key: cord-021491-x8czsmyd authors: Hoefer, Heidi L.; Bell, Judith A. title: Gastrointestinal Diseases date: 2009-05-18 journal: Ferrets, Rabbits, and Rodents DOI: 10.1016/b0-72-169377-6/50005-8 sha: doc_id: 21491 cord_uid: x8czsmyd nan Dental tartar, gingivitis, and periodontal disease are common in middle-aged and older ferrets (see Chapter 34) . Moist or semimoist diets may predispose these animals to dental calculi and periodontal disease. 30 Most ferrets, even on a dry diet, develop tartar that progresses with age. Tartar tends to accumulate most heavily on the second and third upper premolars. Biting and gnawing habits often result in discoloration, wearing, and breaking of the tips of the canine teeth ( Fig. 3-1) . Broken canine teeth do not usually result in obvious discomfort or pain unless the dental pulp is exposed. Root canal restoration or surgical removal of the affected teeth may be necessary in some ferrets. 33 Tooth root abscesses are not common but can occur at any age. Although dysphagia and drooling are sometimes seen, dental disease is often an incidental finding during physical examination. Dental extractions and scaling can be performed with the animal under anesthesia. Follow the basic principles for dental disease management that apply in the care of the dog or cat. FERRETS cele formation. Although this lesion is uncommon in ferrets, mucocele diagnosis and treatment have been described. 3, 39 Diagnosis of a mucocele is relatively straightforward. Facial swellings are often seen in the commissures of the mouth or in the orbital area in the case of a zygomatic mucocele. Other locations also are possible. Aspirate the mass to obtain samples for cytologic analysis. The fluid is viscous or mucinous and clear or blood-tinged. Cytologic examination reveals amorphous debris and occasional red blood cells. Treatment for salivary mucoceles is usually surgery. In one reported case, scalpel blade lancing of the medial wall of the mucocele resulted in drainage and no recurrence. 3 Marsupialization into the mouth with the use of a wide circular incision in the medial wall of the mucocele may be effective for mucoceles that bulge into the oral cavity ( Fig. 3-2 ). Surgical excision of the affected salivary gland is ideal for avoiding recurrence (see Chapter 12) . It may be possible to inject contrast medium into the mucocele in an effort to trace the origin of the saliva. Review the superficial anatomy of the head and neck region of the ferret before attempting surgical excision of a salivary gland. 44 Recurrence is possible. Diseases of the esophagus are rare in ferrets. Acquired megaesophagus has been reported in ferrets, and I have seen the condition several times in my practice. 6, 31 Megaesophagus describes an esophagus that is enlarged (dilated) on radiographic examination and that lacks normal motility. Recognizing this disease is important because the prognosis in ferrets with megaesophagus is poor. Clinical signs include lethargy, inappetence or anorexia, dysphagia, and weight loss. Regurgitation is common. Coughing or choking motions are sometimes described, and some ferrets have labored breathing. Differential diagnosis includes the presence of an esophageal or GI foreign body, gastritis, influenza, and respiratory diseases. Diagnosis is based on clinical signs and radiographic evidence. On radiographs, the esophagus is often dilated in both the cervical and thoracic segments ( Fig. 3-3 ). Food may be visualized in the esophagus. Aspiration pneumonia and gastric gas are sometimes evident in addition to esophageal dilation. Always take radiographs of the abdomen to exclude lower GI disease. Administer barium (10 mL/kg PO) to delineate the esophagus and to evaluate mural lesions, strictures, or obstructions ( Fig. 3-4 ). An endoscope can also be used to evaluate the esophagus. Use fluoroscopy, if available, to determine the motility of the esophagus after a barium swallow. The cause of megaesophagus in ferrets is unknown. Consider possibilities in the differential diagnosis as for dogs, and tailor the diagnostic workup accordingly. The management of ferrets with megaesophagus is similar to that of canine patients but is usually less successful. Supportive care and antibiotics are palliative at best. Administration of a GI motility enhancer such as metoclopramide (0.2-1 mg/kg q6-8h PO or SC) (Reglan, AH Robins Company, Inc., Richmond, VA) may be helpful. Cisapride, which until recently was marketed for gastroesophageal reflux and gastroparesis in humans, reduces the frequency of regurgitation in dogs with megaesophagus when it is given at 0.5 mg/kg q8-24h PO. 55 However, this drug is no longer available commercially in the United States because of adverse cardiac effects in humans. Its use in ferrets has not been evaluated. If esophagitis is suspected, add an H 2-receptor blocker, such as cimetidine, ranitidine (Zantac, Glaxo Pharmaceuticals, Research Triangle Park, NC), or famotidine (Pepcid AC, Johnson and Johnson, Fort Washington, PA). The prognosis for ferrets with megaesophagus is poor; generally, they die or are euthanatized within days of diagnosis. Affected ferrets are debilitated and suffer from malnutrition, hepatic lipidosis, and aspiration pneumonia. Other causes of esophageal disease in the ferret are rare. Esophageal foreign body has been reported in a ferret and was successfully managed surgically. 10 Gastric and duodenal ulceration has been reported in laboratory ferrets and is seen sporadically in pet ferrets. Causes of GI ulceration include foreign body or toxin ingestion, Helicobacter mustelae infection, treatment with ulcerogenic drugs, GI neoplasia, and azotemia caused by renal disease. The laboratory ferret is used as an animal model for the study of H. pylori infection in humans. H. mustelae isolated from the gastric mucosa of ferrets shares many molecular and biochemical features of H. pylori. H. mustelae infection in ferrets is associated with varying degrees of gastritis, with or without duodenitis, and it can result in ulcer formation. 21 (See Part II for a discussion of H. mustelae infection.) Ulcerogenic drugs such as nonsteroidal and steroidal antiinflammatory agents can be associated with ulcer formation. It is rare for ferrets to have GI bleeding when they are treated with corticosteroids at appropriate dosages; however, ulceration is possible with the prolonged use or overdose of other antiinflammatory agents such as ibuprofen (see Chapter 6) . Severe uremia and associated melena can occur in ferrets with primary renal disease, but this is uncommon. Gastritis in ferrets may be acute or chronic. Clinical signs may include weight loss and vomiting. Affected ferrets may hypersalivate and display tooth-grinding, which are indicative of nausea and abdominal pain. Clinical signs of gastric or duodenal ulceration include melena, anorexia, lethargy, and weight loss. Basic diagnostic testing includes whole-body radiography and screening blood tests. Fast the ferret for a short time (6-8 hours) to facilitate visualization of a gastric foreign body or hairball. The diagnosis of H. mustelae gastritis may be a diagnosis of exclusion of other common disorders, such as the presence of a GI foreign body; treatment for H. mustelae gastritis is often based on a presumptive diagnosis. Establish definitive diagnosis of Helicobacter infection by histopathologic study of a gastric mucosal sample obtained by endoscopic or surgical biopsy. Specialized techniques are necessary for culturing the organism, which is not shed consistently in feces of infected ferrets. 