Temporal expression of Toxoplasma stage-specific genes in brain tissue: coincidence with parasitological and histopathological findings in mice models.

In the intermediate hosts, tachyzoites of T. gondii predominate in the acute stage while bradyzoites persist inside tissue cysts with the potential for reactivation. The two stages exhibit different metabolic and antigenic characters. The present study aimed to investigate temporal expression of Toxoplasma SAG1 and BAG1 genes in the brain tissue and the coincident parasitological and histopathological findings in mice models of toxoplasmosis. The study included group A: mice infected with RH strain and sacrificed 7 days post-infection (p.i.); group B: mice infected with RH strain and treated with sulfamethoxazole-trimethoprim (30 mg/kg/day and 150 mg/kg/day respectively) 24 h p.i. until sacrificed at days 5, 10, or 20 post-treatment; group C: mice infected with ME-49 strain and sacrificed at days 7, 27, 47, or 67 p.i; and group D: mice infected with ME-49 strain and received dexamethasone daily starting at day 68 p.i. and scarified at days 6 or 10 post-treatment. All mice were inspected daily for abnormal physical signs. Peritoneal exudate and brain homogenate were examined for detection of Toxoplasma stages. Brain sections were examined histopathologically. SAG1 and BAG1 gene expression was evaluated using reverse transcription real-time polymerase chain reaction and the ΔΔCt method. Results revealed that marked BAG1 upregulation is consistent with detection of Toxoplasma cysts and degenerative changes while predominance of tachyzoites and inflammatory infiltrate is compatible with SAG1 upregulation. The study sheds light on the potential for using stage-specific gene expression pattern as markers for evaluation of toxoplasmosis disease progression in clinical settings.

Detection of Helicobacter pylori infection in Egyptian patients with chronic calcular cholecystitis.

Reports of Helicobacter pylori in biliary tract diseases in humans are very fragmentary, and therefore there is a need for further investigations. This study aims to detect H. pylori in the bile and gall bladder (GB) of patients with chronic calcular cholecystitis (CCC), and to determine the association of H. pylori infection with gallstone type. Thirty patients with CCC admitted for laparoscopic cholecystectomy were investigated, including upper gastro-endoscopy before cholecystectomy. Rapid urease test and histopathological examination were performed on gastric biopsies. The GB specimens were investigated for the presence of H. pylori by immunohistochemistry (IHC). H. pylori antigen in bile was detected by enzyme immunoassay. Chemical analysis of gallstones was performed to determine type. Immunohistochemistry testing showed 73.3% and 66.7% positivity among GB neck and body biopsies, respectively, demonstrating high sensitivity and specificity. A significant association was found between gastric and GB H. pylori positivity (P < 0.01). H. pylori antigen was detected in bile from three CCC cases. The greatest number of stones were of the calcium bilirubinate type. Gall bladder positivity for H. pylori was accompanied by chronic quiescent gastritis (40.9%). In conclusion, H. pylori infection may be an aetiological factor leading to cholecystitis. Gastric colonisation with H. pylori could be a source for GB infection, and the organism may act as a lithogenic component, especially in the context of pure pigmented gallstones.