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 replacement 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 2016 | 21