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Metronidazole
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Metronidazole has also been reported to increase cyclosporine levels in a renal transplant recipient. Once again, this was in the setting of treatment for diarrhea—this time caused by Campylobacter coli (Herzig and Johnson, 1999). When a single dose of intravenous metronidazole 750 mg/m2 daily (equivalent to 1275 mg metronidazole daily) was co-administered with 5-fluorouracil (5-FU) for the treatment of metastatic colorectal cancer, clearance of the 5-FU was decreased, resulting in increased toxicity—74% of patients developed granulocytopenia of < 1500 cells/µl and there was one drug-related death. There was no enhanced therapeutic efficacy of 5-FU noted (Bardakji et al., 1986).
Campylobacter
Published in Dongyou Liu, Laboratory Models for Foodborne Infections, 2017
Martin Stahl, Bruce A. Vallance
The use of colostrum-deprived piglets as a model for C. jejuni infection was first defined by Babakhani et al.64 Although conventionally reared piglets may be susceptible to Campylobacter infection early in life, maternal antibodies are usually sufficient to prevent infection. Adult pigs are also known to be frequent carriers of both C. jejuni and Campylobacter coli65; however, the development of symptoms of gastroenteritis in response to these pathogens is rare. Colostrum-deprived piglets lack the protection of maternal antibodies that usually helps prevent infection in piglets. Additionally, at very young ages, they lack a fully mature immune response or a protective, fully developed intestinal microbiota, making them particularly susceptible to infections by enteric pathogens. This vulnerability has been previously exploited for the study of Escherichia coli66 and Salmonella67 infection, among others, and in a number of studies, it has been successfully used as a model for C. jejuni infection.37,42,68
Helicobacter pylori PqqE is a new virulence factor that cleaves junctional adhesion molecule A and disrupts gastric epithelial integrity
Published in Gut Microbes, 2021
Miguel S. Marques, Ana C. Costa, Hugo Osório, Marta L. Pinto, Sandra Relvas, Mário Dinis-Ribeiro, Fátima Carneiro, Marina Leite, Ceu Figueiredo
To better elucidate the nature of the JAM-A alteration induced by H. pylori infection, we conducted western blot analyses with two antibodies, recognizing epitopes either at the extracellular N-terminus or at the cytoplasmic C-terminus regions of this tight junction protein. Using the antibody directed against the cytoplasmic domain of JAM-A, and after infection of cell monolayers with H. pylori, we observed a significant decrease in the detection of the protein (Figure 2A). Interestingly, the use of the antibody directed against the extracellular region of JAM-A detected a lower-molecular-weight JAM-A protein in H. pylori-infected cells. These results suggest that cytoplasmic cleavage is the most likely phenomenon for the appearance of a lower-molecular-weight JAM-A. Additional experiments incubating lysates of different gastric cell lines and of H. pylori led to equivalent results, suggesting that the factor responsible for this cleavage is bacterial-associated and independent of the cell line used (Supplementary Figure S3A). Similar infection experiments with Campylobacter jejuni, Campylobacter coli, and Escherichia coli suggested that this phenotype is H. pylori-specific (Supplementary Figure S3B).
Functional analysis and cryo-electron microscopy of Campylobacter jejuni serine protease HtrA
Published in Gut Microbes, 2020
Urszula Zarzecka, Alessandro Grinzato, Eaazhisai Kandiah, Dominik Cysewski, Paola Berto, Joanna Skorko-Glonek, Giuseppe Zanotti, Steffen Backert
Campylobacter jejuni is an important Gram-negative human pathogen responsible for gastrointestinal infections known as campylobacteriosis. The European Food Safety Authority (EFSA) and the European Center for Disease Prevention and Control (ECDC) reported in 2017 that campylobacteriosis had become the most commonly reported zoonosis in the European Union, representing almost 70% of all the reported cases of infection in humans.1 Although the infection is self-limiting in most cases, in a subset of individuals campylobacteriosis may lead to Guillain-Barré syndrome (GBS) or Miller Fisher syndrome, which are autoimmune conditions.2 In addition, a correlation was observed between various pathological gastrointestinal conditions such as inflammatory bowel diseases (IBD), Barrett’s esophagus, colorectal cancer and C. jejuni infection.3 The optimum temperature for growth of C. jejuni is 42°C, which means that the bacteria adapted to the body temperature in birds. Thus, C. jejuni can be frequently isolated from chicken and other poultry, which serve as hosts and reservoirs that are colonized asymptomatically.4,5 Moreover, C. jejuni and Campylobacter coli together are responsible for more than 95% of Campylobacter infections in humans.6 The potential sources of C. jejuni infections are handling or consumption of contaminated (undercooked) meat, cross-contaminated other foods, unpasteurized milk, contaminated water, or direct animal contact via household pets and farm animals.7
Campylobacter coli meningitis in a 57-year-old patient
Published in Acta Clinica Belgica, 2018
Audrey Cambier, Delphine Martiny, Marie Hallin, Magali Wautier, Jean-Baptiste Giot, Myriam Z. Khaldi, Jacques Cambier, Philippe Léonard
To our knowledge, only one case of Campylobacter coli meningitis has been reported, in a 60-year-old with chronic alcoholism. However, in this unique case, no route of transmission was identified [5]. Here, we report a recent case of Campylobacter coli meningitis.