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Gastrointestinal disease in ferrets and rabbits (Proceedings)

Article

Sacculus rotundus; spherical thick-walled enlargement at ileocecal junction. The adjacent cecum has a round patch of lymphoid tissue called the cecal tonsil. The increased thickness of these two lymphoid structures is due to aggregates of organized lymphoid tissue and macrophages in lamina propria and submucosa. Important to recognize this palpable thickening as normal.

Rabbit

Anatomy

Sacculus rotundus; spherical thick-walled enlargement at ileocecal junction. The adjacent cecum has a round patch of lymphoid tissue called the cecal tonsil. The increased thickness of these two lymphoid structures is due to aggregates of organized lymphoid tissue and macrophages in lamina propria and submucosa. Important to recognize this palpable thickening as normal.

     • -80% of food eaten should reach the cecum within 12 hours of ingestion.

     • -In the colon ingested contents are separated according to size and density: fluid and nutrient-rich particles of greater density settle into haustra (sacculations), and the less dense fiber particles accumulate in the colon's lumen. Taenia (bands) move the fiber antegrade to be eliminated as hard feces, while reverse peristalsis of the haustra move fluid and nutrient rich particles retrograde into the cecum where bacterial fermentation forms B-complex vitamins, protein, and fatty acids. Some of these nutrients are absorbed directly across cecum wall but most are formed into cecotrophs which are usually passed within 4 hours of hard feces. Large, undigestible fiber particles (lignin) are necessary for normal motility of rabbit's cecum and colon.

Gastrointestinal stasis

Gastrointestinal (GI) stasis is a syndrome where the normal muscular contractions of the stomach and intestines are greatly diminished and with time the normal intestinal/cecal bacterial flora is thrown off balance. Several factors can be involved including environmental stressors, pain from other underlying conditions such as dental/tooth points or spurs, and most commonly inappropriate diet. Feeding simple carbohydrates such as breadstuffs or cereals along with a lack of crude fiber can predispose to GI stasis. In the absence of adequate fiber the gastrointestinal tract slows down, which may result in subsequent changes in the cecum pH fermentation and bacterial populations and subsequent worsening of GI stasis. The rabbit with GI stasis will be anorexic or have a reduced appetite. An affected rabbit produces very small stools or none at all and may be hunched-up or grind its teeth in response to painful gastrointestinal gas formation. Diarrhea with mucous may or may not be present. Abdominal auscultation may reveal normal or hyperactive gut sounds early in the course of the disease with decreased to no gut sounds with disease progression. The sooner the problem is recognized the better the chance for full recovery and survival. Rabbits presented in obvious distress and with a palpably enlarged, non-compressible stomach warrant close monitoring and critical care. Rabbits with intestinal obstruction are occasionally presented and create a diagnostic and therapeutic dilemma. Most commonly due to a small trichobezoar or hair filled cecotroph, the duodenum is a common site of obstruction, followed by pylorus or ileocecocolic junction. Radiographically, the stomach is filled with gas and/or fluid and food and loops of dilated intestine proximal to site of obstruction may be seen. If the obstruction passes through the ileocecocolic junction, gas is seen in the cecum and more gas-filled loops of intestine are seen on serial radiographs and the patient is treated medically. If the obstruction is not moving, as determined by serial radiographs, then the case becomes surgical. If the rabbit is taken to surgery it is ideal to try and gently milk the obstruction down through the ileocolic junction and into the hind gut instead of performing an enterotomy due to thin and friable nature of the rabbit small intestine.

Depending on the severity of the condition and clinician discretion a variety of treatment measures may include:

     • Abdominal massage: Gentle, deep massage of the abdomen to stimulate intestinal contractions and to break down impacted stomach contents. If diagnosed early in the course of the disease; encourage movement and exercise as a way to stimulate gut motility.

     • Fluid therapy in appropriate amounts and properly administered.

     • Analgesics as needed; if showing signs of pain or if evidence of increased GI gas.

     • Syringe feeding an enteral nutrition product such as Oxbow Critical Care in order to provide nutritional supplementation and fiber to stimulate GI motility. Nasogastric (NG) tube placement has been advocated in the treatment of GI stasis with one paper showing that nutritional support through a 5- to 8- Fr Argyle tube (Kendall, Mansfield, MA), passed ventrally and medially into the ventral nasal meatus and advanced to the stomach, not only provided for nutritional support but also helped stimulated gastrointestinal motility and early return to function.

     • Appetite stimulants: The sooner the rabbit eats the sooner the intestinal motility will return to normal. Vitamin B complex injections or 1-4mg/rabbit PO q12-24h cyproheptadine (Periactin®, Merck,West Point, PA) may act to stimulate the appetite.

