Gastric bacteria of a variety of ultrastructural morphologies have been identified in or isolated from domestic carnivores, but their prevalence in different populations of animals and their clinical significance are still unknown. The purposes of this study were (i) to evaluate the prevalence and morphologic types of gastric bacteria in three different populations of dogs; (ii) to determine which of the organisms were culturable, and if the cultured organisms were morphologically similar to the organisms seen in situ; (iii) to identify the isolated organisms; and (iv) to determine if gastric bacteria were associated with gastritis. Three groups of dogs were examined: healthy laboratory dogs, healthy dogs from an animal shelter, and pet dogs with various nongastric illnesses. Of these, 100% of laboratory and shelter dogs and 67% of pet dogs were colonized by large, tightly coiled gastric spiral bacteria morphologically similar to Gastrospirillum hominis or Helicobacter felis (referred to as gastrospirilla). Regardless of the presence or density of gastric bacteria, all of the dogs in the study except one had mild to moderate gastritis. Helicobacter spp. were isolated from only 6 of 39 stomachs cultured, and only three of the organisms isolated were morphologically similar to the bacteria seen in situ. Five helicobacters were identified by 16S rDNA (genes coding for rRNA) sequence analysis. Three were strains of H. felis, one was H. bilis, and one was a novel helicobacter morphologically similar to "Flexispira rappini." Gastrospirilla are almost universal in the stomachs of domestic dogs, and in most infected dogs, they do not appear to be associated with clinical signs or histologic lesions compared with uninfected dogs. Nongastrospirillum helicobacters are rare in dogs and are not histologically detectable. Helicobacter pylori was not isolated from domestic dogs.

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Benign esophageal strictures in 6 cats and 7 dogs were treated with endoscopically guided balloon dilatation. Six of 13 had a history of anesthesia within 3 weeks prior to the onset of signs; 8 animals had a single stricture, and 5 had multiple strictures, for a total of 19 strictures. Four of the 19 strictures were in the upper esophagus, 11 were in the middle esophagus, and 4 were in the lower esophagus. The luminal diameters ranged from 1 to 18 mm, with a mean of 5.1 mm. Twelve animals survived the immediate postprocedure period and had a total of 50 dilatation procedures performed; the mean number of procedures per animal was 4.2 (range, 2 to 8). Complications included mild bleeding and tearing (11 of 13), moderate bleeding (1 of 13), and esophageal perforation (1 of 13). The cat with the perforation was subsequently euthanized. Follow-up information was available on the 12 remaining animals; 9 were known to be alive 6 to 59 months (mean, 28.2 months) after dilatation. Two were euthanized, 1 for persistence of signs and the other for unrelated causes. One animal died of possible aspiration pneumonia. Three of 13 animals had complete and 9 had partial resolution of signs. Of the 9 animals with partial resolution, 7 were substantially better with dietary modification, 1 was moderately better, and 1 had minimal improvement. Eleven of 13 animals (85%) had a successful outcome with moderate to complete resolution of signs. Thus, it is concluded that endoscopically guided balloon dilatation is an effective and relatively safe treatment for benign esophageal strictures in dogs and cats.

Abstract. An outbrea k of vo m iting in a gro up of captive chee tahs (Acinonyx j ubat us) was inves tigated , and histologic examinati on revea led chro nic gastritis characterized by infiltration o f lymphocytes and nume rous pla sma cells and epithel ial erosio ns. Lymphoid follicles, globule leu kocytes, scatte red neutrophi ls, and (in on e ani ma l) abscessed gastric glands were incon sistent finding s. In addi tio n, necrop sy of three cheetahs revea led gastric mu cosal hyperplasia. T wo kinds of bacteria were identified in th e sto mac hs of infected cheetahs. Numerou s long, tightl y coi led motile Gastrospi rillum -like organis ms were seen in gastric mu cu s and in WarthinStarry-stai ned sections of m ucosa . T hese bacteria could not be cultured but were transmi tted to conventional mice in hom ogenates of gastric m ucosa from infected cheetahs. Ultrastructural exami natio n revea led helical filam ents on some of these bacteria. In add itio n, a sma ller Helicobacter sp. was isolated . Th is organism co uld be cultured in vitro und er m icroaeroph ilic co ndi tio ns. O ne or both of th ese bacterial species was proba bly respon sible for th e gastritis in these cheetahs.Key words: Bacteria; cheeta hs; gastritis; Gastrospirillum; Helicobacter pylori.In 1983 , a ba ct eri al organism now known as H elicobacter py lori was first isolated fro m th e sto machs of human pati ents with gastritis." This organism has since be en shown to be a co m m o n cause of gastritis and ha s be en associated with peptic ulcer di sease, gastric ca rcin oma , and a number o f othe r co nd it io ns .'>' Because of its association with peptic ulcer d isease, H. pylori has ev o ked a great deal of interest and stud y. Clinical trials have shown tha t erad icatio n of infection is asso ciated with healing of ulcers and that tr eatment for ulcers is in effecti ve in th e absen ce of bacterial era d ication ," suggesting that H. pylori is a n important fac to r in th e pathogenesis of human peptic ulc er di sea se.' > In addition to H. pylori, other gas tric bact eria ha ve been described in human beings.v-' but th ey are unco m mon and ha ve not been cult ured in vitro and thus cannot be taxonom icall y defin ed. They are m ost o fte n referred to as Gastrospirillum hominis or Gastrospir illum-like ba cteria (GLO). Like H. pylori, they may be as sociated with gastritis.s-" Bact eri a l ga stritis is po orl y docum ented in an imals. R ecent rep orts, however , suggest that gastri c ba ct eri a are relati vely co m m on and that gast ritis ca used by th ese ba cteria ma y ha ve been co m m o nly overloo ked in th e past. 12H. pylori-like o rganis ms ha ve been isolat ed fro m ferrets with gastritis a nd gastric ulce rsv -? and from macaques' a nd pigs" with gastritis. These ba ct eria are probably widespread in a nima ls, but their incidence and associa tio n with di sea se ha ve recei ved little a tte ntion. Althou gh th ey ha ve been incon sist entl y associat ed with hi stologic ga stritis, th ey have not previ ou sly been...