26 Treat gastritis and gastric ulceration with both specific therapy (according to the diagnosis) and supportive care. Hospitalize sick and anorexic ferrets for fluid therapy and parenteral treatment. A broad-spectrum antibiotic, administered parenterally, is indicated for sick ferrets. For ferrets that are not vomiting, offer multiple small feedings of a bland, moist diet; avoid dry, FERRETS high-fiber foods. For vomiting animals, withhold food for 6 to 12 hours while closely monitoring for any sign of hypoglycemia (older ferrets often have subclinical insulinomas); then, if vomiting has resolved, introduce small, frequent feedings. Bismuth compounds have action against pepsin, a proteolytic enzyme believed to be an important factor in the development of peptic ulcers. Administer bismuth subsalicylate at a dose of 1 mL/kg q8h PO. Sucralfate (Carafate, Marion Merrell Dow, Inc., Kansas City, MO) is a cytoprotective agent that binds to the erosion site and helps to form a protective barrier. It is a safe and useful adjunct to ulcer treatment and can be given orally in tablet ( 1 / 8 -1 / 10 of a 1-g tablet) or suspension (100 mg/kg) form every 6 hours. Systemic H 2 -receptor antagonists, such as cimetidine and famotidine, are often used to treat gastric ulcers because they block the histamine receptor on the gastric parietal cell and reduce gastric acid secretion. The proton pump inhibitors, such as omeprazole (Prilosec, Astra Merck, Inc., Wayne, PA), are occasionally used in ferrets. One quarter of the contents of a 10-mg capsule can be mixed with soft food and given orally. Antacid therapy may not be helpful in the early treatment of Helicobacter infection because affected ferrets usually develop hypochlorhydria. 26 A standard treatment for Helicobacter infection in humans is "triple therapy" with amoxicillin, metronidazole, and bismuth (see Part II). Bismuth interferes with the colonization of H. pylori in humans and suppresses colonization of H. mustelae in ferrets. 52 Surgical removal is the treatment of choice for GI foreign bodies. Two ferrets with GI polyps have been seen at the Animal Medical Center (New York, NY). Both ferrets showed lethargy, inappetence, melena, and weakness from anemia. Abdominal radiographs suggested GI abnormalities. On surgical abdominal exploration, one ferret had a gastric polyp and the other had a small intestinal polyp. Both ferrets did well after surgical resection of the polyps, which were histologically benign. Gastric bloat is rarely seen in pet ferrets, but it has been reported on domestic ferret farms and in black-footed ferrets (Mustela nigripes). 16, 48 Clinical signs are usually observed in weanling ferrets and include acute gastric distention, dyspnea, and cyanosis. Sudden death can occur. The cause of gastric bloat is unknown but is thought to be related to an overgrowth of Clostridium perfringens (previously called C. welchii). Certain conditions may predispose to clostridial overgrowth, including increased concentration of carbohydrates in the GI tract from overeating, dietary changes, and intestinal hypomotility. C. perfringens multiplies rapidly, producing enterotoxins that attack the villous epithelial cells of the gut. Gas production by the bacteria results in abdominal distention. Prevention and treatment of the disease are difficult because of the ubiquitous nature of the organism and the short course of disease. These animals are in shock and need immediate aggressive therapy. Relieve gastric pressure by trocharization or placement of an orogastric tube. Follow therapeutic protocols as for bloat in canine patients. GI foreign bodies are very common in ferrets. 40 Ferrets are naturally very inquisitive and like to chew on miscellaneous environmental objects, particularly rubber or sponge products. Rubber foreign bodies are most commonly ingested by young ferrets (younger than 2 years of age); in contrast, trichobezoars (hair balls) are more common in older ferrets. Linear foreign bodies, commonly ingested by cats, are rare in ferrets. The most common clinical signs of a GI foreign body in ferrets are lethargy, inappetence or anorexia, and diarrhea. Vomiting is often not reported by the owner. However, if vomiting is observed, consider a GI foreign body (Table 3-1). Some ferrets display signs of nausea, including bruxism, ptyalism, and face rubbing. Weakness can be profound in acutely obstructed animals; some of these ferrets are recumbent and reluctant to ambulate. If a GI foreign body is suspected, palpate the abdomen carefully. Foreign bodies in the small intestine often are associated with very localized discomfort or pain. Gastric foreign bodies are more difficult to palpate. Take whole-body survey radiographs in these cases. Although uncommon, esophageal disease is an important differential diagnosis in the anorexic, "vomiting" ferret. Abnormal abdominal radiographic findings include segmental ileus, gaseous distention of the stomach, and, occasionally, a visible foreign object or trichobezoar ( Fig. 3-5 ). Contrast (barium) studies can be done but are rarely needed. Base the diagnosis on history, clinical signs, palpation, and the results of radiography. At a minimum, submit a blood sample for a complete blood count (CBC) and plasma biochemical analysis in ferrets that are sick for longer than 2 or 3 days. Ferrets rarely pass GI foreign bodies unassisted. Occasionally, a small, partially obstructing object may pass with the administration of intestinal lubricants (cat laxatives) q8h and replacement fluids. However, most GI foreign bodies must be removed surgically. Stabilize debilitated ferrets before surgery. Parenteral fluids are usually essential because these ferrets often have varying degrees of dehydration. Perform an exploratory laparotomy as soon as possible. Collect biopsy specimens from the liver, the spleen (if enlarged), and the stomach or intestines (if ulcerated or abnormal in appearance). Some of these ferrets may also have H. mustelae-associated gastritis or GI lymphoma. Check the adrenal glands and the pancreas in older ferrets; discovery of concurrent abdominal disease is not unusual during surgery. (See Chapter 12 for a description of the surgical procedure.) In most instances, recovery is rapid after GI foreign body removal, and ferrets are able FERRETS to eat soft foods 24 hours after surgery. Most ferrets can be discharged within 36 to 48 hours after surgery. Prevention of foreign body obstructions includes recommending the regular use of a cat laxative preparation during active shedding seasons and "ferret-proofing" the household. Ferrets should not be left uncaged or unsupervised. Advise owners to avoid giving small rubber "squeak" toys to pet ferrets. GI parasites are uncommon in ferrets. However, any ferret with diarrhea should have a complete fecal parasite check, including a direct fresh wet mount and fecal flotation. In juvenile ferrets, nematodiasis is rare, but coccidiosis and giardiasis are occasionally seen. Coccidiosis can be subclinical in ferrets or it may be associated with diarrhea, lethargy, and dehydration. 7 Rectal prolapse is possible. Base the diagnosis of coccidiosis on fecal testing, either by direct wet mount and microscopic examination or by fecal flotation. Follow the same treatment protocols as for canine and feline patients with coccidiosis. Cryptosporidiosis is described in ferrets but may not result in clinical disease. 4, 46 Young ferrets can have a subclinical infection that can persist for several weeks. The oocysts can be shed in the feces of clinically normal ferrets. Histologically, the organism may be associated with an eosinophilic infiltrate in the lamina propria of the small intestine. It is not known whether zoonotic transmission of ferret cryptosporidia is possible; however, warn immunocompromised owners if the oocysts are detected in their ferrets. Salmonellosis is a contagious disease characterized by fever, bloody diarrhea, and lethargy. Conjunctivitis and anemia also may be present. Salmonella newport, S. typhimurium, and S. choleraesuis may be involved. 35 The incidence of salmonellosis in pet ferrets is very low and the infection may be associated with the feeding of uncooked meat, poultry, and meat by-products. Isolation of Salmonella organisms usually requires the collection of multiple fecal samples and the use of selective media. Treatment consists of aggressive supportive care, use of antimicrobials, and shock therapy as needed. Ferrets may be naturally or experimentally infected by the bovine, avian, and human tubercle bacilli. 