     • GI motility stimulants: Prokinetics such as cisapride (available through a compounding pharmacy) dosed at 0.5mg/kg PO q8-12h and metoclopromide (Reglan®, Schwarz Pharm. Mequon, WI) at 0.5mg/kg PO,SC q8-24h.

     • Simethicone: To help break down gas bubbles associated with bloating.

     • If suspect endotoxin-induced gut mucosal injury consider epidural analgesia to prevent functional and structural mucosal alterations.

Other causes of rabbit GI disease

     • Parasitism-coccidia (Eimeria spp.) more common in juvenile rabbits and can lead to diarrhea and remains a major disease problem in commercial rabbitries. E. intestinalis and E. flavescens are considered most pathologic. Oocysts require 1 or more days to sporulate at room temperature before they are infective. When ingested, sporulated oocysts (sporocysts) release sporozoites, which invade enterocytes and multiply by schizogony. Dx: fecal flotation [don't confuse nonpathogenic GI yeast (Saccharomycoptes gutulatus) with coccidia or suspect as pathogen]

     • Hepatic coccidiosis- Eimeria stiedae Sporozoites can be found in liver within 48 hours post ingestion of sporulated oocysts. Migrate to liver via lymphatics or hematogenous→ invade epithelial cells of the bile ducts and schizogony begins. Following gametogeny, oocysts are formed, released into the bile ducts, and passed into the intestines. Infections may be clinical or subclinical. Weanling rabbits most often affected. Pathology; weight loss, diarrhea, ascites, icterus. Liver periportal mixed inflammatory cell infiltration with bile duct epithelial hyperplasia and ductal dilation. Grossly seen as yellow to gray raised circumscribed lesions.

     • Pinworm (Passalurus ambiguous) Dx, fecal flotation. Weight loss, poor overall performance.

     • Viral: Coronaviral enteritis with mortality in young rabbits 3-8 weeks old, reported in German breeding colony. Rotavirus enteritis usually confined to suckling and weanling animals, secondary E coli infections complicate the disease. Dx: ELISA testing, direct electron microscopy of fecal samples.

     • Clostridial enteropathies/ Enterotoxemia ; C difficile, C perfringens, C spiroforme. Disruption of normal gut flora that act as a microbial barrier and predisposes to Clostridium overgrowth leading to diarrhea with possible subsequent type E iota toxin production leading to enterotoxemia. Enterotoxemia manifest as damage to enterocytes with resulting profuse diarrhea, depression, dehydration and death. Predisposing causes include "carbohydrate overload" with ingestion of large quantities of high-energy foods or treats, and inappropriate oral antibiotic therapy. Pathologic intestinal submucosal edema and hemorrhage common. Dx: clinical signs, history and fecal Grams stains or cytology, special procedures to identify gut Clostridial toxin.

     • Clostridium piliforme; Tyzzers Disease. Not seen in pet population and rarely in lab animal any more. The organism may survive for long periods in the sporulated state and can remain infectious in contaminated bedding for at least a year. It is likely that interspecies infection can occur. Infection from fecal to oral exposure. Following oral exposure→ C piliforme multiplication in intestinal mucosa, with tissue damage, dissemination to the liver by portal circulation with bacteremia and subsequent hepatitis and on occasion myocarditis. Stress from shipping, overcrowding, high env temperatures and poor sanitation predispose. Alterations in normal gut flora may predispose to disease. All ages affected but most severe in weanlings; morbidity variable with high mortality. Disease characterized by sudden onset, watery diarrhea, rapid progression and high mortality. Sudden death with no prior clinical signs possible. Caudal GI (particularly cecum) thickened and edematous, pale miliary foci in liver, pale linear myocardial streaks. Dx: histopathology. Can be harbored as an inapparent or subclinical infection- concurrent E. coli and or coccidiosis can worsen clinical signs on disease progression.

     • Mucoid enteropathy Syndrome involves primarily young rabbits, occasionally adults. Characterized by large accumulation of mucous (in response to non-specific noxious stimuli) in the colon. Many affected rabbits also have cecal impaction and fibrous fecal pellets are not produced. Signs similar to GI stasis. Definitive cause unk. Rx supportive.

     • Saccharomyces guttulatulus- Normal inhabitants of cecum. Overgrowth of GI yeast may occur secondary to a diet too rich in pellets or simple CHO. Dx on fecal analysis. Can result in diarrhea. Rx- diet correction or at time Nystatin when in very high numbers.

