cattle.

Hydatid cysts formed by the metacestodes of Echinococcus granulosus. Cattle suffering from hydatid cyst shows fluid-filled structures, especially in liver. These parasite-induced cysts localized by forming fibrous capsules in the liver. Fibrogenesis is the host immune response in the liver against these parasites. Hepatic stellate cells (HSCs) are localized perisinusoidal space also known as vitamin A-storing cells, characterize the important fibrogenic cell type. In this study, livers from 15 animals with hydatid cyst and 8 healthy animals were used. Hematoxylin and Eosin, masson trichrome staining were performed on the prepared liver sections. Microscopically, cysts were bordered eosinophilic necrotic debris blended with degenerate neutrophils, macrophages, eosinophils, lymphocytes, plasma cells and multinucleated giant cells, which extend into the adjacent fibrous connective tissue. In Masson trichrome staining, the fibrous connective tissue was observed surrounding of hydatid cyst. Glial fibrillary acidic protein (GFAP), collagen I, GFAP/collagen I, positive cells were investigated using either indirect single- or double-labeling immunohistochemical staining. The results indicated that anti-GFAP-positive staining was seen in areas including fibrous tissue just under the foreign body giant cells surrounding the cyst wall. In double immunohistochemical staining, it was observed that HSCs labeled with anti-GFAP antibody in the fibrous connective tissue also labeled anti-collagen I antibody. This study shows that HSCs may responsible for synthesis the collagen I in the development of parasitic fibrosis in cystic echinococcosis in the liver of cattle.

Tracking acute phase protein response during acute and chronic Toxoplasma gondii infection.

Toxoplasmosis is a disease caused by the protozoan Toxoplasma gondii, which occurs worldwide in mammals and birds. Brain is the primary target organ because Toxoplasma gondii is a ubiquitous intracellular parasite that causes most frequently life-threatening encephalitis in immunocompromised patients. Relation of tissue cysts number, histopathology score and acute phase proteins were investigated. In this study, 36 mice are infected with Me49 strain of Toxoplasma gondii. The control group has 6 healthy mice. After inoculation of Toxoplasma gondii, at 10., 15., 20., 30., 45., 60. days, 6 each mice euthanized after collection of blood samples. Hemopexin, haptoglobulin, macroglobulin, serum amyloid A and clusterin levels are determined by ELISA. Then, brain tissues were investigated histopathologically and lesions were scored. The average cyst numbers were determined by counting three samples (25 µl each) of each brain homogenate under light microscopy. Inflammatory reaction was observed on day 10 days after inoculation (d.a.i.) The lesions were characterized by perivascular mononuclear cell infiltration, focal mononuclear cell infiltration in the meninges, and glial proliferation. Tissue cysts were observed in all Toxoplasma gondii-infected groups. The highest lesion score was observed at 60 d.a.i. And the most tissue cyst number were on day 30. d.a.i. Serum levels of hemopexin, haptoglobulin, macroglobulin, serum amyloid A and clusterin were significantly higher than the control group on day 10-20., 10., 10-30., 10.,10-45 d.a.i., respectively. High level of acute phase proteins in mice on certain days infected with Toxoplasma gondii was exhibited a relationship between brain lesions and tissue cysts.

Role of oxidative stress in the pathophysiology of Toxoplasma gondii infection.

Oxidative stress (OS) plays an essential role in the pathogenesis of common neurodegenerative diseases. We have previously shown that Toxoplasma gondii (T. gondii) induces high nitric oxide (NO) production, glial activation, and apoptosis that altogether cause severe neuropathology in toxoplasma encephalitis (TE). The objective of this study was to investigate the cytotoxic effect of OS and to identify a correlation between the causes of T. gondii induced neuropathology. Expression levels of glutathione reductase (GR), Cu/Zn superoxide dismutase (SOD1), neuron specific enolase (NSE), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were investigated. Results of the study revealed that the levels of GR (P <0.005) and NSE (P <0.001) expression in the brain tissue markedly increased while SOD1 activity decreased (P <0.001) in the infected group compared to the non-infected group. In addition, intense staining for 8-OHdG (P <0.05) was observed both in the nucleus and the cytoplasm of neurons and glial cells that underwent OS. These results were reasonable to suggest that T. gondii-mediated OS might play a pivotal role and a different type of role in the mechanism of neurodegeneration/neuropathology in the process of TE. The results also clearly indicated that increased levels of NO and apoptosis might contribute to OS-related pathogenesis of TE. As a result, OS and expression of NSE might give an idea of the disease progress and may have a critical diagnostic significance for patients with T. gondii infection.