8, 15, 49 Mycobacterium bovis and M. avium infections have been recognized in research and farm ferrets in England, Europe, and New Zealand. These infections may have been associated with the feeding of raw meat and poultry and unpasteurized dairy products. More recently, a pet ferret was reported to have a visceral infection caused by M. avium. 49 The ferret had a long-term history of weight loss, diarrhea, and vomiting that was unresponsive to treatment. Intestinal biopsy results revealed granulomatous inflammation and acid-fast bacteria. Base the diagnosis of mycobacteriosis on the findings of tissue biopsy, including histopathologic examination with acid-fast staining, polymerase chain reaction (PCR) testing, and culture. M. avium can be detected in the small intestine, liver, spleen, and lymph nodes of affected ferrets. Because of the zoonotic potential, treatment is not recommended. Campylobacter jejuni is a bacterial enteric pathogen that is associated with diarrhea and enterocolitis in human beings and several animal species, including dogs, cats, calves, and sheep. C. jejuni can be isolated from the feces of normal ferrets. During the 1980s, it was suspected to be the cause of proliferative colitis, which has since been renamed "proliferative bowel disease (PBD)" in ferrets. 19, 20 However, inoculation of C. jejuni in 54 conventionally reared and two gnotobiotic ferrets caused diarrhea but not the full spectrum of clinical signs and histopathologic lesions seen in PBD (see Part II). 4 The agent of porcine proliferative enteropathy, which is identical to that causing PBD in ferrets, 15 has now been assigned the new genus and species name Lawsonia intracellularis. The importance of C. jejuni as a primary pathogen in pet ferrets is not known. Infection with rotavirus causes diarrhea in young ferrets. Farm outbreaks of diarrhea are associated with high morbidity and mortality rates in neonatal kits from 2 to 6 weeks of age. 5, 56 The morbidity is low in adult ferrets, but infection may result in a transient green mucoid diarrhea. No antemortem testing is available for the diagnosis of rotaviral infection in ferrets. Treatment is supportive; administer fluids and antibiotics to affected ferrets. Canine distemper virus is a highly contagious paramyxovirus that causes fatal disease in unvaccinated ferrets. Clinical signs are variable but often include diarrhea in conjunction with nasal and ocular discharges and a generalized orange-tinged dermatitis (see Chapter 7) . Diarrhea may be acute or intermittent. Fortunately, the widespread practice of vaccinating ferrets against canine distemper virus has greatly limited the occurrence of distemper and it has now has become an uncommon disease in ferrets. Coldlike symptoms and diarrhea in newly purchased, unvaccinated ferrets should arouse suspicion. There is no treatment for distemper. Ferrets affected with human influenza virus (an orthomyxovirus) sometimes have transient diarrhea. The virus also causes upper respiratory disease associated with coughing, sneezing, inappetence, and lethargy. Affected ferrets are often febrile (see Chapter 7) . Epizootic catarrhal enteritis (ECE) is a highly transmissible diarrheal disease of ferrets that first appeared in 1993 in several rescue and breeder operations in the eastern United States. The causative agent is thought to be a coronavirus. 57 In intestinal biopsy samples from affected ferrets, histologic findings include lymphocytic enteritis, villous atrophy, and blunting or degeneration of apical epithelium. Ferrets with ECE initially develop a profuse, green mucoid diarrhea that may progress to a loose, grainy stool resembling birdseed. Adult ferrets are most susceptible to ECE, and the typical history includes recent exposure to a new, young ferret that acts as an asymptomatic carrier. The incubation period is 48 to 72 hours, and affected ferrets are anorexic and lethargic. Treat sick ferrets with signs of ECE with aggressive fluid therapy, antibi-otics, and supportive care, and isolate these ferrets from asymptomatic or unexposed ferrets. Although the morbidity rate can be high, the mortality rate is low in ferrets that are treated appropriately. After recovering from ECE, some adult ferrets develop persistent, intermittent malabsorption with diarrhea. The clinical course can be prolonged in these ferrets, lasting weeks to months. Treatment with a short course of steroids (prednisone 1 mg/kg q12h for 14 days) and changing the diet to an easily absorbed food may speed recovery. Inflammatory bowel disease is a relatively common cause of gastroenteritis in ferrets. 9 The cause is unknown but may be related to dietary intolerance, hypersensitivity reaction, or another aberrant immune response. The inflammation typically is lymphoplasmacytic and should be distinguished from eosinophilic gastroenteritis, which often involves multiple tissues. This condition is easily overlooked in ferrets because it resembles viral diarrhea (ECE), eosinophilic gastroenteritis, and Helicobacter-associated gastroenteritis. Affected ferrets can have loose stools, intermittent nausea, occasional vomiting, and weight loss. Clinical signs can be subtle or, in rare cases, can resemble those of a GI foreign body in severity. These ferrets are usually young or middle-aged adults and in multiple-ferret households; typically only one ferret in the household is affected. Results of blood tests may reveal an increase in concentrations of liver enzymes and serum globulins, and lymphocytosis is occasionally present. In some ferrets, laboratory results are unremarkable. Diagnosis is based on clinical signs, a detailed clinical history that eliminates the possibility of exposure to ECE, and results of diagnostic tests such as radiographs and routine blood tests. Diseases such as Helicobacter gastroenteritis and Aleutian mink disease should be ruled out. Definitive diagnosis can only be made by histologic examination of full-thickness gastric and intestinal biopsy samples. Treatment is aimed at suppressing the immune response and dietary management. Corticosteroids such as prednisone (1 mg/kg PO q12-24h) can be used, but some ferrets with inflammatory bowel disease respond poorly to long-term treatment with steroids. Azathioprine (Imuran, Prometheus Laboratories, San Diego, CA) (0.9 mg/kg PO q24-72h) is another treatment option and seems to be well tolerated in ferrets. 3 Hypoallergenic diets made for cats (z/d feline; Hill's Pet Nutrition, Topeka, KS) can be tried. Lymphoma is the most common hepatic neoplasm seen in ferrets. Other reported hepatic neoplasms include hemangiosarcoma, adenocarcinoma, and hepatocellular adenoma. 29 Pancreatic islet cell tumors can eventually metastasize to the liver. Prognosis is guarded regardless of tumor type. Other than neoplastic diseases, primary hepatopathies are uncommon in ferrets. Vascular shunts have not been reported. Hepatic lipidosis can be found in association with long-term anorexia. Chronic GI diseases (e.g., trichobezoar formation) can lead to hepatic lipidosis. Steroid hepatopathy is rare in ferrets, even with long-term steroid administration or hyperadrenocor-ticism. Chronic-lymphocytic portal hepatitis has been found on histologic examination of hepatic biopsy samples. The cause of these entities is unknown but may be related to chronic visceral inflammation such as inflammatory bowel disease. Chronic cholangiohepatitis with biliary hyperplasia of variable intensity was reported in 8 of 34 cohabitating ferrets. 28 Three ferrets had neoplastic lesions in the liver. Spiral-shaped bacteria were identified in the livers of three ferrets, and bacteria with 97% similarity to Helicobacter species were identified by PCR in the feces of one ferret. Because of the clustering of cases and the pathologic findings, a possible infectious cause was suggested. Copper toxicosis was diagnosed in two sibling ferrets on the basis of high hepatic copper concentrations and histologic changes in hepatic tissue. 