We report the first study to evaluate the intestinal mucosal microbiota of dogs with inflammatory bowel disease (IBD) and dogs with food-responsive diarrhea (FRD) before and after treatment. It was hypothesized that differences in the microbial composition exist between both disease groups and within groups pre- vs. post-treatment. Duodenal and colonic biopsies were obtained endoscopically from 24 dogs (15 FRD, 9 IBD) before and after treatment. The intestinal microbiota was evaluated by Illumina sequencing of the bacterial 16S rRNA gene. The global bacterial composition did not differ between IBD and FRD dogs, nor between treatment status. However, several bacterial taxa showed a difference in abundance. Comparing disease groups, an unclassified genus of Neisseriaceae was abundant in the duodenum in the IBD group, whereas Bilophila occurred more frequently in the duodenum and Burkholderia in the colon of FRD dogs. Comparing the microbiota pre- and post-treatment revealed Enterococcus, Corynebacterium and Proteobacteria to be enriched in the duodenum of FRD dogs pre-treatment, while Bacteroides was abundant in the colon post-treatment. In dogs with IBD, Bacteroides also reached significant abundance in the colon post-treatment. In conclusion, some differences in individual bacterial taxa were identified between IBD and FRD dogs and between treatment status.

Background Inflammatory bowel disease (IBD) and food-responsive diarrhea (FRD) are common chronic enteropathies in dogs, of which the exact pathogenesis has not been fully understood. In people dyslipidemia has been reported in patients with IBD, and potential therapeutic benefits of polyunsaturated fatty acids (PUFA) in the treatment of IBD have been investigated. Studies on the phospholipid profile in dogs with IBD and FRD are still lacking. Aim To investigate the systemic phospholipid profile of dogs with IBD or FRD and to evaluate possible differences in phospholipids before and after treatment. Methods The phospholipids in whole blood and EDTA plasma of 32 dogs diagnosed with either IBD (n = 16) or FRD (n = 16) were analyzed by hydrophilic interaction liquid chromatography (HILIC) prior to and after initiation of treatment, which included an elimination diet enriched with PUFAs. Results A clear separation of the phospholipids between whole blood and plasma was demonstrated on principal component analysis plots. In addition to the type of specimen, treatment and disease severity were the most significant factors determining the variance of the phospholipid profile. An increase in lysolipids was observed after treatment. The phosphatidylcholine (PC) species changed from PC 38:4 before treatment to mainly lysophosphatidylcholine 18:0 after treatment. Furthermore, several differences in the abundance of individual phospholipids were identified between dogs with IBD and dogs with FRD and between treatment statuses using random forest analysis. Conclusion Significant variances were identified in the phospholipid profiles of dogs with IBD and FRD. These were particularly determined by type of specimen used, disease severity and treatment status. After treatment, a shift of phospholipid species towards lysophosphatidylcholine 18:0 was observed. Future studies should further investigate the role of lipids in the pathophysiology of IBD and FRD as well as their potential therapeutic benefits.

ZusammenfassungEin Hypoadrenokortizismus (HoAK) entsteht durch eine in der Regel primäre (immunmediierte) Entzündung der Nebennierenrinde mit der Folge einer unzureichenden Gluko-und Mineralokortikoidproduktion. Als Sonderform können Patienten mit einem “atypischen” HoAK eine reine Glukokortikoidoder eine Glukokortikoid-und Mineralokorti-koiddefizienz mit dabei stabilen Elektrolytkonzentrationen aufweisen. Das klinische Bild eines HoAK ist beim Hund sehr unspezifisch. Die Symptome reichen von Zittern, Schwäche, milden bis rezidivierenden gastrointestinalen Symptomen bis hin zu Anfällen, hypovolämischem Schock und Kollaps. Die ebenfalls unspezifischen Befunde der Routineuntersuchungen gleichen häufig denen anderer Erkrankungen. Ein fehlendes Stressleukogramm, Eosinophilie, Hyponatriämie, Hyperkaliämie, Azotämie und sonographisch kleine Nebennieren stellen die charakteristischsten Befunde eines HoAK dar. Der ACTH-Stimulationstest gilt als Goldstandard zur Diagnosesicherung. Weitere endokrinologische Tests, wie Bestimmung der endogenen ACTH-Konzentration, der basalen und ACTH-stimulierten Aldosteronkonzentration, des Kortisol:ACTH-Verhältnisses sowie des Aldosteron:Renin-Verhältnisses, helfen bei der Differenzierung zwischen primärem, sekundärem und “atypischem” HoAK. In der akuten Krise bestehen die Eckpfeiler der Therapie in einer aggressiven Flüssigkeitstherapie zur Wiederherstellung der Normovolämie und Korrektur der Elektrolytverschiebungen. Die langfristige Therapie besteht in der Supplementierung von Gluko (Prednisolon) und Mineralokortikoiden (Desoxycortonpivalat) mit dem Ziel stabiler Elektrolytkonzentrationen und eines guten Allgemeinbefindens des Hundes. Die Einstellung eines Patienten unter Desoxycortonpivalat erfolgt anhand der Natrium-und Kaliumkonzentration nach einem standardisierten Protokoll. Beim “atypischen” HoAK sind ebenfalls regelmäßige Kontrollen der Elektrolyte zwingend, um einen späteren Substitutionsbedarf an Mineralokortikoiden möglichst frühzeitig zu erkennen. Mit einer adäquaten Therapie und einer guten Besitzercompliance haben Hunde mit HoAK eine exzellente Langzeitprognose.

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