High prevalence of DNA from non-H. pylori helicobacters in the gastric mucosa of Venezuelan pet dogs and its histological alterations.
ABSTRACT Non-H. pylori helicobacters (NHPH) have been demonstrated as gastric spiral-shaped bacteria in specimens obtained from dogs; however, their roles in the pathogenesis of upper gastrointestinal disease have not yet been clearly established. The purpose of this study was to evaluate the prevalence of NHPH DNA in the gastric mucosa of dogs and its association with histopathology. Helicobacter was detected through histopathological techniques, PCR, and FISH analysis from fundic biopsies of twenty dogs with or without signs of gastrointestinal disease. PCR and FISH were based on partial 16S rRNA gene sequences. Nineteen dogs showed mild to marked gastritis in the fundus, and only one dog had a healthy gastric mucosa. NHPH DNA was detected in 18 dogs with gastritis and one with normal gastric mucosa. However, there was no significant correlation between the presence of NHPH DNA and the degree of gastritis. These results show a high prevalence of NHPH DNA in the gastric mucosa of dogs from Venezuela. Further studies are necessary to determine a possible association between a specific NHPH species and the degree of gastritis.
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ABSTRACT: The results of studies examining the role of Helicobacter spp. in the pathogenesis of canine and feline gastritis are inconclusive. Furthermore, data evaluating the effectiveness of medical therapy for eradication of Helicobacter infection are limited. To detect Helicobacter spp. in mucosal biopsies of dogs and cats diagnosed with gastritis, with fluorescence in situ hybridization (FISH). Three dogs and 2 cats with signs of chronic gastrointestinal disease. Dogs and cats infected with Helicobacter spp. were treated with triple antimicrobial therapy and fed an elimination diet for 21 days. Helicobacter spp. status in endoscopic (3 dogs, 1 cat) or surgical biopsies (1 cat) of gastric mucosa was compared pre- and posttreatment in each animal by histology, FISH analysis, and polymerase chain reaction (PCR). Gastritis of varying severity with intraglandular spiral bacteria was observed in all animals. Pretreatment diagnostic tests confirmed the presence of mucosal Helicobacter spp. in all animals by FISH and histopathology and in 4/5 animals by PCR. Rapid resolution of vomiting episodes was observed in all animals. Gastric biopsies performed after triple therapy revealed clearance of visible Helicobacter spp. by histopathology and negative FISH analysis, as well as PCR in all animals. Application of FISH to routine biopsy specimens enabled rapid and specific identification of Helicobacter spp. within the gastric mucosa of dogs and cats. Although medical therapy was useful in resolution of clinical signs and clearance of visible Helicobacter spp. in gastric biopsies, gastric inflammation persisted.Journal of Veterinary Internal Medicine 12/2008; 23(1):16-23. · 2.06 Impact Factor
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ABSTRACT: The discovery of the spiral bacterium Helicobacter pylori and its causative role in gastric disease in humans has brought a dramatic change to gastroenterology. Although spiral bacteria have been known for more than a century to infect the stomachs of dogs and cats, recent research has been conducted mainly in the wake of interest in H. pylori. H. pylori has not been found in dogs and only very rarely in cats and zoonotic risk is minimal. A variety of other Helicobacter spp. can infect the stomach of pets; however, their pathogenic role is far from clear, and they have a small but real zoonotic potential. The prevalence of gastric Helicobacter spp. in dogs and cats is high, irrespective of clinical signs, and as in human medicine, mode of transmission is unclear. The relationship of Helicobacter spp. to gastric inflammation in cats and dogs is unresolved, with inflammation, glandular degeneration, and lymphoid follicle hyperplasia accompanying infection in some but not all subjects. Circulating anti-Helicobacter immuno-globulin G antibodies have been detected in 80% of dogs with naturally acquired infection and most dogs and cats with experimental infection. The gastric secretory axis is similar in infected and uninfected cats and dogs and no relationship of infection to gastrointestinal ulcers has been found. Differences in the pathogenicity of Helicobacter spp. are apparent, because infection with H pylori is associated with a more severe gastritis than infection with other Helicobacter spp. in both cats and dogs. Rapid urease test, histopathology, and touch cytology are all highly accurate invasive diagnostic tests for gastric Helicobacter-like organisms in dogs and cats, whereas culture and polymerase chain reaction are the only means to identify them to the species level. Urea breath and blood tests or serology can be used to diagnose Helicobacter spp. noninvasively in dogs and cats. Most therapeutic studies in pets have not shown long-term eradication of Helicobacter spp. Whether this is due to reinfection or recrudescence has not been established.Journal of Veterinary Internal Medicine 02/2000; 14(2):125 - 133. · 2.06 Impact Factor
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ABSTRACT: The development of macrolide resistance in Helicobacter pylori is considered an essential reason for failure of antibiotic eradication therapies. The predominant mechanism of resistance to macrolides, particularly clarithromycin, is based on three defined mutations within 23S rRNA, resulting in decreased binding of the antibiotic to the bacterial ribosome. To develop an rRNA based whole cell hybridisation method to detect Helicobacter species in situ within gastric tissue, simultaneously with its clarithromycin resistance genotype. A set of fluorescent labelled oligonucleotide probes was developed, binding either to H pylori 16S rRNA or 23S rRNA sequences containing specific point mutations responsible for clarithromycin resistance. After hybridisation and stringent washing procedures, labelling of intact single bacteria was monitored by fluorescence microscopy. The new approach was compared with PCR based assays, histology, and microbiological culture. In comparison with the phenotypic resistance measurement by E test, the genotypic clarithromycin resistance correlated perfectly (100%) for 35 H pylori isolates analysed. In a set of gastric biopsy specimens (27) H pylori infection was confirmed by histology (17/27) and correctly detected by whole cell hybridisation. Five clarithromycin resistant strains were identified in gastric tissue specimens directly. Furthermore, non-cultivable coccoid forms of H pylori were easily detectable by whole cell hybridisation. Whole cell hybridisation of rRNA holds great promise for cultivation independent, reliable, and rapid (three hours) genotypic determination of clarithromycin resistance in H pylori. Compared with PCR techniques it is independent of nucleic acid preparations, not prone to inhibition, and allows semiquantitative visualisation of the bacteria within intact tissue samples.Gut 06/2000; 46(5):608-14. · 10.73 Impact Factor