27 Clinical signs in these two ferrets were mostly nonspecific and included severe central nervous system depression with hypothermia and hyperthermia, respectively. One ferret was icteric. Both ferrets died within a few days of clinical evaluation despite supportive care. A genetic predisposition to copper toxicosis in these two ferrets was proposed because they were siblings with the same phenotypic coat color and because no environmental source of copper could be identified. A high concentration of alanine aminotransferase (>275 IU/L) is present on biochemical analysis in most ferrets with liver disease. Alkaline phosphatase concentration is sometimes elevated. High total bilirubin levels are uncommon, and ferrets are rarely icteric. Base the diagnosis of liver disease on observation of persistently high concentrations of liver enzymes, radiographic and ultrasound findings, and for definitive diagnosis, analysis of liver biopsy samples. Ultrasound-guided needle biopsy of the liver is possible, but full abdominal exploration is often recommended because of the likelihood of concomitant disease in ferrets. The GI tract is not a common site of primary neoplasia in ferrets. The oral cavity is a rare location for neoplastic lesions. Pyloric adenocarcinoma has been reported, 47 and I have seen intestinal adenocarcinoma in one ferret. Lymphoma frequently affects the GI tract of ferrets (see also Part II). Visceral and mesenteric lymph nodes and the liver are common sites for lymphoma; intestinal lymphoma is uncommon. Treatment involves surgical resection and debulking whenever possible. Chemotherapy for lymphoma is described in Chapter 9. Rectal prolapse can occur in ferrets. It is most often associated with diarrhea and is usually a disease of young ferrets. Possible causes include coccidiosis, PBD, colitis, campylobacteriosis, and neoplasia (see Part II). Diagnostic tests should include a fecal wet mount and flotation to check for parasites. GI parasitism other than coccidiosis is uncommon. Treat with antibiotics and antiparasitics, as indicated. Prolapses often resolve with treatment of the causative condition. Although rarely needed, rectal purse-string sutures can be placed if the prolapse is extensive; these sutures can be left in place for 2 to 3 days. Include a careful rectal examination (visualization and palpation) in all ferret examinations. Undescented ferrets may develop anal gland disease, including impactions and abscessation. Palpation of the anal area may reveal either unilateral or 360-degree perianal swelling. Manage anal gland disease as in the dog. Be forewarned: anal gland odor is quite noxious. Anal gland removal is described in Chapter 12. Neoplasia is rare in the rectal area, although I have seen one descented ferret with leiomyosarcoma that surrounded the rectal opening ( Fig. 3-6 ). The ferret presented for a rectal prolapse, and a tumor was found on palpation. Treatment involves surgical debulking and, possibly, a rectoplasty. Prognosis is poor. Owners may describe "vomiting" in their ferrets, but some of these animals may actually be regurgitating. In light of this, the differential diagnoses for emesis in ferrets include both esophageal diseases and gastroenteric disorders. In the clinical history, vomiting is not as frequently described in ferrets as it is in canine or feline patients. For example, ferrets rarely vomit hairballs, and often vomiting is not part of the history associated with foreign body ingestion. The reason for this is unclear. No anatomic feature prevents emesis in ferrets; in fact, ferrets have long been laboratory animal models for human emesis studies because vomiting can readily be induced in them in a laboratory setting. 14 The major differential diagnoses for vomiting or regurgitation in ferrets include the presence of a GI foreign body, H. mustelae gastritis, gastroenteritis, and, rarely, megaesophagus. It is uncommon for ferrets with metabolic problems such as azotemia or hepatic disease to vomit. Although definitive diagnosis is not always possible, it is important to recognize whether medical or surgical treatment is required. For example, most obstructions caused by a foreign body require surgery, whereas gastroenteritis is a medical disease. However, differentiating these two diagnoses is often quite challenging (see Table 3 -1). Diagnosis begins with the history. Pointedly question an owner regarding the chewing habits of the ferret: Does the ferret have a squeak toy? Is it unsupervised in the household or usually caged? Has vomiting been observed? The description of any vomiting behavior is significant. Also question the owner regarding the animal's appetite and obtain a description of the feces. On physical examination, some foreign bodies in the small intestine can be distinctly palpated. However, enlarged mesenteric lymph nodes can sometimes feel like foreign objects. Also remember that foreign bodies in the stomach are difficult to detect on palpation. PBD may result in palpably thickened intestines in the ferret; however, vomiting is not usually a feature of this disease. Radiography is the most important diagnostic test in the workup of a vomiting ferret. Survey radiographs should include the whole body. Radiographic signs of megaesophagus can be subtle. The heart may appear small because of hypovolemia from dehydration. Varying amounts of gas can be seen with foreign body-related obstruction, and sometimes the incriminating object is visible. Segmental ileus or a dilated and gas-or fluidfilled stomach is a typical radiographic sign of obstruction (see Fig. 3 -5) . Not all cases of GI foreign body are radiographically obvious. If evidence of foreign body obstruction is not well defined, consider medical therapy and perform repeat radiography in 24 hours. Alternatively, give barium contrast for a series of contrast-enhanced films. If there is a strong indication of the presence of a foreign body, perform abdominal exploratory surgery the same day, preferably after parenteral fluid therapy has been started (see Chapter 12) . Obtain tissue for biopsy as needed (e.g., the liver or spleen), and save any foreign object to show to the owner. Always check the entire gut for lesions and examine the pancreas and adrenal glands, especially in older ferrets. If a foreign body is not found, collect gastric and duodenal biopsy samples and request special staining for Helicobacter species. Helicobacter infection is associated with gastritis, especially in the antral region and the proximal duodenum (see Part II). Although results of exploratory surgery may be negative for a foreign object, histologic examination of biopsy samples may or may not reveal a diagnosis. The possibility of negative findings should be discussed with the owner before surgery. If surgery is not an option or is not recommended, consider treatment for H. mustelae-associated gastritis (see Part II). If obstruction is still a possibility, administer a cat hairball preparation (Laxatone [EVSCO Pharmaceuticals, Buena, NJ] or Petromalt [VRx Products, Harbor City, CA]) at 1 mL q8-12h. Carefully examine all feces passed in the hospital; foreign objects or matter may sometimes be found in the stool. Normal ferrets nibble on food all day. Their GI transit time is short (3 hours), so defecation is frequent in the healthy state. The normal stool is slightly soft and formed. Diarrhea can range from mucoid and green to hemorrhagic. Some owners describe a "birdseed" type of diarrhea that may be caused by malabsorption. Anorexic ferrets may produce a very dark green (bile) stool that can resemble melena. Unlike canine patients, diarrhea in ferrets is difficult to classify as originating in the small intestine or the large intestine. More important are the onset, duration, and severity of the diarrhea as well as concurrent