Gastroenteritis

Gastroenteritis is a broad term used to indicate inflammation of the stomach and the intestinal tract. It is a common cause for acute-onset vomiting, anorexia, and diarrhea in dogs and cats but should be differentiated from other problems that may cause similar clinical signs, such as pancreatitis, azotemia, hepatitis, and intestinal obstruction (see additional chapters in Intraabdominal Disorders section).¹ Inflammation of the alimentary tract may occur in dogs and cats and can be due to a wide variety of underlying causes, including dietary indiscretion, infectious organisms, toxins, immune dysregulation, and metabolic disorders (see Chapters 120 and 121). A thorough history and physical examination may aid in uncovering an underlying cause, but often a specific cause is not identified. In most cases, supportive therapy, including appropriate fluid support, dietary modification, antiemetics, and gastric protectant agents, are sufficient for resolution of clinical signs. However, acute decompensation can occur in severe cases. This is usually secondary to volume depletion, fluid losses, electrolyte imbalances and acid-base disturbances that occur because the intestinal tract cannot perform its normal hemostatic functions.

Anatomy and Physiology

The stomach is the compartment between the esophagus and small intestine that functions as a storage reservoir for food and a vessel for mixing and grinding food into smaller components that then enter the small intestine.² The stomach is made up of muscular layers, glandular portions, and a mucosal barrier. The muscular layers grind food into smaller particles and move it forward into the small intestine through the pyloric sphincter. Of equal importance are the glandular portions of the stomach, which include parietal cells (for secretion of hydrochloric acid), chief cells (for secretion of pepsinogen), and mucus-producing cells (which also secrete bicarbonate). Normally, the gastric mucosal barrier keeps hydrochloric acid and digestive enzymes within the lumen and prevents loss of plasma constituents into the stomach.² Once the food particles are ground into small enough components, they pass through the pyloric sphincter into the beginning of the small intestine, known as the duodenum.

The small intestine of cats and dogs functions in digestion and absorption of food and its nutrients and is divided arbitrarily into the duodenum, jejunum, and ileum.³ The mucosa of the small intestine is involved in secretory and absorptive functions and contains a single layer of epithelial cells called enterocytes. The mucosa along the length of the small intestine is formed into villi, which are fingerlike projections into the intestinal lumen that enlarge the surface of the small intestine. Microvilli then form the “brush border” to further increase the surface area available for digestion and absorption of nutrients. Enzymes within the brush border aid in digestion of larger food molecules into smaller, more readily absorbable particles. Absorption may occur via specific transport mechanisms or by pinocytosis. The epithelial cells also are involved with absorption and secretion of electrolytes and water.³ Enterocytes are connected to each other by tight junctions, limiting absorption between cells, as well as preventing backflow of nutrients from the interstitium into the intestinal lumen. The enterocytes start at the crypt (base of the villus) and migrate toward the intestinal lumen where they are shed, with a lifespan of approximately 2 to 5 days. A healthy, intact mucosal lining is important for the integrity of the intestine. Any type of inflammation that disrupts this layer can lead to significant intestinal disease.⁴ The gastrointestinal (GI) tract absorbs approximately 99% of the fluid presented to it; therefore any damage can cause significant alterations in acid-base and fluid balances.5, 5a

History and Clinical Signs

A thorough history is critical to identifying an underlying cause for gastroenteritis. Questions may be related to the patient's current diet, recent change in diet, and exposure to unusual food, foreign materials, garbage, or toxins. It is also important to find out about the patient's environment, including exposure to other animals, and if other exposed animals have similar signs or a history of similar signs. Vaccination status, deworming history, and medication use are also important.

Clinical signs of gastroenteritis are often similar regardless of the underlying cause. Vomiting, diarrhea, and anorexia are most common, and certain combinations of these signs may make one cause more or less likely than another. Severe inflammation or ulceration, depending on the cause, can lead to hematemesis or melena.

Physical examination is often unrewarding towards finding an underlying cause. Patients may have varying degrees of dehydration, as well as abdominal pain. In severe cases, such as those animals with hemorrhagic gastroenteritis (HGE) or parvoviral enteritis, patients may have signs of hypovolemia and shock because of the severe fluid losses and acid-base disturbances.

Causes

Infectious Gastroenteritis

A variety of infectious agents can affect the GI tract. Viruses, bacteria, parasites, protozoa, and fungi have been shown to cause gastroenteritis of varying severity. The descriptions in the text are limited to the most common. Please see Box 117-1 for a more complete list of potential infectious causes of gastroenteritis.

