muramidase and Typhoid-Fever

Protein secretion mechanisms are essential for the virulence of most bacterial pathogens. Typhoid toxin is an essential virulence factor for Salmonella Typhi, the cause of typhoid fever in humans. This toxin is unique in that it is only produced within mammalian cells, and it must be trafficked to the extracellular space before intoxicating target cells. An essential and poorly understood aspect of this transport pathway is the secretion of typhoid toxin from the bacterium into the S. Typhi-containing vacuole. We show here that typhoid toxin secretion requires its translocation to the trans side of the peptidoglycan layer at the bacterial poles for subsequent release through the outer membrane. This translocation process depends on a specialized muramidase, the activity of which requires the localized editing of peptidoglycan by a specific ld-transpeptidase. These studies describe a protein export mechanism that is probably conserved in other bacterial species.

Topics: Bacterial Proteins; Bacterial Toxins; Cell Line; Cell Wall; Humans; Muramidase; Peptidoglycan; Peptidyl Transferases; Protein Transport; Salmonella typhi; Typhoid Fever; Virulence

Topics: Cell Wall; Humans; Muramidase; Peptidoglycan; Peptidyl Transferases; Typhoid Fever

Enteric fever is a systemic illness caused by Salmonella infection, with S. typhi, S. paratyphi, and S. enteritidis being the most common serotypes. Humans are the only reservoir for S. typhi, and its predilection for the ileum is due to the fact that organisms enter the body by translocation across specialized Peyer's patch epithelium and then proliferate in the mucosal macrophages. The lesions in bowel and mesenteric lymph nodes are distinctive and mimic Kikuchi-Fujimoto disease and Rosai-Dorfman disease as well as infections caused by some non-salmonella bacteria. The four cases presented in this report, two culture-confirmed, all exhibited ileal mucosal hypertrophy caused by a neutrophil-poor monocyte/macrophage-rich hyperplasia. Though diffuse areas were present, much of the lesional proliferation was nodular, representing macrophage infiltration and colonization by the monocytes and macrophages. Immunophenotypic studies, which showed a CD68+, lysozyme+, UCHL-1+, OPD4-, CD4-, s100- profile, were helpful in distinguishing these lesions from other processes, including Kikuchi-Fujimoto disease and Rosai-Dorfman disease. Although rare in developed countries, enteric fever should be considered in any patient with recent travel to endemic areas and in the context of illness thought to be related to contaminated foods.

Topics: Adult; Antigens, CD; Antigens, Differentiation, Myelomonocytic; Child; Child, Preschool; Enteritis; Female; Humans; Ileum; Immunophenotyping; Leukocyte Common Antigens; Male; Muramidase; Typhoid Fever

Topics: Adolescent; Adult; Child; Child, Preschool; Chloramphenicol; Humans; Middle Aged; Muramidase; Phenylbutazone; Prednisolone; Typhoid Fever

Topics: Animals; Antibody Formation; Antigens; Dysentery, Bacillary; Escherichia coli; Muramidase; Rabbits; Typhoid Fever; Vaccination

Topics: Animals; Antibodies; Blood; Blood Bactericidal Activity; Complement System Proteins; Immunity; Mouth; Muramidase; Rabbits; Salmonella; Shigella; Staphylococcus; Typhoid Fever; Vaccination

Topics: Acid Phosphatase; Animals; Cathepsins; Electron Transport Complex II; Glucuronidase; Immunity; Metabolism; Mice; Muramidase; Peritoneum; Pharmacology; Research; Succinate Dehydrogenase; Typhoid Fever; Typhoid-Paratyphoid Vaccines

Topics: Animals; Anti-Infective Agents, Local; Antitoxins; Injections; Muramidase; Newcastle Disease; Plasma; Toxins, Biological; Typhoid Fever; Typhoid-Paratyphoid Vaccines

Topics: Agglutinins; Anti-Infective Agents, Local; Blood Proteins; Brucellosis; Humans; Muramidase; Typhoid Fever