clinical signs. Several causes of diarrhea in ferrets are recognized. These can be separated into diseases of young or older ferrets as well as infectious or noninfectious causes. The most common noninfectious causes of diarrhea include dietary indiscretion, foreign body ingestion, trichobezoar, and inflammatory bowel disease. Occasionally, severe metabolic disease can result in a green (biletinged) mucoid diarrhea. Eosinophilic gastroenteritis typically affects mature ferrets but is uncommon (see Table 3 -1 and Part II). Infectious agents are rare causes of diarrhea in closed groups or isolated ferrets, such as those kept as individual household pets. Ferrets do not usually have GI parasites, but coccidia can be present in young, newly purchased ferrets. Rotavirus can cause outbreaks of severe diarrhea, but most reports of this are in very young, unweaned ferrets. Ferrets that have been exposed to unfamiliar ferrets, such as show ferrets, may be susceptible to ECE. Newly acquired young ferrets can also act as asymptomatic carriers of ECE and expose naïve, older ferrets in a household group. In contrast, PBD usually affects young ferrets. Canine distemper virus in the epitheliotropic form causes diarrhea in conjunction with respiratory and integumentary disease in unvaccinated ferrets. The clinical approach to the diagnosis of diarrhea depends on the severity and duration of clinical signs. Obtain a vaccination and dietary history and perform a direct fecal wet mount and flotation to check for GI parasites. Treat ferrets with mild diarrhea, without anorexia or vomiting, on an outpatient basis with an antibiotic such as chloramphenicol or sulfadimethoxine or with a cat hairball preparation if a trichobezoar is a possibility. Sick ferrets need a more comprehensive workup that includes radiographs to check for obstructive lesions and a CBC and a plasma biochemical analysis to assess metabolic conditions. If simple diagnostic tests do not reveal a cause and therapy is unsuccessful, consider exploratory surgery to evaluate the GI tract and obtain biopsy samples. Endoscopy can be difficult in ferrets because of their small size but may be an alternative to surgery. Perform colonoscopy in ferrets with chronic colitis. Culture the feces for C. jejuni or Salmonella species, especially if the ferret is febrile or the feces are hemorrhagic. Hospitalize sick or dehydrated ferrets for supportive care and a diagnostic workup. Give fluids subcutaneously if a ferret is stable or intravenously if it is weak and dehydrated. Administer antibiotics parenterally if possible. Metronidazole, chloramphenicol, and amoxicillin are good choices for GI disease in the ferret. Oral chloramphenicol does not usually cause the nausea and anorexia that it produces in some cats. A short course of a kaolin/pectin suspension (1-2 mL/kg PO q2-6h prn) can be administered as a GI protectant until a more definitive diagnosis is established. Drugs that affect the motility of the GI tract should never be administered without an initial diagnosis. Motility-enhancing drugs such as metoclopramide and cisapride are contraindicated if a GI obstruction is present, and anti-cholinergic drugs can produce an ileus that may be difficult to interpret radiographically. Judith A. Bell, DVM, MSc, PhD H. mustelae gastritis, PBD, and eosinophilic gastroenteritis all cause diarrhea and wasting in ferrets. Eosinophilic gastroenteritis has been infrequently diagnosed, and no specific causative agent has been identified. Virtually all North American ferrets are likely to be exposed to H. mustelae as kits, becoming persistently infected at weaning and developing some degree of gastritis. 17 PBD, also known as proliferative colitis or ileitis, is caused by an intracellular bacterium and is associated with chronic diarrhea and marked weight loss in ferrets. 18 Clinical or subclinical gastritis may develop concurrently with PBD and other GI or systemic diseases. Other entities to be ruled out include partial GI obstruction by a foreign body, lymphosarcoma or other gastric neoplasia, Aleutian mink disease, and persistent ECE. H. mustelae is a gram-negative rod morphologically similar to Campylobacter species that requires a microaerophilic environment for growth on artificial media. It is antigenically related and biochemically similar to H. pylori, a human pathogen associated with gastritis and ulcers. 21 Colonization of the antral area of the stomach and pyloric area of the duodenum with H. mustelae is very common in domestic ferrets, unless they are specifically treated or hand reared in isolation. 12, 17 Colonization is accompanied by a specific immune response, but infection persists despite high serum antibody titers. 17 Although infection is common, clinical gastritis and ulcers occur relatively infrequently. Severe gastritis may be evident in gastric biopsy samples from ferrets showing no signs of clinical disease. 17 The histopathologic lesions of H. mustelae-associated gastritis in human beings and ferrets consist of mucus depletion, gland loss and regeneration, and leukocyte infiltration. The organism can be observed in silver-stained histologic sections of gastric mucosa. 21 Affected ferrets that die usually have a single large pyloric ulcer or many small ones (Fig. 3-7) , and the stomach and intestinal tract contain digested blood and mucus, causing the ingesta to appear very dark. Cultures of H. mustelae from fecal samples are usually difficult to obtain, even when the organism is readily identified histologically in gastric biopsy samples. In humans, chronic infection with H. pylori leads to different clinical and pathologic outcomes, including chronic gastritis, peptic ulcer disease, and gastric neoplasia. 42 The severity and distribution of the H. pylori-induced inflammation are key deter-FERRETS minants of these outcomes. Gastritis involving the antrum is associated with excessive acid secretion and a high risk of duodenal ulcer. Gastritis involving the acid-secreting corpus region of the stomach is associated with hypochlorhydria, gastric atrophy, and increased risk of gastric cancer. 41 As in humans infected with H. pylori, transient hypochlorhydria develops in ferrets approximately 4 weeks after experimental infection. 36 This condition probably facilitates fecal-oral transmission as well as recovery of H. mustelae from feces. 37 Hypochlorhydria is associated with urease production, which is detectable in gastric biopsy samples. It also correlates with the degree of colonization and the occurrence of gastritis in biopsy results. 17 Urease production is associated with the ability of H. mustelae to colonize the stomach, with non-urease-producing strains being nonpathogenic. 17 A urease breath test is available for humans to aid in diagnosis, and a similar test has been used in ferrets under research conditions but is not practical for clinical use. 37 H. mustelae inhibits secretion of acid by parietal cells in vitro, and this mechanism may also contribute to hypochlorhydria. 21 In humans, chronic infection with H. pylori is associated with release of cytokines that impair function of enterochromaffin cells, which are neuroendocrine cells in the gastric mucosa that control acid secretion by releasing histamine. The impaired secretory function of these cells may predispose to hypochlorhydria and gastric carcinogenesis. 45 Gastrin is a hormone that stimulates gastric acid secretion and is secreted by the G cells of the gastric antrum. In humans and probably in ferrets, high levels of gastrin may initiate GI mucosal damage and ulceration. Hypergastrinemia is probably a response to the presence of H. mustelae in the antrum or to its associated inflammation. Hypergastrinemia is abolished after antibiotic therapy eradicates the Helicobacter infection. 17 In humans, Helicobacter-associated gastritis has been implicated as a risk factor for gastric adenocarcinoma and gastric lymphoma. 