Box 117-1. Infectious Causes of Gastroenteritis in Dogs and Cats.

Bacterial

• Campylobacter spp.

• Clostridium spp.

• Escherichia coli

• Salmonella spp.

• Helicobacter spp.

Viral

• Parvovirus

• Rotavirus

• Enteric coronavirus

• Feline infectious peritonitis

• Canine distemper virus

• Feline leukemia virus

• Feline immunodeficiency virus

Fungal, Algal, and Oomycoses

• Histoplasmosis

• Protothecosis

• Pythiosis

Parasitic

• Ascarids (Toxocara canis, Toxocara cati, Toxascaris leonina)

• Hookworms (Ancylostoma spp., Uncinaria stenocephala)

• Strongyloides stercoralis

• Whipworms (Trichuris vulpis)

• Coccidiosis (Isospora canis or felis, Toxoplasma gondii, Cryptosporidium parvum)

• Giardia

• Tritrichomonas

• Balantidium coli

Rickettsial

• Neorickettsia helminthoeca (salmon poisoning)

Viral enteritis

Canine parvovirus-2 (CPV-2) is one of the most common infectious diseases in dogs and may be characterized by severe enteritis, vomiting, hemorrhagic diarrhea, and shock.⁴ The pathophysiology and treatment of CPV-2 are discussed in Chapter 97. Other viral diseases that can lead to severe GI inflammation include coronavirus and rotavirus infection, although clinical manifestations of these viral diseases are typically milder than those of CPV-2, possibly because they affect the tips of the villi, whereas CPV-2 affects the crypts.⁶ Feline panleukopenia, also caused by a parvovirus, can cause similar signs of severe gastroenteritis in cats.

Bacterial enteritis

The bacterial organisms most commonly associated with acute gastroenteritis in dogs and cats include Clostridium perfringens and Clostridium difficile, Campylobacter jejuni and Campylobacter upsaliensis, Salmonella spp., Helicobacter spp., and enterotoxigenic E. coli. 7, 8, 9, 10 Controversy continues regarding whether some of these organisms truly cause clinical disease because some of them can be found in nondiarrheic patients as well as animals with diarrhea. With emerging and improved diagnostic techniques such as ELISA and PCR testing, newer recommendations for definitive diagnosis rely on a multimodal evaluation for some of these organisms.¹¹ Evidence does support the role of Clostridium spp. in gastroenteritis.8, 9, 12 However, because many dogs have C. perfringens and its CPE toxin in their GI tracts without developing clinical signs, evaluation of the roles of these organisms, as well as those of Campylobacter and Helicobacter spp. in GI disease of companion animals, is ongoing.¹³

Although the majority of Salmonella infections in dogs are self-limiting and resolved by the host's local immune response, bacterial translocation and septicemia can occur, leading to systemic inflammatory response and multi-organ dysfunction in some patients (see Chapters 6 and 7). Those most at risk are the young or immunocompromised, those that have concurrent infections, or those that have received prior antibiotic or glucocorticoid therapy. As is the case with many bacterial organisms, Salmonella can be found in a population of healthy, nonclinical patients, so its documentation in the GI tract should be correlated with clinical signs.¹³

In addition to the aforementioned more commonly diagnosed bacterial infections, evidence is beginning to suggest that histiocytic ulcerative colitis in Boxer dogs may be due to invasive E. coli organisms within the colonic mucosa of affected dogs.14, 15 Fluoroquinolones have become the standard treatment for these patients, with the use of fluorescent in situ hybridization (FISH) to confirm the presence of these organisms.14, 15 Culture and susceptibility testing of colonic tissue can be used to isolate and guide therapy because antimicrobial resistance has become of increasing concern.14, 15

Parasitic gastroenteritis

Although most dogs and cats with GI parasites have mild clinical signs, ascarids (Toxocara spp., Toxascaris leonina, Ollulanus tricuspis, and Physaloptera spp.), hookworms (Ancylostoma spp., Uncinaria stenocephala), and whipworms (Trichuris spp.) can cause significant GI tract inflammation, vomiting, and diarrhea. GI blood loss is also common with severe hookworm infestations. Protozoans that cause canine and feline gastroenteritis include Giardia spp., coccidia, and Cryptosporidia spp. Tritrichomonas foetus infection is another protozoal cause of diarrhea in cats (primarily large bowel) with waxing and waning signs. Although patients may appear unthrifty, it is rarely the cause of critical illness.⁶

Fungal gastroenteritis

Fungal disease can affect the GI tract of dogs and cats, although the likelihood greatly depends on the animal's geographic location or recent travel destinations. Histoplasmosis is the fungal pathogen that most commonly affects the GI tract, causing a severe protein-losing enteropathy (PLE). Pythium spp., an oomycete, also can cause similar disease.

