Vet360 Vol 3 Issue 04 August 2016 - Page 21

GASTROENTEROLOGY Pathogenesis The pathogenesis of IBD is unknown. Current theories include hypersensitivities as a result of immune system dysregulation and loss of tolerance to luminal antigens; pathological events increasing mucosal barrier permeability and exposing previously privileged innate immune system receptors to luminal commensals and dietary components; genetic mucousal innate immune system derangements predisposing the host to invasion by its own microbiota; loss of inflammatory cell apoptosis; food intolerance or other nutrition induced host microbiota dysbiosis and host microbiota mutations. Diagnosis Diagnosis of IBD requires that systematic elimination process is followed. Clinical examination A clinical examination always includes signalment, history, hands off examination and physical examination. It is used to localise the patient’s disease to at least include the intestine, determines the chronicity (> 3 weeks), and determines the distribution and severity of the disease. The severity of the disease and the detection of extra-intestinal clinical signs determine the urgency and extent of diagnostic investigations and therapeutic intervention. For example severe IBD may cause protein losing enteropathy (PLE) with consequential loss of muscle condition score, body condition score, development of hypoproteinemia and cavity effusions; these patients need to be aggressively worked-up and treated. Other patients may have relatively mild clinical signs without weight loss or debilitation allowing a progressive methodical work up which may include empirical treatment for parasites, a therapeutic dietary intervention and an empirical antibiotic trial. A minimum database for potential IBD patients The first diagnostic challenge faced is ruling out primary intestinal pathogens, extra-intestinal disease, and concomitant diseases. A complete blood count (CBC), serum chemistry profile, urine analysis, and multiple faecal wet preparations and faecal flotations, are recommended in all cases to help rule out extraintestinal disease and to help establish the severity of the intestinal disease. An extended database selected for individual IBD patients Faecal α1-protease inhibitor is useful to document PLE in untreated canine IBD cases. Faecal culture may be useful for the detection of salmonellosis or campylobacteriosis in some severe cases; cultured E.coli is not significant unless they are determined to be attached invasive type, which can only be determined with highly specialised techniques. Evaluation of serum cobalamin levels may be useful in cats and dogs with IBD to help guide replace- ment therapy; it is also low in cats with lymphoma and pancreatic disease. Clinically significant hypocalcaemia and hypomagnesemia has been reported in cases of PLE in Yorkshire Terriers. Canine and feline pancreatic lipase immunoassay may be useful to help rule out pancreatitis in selected cases. A canine trypsin-like immunoassay (TLI) is used to rule out exocrine pancreatic insufficiency (EPI), especially in German Shepherd dogs (GSDs). Dogs with concurrent EPI and IBD have severe weight loss and may exhibit coprophagia and an increased appetite in addition to typical IBD signs. Thyroid hormone levels and FIV and FeLV status should be known in cats. Radiography and ultrasonography are useful to detect extra-intestinal disease, intestinal obstruction as well as to help define intestinal disease. As the work up evolves, endoscopy or laparoscopy/laparotomy procedures are conducted. In severe cases they are ordered immediately. Stepwise work up of non-critical patients with symptoms of IBD What follows is a step wise approach that attempts to encompass the many clinical variations seen in practice. 1. Rule out intestinal helminths and protozoal infections It is considered standard practice to thoroughly screen all dogs and cats with a CE for helminths and protozoa multiple times (at least 3X) very early in the diagnostic work up. Faecal tests for giardia can be supplemented by a faecal ELISA that is highly sensitive and specific. It is also considered standard practice to empirically treat for helminths and protozoa even if the screening tests are negative. Giardia has variable therapeutic sensitivities. Possible treatments are metronidazole, febantyl and fenbendazole. Success of therapy should be reassessed with appropriate tests. In cases resistant to treatment environment, therapeutic sensitivity and a genetic immunopathology which may predispose the patient to infection are considered. In these cases drug combinations are used together with a high fibre diet and environmental decontamination. In cats especially, Pentatrichomonas spp and Tritrichomonas spp must also be considered. These parasites can be seen on faecal wet prep mounts, diagnosed on faecal polymer PCR or in the case of Trichomonas spp cultured from faeces using the bovine TTF culture medium. Tritrichomonas is treated with ronidazole. Spontaneous remissions do occur and an asymptomatic carrier state is recognised. Ronidazole resistance has also been encountered. Other more obscure intestinal pathogens, for example Cryptosporidium spp, Histoplasma spp., Toxoplasma spp., Mycobacteria spp., Protothecosis and Issue 04 | AUGUST 2 M BU ͌UQT Mܚ[˚[ B M ̍H LN B