17 There is some evidence that this is also the case in ferrets. As H. pylori does in humans, 32 infection with H. mustelae in ferrets apparently stimulates cell proliferation in the gastric mucosa. 22 Under research conditions, gastric adenocar-cinoma eventually developed in ferrets that were naturally infected with H. mustelae and treated with a known gastric carcinogen. 17 Spontaneously occurring gastric adenocarcinoma has been reported in pet ferrets. Although H. mustelae was neither cultured from the lesions nor identified histologically in some cases, 47, 51, 53 in others, silver-stained organisms that were morphologically compatible with H. mustelae were present in the neoplastic tissues. 22 Lymphoid follicles (mucosa-associated lymphoid tissue [MALT]) are observed in the gastric mucosa of humans colonized with H. pylori 59 and in that of ferrets colonized with H. mustelae 21 but not in uninfected individuals. In humans this condition may progress to MALT lymphoma. Eradicating H. pylori usually causes early tumors to regress, implicating the infection as the cause of neoplasia. 58, 59 Gastric MALT lymphoma associated with H. mustelae infection has also been reported in four ferrets 5 to 10 years of age. 12 None of the affected ferrets were treated with antibiotics to eradicate H. mustelae either before or during the illness associated with neoplasia. Illness may develop in ferrets 12 to 20 weeks of age under conditions of stress caused by a combination of factors, such as rapid growth, dietary changes or inadequacy, and concurrent diseases. Infection is lifelong in untreated ferrets, and the severity of chronic gastritis increases with age. 24 In mature ferrets, the disease may become clinically apparent in animals that are stressed by concurrent disease or by surgery for other conditions such as adrenal disease or insulinoma. Ferrets with severe H. mustelae gastritis and ulcers are lethargic and anorexic, and they rapidly become emaciated. Chronic vomiting may occur. Excessive salivation and pawing at the mouth, which are signs of nausea in ferrets, may be evident. Affected ferrets are often moderately to severely dehydrated and may have mild anemia. Black, tarry fecal material often stains the fur of the tail and perineal region. PBD has been recognized for decades in pigs, hamsters, and ferrets. The cause in swine is a bacterium classified in a new genus and species, Lawsonia intracellularis. 38 The same agent causes PBD in hamsters and in ferrets 18 and has more recently been implicated in proliferative enteropathies of other species, including white-tailed deer, ratite birds, and domestic horse foals. 11 L. intracellularis is an obligate intracellular organism that cannot be propagated on artificial media. Two tests that detect this organism have been developed and are used in ferret tissues under research conditions: a PCR test specific for the swine isolate, and an indirect fluorescent antibody test that identifies the omega antigen common to organisms found in PBD lesions of swine, hamsters, and ferrets. 18 However, diagnosis of clinical cases usually depends on observing clinical signs and gross or histopathologic lesions. Areas of intestine affected by PBD feel firm, appear grossly thickened, and are often discolored on the serosal surface. The colon, small intestine, or both may be involved. Ridges of proliferative tissue, distinct from adjacent normal tissue, are obvious on the mucosal surface ( Fig. 3-8) . Occasionally the affected bowel perforates and causes fatal peritonitis. On histologic examination, epithelial proliferation with hypertrophy of the muscularis and infiltration of the bowel wall with either monocytic or granulocytic inflammatory cells, or both, are present. 25 In silver-stained sections, comma-shaped organisms can be found inside enterocytes lining crypts or glands. The normal architectural pattern of the mucosa is lost. Normally, straight tubular glands are covered evenly with enterocytes and numerous goblet cells. In PBD the irregular, branching, proliferative glands lack goblet cells, and necrotic debris accumulates in the crypts. Severe glandular hyperplasia resembles neoplasia and may metastasize to extraintestinal sites. 18 PBD occurs most frequently in rapidly growing juveniles, 10 to 16 weeks of age. Environmental and nutritional stress factors appear to play a role in resistance of infected animals to clinical disease. L. intracellularis is probably transmitted by the oral-fecal route, 18 and it may be assumed that all ferrets that are housed in groups will be equally exposed to the agent. However, clinical disease develops in only a small percentage (usually 1%-3%) of group-housed juvenile ferrets. Improvements in the quality of care and nutrition of pet ferrets may be responsible for the apparently decreasing incidence of PBD in recent years. Affected ferrets have chronic diarrhea that may vary from dark, liquid feces streaked with bright red blood to scant, mucoid stool, often with bright green mucus. The fur of the tail and perineal area may be stained and wet with fecal material, and the preputial area of males is often wet with urine. Rectal tissue may continuously or intermittently prolapse (Fig. 3-9 ). Affected animals moan or cry while straining. Some continue to eat but lose weight at an alarming rate. If not appropriately treated, a ferret weighing 800 g may lose 400 g in less than 2 weeks. These animals are moderately to severely dehydrated and may be hypoalbuminemic. They are weak and sleep most of the time. Because of their general debility, ferrets with PBD are more susceptible to other infectious diseases. They may have upper respiratory tract infections that do not affect other healthy ferrets housed with them and often develop clinical gastritis or ulcers. Severely affected animals will die if not treated appropriately, and most of those that die despite treatment have proliferative ileitis alone or in combination with colitis. Eosinophilic gastroenteritis is a rare type of inflammatory bowel disease that occurs in ferrets as in other animals. In all reported cases, the ferrets were older than 6 months of age; however, because of the small number of reports available, finding this disease in a younger animal may be possible. No specific causative agent has been found in ferrets, 13, 43 dogs, 50 or humans, 54 but food allergy is implicated in most humans and in some dogs. In specific cases in humans and in other species, clinical signs were relieved when appropriate treatment for food allergies or parasitism was instituted. Peripheral eosinophilia is a common but not a constant finding in affected dogs and humans 50 but has been reported in most of the relatively few ferrets diagnosed with this disease. 43 No reports of food elimination tests in affected ferrets have been published. The lesion of eosinophilic gastritis in ferrets, as in other animals and humans, is a mild to extensive infiltration of the mucosa, submucosa, and muscularis of the stomach and small intestine with eosinophils. Focal eosinophilic granulomas may be found in the mesenteric lymph nodes of affected ferrets. 