The patient, an 8-year-old, male castrated mixed breed dog, was presented to Cornell University Hospital for Animals (CUHA) for intractable diarrhea, vomiting, inappetance, weight loss, muscle wasting and ascites. In March 2018 the patient was seen by his primary care veterinarian for vomiting and diarrhea. He was hospitalized several times over three months but did not improve despite supportive care and multiple therapeutic trials. He was ultimately diagnosed with lymphoplasmacytic and neutrophilic inflammatory bowel disease (IBD) via surgically obtained intestinal biopsies. By May 2018, the patient had developed peritoneal effusion, causing increased respiratory effort, and dependent hind limb edema. Euthanasia was recommended due to lack of response to therapy. Upon presentation to the CUHA Emergency Service on 6/1/18, the patient was quiet, alert, and responsive with increased respiratory rate and effort. His mucous membranes were pale pink and his capillary refill time (CRT) was prolonged ( >3 seconds). His body condition score was 3/9 with significant muscle wasting. Abdominal palpation disclosed a pendulous abdomen with a palpable fluid wave and mild discomfort. The patient also had perianal pyoderma and dependent edema in both hind limbs. An abbreviated abdominal ultrasound showed free fluid in the peritoneal cavity. One liter of fluid was removed via abdominocentesis, resulting in significant improvement in respiratory rate and effort. The patient was hospitalized with supportive care and transferred to the Internal Medicine Service the following day. The problem list for the patient included intractable vomiting and diarrhea, weight loss, dehydration, inappetance, abdominal effusion, dependent hind limb edema and increased respiratory effort. Given the clinical signs, clinicopathologic data, and intestinal histopathology, the patient was diagnosed with protein losing enteropathy (PLE) secondary to IBD. Under the care of the Internal Medicine Service, fecal smears were performed revealing a diminished bacterial population. Given the colonic dysbiosis and severity of disease, placement of an esophageal feeding tube and fecal microbiota transplant were implemented. The procedure was performed without complications and the patient recovered uneventfully. He was hospitalized with supportive care, immunosuppressant therapy (dexamethasone-SP 0.1mg/kg IV q24), diuretic therapy, and a strict diet of Vivonex via esophagostomy tube. Antibiotic therapy was withheld. Throughout his hospitalization, serial bloodwork showed improvements in his biochemical parameters and repeated fecal smears showed a normal population of bacteria. Three days after the fecal transplantation was performed, the patient’s abdominal effusion and hind limb edema had dissipated, his protein levels had improved on bloodwork, and his diuretics were discontinued. He was discharged to the care of his owners on June 4th, three days after initial presentation. At this time, 8 months later, the patient has no remaining clinical signs, is eating a hypoallergenic diet and has returned to his pre-illness weight. Though he is on long term medical management, he has a ravenous appetite and is clinically healthy.