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Helicobacter Spp. — Food- Or Waterborne Pathogens?

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Helicobacter Spp. — Food- Or Waterborne Pathogens? FRI FOOD SAFETY REVIEWS Helicobacter spp. — Food- or Waterborne Pathogens? M. Ellin Doyle Food Research Institute University of Wisconsin–Madison Madison WI 53706 Contents34B Introduction....................................................................................................................................1 Virulence Factors ...........................................................................................................................2 Associated Diseases .......................................................................................................................2 Gastrointestinal Disease .........................................................................................................2 Neurological Disease..............................................................................................................3 Other Diseases........................................................................................................................4 Epidemiology.................................................................................................................................4 Prevalence..............................................................................................................................4 Transmission ..........................................................................................................................4 Summary .......................................................................................................................................5 Appendix — FRI Briefing, January 1997: Helicobacter pylori INTRODUCTION detected in other animals. H. pylori has been associated Helicobacter spp. are Gram-negative, curved or spiral- with humans for at least 50,000 years and during that shaped bacteria that live in the stomach, intestine, and time has evolved to adapt to conditions in the human liver of mammals, birds, and reptiles. Helicobacters are gut as humans have also adapted to the presence of fastidious, difficult to cultivate, and are notorious for these bacteria. H. pylori was first described in 1984 entering a viable but non-culturable state when exposed from the stomach of patients with gastritis and peptic to adverse environmental conditions (9). These ulcers (35). Approximately 70–90% of persons in characteristics make it difficult to determine the species developing countries and 25–50% of those in of different isolates. Numerous species have been developed countries are colonized by H. pylori. Some described, but the taxonomy of this genus is still in flux strains are more virulent than others and are more often because many isolates have not been completely associated with more severe gastric diseases, including characterized (24). ulcers and cancer. Most people colonized with Most Helicobacter isolates from humans are H. pylori, perhaps as many as 90%, experience only a classified as H. pylori, but this species is rarely mild inflammatory response and are asymptomatic. Corresponding author: M. Ellin Doyle, Ph.D., [email protected] February 2012 http://fri.wisc.edu/docs/pdf/FRI_Brief_Helicobacter_Feb2012.pdf Food Research Institute, University of Wisconsin–Madison 2 FRI FOOD SAFETY REVIEW: Helicobacter spp. — Food- or Waterborne Pathogens? In fact, it has been suggested that colonization with Numerous other proteins associated with H. pylori is the “normal” condition for humans and that pathogenicity have been identified, including adhesins the recent “loss” of H. pylori in people in more that facilitate binding to intestinal epithelial cells and developed societies (living in more hygienic condi- enzymes. For example, in order to survive stomach tions) may be one factor causing increases in some acidity, helicobacters synthesize urease enzymes to “modern” diseases (6). degrade urea. The ammonia produced by these Some Helicobacter species usually associated with reactions neutralizes hydrochloric acid around the cells, animals have also been detected in humans. These are thereby providing a safe microniche for bacterial sometimes referred to as “H. heilmannii,” but this growth. Some mucoid strains of H. pylori have been group probably includes several distinct species. isolated from gastric biopsies. The exopolysaccharide Estimates of the prevalence of human infection with produced by these strains may protect cells from acid, non-H. pylori helicobacters (NHPH) range from 0.2– antibiotics, and high oxygen levels (55). 