43 No pathogens have been observed in or isolated from the lesions of affected ferrets. In humans and other affected species, granulomas may cause partial bowel obstruction. Affected animals typically have chronic diarrhea, with or without mucus and blood, and severe weight loss. Granulomas may be palpable. Vomiting, anorexia, and dehydration are variable signs. Signs may be clinically indistinguishable from those of gastritis, persistent ECE, or GI obstruction by a foreign body. H. mustelae-associated gastritis and PBD may occur independently, sequentially, or concurrently in the same animal. PBD is a sufficient stressor to induce clinical gastritis in a ferret colonized with H. mustelae. Although these two diseases are most common in ferrets 12 to 16 weeks of age, sufficiently stressed mature ferrets may also be affected. However, clinical disease in adult animals is more often associated with Helicobacter-associated gastritis than with PBD. Although eosinophilic gastroenteritis has been confirmed only in adults, it also may be occurring undiagnosed in younger animals. Any of the wasting diseases can be diagnosed by gastric and intestinal biopsy. However, often a presumptive diagnosis may be based on clinical examination, an accurate history, and results of a CBC, without results from a complex or expensive laboratory workup. Diagnosis may be "confirmed" by the response to appropriate treatment. Characteristics of GI diseases that cause diarrhea and weight loss are summarized in Table 3 -1. Other important differential diagnoses for diarrhea and weight loss in domestic ferrets include lymphoma and Aleutian disease. History Question the owner of a lethargic, anorexic ferret with diarrhea and sudden weight loss about changes in the ferret's diet, feeding schedule, and access to water. The stress factor most commonly associated with wasting diseases is restriction of food for any reason, including the following: Self-denial of food Ferrets resist changing to a food that differs in flavor and texture from the one to which they are accustomed and may fast for several days rather than eat the new food. Fasting depletes fat stores, which should not be confused with the loss of muscle mass associated with wasting diseases. Ferrets consume about three times as much water as dry food pellets and cannot meet their nutritional requirements if water is restricted. Restriction of access to food Food hoppers used with some types of ferret cages may be easily blocked by large food pellets or pellets with unusual shapes, and the owner may not realize that the ferret is unable to get its food. Children caring for ferrets are less likely than adults to understand the significance of an unchanging level of food in the hopper for several days. In addition, some ferrets habitually dig their food out of the container and refuse to eat food that becomes wet or contaminated on the cage floor. Inappropriate, nutritionally deficient diet Occasionally, new owners provide ferrets with inappropriate foods, such as dog food or poor-quality cat food, or offer them excessive amounts of treats, especially raisins, which are palatable but contain almost 100% sugar and no protein. Rapidly growing young animals with nutritional deficiencies are much more susceptible to all infectious diseases. Environmental stress Exposure to extremes of temperature, particularly heat, is very stressful to ferrets. Animals may be stressed during inclement weather if they are housed outdoors without adequate protection from wind and rain, especially if their food is of poor quality or subject to wetting, caking, and molding. Ask the owner if the affected pet is their first ferret. You may identify stressors that the owner would not have taken into consideration. Physical examination Palpate the abdomen of an emaciated ferret. Grossly thickened areas of gut in ferrets with PBD and eosinophilic gastroenteritis are usually palpable. A focal area of pain in the abdomen is more typical of the presence of a GI foreign body. Splenomegaly is common in ferrets in association with many diseases, and mesenteric lymph nodes are likely to be enlarged in ferrets with any of the wasting diseases. Projectile vomiting has been reported in one ferret with eosinophilic gastroenteritis. 13 Although rectal prolapse is not pathognomonic for PBD, it is safe to assume this diagnosis in a ferret with prolapse associated with diarrhea and weight loss. In young ferrets (younger than 16 weeks of age and usually younger than 10 weeks), coccidiosis may be associated with diarrhea and rectal prolapse, but coccidiosis is rarely associated with significant weight loss. Both Aleutian mink disease and lymphosarcoma are insidious; thin ferrets will have lost condition over a period of weeks or months and may not have diarrhea. Radiography is the most useful tool for detecting a GI foreign body (see Part I). Contrast radiographs are sometimes helpful in identifying obstruction with a radiolucent foreign body, but radiographs may also suggest areas of gastric ulceration or intestinal mucosal proliferation in ferrets with either PBD or eosinophilic gastroenteritis. Obtain a blood sample for a CBC to help eliminate the possibility of lymphosarcoma and eosinophilic gastroenteritis. Ferrets with eosinophilic gastroenteritis usually have dramatic eosinophilia (10%-35% eosinophils compared with 3%-5% in normal ferrets). Ferrets with lymphosarcoma may not be leukemic, and further tests, such as peripheral lymph node biopsy or a splenic aspirate, are necessary for diagnosis. Inflammation associated with PBD often causes leukocytosis with neutrophilia and a left shift. Ferrets with bleeding ulcers are usually anemic (normal hematocrit is 40%-55% in spayed or neutered pets, lower in jills in estrus). Dehydration may mask mild anemia and hypoproteinemia in emaciated animals; therefore repeat a CBC after rehydration. Aleutian disease may cause diarrhea, anemia, leukocytosis, and wasting. Serologic tests for Aleutian disease virus are available (see Chapter 6), but many ferrets with positive test results show no clinical signs of Aleutian mink disease. Clinicians should not assume that any illness in ferrets serologically positive for Aleutian disease virus is caused by the virus. L. intracellularis is sensitive to chloramphenicol. No other antibiotic consistently resolves PBD in ferrets. Chloramphenicol is administered at a dose of 50 mg/kg q12h IM or SC (chloramphenicol sodium succinate) or orally (chloramphenicol palmitate oral suspension) for at least 10 days. A ferret with colitis of recent onset improves quickly with this treatment and gains 50 to 100 g/day within a few days of the first dose. L. intracellularis is also sensitive to tylosin, tetracyclines, tiamulin, and several other antimicrobials that are used to treat PBD in pigs 38 and to erythromycin, which is commonly used in affected foals, 34 but treatment of ferrets with any of these drugs is disappointing. Treatment of infected but clinically normal 6-to 9week-old ferrets with oral tylosin (5 mg/kg mixed in soft food once daily) appears to reduce the incidence of clinical PBD in a colony, but only chloramphenicol produces a dramatic improvement in sick ferrets. Repair of rectal prolapse with a purse-string suture is rarely necessary because, as the colon heals, the prolapse usually disappears spontaneously. It may appear intermittently for weeks but causes no apparent distress. If a purse-string suture is used, the owner must closely monitor the ferret to make sure that it can defecate, especially when the stool regains its normal consistency. Sutures should be removed in 2 to 3 days. Chloramphenicol has no effect on H. mustelae. 42 The original treatment for Helicobacter in humans and ferrets was "triple therapy," a combination of amoxicillin, metronidazole, and bismuth subsalicylate, administered q12h for at least 2 weeks (see Table 3 -2 for dosages). Colloidal bismuth subcitrate (8 mg/kg PO q8h) may be substituted for bismuth subsalicylate. Although H. mustelae is sensitive to either amoxicillin or metronidazole, drug resistance quickly develops unless both are given simultaneously. Cimetidine (10 mg/kg PO q8h), other H 2 -receptor blockers, or sucralfate suspension (25-100 mg/kg PO q8h) may be helpful in very sick animals that are bleeding from extensive gastric ulcers. Compounding pharmacists can prepare palat-able suspensions of many drugs available in tablet form. Avoid fish-flavored suspensions when having drugs compounded because ferrets do not like this taste. When administering oral medications, scruff the ferret firmly and use a plastic dropper or dosing syringe. Oral veterinary or pediatric amoxicillin suspensions are palatable and well accepted by most ferrets. Other drug combinations have been used in ferrets to eradicate H. mustelae, with advantages of improved palatability and convenience of dosing (see Table 3 -2). A combination of ranitidine bismuth citrate and clarithromycin, recommended for treatment of H. pylori in humans, has been effective in treating ferrets under research conditions and has been used clinically. 