Does bosentan protect diabetic brain alterations in rats? The role of endothelin-1 in the diabetic brain.

Diabetes mellitus (DM) is a major problem all over the world, affecting more people in recent years. Individuals with diabetes are more prone to disease than non-diabetics, especially vascular complications. The aim of this study was to examine the roles of the endothelin (ET)-1 in brain damage formed in a streptozocin (STZ)-induced diabetes model, and the effect of bosentan, which is the non-specific ET1 receptor blocker in the prevention of the diabetes-induced brain damage. To examine the effects of bosentan (50 mg/kg and 100 mg/kg) in this study, the rats were given the drug for 3 months. The rats were divided into four groups: the sham group (n = 10), the diabetic control group (n = 10), the group of diabetic rats given bosentan 50 mg/kg (n = 10) and the group of diabetic rats given bosentan 100 mg/kg (n = 10). Diabetes was induced in the rats by STZ (60 mg/kg i.p.). On day 91, all rats were killed. Brain tissues of the rats were measured by molecular, biochemical and histopathological methods. Antioxidant levels in the therapy groups were observed as quite near to the values in the healthy group. In this study, while the brain eNOS levels in the diabetic groups decreased, the ET1 and iNOS levels were found to be increased. However, in the diabetes group, hippocampus and cerebellum, pericellular oedema and a number of neuronal cytoretraction were increased in neuropiles, whereas these results were decreased in the therapy group. Based on all of these results, ET1 will not be ignored in diabetes-induced cerebral complications.

Tnf-α inhibition by infliximab as a new target for the prevention of glycerol-contrast-induced nephropathy.

Contrast medium-induced nephropathy (CIN) remains as a problem with high incidence and mortality rates. The aim of this study is to examine the roles of infliximab (INF) in the glycerol (GLY) and CIN model in rats. The rats were separated into five groups (n=8): Healthy, GLY, GLY+CM, GLY+CM+INF 5mg/kg intraperitoneally (i.p.), and GLY+CM+INF 7 mg/kg (i.p.). Antioxidant levels in the therapy groups were observed to be quite similar to those in the healthy group. In this study, while the kidney TNF-α, IL-1ß, TGF-1ß and Caspase 3 gene expressions' levels increased in the nephrotoxic groups, these levels were found to have decreased in the treatment groups. Moreover, histopathologic examination showed that hyaline, haemorrhagic casts and necrosis were increased in nephrotoxicity group, whereas they decreased in the therapy group. Furthermore, TNF-α and NF-κB expression were decreased with infliximab administrated groups similar to control group. In conclusion, we suggest that infliximab have protective roles on CIN.

Protective effect of resveratrol on sodium fluoride-induced oxidative stress, hepatotoxicity and neurotoxicity in rats.