Hemorrhagic Gastroenteritis

Hemorrhagic gastroenteritis (HGE) is a disease of unknown cause. It typically affects young to middle-age, small breed dogs, and its clinical course usually includes a peracute onset of clinical signs that can progress rapidly to death without appropriate therapy.7, 16 Affected animals are often previously healthy dogs with no pertinent historical information. The syndrome is characterized by acute onset of bloody diarrhea, often explosive, along with an elevated packed cell volume (PCV) (at least 60%).7, 16 Although the cause remains unknown, it has been suggested that abnormal immune responses to bacteria, bacterial endotoxin, or dietary ingredients may play a role.¹⁷ C. perfringens has been isolated from cultures of GI contents in dogs with HGE; however, its exact role in the syndrome has not been determined. Fatal acute HGE was reported in a dog with large numbers of enterotoxin-positive A C. perfringens isolated from the intestinal tract.¹²

Clinical signs of vomiting and depression, progressing to explosive, bloody diarrhea and anorexia are classic, and the diarrhea often is described as having the appearance of raspberry jam.⁷ Thorough investigation to rule out other causes of hemorrhagic diarrhea such as parvovirus, bacterial infections, or GI parasites should be undertaken before arriving at a diagnosis of HGE. Along with hemoconcentration, the total protein concentration typically increases little or not at all (it may actually decrease). The elevated PCV occurs because of hemoconcentration and/or splenic contraction, whereas GI loss of serum proteins or redistribution of body water into the vascular space explains the lack of rise in total protein levels.⁷

Aggressive therapy is warranted in these animals because rapid decompensation may occur. Adequate replacement of fluid volume is essential; more specific fluid management strategies can be found in Chapters 59 and 60. General goals are to replace quickly the fluid deficits from the acute diarrhea and vomiting then adjust fluid rates to maintain proper hydration. The GI tract is a “shock organ” in the dog, and lack of proper perfusion to the GI tract can lead to worsening GI inflammation, bacterial translocation, sepsis, and disseminated intravascular coagulation (see Chapter 91).18, 19 Because serum proteins are lost through the intestinal tract, close attention should be paid to the patient's colloid osmotic pressure and colloidal support given when necessary. Fluid therapy is the mainstay of treatment for patients with HGE. Antiemetic and gastric protectant drugs should be used as indicated. Although antimicrobials may be warranted in patients with suspected bacterial translocation, caution is advised because inappropriate use of these drugs may promote antimicrobial resistance or other unwanted side effects. In some dogs with HGE but no signs of sepsis, antimicrobial therapy may not be indicated.²⁰ With rapid and appropriate therapy, the prognosis for full recovery from HGE is excellent.

Dietary Indiscretion

Gastroenteritis caused by ingestion of toxins (i.e., organophosphates), foreign materials, or garbage is common in dogs, and less so in cats. Some toxins lead directly to inflammation of the GI tract, although ingestion of other foreign materials may lead to direct GI trauma or an osmotic diarrhea secondary to nondigestible substances within the intestinal tract. Ingestion of excessive fatty products also may cause pancreatitis in these animals. Many drugs are associated with vomiting and diarrhea (antimicrobials, antineoplastics, anthelminthics), and garbage ingestion can lead to exposure of the intestinal tract to preformed bacterial toxins. Most commonly, dietary indiscretion leads to acute onset of vomiting, diarrhea, and anorexia. The patient's history is useful because the owner may be aware of exposure to a specific toxicant or garbage. The diagnosis is usually presumptive, and treatment involves supportive care such as fluid therapy to maintain hydration, antiemetic drugs, and gastric protectants as needed. The prognosis is excellent, and most animals recover within 24 to 72 hours.