36 Ranitidine bismuth citrate tablets may be crushed and mixed with a palatable liquid, and clarithromycin is available as a pediatric suspension (Biaxin, Abbott Laboratories, North Chicago, IL). Both drugs are administered for 14 days (dosages given in Table 3 -2). A combination of clarithromycin, metronidazole, and omeprazole has proved more effective than the original "triple therapy" in eradicating H. mustelae in research ferrets. 1 Resistance to clarithromycin has not yet been reported in ferrets but does occur in humans. 36 To prevent development of macrolide-resistant strains, clarithromycin should be combined with a second antibiotic not in the macrolide class. 1 Although eradication of H. mustelae is accompanied by decreasing antibody titers, lesions may take longer to resolve. 36 Ferrets from which the infection has been eradicated by antibiotic therapy may be reinfected with H. mustelae through contact with infected ferrets. 2 For treated ferrets to remain free of H. mustelae, they should not be exposed to ferrets of unknown Helicobacter status until the new ferrets have also been treated. Humans, dogs, and cats with eosinophilic gastroenteritis usually respond to steroid treatment. Because the disease in ferrets resembles that in other species, prednisone administration has been the treatment of choice. 43 Remission has occurred in ferrets treated with prednisone (1.25-2.5 mg/kg PO q24h for 7 days and q48h thereafter) until the ferret is clinically normal. Immediate recovery also followed removal of an enlarged mesenteric lymph node in one ferret and treatment with ivermectin (0.4 mg/kg SC) in another. 43 When eosinophilic gastroenteritis is a response to the presence of a parasite, eliminating the parasite is preferable to prolonged treatment with corticosteroids to relieve clinical signs. Rehydrate sick ferrets with either intravenously (preferred) or subcutaneously administered balanced electrolyte solutions. These animals are often very weak and may allow a saphenous or cephalic catheter to be inserted with little resistance. Among the advantages of giving intravenous fluids is that glucose can be administered by this route. However, if a catheter cannot be placed, fluids administered subcutaneously are well and rapidly absorbed. Hospitalize an emaciated, dehydrated ferret until fluid and electrolyte balances are reestablished. When the life-threatening episode is over, the owner will probably be willing and able to give the supportive care needed to restore the ferret to health. While waiting for results of diagnostic tests, one can assume that most cachectic ferrets with diarrhea that do not have a GI foreign body or eosinophilia have both ileitis/colitis and H. mustelae gastritis with ulcers. If the ferret is treated for only one disease when it has both, the time required for recognizing treatment failure may be the factor that ultimately decides if the ferret will survive. Unfortunately, the effective drugs used for treatment of the two diseases are different, and therapy necessitates multiple daily doses of several drugs for at least 2 weeks. Because the gut flora of ferrets is very simple and plays no vital role in digestion, long-term administration of broadspectrum antibiotics does not cause diarrhea in ferrets as it does in most animals. Emaciated animals that die despite proper treatment usually have either very extensive gastric ulcers or severe ileitis, each of which drastically reduces the absorption of essential nutrients. Age of the animal may help in the differential diagnosis; young ferrets are more likely to develop PBD, whereas older ferrets can develop severe, chronic gastritis associated with H. mustelae infection. 24 Also, H. mustelae-associated disease is more often associated with stress factors common in mature pet ferrets, such as concurrent disease or surgery (see Table 3 -1). Emaciated animals have no energy reserve and should receive intensive care. Offer a smorgasbord of premium cat foods and ferret diets. Some animals refuse to eat their regular diet of dry pellets but do accept the same food mixed with water and heated in a microwave until it develops a porridge-like consistency. Some ferrets eat meat baby foods, especially liver and chicken, and most drink milk. Milk causes loose stool in normal ferrets and in those with colitis, but it is very palatable. If milk fat is increased to 10% to 20% with cream, it appears to be absorbed well and contributes to weight gain even though diarrhea continues. Most sick ferrets accept Nutri-Cal (Tomlyn, Buena, NJ) at numerous times during the day. Many ferrets like the human food supplements such as Ensure Plus (Abbott Laboratories, Ross Products Division, Columbus, OH), Boost Plus (formerly Sustacal; Bristol Myers, Evansville, IN), or Isocal HN (Mead Johnston, Evansville, IN), and they sometimes eat softened pellets mixed with one of these products when they refuse pellets alone. Alternatively, offer nutritional recovery foods such as Maximum-Calorie (The Iams Company, Dayton, OH) or Canine a/d (Hill's Pet Nutrition); most sick ferrets accept these foods readily. Nutritional recovery diets such as Max-Cal can be used as the sole source of nutrition for weeks at a time if necessary. When using these diets, calculate a minimum daily intake of 400 kcal per kilogram of body weight. Sick ferrets may not make the effort to get up and drink from a water bottle but do usually drink from a dish. Offer fresh food and water by hand several times daily during hospitalization and home care; ferrets often take a few mouthfuls of every new offering but never go back for more. The first 2 days are critical for an animal that has lost 40% to 50% of its body weight, and intensive supportive care is essential. When ferrets with PBD or ulcers regain their appetites, often within 48 hours of the first doses of medication, and diarrhea has resolved significantly, owners may be tempted to stop treatment. However, ferrets treated for less than 2 weeks often relapse, and some ferrets need antibiotic therapy for an additional 2 to 3 weeks if they are to recover completely. Ferrets with eosinophilic gastroenteritis that do not respond to ivermectin require longer periods of monitoring and prednisone therapy. Most ferrets with these wasting diseases can be saved with aggressive and persistent treatment. Eosinophilic gastroenteritis Prednisone 1.25-2.5 mg/kg q24h PO Ivermectin 0.4 mg/kg SC, PO once ranitidine bismuth citrate, azathioprine, and metronidazole can be prepared as suspensions by compounding pharmacists. *Treat for a minimum of 14 days Relevance of the ferret model of Helicobacter-induced gastritis to evaluation of antibacterial therapies Natural and experimental Helicobacter mustelae reinfection following successful antimicrobial eradication ferrets Salivary mucocele in 2 ferrets Evaluation of Campylobacter jejuni colonization of the domestic ferret intestine as a model of proliferative colitis Biology and diseases of ferrets Megaesophagus in nine ferrets Enteric coccidiosis in a ferret A chronic granulomatous intestinal disease in ferrets caused by an acid-fast organism morphologically similar to Mycobacterium paratuberculosis Clinical aspects of inflammatory bowel disease in ferrets Medical and surgical management of esophageal foreign body in a ferret Diagnosis of proliferative enteritis in frozen and formalin-fixed, paraffin-embedded tissues from a hamster, horse, deer and ostrich using a Lawsonia intracellularis-specific multiplex PCR assay Helicobacter mustelae-associated gastric MALT lymphoma in ferrets Eosinophilic gastroenteritis in a domestic ferret Cisplatin-induced emesis in the ferret: a new animal model Bacterial and mycoplasmal diseases Systemic diseases. 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