Canine histiocytic ulcerative colitis (HUC) is characterized by colonic inflammation with predominantly periodic acid-Schiff (PAS)-positive macrophages. The inflammation results in colonic thickening, ulcerations, and distortion of normal glandular architecture. Resultant clinical signs consist of chronic large bowel diarrhea, tenesmus, and marked weight loss, and the disease frequently results in euthanasia. Conventional therapy consists of some combination of prednisone, azathioprine, sulfasalazine, and metronidazole. Nine dogs (8 Boxers and 1 English Bulldog) with histologic confirmation of HUC were treated with antibiotic therapy (either with enrofloxacin alone or in combination with metronidazole and amoxicillin). Clinical signs, physical examination findings, laboratory abnormalities, and the histologic severity of the disease were evaluated. Four of the 9 dogs had been treated previously with conventional therapy and had failed to respond favorably; then, these dogs were placed on antibiotic therapy (enrofloxacin, n ϭ 1; enrofloxacin, metronidazole, and amoxicillin, n ϭ 3) and had resolution of clinical signs within 3-12 days. Five dogs were treated solely with antibiotic therapy (enrofloxacin, n ϭ 1; enrofloxacin and metronidazole, n ϭ 1; enrofloxacin, metronidazole, and amoxicillin, n ϭ 3), and clinical signs resolved in 2-7 days. Repeated biopsy specimens were obtained from 5 dogs after treatment, and all showed marked histologic improvement. The increase in body weight after treatment was statistically significant (P ϭ .01). Three dogs currently are not on any treatment and have had resolution of clinical signs for up to 14 months. These observations suggest that an infectious agent responsive to antibiotics plays an integral role in the clinical manifestation of canine HUC, and they support the use of antibiotics in its treatment.

These results indicate that dietary management of protein-losing enteropathy is a potential management strategy in Yorkshire terriers. Randomised clinical trials in Yorkshire terriers with protein-losing enteropathy are necessary to compare success rate, survival and quality of life with dietary management versus combined dietary and immunosuppressive/anti-inflammatory therapy.

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Spontaneous hyperlipidemia in rats causes glomerular disease. Idiopathic hypertriglyceridemia (HTG) is prevalent in Miniature schnauzers, but its relationship with proteinuria is unknown. Decreased activity of major lipid metabolism enzymes, lipoprotein lipase (LPL) and hepatic lipase (HL), may play a role in the cyclic relationship between hyperlipidemia and proteinuria. These enzymes have also not been previously investigated in Miniature shnauzers. The aims of this study were to determine the relationship between HTG and proteinuria in Miniature schnauzers and to measure LPL and HL activities in a subset of dogs. Fifty-seven Miniature schnauzers were recruited (34 with and 23 without HTG). Fasting serum triglyceride concentrations and urine protein-to-creatinine ratios (UPC) were measured in all dogs, and LPL and HL activities were determined in 17 dogs (8 with and 9 without HTG). There was a strong positive correlation between triglyceride concentration and UPC (r = 0.77–0.83, P < 0.001). Proteinuria (UPC ≥ 0.5) was present in 60% of dogs with HTG and absent from all dogs without HTG (P < 0.001). Proteinuric dogs were not azotemic or hypoalbuminemic. Dogs with HTG had a 65% reduction in LPL activity relative to dogs without HTG (P < 0.001); HL activity did not differ. Proteinuria occurs with HTG in Miniature schnauzers and could be due to lipid-induced glomerular injury. Reduced LPL activity may contribute to the severity of HTG, but further assay validation is required.