Protective effect of resveratrol on sodium fluoride-induced oxidative stress, hepatotoxicity and neurotoxicity were studied in rats. A total of 28 Wistar albino male rats were used. Four study groups were randomly formed with seven animals in each. The groups were treated for 21days with distilled water (control group), with water containing 100ppm fluoride (fluoride group), with resveratrol (12.5mg/kg i.p., resveratrol group), or with 100ppm fluoride+12.5mg/kg resveratrol i.p. (fluoride+resveratrol group). At the end of the trial, blood samples were collected by cardiac puncture and tissue samples were taken simultaneously. The total antioxidant and oxidant status in plasma and tissues as well as plasma 8-hydroxydeoxyguanosine levels were measured. Histopathological analyses of rat liver and brain tissues were performed in all groups to identify any changes. In the fluoride group, the total oxidant levels increased in plasma, liver and brain and total antioxidant levels decreased, as did the plasma 8-hydroxy-deoxyguanosine levels. These changes were prevented by co-administration of resveratrol. In addition, fluoride-associated severe histopathological changes in brain and liver tissues were not observed in the fluoride+resveratrol group. Consequently, these data suggested that resveratrol had beneficial effects in alleviating fluoride-induced oxidative stress.

Effects of ozone therapy and taurine on ischemia/reperfusion-induced testicular injury in a rat testicular torsion model.

BACKGROUND/AIM: To investigate the effect of ozone and/or taurine treatment comparatively on testicular damage due to ischemia/ reperfusion (I/R) injury in an experimental torsion model in rats. MATERIALS AND METHODS: Adult Wistar rats with and without torsion/detorsion were used. In order to monitor the effect of ozone and/or taurine treatment on testicular damage due to I/R injury, following histopathological investigation apoptotic indexes were scored by TUNEL method. Moreover, tumor necrosis factor receptor 1 (TNFR1), caspase 3, caspase 8, endothelial nitric oxide synthase (eNOS), tumor necrosis factor alpha (TNFα), and cytochrome C immunostainings were performed and the levels of malondialdehyde, glutathione peroxidase, superoxide dismutase, catalase, total sulfhydryl, and nitric oxide were determined in the testicular tissue. RESULTS: Intraperitoneal ozone and/or taurine treatment prevented both histopathological damage and increase in the apoptotic index. Torsion did not exert an effect on the levels of TNFα and cytochrome C. Ozone and/or taurine treatment prevented increases in TNFR1, caspase 3, and caspase 8. The level of oxidative stress markers was unchanged. The increases in NO level and eNOS expression were prevented by ozone and/or taurine treatment in I/R groups. CONCLUSION: Using ozone therapy and/or taurine before reperfusion may be a solution for germ cell degeneration resulting from testicular torsion and related infertility.

The ocular endothelin system: a novel target for the treatment of endotoxin-induced uveitis with bosentan.

PURPOSE: We compared the anti-inflammatory effects of bosentan and dexamethasone in endotoxin-induced uveitis (EIU). METHODS: Endotoxin-induced uveitis was induced by subcutaneous injection of lipopolysaccharide (LPS, 200 µg) in Wistar rats. Rats were divided randomly into 10 groups (n = 6). Bosentan at doses of 50 and 100 mg/kg were administered orally 1 hour before and 12 hours after LPS injection, and dexamethasone was administered by intraperitoneally 30 minutes before and 30 minutes after LPS injection at a dose of 1 mg/kg. Data were collected at two time points for each control and treatment; animals were killed at either 3 or 24 hours after LPS injection. Histopathologic evaluation and aqueous humour measurements of TNF-α level were performed, and endothelin-1 (ET-1), inducible nitric oxide synthase (iNOS), and endothelin receptor A and B (EDNRA and B) expression were analyzed. RESULTS: The group treated with 100 mg/kg bosentan at 24 hours displayed significantly milder uveitis and fewer inflammatory cells compared to LPS-injected animals, and there were similar findings in the dexamethasone-treated group at 24 hours. The TNF-α levels in the dexamethasone treatment group were lower than those in the LPS-induced uveitis control group (P < 0.05); however, there was no difference between the dexamethasone and bosentan treatment groups at 3 and 24 hours after LPS administration. Bosentan treatment at doses of 50 and 100 mg/kg significantly decreased iNOS expression compared to LPS-injected animals (P < 0.001). The ET-1 expression was suppressed significantly by bosentan and dexamethasone at 3 and 24 hours after LPS administration (P < 0.001). The EDNRA expression in the bosentan treatment groups was statistically significantly lower than that in the LPS-induced uveitis control group at 3 and 24 hours after LPS administration (P < 0.05). CONCLUSIONS: Bosentan reduces intraocular inflammation and has similar effects as dexamethasone in a rat model of EIU.