     • Rectoanal papillomas- benign friable papillomas at the rectoanal junction. Relatively small cauliflower-like masses extends 360° around anus. Can cause discomfort and result in intermittent rectal bleeding. Rx: surgical excision. Etiology unk.

     • Lead toxicosis. Leads to anorexia and ileus. Vomiting, seizures, anorexia, hysteria, lethargy, and diarrhea were the most common clinical signs, and nucleated RBC and basophilic stippling were the most common laboratory abnormalities. Blood lead > 10ug/dl is considered significant. Rx: chelation with Calcium Disodium Versenate (Abbott Labs, N Chicago, IL).

Ferret

Nutritional.

The ferret is an obligate carnivore with a short intestinal tract that lacks a cecum and ileocolic valve. GI transit time is as short as 3 hours from stomach to rectum. This rapid transit time along with the ferret's lack of intestinal brush border enzymes, esp. lactase, contribute to an inefficiency in absorption. As a result, they are less able than cats to absorb enough calories from carbohydrates. Ferrets snack and eat multiple small meals throughout the day. Milk products can result in a very soft stool within hours of ingestion. Ferrets possess an unsophisticated gut flora and the usual anaerobic flora abundant in most mammals is scanty in the ferret, probably as a result of the short 10cm large colon. Ferrets treated for weeks to months with antibiotics do not experience GI upsets such as diarrhea. To compensate for the inefficiency of its digestive tract, the ferret requires a concentrated diet, high in protein and fat and low in fiber. Unless fed very high fat foods ferrets generally eat as much as they want without becoming obese. Ferrets normally increase food intake approx 30% in the winter and gain weight by depositing SQ fat. This will reverse as daylight lengthens in the spring. For maintenance, ferrets may consume between 200-300 kcal/kg bw daily

Physiological.

The ferret GI tract is spontaneously active even under anesthesia. The ferret GI tract is designed to be excitatory and have rapid motility, and be highly secretory. Exogenous stressors, chemical and neurologic stimulations, further increase motility and secretion. During any hypoglycemic episode, whether due to inanition, GI loss or insulinoma, the clinician needs to be aware of pancreatic and gastric physiology and treat the nausea and secretions in addition to the hypoglycemia. The ferret stomach secretes acid in response to histamine, pentagastrin, and calcium. There is a low concentration of free histamine in the stomach. Histamine H2 receptor antagonists abolish the acid secretion response to exogenous histamine. The author treats any stressful ill, pre-surgical or hypoglycemic ferret with famotidine in order to prevent gastric ulcerative disease.

Parasitism-

     • coccidia, giardia, ascarids

Gastrointestinal Obstruction /Foreign Bodies

Ferrets, most commonly less than one year of age, have a tendency to chew and ingest rubber objects of any kind, especially foam rubber, and will occasionally ingest cloth or other foreign materials. This behavior tends to greatly decrease in mature ferrets. In the older animal, obstruction with trichobezoars becomes a more frequent cause of gastrointestinal obstructive disease.

In ferrets, the clinical signs associated with GI foreign bodies vary greatly. In cases of gastric foreign bodies that are not causing acute obstructive disease, the signs can be vague and include any combination of the following: intermittent anorexia, decreased volume of stools, tarry stools, depression, gradual weight loss with eventual severe wasting, pawing at the mouth, teeth grinding and salivation. Vomiting does occur, but is not as frequent a finding as in dogs or cats with gastric foreign bodies. The ferret may become irritable due to chronic pain. When a complete obstruction occurs, whether it is at the pylorus or in the small intestine, the signs are much more dramatic. The patient will exhibit severe depression and dehydration, vomiting is more common, stools are scant and tarry. These patients also demonstrate abdominal pain/splinting and may grind their teeth and paw at their mouths.

The diagnosis is based primarily on history, physical examination and radiography. The ferret abdomen is easily palpated and foreign material in the stomach or intestine may be identifiable. Survey radiographs are used to look for signs of gastrointestinal tract obstruction or the foreign body itself. Barium series may be necessary to Dx; barium dosage is 12-15ml/kg, and due to the ferret's short gastrointestinal transit time, a full barium series may be completed in two hours.

If severely debilitated, placement of an esophagostomy tube is a convenient way to provide nutritional support for extended periods. The resting energy requirement (RER) of ferrets is 70 kcal/day.

     • Hairball syndrome - see above. Dx via history, signs, abdominal palpation and imaging

     • Neoplasia- lymphoma, adenocarcinoma- association with chronic Helicobacter infection?

