BackgroundRecent studies have shown that the fecal microbiota is generally resilient to short-term antibiotic administration, but some bacterial taxa may remain depressed for several months. Limited information is available about the effect of antimicrobials on small intestinal microbiota, an important contributor to gastrointestinal health. The antibiotic tylosin is often successfully used for the treatment of chronic diarrhea in dogs, but its exact mode of action and its effect on the intestinal microbiota remain unknown. The aim of this study was to evaluate the effect of tylosin on canine jejunal microbiota. Tylosin was administered at 20 to 22 mg/kg q 24 hr for 14 days to five healthy dogs, each with a pre-existing jejunal fistula. Jejunal brush samples were collected through the fistula on days 0, 14, and 28 (14 days after withdrawal of tylosin). Bacterial diversity was characterized using massive parallel 16S rRNA gene pyrosequencing.ResultsPyrosequencing revealed a previously unrecognized species richness in the canine small intestine. Ten bacterial phyla were identified. Microbial populations were phylogenetically more similar during tylosin treatment. However, a remarkable inter-individual response was observed for specific taxa. Fusobacteria, Bacteroidales, and Moraxella tended to decrease. The proportions of Enterococcus-like organisms, Pasteurella spp., and Dietzia spp. increased significantly during tylosin administration (p < 0.05). The proportion of Escherichia coli-like organisms increased by day 28 (p = 0.04). These changes were not accompanied by any obvious clinical effects. On day 28, the phylogenetic composition of the microbiota was similar to day 0 in only 2 of 5 dogs. Bacterial diversity resembled the pre-treatment state in 3 of 5 dogs. Several bacterial taxa such as Spirochaetes, Streptomycetaceae, and Prevotellaceae failed to recover at day 28 (p < 0.05). Several bacterial groups considered to be sensitive to tylosin increased in their proportions.ConclusionTylosin may lead to prolonged effects on the composition and diversity of jejunal microbiota. However, these changes were not associated with any short-term clinical signs of gastrointestinal disease in healthy dogs. Our results illustrate the complexity of the intestinal microbiota and the challenges associated with evaluating the effect of antibiotic administration on the various bacterial groups and their potential interactions.

The microbiota of the small intestine is poorly known because of difficulties in sampling. In this study, we examined whether the organisms cultured from the jejunum and feces resemble each other. Small-intestinal fluid samples were collected from 22 beagle dogs with a permanent jejunal fistula in parallel with fecal samples. In addition, corresponding samples from seven of the dogs were collected during a 4-week period (days 4, 10, 14, and 28) to examine the stability of the microbiota. In the jejunal samples, aerobic/facultative and anaerobic bacteria were equally represented, whereas anaerobes dominated in the fecal samples. Despite lower numbers of bacteria in the jejunum (range, 10 2 to 10 6 CFU/g) than in feces (range, 10 8 to 10 11 CFU/g), some microbial groups were more prevalent in the small intestine: staphylococci, 64% versus 36%; nonfermentative gramnegative rods, 27% versus 9%; and yeasts, 27% versus 5%, respectively. In contrast, part of the fecal dominant microbiota (bile-resistant Bacteroides spp., Clostridium hiranonis-like organisms, and lactobacilli) was practically absent in the jejunum. Many species were seldom isolated simultaneously from both sample types, regardless of their overall prevalence. In conclusion, the small intestine contains a few bacterial species at a time with vastly fluctuating counts, opposite to the results obtained for the colon, where the major bacterial groups remain relatively constant over time. Qualitative and quantitative differences between the corresponding jejunal and fecal samples indicate the inability of fecal samples to represent the microbiotas present in the upper gut.