Hepatic stellate cells increase in Toxoplasma gondii infection in mice.

BACKGROUND: Toxoplasma gondii is a ubiquitous protozoan parasite that can infect humans and animals. The severity of toxoplasmosis varies according to the immune status of the individual, parasite strain, and host species. In mammalian species, it has been observed that severe lesions of acute toxoplasmosis form in visceral organs such as the liver, lung, and spleen. Some epidemiological studies have reported an association of T. gondii infection with liver cirrhosis. METHODS: Acute infection was induced in fifteen 30-day-old normal Swiss albino mice. The mice were infected by intraperitoneal inoculation of 5000 T. gondii RH strain tachyzoites. The mice were sacrificed in groups of 5 at 2, 4, and 6 days after inoculation. Another group of 5 mice were used as the controls. Anti-glial fibrillary acidic protein (GFAP) and anti-T. gondii antibodies were used to compare GFAP-immunoreactive cells and anti-T. gondii-immunopositive areas in the liver between the T. gondii-infected groups and the healthy controls, respectively. RESULTS: There was a significant correlation between the numbers of GFAP-positive hepatic stellate cells (HSCs) when they were compared with T. gondii antigen immunostaining (p < 0.05). The amount of T. gondii immunostaining increased significantly with the increase in the number of HSCs. CONCLUSIONS: There is a significant relationship between the number of HSCs and T. gondii antigens, which may represent an active role of HSCs in liver pathology and the pathobiology of T. gondii-related hepatitis.

A rare case of feline congenital Toxoplasma gondii infection: fatal outcome of systemic toxoplasmosis for the mother and its kitten.

This report describes a case of fatal systemic toxoplasmosis in a 2.5-year-old mixed breed pregnant cat and its kittens. The pregnant cat was presented to the gynecology clinic with symptoms of dystocia. The ultrasound examination revealed the presence of five fetuses in the uterus, three of which were not alive, and consequently a cesarean section was performed. However, the mother cat and the remaining two live kittens died two and ten days after cesarean section, respectively. Pathologically, severe alveolar edema, tachyzoite-like structures in the alveolar macrophages and multifocal necroses in the lungs of mother cat were observed. An intense Toxoplasma gondii immunopositive reaction was observed in the cytoplasms of alveolar macrophages, bronchial and bronchiolar epithelia, necrotic foci in the lungs, and Kupffer cells of the liver. PCR analyses amplified T. gondii DNA in tissue samples of the mother cat and kittens. The present study provides strong evidence for a transplacental transmission of T. gondii infection with deadly outcome for the mother cat, fetuses and kittens. As to the authors' knowledge, this report is the first case of fatal congenital toxoplasmosis in domestic cats in Turkey.

In-vivo efficacy of toltrazuril on experimentally induced Toxoplasma gondii tissue cysts in lambs: a novel strategy for prevention of human exposure to meat-borne toxoplasmosis.