Protein-Losing Enteropathy

Protein-losing enteropathy (PLE) is a broad diagnosis that includes any cause of GI disease that results in excessive loss of plasma proteins. The diseases most commonly associated with PLE are severe lymphocytic-plasmacytic, eosinophilic, or granulomatous inflammatory bowel diseases, lymphangiectasia, diffuse GI fungal disease, and diffuse neoplasia such as lymphosarcoma. Some of the aforementioned GI diseases can cause PLE if the inflammation and damage to the intestinal mucosa are severe enough.

The mechanism of protein loss may be related to inflammation or loss of the GI barrier.²¹ Protein loss likely arises because of disruption to the normal enterocyte function, as well as deranged permeability through the tight junctions.²¹ Clinical signs of PLE usually are associated with chronic wasting because of lack of nutrient integration into the body. However, the proteins lost into the intestinal tract can include large proteins such as albumin and antithrombin, both of which have important roles in homeostasis. Albumin, with a molecular weight of 69,000 daltons, contributes significantly to oncotic pressure. Loss of albumin through the GI tract can lead to a reduced colloid osmotic pressure and subsequent loss of fluid from the intravascular space. Although this is typically a gradual process, it can cause significant changes in the compartmentalization of fluids in some patients. If third spacing has occurred, it may be necessary to use colloidal fluids such as hydroxyethyl starch or human albumin, in addition to crystalloids, to prevent further intravascular fluid losses (see Chapter 58).²²Albumin also has additional beneficial effects, such as its antioxidant and antiinflammatory properties.²³

Antithrombin plays a critical role in the coagulation and fibrinolytic cascade by inactivating thrombin and other clotting factors. Even a small reduction in antithrombin levels can cause a large propensity toward thrombosis and thromboembolism. This becomes important in patients with PLE that lose large amounts of protein and are predisposed to developing thromboemboli in various parts of the body, including the pulmonary vessels, portal vein, or coronary or cerebral vessels. Therapy for PLE often involves glucocorticoids, which also increase the risk of thromboembolic disease. Therefore anticoagulant or antiplatelet therapy, or both, may be warranted in these cases.

Therapy for PLE is aimed at treating the underlying cause. Animals with diffuse neoplasia such as lymphosarcoma should be treated with chemotherapy, and those with severe inflammatory bowel disease may benefit from antiinflammatory drugs and a hypoallergenic diet. Lymphangiectasia may be primary or secondary, and administration of a diet low in fat may be more important than feeding a hypoallergenic diet, depending on the degree of inflammation.

Extraintestinal Diseases

Hypoadrenocorticism, liver or kidney disease, acute pancreatitis, and peritonitis are common extraintestinal causes of gastroenteritis in small animals.

Diagnosis

The extent of diagnostic testing in a dog that is presented with signs of acute gastroenteritis depends on factors such as historical information, prior occurrence of similar clinical signs, and stability of the patient. Fecal samples should be evaluated for parasitic diseases and bacterial infections in most animals with clinical signs of acute gastroenteritis. A culture and Gram stain evaluation also should be performed. Feces should be tested at least three times before a negative result is confirmed. Testing for clostridial enterotoxins may include use of a C. perfringens enterotoxin enzyme-linked immunosorbent assay (ELISA), or an ELISA that detects C. difficile toxins A and B. Recent developments with real PCR testing have provided another diagnostic method for detection of many organisms that are seen commonly in small animals. A Giardia antigen test also exists. If parvovirus is suspected, a fecal antigen test (ELISA) should be performed.

Systemic evaluation should include a complete blood count, chemistry screen, and urinalysis. Typically results of these tests are normal and do not aid in determining an underlying cause for the gastroenteritis. However, in certain circumstances such as HGE (in which the PCV is elevated with a normal to decreased total protein concentration), PLE (which may cause a decrease in total protein, globulin, albumin, and cholesterol levels), these tests can aid in making a diagnosis. Electrolytes should be checked regularly to confirm adequate fluid management.

Abdominal radiographs may be unrewarding or may show signs of fluid-filled bowel loops. Radiographs are indicated if a GI obstruction (i.e., foreign body, neoplasia) is suspected. Abdominal ultrasonography is an excellent tool to evaluate all abdominal organs, including the thickness and layering of the stomach and small intestine. These findings may be insensitive and nonspecific, however, and always should be used in conjunction with other diagnostic tests.

