Relation between cytotoxin producing Helicobacter pylori and Helicobacter pylorielated upper gastrointestinal disease

Helicobacter pylori [H. pylori], a major aetiological agent in gastritis, peptic ulcer and gastric cancer, is estimated to infect more than 50% of the world's population. However, only about 10% will develop peptic ulcer disease and 1 - 2% gastric malignancy. Virulent strains carrying the cag A gene and vac A s1 genotype and capable of cytotoxin production have been proposed to be associating with the severer forms or disease, although this was not universal. We were interested in studying the relation between cytotoxin-producing H. pylori strains and the H. pylori-related upper gastrointestinal disease in our community. Sixty patients were allocated into 3 predefined groups according to their endoscopic picture: gastroesophageal reflux disease [GERD], peptic ulcer disease, and gastritis groups. Gastric biopsies from the patients were examined for the presence of H. pylori by urease test and culture. The isolated H. pylori strains were subjected to cytotoxic assay to detect cytotoxin-producing strains. Forty-one patients [68.3%] were H. pylori positive, of them 19 [46.3%] were positive for cytotoxin production. Cytotoxin-producing H. pylori strains significantly associated peptic ulcer disease where 73.3% of peptic ulcer patients were infected with cytotoxin-producing strains. GERD was significantly associated with absence of H. pylori infection [66.7% of GERD patients were free of H. pylori infection]. The presence of gastritis did not correlate with the H. pylori status, however, there was a significant association between cytotoxin-producing strains and atrophic gastritis. Cytotoxin-producing H. pylori strains are associated with severer H. pylori-related upper gastrointestinal diseases such as atrophic gastritis and peptic ulcer disease. Our findings support the hypothesis of cag A [+] H. pylori being protective against GERD. Determination of cag A status of H. pylori strains bears importance in clinical practice in detecting patients at increased risk for developing gastric cancer and in helping planning treatment strategies

Chloramphenicol drug failure in typhoid fever

Two hundred positive blood culture typhoid patients admitted to Embaba Fever Hospital, Giza province, were subjected to: 1] Careful history and thorough clinical examination. 2] Complete blood picture. 3] Widal agglutination teat. 4] Urine and stool cultures for Salmonellae. 5] To the isolates of the cultures, disk diffusion chloramphenicol susceptibility test, minimum inhibitory concentrations and chloramphenicol acetyl transferase test were performed. The dose of chloramphenicol was restricted to 50 mg per Kg body weight daily, whatever the route used; whether oral, rectal or intravenous. When fever did not drop up to 5 days or the patient presented with typhoid complications or the blood culture revealed resistant Salmonellae, quinolones or third generation, cephalosporins were administered. Measurement of the level of chloramphenicol in the blood was performed for every patient. Fifty [25%] patients were found to be resistant in vitro and in vivo to chloramphenicol. All their Salmonellae isolates were resistant to chloramphenicol the mean zone size was 10 mm, the mean inhibitory concentration was 64 microgram per ml. and all were positive for chloramphenicol acetyl transferase. There was no significant difference in the serum level of chloramphenicol between susceptible and resistant groups to the drug. Results were interpreted and discussed

Histochemical studies on rectal mucosa in active intestinal schistosomiasis

Thirty patients suffering from active intestinal S. mansoni infection, were classified into 3 groups. The first group: 13 cases with early active intestinal schistosomiasis without hepatosplenomegaly. The second group: 11 cases with hepatoslenomegaly and the third group: 6 cases with splenomegaly and ascites. Also 10 normal individuals were included as a normal control group. Histopathological examination of rectal mucosa showed hyperaemia with extravasation of blood in early cases and grarulomatous lesions in the second group with hepatosplenomegaly. The structural changes were severe in the late ascitic group. In this group the rectal mucosal glands showed distorted irregular tubular branching in addition to the granulomatous and the fibrous reactions. Histochemical studies including periodic acid schiff, alkaline phosphatase and acetyl cholinestrase reactions were done. Using the periodic acid shiff stain, the goblet cells showed strong reaction for neutral mucin in cases of group I [early cases] and group II [late hepatosplenomegalic cases]. In group III [late ascitic cases] the goblet cells were faintly stained. A notable difference was observed between the lightly and heavily infected patients of this group. No alkaline phosphatase reactivity could be identified in rectal crypts of patients and controls. Alkaline phatase reactivity was sharply localised in S. mansoni egg shell. There was obvious decrease in the acetyl cholinesterase stained nerve fiber in the rectal mucosa of all studied patients. The decrease was more in chronic and heavily infected cases rather than in the acute and lightly infected ones

role of plasma prolidase enzyme assay in the diagnosis of early cases of bilharzial hepatic fibrosis

In this work, 40 male Egyptian patients having schistosomiasis were classified into early and late cases of bilharziasis accoding to the duration of the disease, they were subjected to the estimation of their plasma prolidase levels in an attempt to elucidate its role in the diagnosis of hepatic fibrosis. Our results indicate that the prolidase enzyme could help as a marker for the diagnosis of hepatic fibrosis in cases of early hepatic schistosomiasis. To the last of our Knowledge, this was the first attempt for the estimation of this enzyme in liver fibrosis concurrently occurring in cases of intestinal schistosomiasis. The results were analysed and discussed

Delayed hypersensitivity skin and leukocyte migration inhibition tests in chronic liver disease

Cell mediated immunity was evaluated in 30 patients with chronic liver disease and 10 healthy controls The patients were 14 with chronic active hepatitis or active cirrhosis, 9 with bilharzial hepatic fibrosis 4 with liver cirrhosis of mixed etiology and 3 with primary liver cell carcinoma. Delayed hypersensitivity skin test to PPD antigen and leucocyte migration inhibition test was performed. Results indicate that patients with chronic active hepatitis or active cirrhosis, bilharzial hepatic fibrosis and primary liver cell carcinoma exhibit marked depression of cell mediated immunity and also failure to secrete migration inhibition factor