The aim of the present study was to investigate in vivo efficacy of toltrazuril on Toxoplasma gondii tissue cysts following induction of chronic toxoplasmosis in 4-week-old lambs (n=27) by inoculation of 1×10(5) T. gondii ME 49 strain oocysts (day 0). Beginning at the 15th day after inoculation, lambs in Group T20 and Group T40 were given toltrazuril orally 2 times, once every week (Baycox 5%, Bayer Animal Health) at a dose of 20 mg/kg and 40 mg/kg, respectively. Positive control (PC) lambs were not given any therapy, and 2 clinically healthy non-infected lambs were used as negative controls (Group NC). Two out of 9 lambs in PC group (oocyst inoculated but non-treated) were killed on toltrazuril treatment days (day 15 and 22) to evaluate the tissue cyst presence in their muscles. On day 90, the remaining 25 lambs were necropsied, and samples from the brain and 11 different muscle groups were collected. The tissues were examined for the presence of tissue cysts by histopathology, immunohistochemistry, nested-PCR and percoll gradient centrifugation. Anti-T. gondii antibodies were screened by IFAT throughout the experiment. The increased T. gondii seropositivity beginning from the 15th day of inoculation remained steady at Day 45 and Day 90 in Groups PC while it was significantly lower at Day 90 in toltrazuril receiving groups. In toltrazuril treated groups, histopathological findings included degenerative changes in the cyst wall, complete macrophage invasion to the cysts, and reduction or removal of the cysts in toto. Four out of 9 lambs (44.4%) in both toltrazuril treated group (Group T20 and T40) did not contain tissue cyst in any examined tissues while all positive control animals had T. gondii tissue cysts at least in one muscle group. The toltrazuril treatment efficacy on the cyst presence was determined as 44.4%. The number of the cysts in the musculature was significantly different between non-treated and toltrazuril treated lambs (X(2)=6.613; p=0.037). For the total number of cysts, the positive control lambs had higher number of cysts compared to both toltrazuril treated lambs (T20 and T40) (X(2)=5.629; p=0.018 and X(2)=5.629; p=0.018, respectively) while there were no differences between Group T20 and Group T40 (X(2)=0.000; p=1.000). According to PCR results, the brain and M. semitendinosus were positive in all 7 control lambs while 12 out of 18 lambs were positive in toltrazuril treated lambs. In conclusion, the results are promising as the toltrazuril treated lambs had markedly less parasite counts compared to those of untreated lambs. Further research should be conducted to reveal if toltrazuril treatment in sheep could be used as a strategy to minimize the cyst exposure of humans through consumption of raw or undercooked mutton.

Clinicopathologic diagnosis of cutaneous toxoplasmosis in an Angora cat.

This report deals with a case of cutaneous toxoplasmosis in a 2 year-old female Angora cat. Cutaneous lesions were characterized by prescapular ulcers and hyperemic nodules in the skin of the inguinal and dorsosacral regions. A skin biopsy sample was collected from the lesioned area and processed for histopathologic examination and immunoperoxidase test using Toxoplasma gondii and Neospora caninum specific antibodies. Toxoplasma gondii immunopositive reactions were detected in keratinocytes and dermal macrophages while no immunoreactivity was detected for N. caninum. The case of cutaneous toxoplasmosis was further confirmed by PCR analysis using T. gondii B1 gene-specific primers. In conclusion, we report the first case of cutaneous toxoplasmosis in Angora cats.

[The prevalence of Sarcocystis species in sheep slaughtered in municipality slaughterhouse in Kirikkale]. / Kirikkale belediye mezbahasi'nda kesilen koyunlarda Sarcocystis türlerinin yayginligi

This study was undertaken for the determination of Sarcocysts species in sheep slaughtered in Kirikkale Municipality Slaughterhouse. For this study, oesophageal, diaphragm and intercostal muscles were collected from randomly selected 112 sheep out of 1131 sheep (814 sheep and 317 lambs) that were slaughtered from October 2005 to May 2006. The samples were examined for macro and microcyst of Sarcocysts spp. Macrocysts and microcysts were found in 58.92% of the overall samples. Microcysts were found in 47.32% and macrocysts were perceived in 20.53% of the sheep that were under examination. The distribution of the microcysts with respective to the age of the sheep was studied and it has been observed that 16.12% (5 in every 31 lambs) of the lambs under 1 year old and 59.25% (48 in every 81 sheep) of the sheep equal or older than 1 year old had possessed microcysts. Sarcocystis ovicanis (47.32%) and S. arieticanis (1.23%) were the species with the highest and lowest number of recurrences respectively. Macrocysts were observed in every sheep over one age. In addition, randomly selected oesophagi with macrocyst were examined histopathologically. Sarcocystis sporocysts were not found in dog feces.