     • Inflammatory Bowel Disease (IBD) - muscle wasting, chronic diarrhea of varying character (green mucous, bird seed, melena, watery), vomiting, bruxism. Repeated trichobezoars due to decreased gastric motility due to underlying inflammation

          o Clin path: elevated lipase, globulin, +/- lymphocytosis, elevated liver enzy (ALT, GGT) due to ascending lymphocytic portal hepatitis may all be seen.

          o Surgically biopsy stomach, duodenum, jejunum, gastric as well as duodenal lymph nodes and liver

          o Histopath: primarily lymphoplasmacytic with lesser eosinophilic infiltrate. LN biopsy interpretation may be difficult to differentiate, hyperplasia/advanced atypia vs. lymphoma

          o Theoretical causes; hypersensitivity, infectious disease, dietary intolerance, metabolic disease or other factors triggering an aberrant immune response.

          o May lead to megaesophagus or lymphoma

          o Therapy aimed at long term suppression of the inflammatory response including prednisolone (1 mg/kg PO qd) and/or azathioprine (0.9mg/kg PO q72h) (response may take several months, dose varies with severity of disease) and eliminating possible contributing factors. Novel protein diets may help.

Coronavirus-associated disease

Usually young ferrets < 24 mo, rapid onset, high fever, lethargy, recumbency, ataxia, posterior paresis, pain when moving, bruxism, anorexia or difficult swallowing or drinking. Clin path: many times see a neutrophilic leukocytosis, anemia, thrombocytopenia, and hypergammaglobulinemia. Grossly, whitish nodules were found in numerous tissues, most frequently the mesenteric adipose tissue and lymph nodes, visceral peritoneum, liver, kidneys, spleen, and lungs. One ferret had a serous abdominal effusion. Microscopically, pyogranulomatous inflammation involved especially the visceral peritoneum, mesenteric adipose tissue, liver, lungs, kidneys, lymph nodes, spleen, pancreas, adrenal glands, and/or blood vessels. Immunohistochemically, all cases were positive for coronavirus antigen using monoclonal antibody. FIPV3-70.

Idiopathic megaesophagus also reported in the ferret: Clinical history included regurgitation, difficulty swallowing, partial anorexia, and lethargy. Diagnosed via contrast radiography. Etiology unknown. Symptomatic treatment was unrewarding. Bronchopneumonia, hepatic lipidosis, mild esophagits, and gastritis found on necropsy.

Helicobacter

Helicobacter mustelae has been found in ferrets worldwide and can be considered a normal inhabitant of ferret stomachs. H. mustelae colonizes nearly 100 percent of ferrets shortly after weaning via the fecal-oral route. Increased gastric pH permits bacteria to exit the stomach and enter the lower GI tract, where they can be recovered in the feces. Helicobacter may cause a progressive inflammatory response in the stomach lining over the lifetime of the ferret. Naturally infected ferrets have a predominantly mononuclear gastritis composed of lymphocytes and plasma cells, with only occasional eosinophilic and polymorphonuclear leukocytes. The ferret Helicobacter is morphologically and biochemically similar to human Helicobacter pylori, but DNA relatedness and 16S rRna sequence analysis prove that it is a unique species. H. pylori, has been definitively incriminated in development of ulcers in humans, therefore the ferret has been studied extensively as a model for several human gastrointestinal tract disease.

H. mustelae has been associated with the development of gastric and duodenal hemorrhagic ulcers. The role of H mustelae in gastric tumors and inflammatory bowel disease is less clear. The signs of gastric ulceration can be difficult to detect. Some ferrets show subtle signs of lethargy and poor appetite. The stools may become soft and occasional vomiting may be seen. As the disease progresses, the ferret will start to pass dark, tarry stools indicative of upper gastrointestinal bleeding, as well as show signs of abdominal discomfort; grinding of the teeth and increased salivation. Anemia, more severe weakness, dehydration and anorexia may follow.

GI biopsies may be obtained for histopathology, with Warthin-Starry and H&E stains used for assessment of colonization and mucosal histopathologic morphology respectively. Microbiology of biopsy specimens can be attempted, but the clinician needs to be aware that special handling of samples is required and finding a diagnostic lab that can handle such specimens may be difficult. Immunohistochemical staining to demonstrate the presence of Helicobacter organism in biopsy samples as well as gastric and fecal swabs is available through Research Associate Laboratory (RAL), Dallas, TX, www.vetdna.com. RAL will also perform real-time PCR confirming the presence of H mustelae DNA on gastric swabs taken at the time of surgery or from a culture swab inserted in red rubber tubing and passed into the stomach of the anesthetized ferret.

