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Final Diagnosis: Helicobacter gastritis in a dog

History:  This four-year-old, spayed female, Chinese crested dog had been losing weight for one year.  No vomiting or diarrhea had been observed by the owner and the dog had been clinically normal otherwise.  There were no apparent findings in the stomach on gross post mortem examination.      

Histopathologic description:  There was irregular thickness of the gastric pyloric mucosa.  The lamina propria of the pylorus was markedly diffusely infiltrated by lymphocytes and plasma cells with scattered lymphoid follicle formation in the deeper mucosa.  The pyloric glandular epithelium was often attenuated (degeneration) and/or infiltrated by few lymphocytes and plasma cells. Rarely, pyloric glands were dilated with mucus and scanty cell debris.  In the pylorus, some gastric pits and glands had varying numbers of 6-10 µm long, spiral, gram-negative bacteria.  In the fundus, mucosal inflammation and bacterial colonization were minimal.

The pyloric lamina propria is infiltrated by many lympho-cytes and plasma cells.  (HE, bar = 20µm  

Spiral bacteria are present in the lumen and intercellular spaces of pyloric glands (Warthin-Starry silver stain, bar = 10µm

Spiral bacteria in the pyloric glandular lumen (L) have periplasmic fibrils (smaller arrows) and flagella (larger arrow). Pyloric glandular epithelial cells (E) contain numerous electron-dense secretory granules. Trans-mission electron microscopy, bar = 1µm


Discussion:
  Severe lymphoplasmacytic gastritis in this dog was associated with intralesional spiral bacteria.  Light and electron microscopic characteristics of this bacteria are compatible with Helicobacter species.  The gastritis might have played a role in the emaciation and weight loss of this dog.

  Genus Helicobacter encompasses gram-negative, microaerophilic, curved to spiral-shaped bacteria.  Chronic gastric inflammation due to H. pylori has been associated with increased risk of gastric adenocarcinoma and other malignancies in humans and some animal species.

  Several gastric Helicobacter species have been isolated from apparently healthy animals or animals with clinical signs of gastrointestinal problems.  In dogs, four gastric Helicobacter species have been described and the prevalence of these bacteria is generally very high regardless of concurrent clinical signs.  H. (Flexispira) rappini (sheep, humans, dogs) 4-5 µm, is fusiform, entwined with multiple periplasmic fibers, and has multiple bipolar sheathed flagella. H. felis (cats, dogs, humans) is 7-10µm with superficial, sparse periplasmic  fibers and multiple bipolar sheathed flagella.  H. heilmannii and H. Gastrospirilium hominis as synonyms (dogs, cats, humans, nonhuman primates, pigs) is 7-10 µm long, has multiple bipolar sheathed flagella, but lacks periplasmic fibers.  H. salomonis (dogs) is 5-7 µm long with tufts of sheathed flagella at each end.  Based on this classification, the majority of bacteria in this dog's stomach are most consistent with H. felis.

  The majority of gastric Helicobacter species infections in animals has been reported to be asymptomatic; however, some animals may show intermittent vomiting, weight loss, or diarrhea.  Clinical signs less frequently seen include pica, belching, anorexia, or emaciation.  The mode of transmission of Helicobacter species is yet to be elucidated although fecal-oral or oral-oral transmission is likely.  Until now, there has been no report pointing to a direct relationship between human infection by animal Helicobacter species and gastric disorders in humans, even in the case of H. pylori.

  Diagnosis of Helicobacter species infection is usually made by histologic examination of endoscopic or postmortem stomach specimens through demonstration of mucosal inflammation accompanied by organisms.  Endoscopic collection of gastric mucus using a brush has been reported to be equally or more sensitive in detection of the organisms although the degree of gastric inflammation is difficult to assess.  Commercial rapid urease testing on gastric mucus samples has been used although sensitivity and specificity are variable.  Culture of these fastidious bacteria requires modification of routine methods and, thus, is not practical.  Electron microscopy and PCR amplification of 16S ribosomal RNA amplicons can be used to differentiate Helicobacter species.

  Pathogenicity of gastric Helicobacter species relies on their urease production, which increases pH just around the bacterial wall and provides them with an appropriate milieu.  Interestingly, because not all animals and humans that harbor these bacteria develop clinical signs, both bacterial virulence and host genetic diversity are thought to be involved in disease initiation, progression and, in some instances, carcino-genesis.  The reason the pylorus was selectively inflamed and colonized by Helicobacter species in this dog is not clear, although the difference in intragastric distribution of inflammation and bacterial colonization has often been described in human and animal infections.

-by Dr. Ikki Mitsui, ADDL Graduate Student

References:

  1. Fox JG: 2006.  Gastric Helicobacter infections. In: Infectious Diseases of the Dog and Cat. Ed. Greene CE, 4th ed W.B. Saunders Company, Philadelphia.  PP 343-351.

  2. Happonen I et al: 1996.  Occurrence and topographical mapping of gastric Helicobacter-like organisms and their association with histological changes in apparently healthy dogs and cats.  J Vet Med 43:305-315.

  3. Jenkins CC, Bassett JR: 1997.  Helicobacter infection.  The Compendium 19:267-309.

  4. Neiger R, Simpson KW: 2000.  Helicobacter infection in dogs and cats: facts and fiction. J Vet Intern Med 14: 125-133.

  5. Peek Jr RM, Crabtree: 2006.  Helicobacter infection and gastric neoplasia. J Pathol 208:233-248.

  6. Simpson KW et al: 1999. Helicobacter felis infection in dogs: effect on gastric structure and function. Vet Pathol 36:237-248.

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