If PLE is suspected and biopsies of the stomach and intestine are required, there are two main ways of achieving this. Endoscopy is a noninvasive method for visualizing the esophageal, gastric, and duodenal mucosa, as well as for obtaining small (1.8- to 2.4-mm) biopsy samples. Disadvantages of this method are that the samples are small and biopsies cannot be obtained distal to the duodenum. Ileal samples can be obtained if colonoscopy is performed, but this requires patient preparation (i.e., administration of cleansing enemas), which can cause decompensation in unstable animals resulting from fluid and electrolyte shifts. Another method for obtaining samples is via exploratory laparotomy. This is an excellent method for acquiring full-thickness biopsy samples of multiple areas of the GI tract (and other organs if they are found to be abnormal). The disadvantages are that it is much more invasive, and poor wound healing may be a concern in patients with reduced albumin levels. This has been reported in human surgical patients as well as canine surgical patients.24, 25, 26 In addition, diseased gastric and intestinal walls may heal poorly. Laparoscopy is another technique that can be used to obtain excellent visualization of the abdominal cavity along with full-thickness biopsies of the GI tract (and other organs as needed). Laparoscopy is less invasive than exploratory laparotomy and may be associated with less morbidity because of smaller incisions; however, healing of gastric and intestinal biopsy sites would remain a concern in patients with low albumin levels or diseased walls.

The most common clinical signs of gastroenteritis are vomiting, diarrhea, and anorexia. These are common to a variety of diseases; therefore gastroenteritis is often a diagnosis of exclusion. Differential diagnosis may include systemic diseases such as kidney disease, liver disease, hypoadrenocorticism, complicated diabetes mellitus (diabetic ketoacidosis), vestibular disease or other neurologic abnormalities, pancreatitis, pyometra, prostatitis, and peritonitis. Additional primary GI diseases to consider include intussusception, foreign body or mass obstruction, infiltrative disease (neoplasia, infectious), or ischemia. It is important to rule out these other disorders, as indicated, before making a diagnosis of gastroenteritis.

Treatment

Most cases of gastroenteritis respond well to supportive care. Aggressiveness of treatment depends on the severity of clinical signs and the underlying cause. Because the most common clinical signs of gastroenteritis, regardless of underlying cause, are vomiting, diarrhea, and anorexia, dehydration is a common occurrence, and initial therapy should be aimed at addressing the patient's hydration status and perfusion parameters (see Chapters 57, 59, and 60Chapter 57Chapter 59Chapter 60).

Other treatments can be divided into specific or symptomatic therapies. Specific drugs can be used to treat some of the underlying causes of disease. For the most part, drugs used to eradicate many of the infectious causes for gastroenteritis are available. GI parasites may be treated with fenbendazole or other antihelminthic drugs. Campylobacter spp. have responded well to such drugs as erythromycin, enrofloxacin, and cefoxitin,²⁷ and Clostridium spp. may respond to metronidazole or ampicillin.²⁸ The choice of drug depends on many factors, including patient age and ability to take oral medications. Few antiviral drugs are effective in veterinary medicine; therefore diseases such as parvoviral enteritis are treated supportively. As stated before, the aims of therapy for animals with PLE are to treat the underlying cause, commonly with diet change and antiinflammatory agents.

Many of the drugs used to treat gastroenteritis are nonspecific. In addition to fluids, most animals respond well to resting the GI tract by withholding food for 24 to 48 hours. When food is offered, a wet, easily digestible diet is recommended. Addition of GI protectants (see Chapter 161) or antiemetics (see Chapter 162), or both, may hasten recovery of the enterocyte damage, give the GI tract time to heal, and decrease nausea. In animals with severe GI damage, in which bacterial translocation is a concern (especially in puppies with parvoviral enteritis), antimicrobials may be indicated and should aim at treating the common organisms expected in the intestinal tract. This usually consists of drugs with good gram-negative and anaerobic coverage. More recently, use of probiotics has been evaluated in veterinary medicine for treatment of acute and chronic GI disease. Two recent prospective studies have shown that the use of probiotics in acute gastroenteritis may hasten recovery and reduce the severity of diarrhea in affected patients. Although specific mechanisms for their benefit still are poorly understood, probiotics may compete with pathogenic organisms for nutrition, they may produce antimicrobial substances, and they may stimulate the immune system.29, 30

Conclusion

Prognosis for animals with mild to moderate gastroenteritis is typically excellent. However, early diagnosis and timely therapy are important to prevent multiple organ involvement and maximize outcome.