Many practitioners choose to treat based on the ubiquitous nature of the organism, clinical signs and lab work and/or radiographs to rule out other causes of similar GI signs. A treatment regimen similar to the one employed for humans can be initiated on the clinician's discretion ; amoxicillin (30 mg/kg PO q8hr) or clarithromycin (12.5mg/kg q12h), metronidazole (20 mg/kg q8hr) and bismuth subsalicylate (pepto-bismol, 17.5 mg/kg q8hr). A H2 blocker; famotidine( pepcid, Merck 0.25-0.5mg/kg PO, IV q 24h) or cimetidine (10 mg/kg PO q8hr) or a proton pump inhibitor; omeprazole (0.7 mg/kg q24hr) can be used in conjunction with the antibiotics. An alternative regimen is ranitidine bismuth (24 mg/kg q8hr) and clarithromycin (50mg/kg q24h or divided q12h). The author has found good success with a combination of amoxicillin, metronidazole and famotidine at above dosages. With all treatment regimens continue treatment for 2 to 4 weeks. Prior confirmed infection is not protective against subsequent challenge.

Hamster

Summary of findings from one study of GI disease found in a large hamster colony (18) :

     • No one etiologic agent as cause and no magic bullet treatment found to be universally effective

     • etiology multifactorial and GI disease found to be a common cause of hamster morbidity and mortality

     • Stress will exacerbate- weaning, shipping, environment/diet changes all occurring with a 1-2 day period in many cases.

     • 3% die annually with diarrhea in this two large breeder study involving 5-6 week old hamsters. Panels for various diseases run at U of Missouri RADL. They have a sick hamster panel.

Etiologic agents responsible for GI disease in this study of nine sick hamsters:

     • 9/9 positive for Clostridium pilliforme (Tyzzer's) [ note: all Normal hamsters tested negative]

     • 8/9 positive for Campylobacter

     • 2/9 positive for Clostridium dificile toxins

     • Numerous protozoa including giardia, trichomonads, entamoeba, Spironucleus muris

     • Stomachs heavily colonized with yeast (Candida)

     • All hamsters healthy and sick: positive for Sendai and PVM (Pneumonia Virus of Mice)

     • All hamsters healthy and sick: positive for Hymenolepis nana (tapeworm) with increased number of organisms found in sick hamsters. Praziquantal treatment of choice

     • Of note: no proliferative enteritis seen in this study

References

Harcourt- Brown TR: Management of acute gastric dilation in rabbits. In: Rabbits (Harcourt- Brown FM, ed), Journal of Exotic Pet Medicine 16: 168-174, 2007.

Lichtenberger M: Rabbit gastrointestinal stasis treated with NG tube feeding. In: Proceedings AEMV Scientific Program, Providence 107-111, 2007.

Kosugi S, Morisaki H, Satoh T, et al: Epidural analgesia prevents endotoxin-induced gut mucosal injury in rabbits. Anesthesia and Analgesia 101: 265-272, 2005

Percy DN, Barthold SW. Rabbit, In: Pathology of Laboratory Rabbits and Rodents., 3rd ed. Blackwell Publishing, Ames, Iowa, 253-307, 2007

Morgan RV, Moore FM, et al. Clinical and laboratory findings in small companion animals with lead poisoning: 347 cases (1977-1986) JAVMA 1991, 199:1, 93-97.

Bell JA, Ferret nutrition. In: VCNA,Exotic Anim Practice. 1999; 2: 169-192.

Burgess M, Garner, Clinical Aspects of Inflammatory Bowel Disease in Ferrets. Exotic DVM 4: 29-34, 2002

Garner MM, Ramsell K, et al. Clinicopathologic Features of a Systemic Coronavirus-Associated Disease Resembling Feline Infectious Peritonitis in the Domestic ferret (Mustela putorius). Veterinary Pathology 45; 236-246, 2008.

Blanco MC, et al. Megaesophagus in nine ferrets. JAVMA 205:3; 444-447, 1994

Johnson-Delaney C. The ferret gastrointestinal tract and Helicobacter mustelae infection. VCNA, Exotic Animal Practice. 8; 198-212, 2005.

Fox JG, Marini RP. Helicobacter mustelae infection in ferrets: Pathogenesis, Epizootiology, Diagnosis and Treatment, Seminars in Avian and Exotic Pet Medicine, 10 ; 36-44, 2001.

Wilson HB. Etiology, pathology and control of enterocolitis in a group of hamsters. Proceedings, AEMV Scientific Program, Providence. 123-126, 2007.

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