Gastroenteritis

INTRODUCTION

Gastroenteritis is a broad term used to indicate inflammation of both the stomach and the intestinal tract. It is a common cause for acute-onset vomiting, anorexia, and diarrhea in both dogs and cats, but should be differentiated from other problems that may cause similar clinical signs such as pancreatitis, hepatitis, and intestinal obstruction (see additional chapters under the textbook section Intraabdominal Disorders).¹ Inflammation in the alimentary tract can be due to a wide variety of underlying causes, including dietary indiscretion, infectious organisms, toxins, immune dysregulation, and metabolic disorders, and may occur in both dogs and cats. 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, in severe cases acute decompensation can occur. This is usually secondary to volume depletion, fluid losses, 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 both 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 serve to 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 mucous-producing cells (which also secrete bicarbonate). The gastric mucosal barrier is able to keep hydrochloric acid and digestive enzymes within the lumen, and it 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 both 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 both 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 increase the surface area even more for digestion and absorption of nutrients. Enzymes found in this 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 are also 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 intestine. The life span of these enterocytes is likely somewhere between 2 and 5 days, and they start at the crypt (base of the villus) and migrate toward the intestinal lumen where they are shed. 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 It is also important to remember that the gastrointestinal (GI) tract absorbs about 99% of the fluid presented to it; therefore any damage to it can cause significant alterations in acid-base and fluid balances.⁵

HISTORY AND CLINICAL SIGNS

A thorough history is extremely important in 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 in terms of helping to find 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 due to the severe fluid losses and acid-base disturbances.

ETIOLOGIES

Infectious Gastroenteritis

A variety of infectious agents can affect the GI tract. Viruses, bacteria, parasites, and fungi have all been shown to cause gastroenteritis of varying severity. The descriptions in the text are limited to the most common. Please see Box 128-1 for a more complete list of potential infectious causes of gastroenteritis.

Box 128-1. 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

• Trichomonas

• 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 112, Canine Parvovirus Infection. Other viral diseases that can lead to severe GI inflammation include coronavirus and rotavirus infection, although clinical manifestations of these viral diseases are thought to be milder than those of CPV-2, likely 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.

Bacterial Enteritis

The bacterial organisms most commonly associated with acute gastroenteritis in dogs and cats include Clostridium perfringens and C. difficile, Campylobacter jejuni and C. upsaliensis, Salmonella spp, Helicobacter spp, and enterotoxigenic E. coli. ^7-10 There is still controversy as to whether some of these organisms truly cause clinical disease. Evidence does support the role of Clostridium spp in gastroenteritis.^8-9 Evaluation of the roles of these organisms, as well as those of Campylobacter and Helicobacter, in GI disease of companion animals is ongoing.

Parasitic Gastroenteritis

Although most dogs and cats with GI parasites have mild clinical signs, ascarids (Toxocara spp, Toxascaris leonina, Ollulanus tricuspis, and Physaloptera), hookworms (Ancylostoma spp, Uncinaria stenocephala), and whipworms (Trichuris spp) can cause significant inflammation, vomiting, and diarrhea. Protozoans that cause canine and feline gastroenteritis include Giardia, coccidia, and Cryptosporidia.

Fungal Gastroenteritis

Fungal disease can affect the GI tract of both dogs and cats, although the likelihood greatly depends on the geographic locations to which the patient has been exposed. Histoplasmosis is the fungal pathogen that affects the GI tract most commonly and can cause a severe protein-losing enteropathy (PLE). Pythium spp, an oomycete, can also cause similar disease.

Hemorrhagic Gastroenteritis

HGE is a disease of unknown etiology. It typically affects young to middle-aged, small breed dogs, and its clinical course usually includes a peracute onset of clinical signs that can progress rapidly to death without appropriate therapy.^7,11 Affected animals are usually 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) (≥60%).^7,11 Although the etiology remains unknown, it has been suggested that abnormal immune responses to bacteria, bacterial endotoxin, or dietary ingredients may play a role.¹² Although C. perfringens has been isolated from cultures of GI contents in dogs with HGE, its exact role in the syndrome has not been determined.