6.0% (7;57). H. suis is the most common NHPH isolated from humans, accounting for up to 31% of human NHPH infections (65). Genetic analyses of ASSOCIATED DISEASES some NHPH reveal that they do not produce some Infection with H. pylori irritates the stomach lining, of the major virulence factors of H. pylori but they do causing gastritis. Some individuals may mount an have wide metabolic flexibility, react to a range of effective defense clearing the infection, although this is environmental signals, and produce other enzymes that considered uncommon. Most infections progress to may act as virulence factors (52). chronic active gastritis. However, in 80–90% of Helicobacters have been detected in 142 vertebrate people, these inflammatory reactions are mild and there species, including livestock, companion animals, are no obvious symptoms of infection. In other people, horses, ferrets, geese, tortoises, possums, whales, and depending on the extent and location of the gastritis, dolphins. Several reviews discuss important veterinary either duodenal ulcers or gastric ulcers and gastric Helicobacter spp. (24;26;57). Strains associated with cancer may develop. It has been estimated that about livestock and companion animals include H. suis (pigs, 10% of all infected persons develop peptic ulcers, monkeys), H. felis (cats, dogs, rabbit), H. bizzozeronii another 1–3% develop gastric cancer, and <0.1% (dogs, cats), H. pullorum (chickens, turkeys), and develop another type of gastric tumor, mucosa- H. bovis (cattle). Prevalence of H. suis in pigs is associated lymphoid tissue (MALT) lymphoma (66). usually reported as 60% or more and is sometimes There are reports that infection with H. pylori is associated with gastritis and stomach ulcers. Helico- associated with other human diseases, but in many bacter spp. have been detected in 67–86% of healthy cases evidence is not compelling. dogs and in 41–100% of healthy cats. Higher preva- Several factors, such as smoking, diet, and use of lences have been reported in animals with chronic non-steroidal anti-inflammatory drugs, influence the vomiting (7). As in humans, many animals colonized development of gastrointestinal illnesses. Genetic with Helicobacter spp. are asymptomatic. However, characteristics of infecting strains of Helicobacter and these bacteria can induce a chronic inflammatory of the human host also determine the nature and response that results in lesions in the stomach, intes- severity of illness. Certain genotypes of H. pylori were tine, or liver. found to be more often associated with esophagitis or with peptic ulcer disease in 286 symptomatic, H. pylori-positive Alaskan adults (37). A study of VIRULENCE FACTORS low income African-Americans found that those with Two important virulence factors in H. pylori are the the greatest percentage of genetic markers indicating vacuolating cytotoxin (VacA) and the CagA protein African ancestry had a higher prevalence of antibodies encoded by a cytotoxin-associated gene pathogenicity to H. pylori and to CagA. Some genotypic charac- island (cagPAI). VacA interacts with receptors on the teristic or lifestyle variations associated with African surfaces of cells lining the gastrointestinal tract, ancestry may explain the higher prevalence of virulent modifying some cell functions and causing vacuolation H. pylori in this population (14). and apoptosis. CagA protein is injected into cells by a type IV secretion system also encoded by cagPAI. Gastrointestinal Disease Once internalized, CagA is phosphorylated by host cell Ulcers. H. pylori infection is the most prominent kinases and then acts as a signaling molecule risk factor associated with gastroduodenal ulcers. disrupting cellular activities. These toxins not only Infections are reported in 60% to 80% of those with adversely impact intracellular metabolism but can also gastric ulcers and in 95% of those with duodenal ulcers attack tight junctions between cells, causing tissue (2). When H. pylori gastritis occurs primarily in the damage and allowing H. pylori cells to penetrate the antrum area of the stomach, acid secretion is increased intestinal epithelial layer (59). and this is associated with ulcer formation (5). Corresponding author: M. Ellin Doyle, Ph.D., [email protected] February 2012 http://fri.wisc.edu/docs/pdf/FRI_Brief_Helicobacter_Feb2012.pdf Food Research Institute, University of Wisconsin–Madison FRI FOOD SAFETY REVIEW: Helicobacter spp. — Food- or Waterborne Pathogens? 3 Cancer. In 1994, an IARC monograph reviewed relationship between H. pylori status and symptomatic 4 cohort and 9 case–control studies and concluded that GERD or endoscopic evidence of reflux esophagitis, H. pylori was a cause of gastric cancer in humans. A there was a significantly lower incidence of GERD more recent analysis of a substantial number of symptoms after H. pylori was eradicated from patients. prospective cohort and nested case–control studies Inflammatory bowel diseases (IBD), Crohn’s revealed a significant association between H. pylori disease, and ulcerative colitis
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