s-aryThe occurrence and topographical mapping of the gastric Helcobacter-like organisms (GHLOs) and their association with histological changes were studied in apparently healthy dogs and cats. Multiple samples were collected for histological examination from the fundus, corpus and antmm of the stomach of 10 dogs and 10 cats. Fundus and corpus were also sampled for transmission electron microscopy (three dogs, six cats), and for culture (eight dogs, six cats). In all dogs, GHLOs were detected in the fundus and corpus, and in the anmm of nine dogs, and significantly more often in the fundus and corpus (in all sample sites examined) than the antmm (P < 0.01). In cats, GHLOs were demonstrated in 6/10 individuals, and in all regions and sample sites. In dogs GHLOs were detected in all sample sites of the fundus and corpus. Lymphocytes, plasma cells and lymphocyte aggregates were found in all dogs in all regions; there were significantly more plasma cells in the antmm than in the corpus (P < 0.05). Neutrophils were found in six dogs, and eosinophils in seven dogs. In cats, lymphocyte aggregates were found only in GHLO-positive cats, which also had more lymphocytes in the fundus and corpus than GHLO-negative ones (P < 0.05). In dogs, no statistically significant association was found between the number of GHLOs and inflammatory parameters. Four dogs showed histological changes comparable to mild chronic gasmtis and another six dogs to mild active chronic gastritis. Mild chronic gastritis was found in the antmm of all cats, and it occurred significantly more often in the anmm than in other regions (P < 0.01). In cats, there was a statistically significant association between GHLOs and chronic gastritis in the fundus and corpus (P < 0.05). GHLOs resembhng human 'Hehobuctcr hdmannii' were identified in all the dogs and cats studied by electron microscopy, and Helicobacterfe~ir in one dog in addition. Culture was successful in three dogs and one cat; 'H. hedmunnii' was identified in two of the dogs, and H j f r j in the third dog and the cat. GHLOs were found to be common in apparently healthy dogs and cats. Based on the results of this study, one sample from the fundus and corpus is enough to demonstrate GHLOs. In cats, GHLOs may cause histological changes comparable to chronic gastritis, but in dogs this association remained unclear. It is also questionable if the histological criteria for human gastritis, used in the present study, are suitable for dogs and cats.

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Fourteen dogs had shown chronic or intermittent diarrhea for more than 1 year. Diarrhea had been successfully treated with tylosin for at least 6 months but recurred when treatment was withdrawn on at least 2 occasions. Tylosin-responsive diarrhea (TRD) affects typically middle-aged, large-breed dogs and clinical signs indicate that TRD affects both the small and large intestine. Treatment with tylosin eliminated diarrhea in all dogs within 3 days and in most dogs within 24 hours. Tylosin administration controlled diarrhea in all dogs, but after it was discontinued, diarrhea reappeared in 12 (85.7%) of 14 dogs within 30 days. Prednisone given for 3 days did not completely resolve diarrhea. Probiotic Lactobacillus rhamnosus GG did not prevent the relapse of diarrhea in any of 9 dogs so treated. The etiology of TRD, a likely form of antibiotic-responsive diarrhea (ARD) is unclear. The following reasons for chronic diarrhea were excluded or found to be unlikely: parasites, exocrine pancreatic insufficiency, inflammatory bowel disease, small intestinal bacterial overgrowth, enteropathogenic bacteria (Salmonella spp., Campylobacter spp., Yersinia spp., or Lawsoni intracellularis), and Clostridium perfringens enterotoxin and Clostridium difficile A toxin. A possible etiologic factor is a specific enteropathogenic organism that is a common resident in the canine gastrointestinal tract and is sensitive to tylosin but difficult to eradicate. Additional studies are required to identify the specific cause of TRD.

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Dogs (n = 158) with serum trypsinlike immunoreactivity (TLI) concentrations < or = 5.0 microg/L were studied. The diagnosis of clinical exocrine pancreatic insufficiency (EPI) was made in 114 of 158 dogs based on TLI concentration < 2.5 microg/L and clinical signs typical of EPI (eg, polyphagia, voluminous feces, weight loss). In 44 of 158 dogs, a single TLI measurement and clinical signs were not diagnostic. In 9 of 44 dogs, TLI was < 2.5 microg/L, indicating EPI, but the gastrointestinal signs were atypical or the dogs were asymptomatic. In 35 of 44 dogs, TLI was 2.5-5.0 microg/L. All 44 dogs were retested for TLI within 1-27 months (mean, 11.9 months). In 20 of 44 dogs, the retested TLI was normal (> 5.0 microg/L). In 4 of 44 dogs with clinically diagnosed EPI, the retested TLI was < 2.5 microg/L. In the remaining 20 of 44 dogs, TLI was persistently < 5.0 microg/L (range, 1.0-4.9 microg/L; mean, 3.1 microg/L). Of these dogs, 15 had no clinical signs of gastrointestinal disease, and 5 had occasional clinical signs atypical for EPI. Gross examination of the pancreas (12 dogs) showed that the amount of normal pancreatic tissue was remarkably diminished. These dogs were diagnosed with subclinical EPI. The TLI-stimulation test, in which TLI is measured before and after stimulation with secretin and cholecystokinin, showed a significant response (P < .05) both in dogs with subclinical EPI and in control dogs, but showed no response in dogs with clinical EPI. In this study, EPI was diagnosed in its subclinical phase by TLI concentrations persistently < 5.0 microg/L, and a single TLI concentration < 5.0 microg/L was not diagnostic. Retesting after TLI concentrations < 5.0 microg/L is recommended even in clinically normal dogs, because of the possibility of subclinical EPI.

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