Cheryl
Stanley, DVM, dipl ABVP (feline)
Lexington Boulevard Animal Hospital
Sugar Land Texas77469
“Annie”, a one- year old intact female beagle presented in December 2001 for anorexia and reluctance to move. She had a normal physical examination except for cervical pain on manipulation and palpation. She was prescribed a reducing dose of dexamethasone over 2 weeks. Annie showed such dramatic improvement in the first 24 hours of medication that the owners discontinued the drug after 4 days.
Three weeks later, Annie presented again with same symptoms but now also seemed to have cervical muscle spasms. Due to her previous dramatic improvement , she was placed back on dexamethasone with instructions to give the entire course of medication over the prescribed 2 weeks and methocarbomal was added to help with the muscle spasms.
Annie did well while on the medications with again an almost immediate response. However, when the drugs were weaned her symptoms returned. At this point, we had a high index of suspicion for a cervical disc, discospondylitis, or beagle pain syndrome (steroid responsive meningitis). We also knew a close relative to this dog had previously been diagnosed with beagle pain syndrome so our rule outs strongly leaned in this direction.
The following day we performed scout cervical radiographs. These showed no evidence of discospondylitis. The plan was to perform a CSF tap to evaluate for any significant inflammatory changes and if none were seen we would then pursue a myelogram. CSF analysis revealed no red blood cells but a marked increase in leukocytes with 90% of the cells being granulocytes and 10% being mononuclear cells. Based on these findings, we did not perform a myelogram . A diagnosis of beagle pain syndrome was made and we instituted a prolonged course of prednisone. The drug was given with very slow weaning over a 10 month period. Annie was eventually successfully taken off the prednisone with no further episodes. She did very well for many years with no major medical problems.
In April 2008, Annie presented to the hospital with a history of chronic diarrhea. Upon examination, the only major medical finding was the presence of ascites. The previous hospital had performed multiple fecal examinations. She had been treated with several courses of metronidazole and pyrantal pamoate. Her diet had been changed to Science Diet I/d and then later to Purina EN. None of these protocols had shown any improvement in her clinical signs. When evaluating the blood work performed by the previous hospital, we noted a significant hypoproteinemia and hypoalbuminemia. Due to her symptoms, the cause of the protein loss was highly suspected to be protein losing enteropathy. For completeness, her liver and kidneys were evaluated and confirmed to not be associated with the protein loss. Our differentials included inflammatory bowel disease, intestinal lymphoma or other neoplasia, infiltrative / granulomatous diseases of the bowel and lymphangectasia.
Endoscopic intestinal biopsies were performed and a diagnosis of lymphocytic, eosinophilic, plasmacytic enteritis and colitis was found. She also had moderate to marked lymphangectasia with significant blunting and effusion on intestinal villi. Treatment involved Purina HA diet, vitamin B12, budesonide and imuran. Annie did well for a little more than a year then succumbed to the progressive nature of this disease. Her symptoms at the time seemed to suggest the possibility that the lesions had changed to intestinal lymphoma but no biopsies were taken to confirm this suspicion.
In retrospect, it is of interest that this dog had two steroid responsive inflammatory diseases. Could there be a link to the process or underlying genetics to predispose her to both conditions? This dog was actually the daughter of another dog that also had severe inflammatory bowel disease. Could there be an inherited trait responsible for these conditions?
“Handsome”, a six-year old intact male beagle presented to the hospital in November 2004 with the complaint of chronic diarrhea. It is important to note that prior to coming to our hospital, he too had a diagnosis of beagle pain syndrome confirmed by CSF analysis many years earlier. Also, Handsome is a son of the same dog that “Annie” in the previous case overview was born to.
Upon presentation, Handsome had hypoproteinemia, hypoalbumenemia, mild anemia and weight loss. Laboratory evaluations again demonstrated an enteropathy as the cause to the protein loss. Endoscopy and intestinal biopsy was discussed but based on his clinical history and familial historic information the owners elected to pursue treatment of inflammatory bowel disease without a definitive diagnosis. He was treated with Purina HA, prednisone and imuran. Handsome did fairly well with this protocol for about 1 and ½ years. He was eventually euthanized due to obstructive intestinal disease associated with severe pica secondary to the cortisone administration.
Here again is a case where the dog had beagle pain syndrome/ steroid responsive meningitis early in his life and later developed severe inflammatory bowel disease. There continues to be a question as to whether there is a commonality to the development of these diseases.