Clinical signs of vomiting and depression, progressing to explosive, bloody diarrhea and anorexia, are classic, and the diarrhea is often 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, there is typically little to no increase in the total protein concentration. The elevated PCV occurs due to hypovolemia 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 cases because rapid decompensation may occur. Adequate replacement of fluid volume is essential for these dogs. More specific fluid management can be found in Chapters 64 and 65, Daily Intravenous Fluid Therapy and Shock Fluids and Fluid Challenge, respectively, but general goals are to quickly replace the fluid lost from acute diarrhea and vomiting, and then adjust fluid rates to maintain proper hydration. It is important to remember that the GI tract is a “shock organ” in the dog, and lack of proper perfusion to the gut can lead to worsening GI inflammation, bacterial translocation, sepsis, and disseminated intravascular coagulation.^13,14 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. Although fluid therapy is the mainstay of treatment for HGE, antiemetic drugs may be indicated, as well as antibiotics if bacterial translocation is suspected. 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 may also cause pancreatitis in these animals. Many drugs are associated with vomiting and diarrhea (antibiotics, 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. History is useful because the owner may be aware that the patient was exposed to a specific toxicant or garbage. Diagnosis is usually presumptive, and treatment involves supportive care such as fluid therapy to maintain hydration, antiemetic drugs, and gastric protectants as needed. Prognosis is excellent, and most animals recover within 24 to 72 hours.

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.¹⁵ Protein loss very likely arises because of disruption to the normal enterocyte function, as well as deranged permeability through the tight junctions.¹⁵ Clinical signs of PLE are usually associated with chronic wasting because of the lack of nutrient integration into the body. However, the proteins lost into the intestinal tract can include large proteins such as albumin and antithrombin III, 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 reduced colloid osmotic pressure, which often leads to 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 the patient, which may require consideration when prescribing fluid therapy. If third spacing has occurred, it may be necessary to use colloidal fluids such as hydroxyethyl starch (Hetastarch) or human albumin, in addition to crystalloids, in order to prevent further intravascular fluid losses. Albumin has additional beneficial effects, such as its antioxidant and antiinflammatory properties.¹⁶

Antithrombin III plays a critical role in the coagulation and fibrinolytic cascade by inactivating thrombin and other clotting factors. Even a small reduction in antithrombin III 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 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 should receive 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 presents 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 both parasitic diseases and bacterial infections in most animals with clinical signs of acute gastroenteritis. A culture can be performed in addition to a Gram stain evaluation. Feces should be evaluated 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. 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 total protein concentration) and PLE (which causes a decrease in total protein, globulin, albumin, and cholesterol levels), these tests can aid in 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 should always 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 performed 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. The other option for obtaining samples requires 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.^17,18 Additionally, diseased gastric and intestinal walls may heal poorly.

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 might 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 rule out might include intussusception, foreign body or mass obstruction, infiltrative disease (neoplasia, infectious), or ischemia. It is important to rule out these other disorders, as indicated, to make a diagnosis of gastroenteritis.

TREATMENT

Most cases of gastroenteritis will 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 (see Chapters 64 and 65, Daily Intravenous Fluid Therapy and Shock Fluids and Fluid Challenge, respectively).

Other treatments can be divided into specific therapies or symptomatic treatments. 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,¹⁹ and Clostridium spp may respond to metronidazole or ampicillin.²⁰ 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 in animals with PLE are to treat the underlying cause, commonly with diet change and antiinflammatory drugs.

Many of the drugs used to treat gastroenteritis are nonspecific. In addition to fluids, many animals will 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 181, Gastrointestinal Protectants) or antiemetics (see Chapter 182, Antiemetics), or both, may hasten recovery of the enterocyte damage and give the GI tract time to heal. In cases of severe GI damage, in which bacterial translocation is a concern (especially in puppies with parvoviral enteritis), antibiotics may be indicated. Antibiotic therapy should be aimed at treating the common organisms expected in the intestinal tract and usually consists of antibiotics with good gram-negative and anaerobic coverage.

PROGNOSIS

In conclusion, prognosis for animals with mild to moderate gastroenteritis is typically excellent. However, early diagnosis and timely therapy are important for positive outcomes.