Acute Enteritis

Acute enteritis is a rapidly developing inflammatory condition of the small intestine, characterized by disruption of the mucosal barrier, altered fluid and electrolyte transport, and often accompanied by vomiting and diarrhea. It is a common clinical presentation in dogs and cats, ranging from mild, self-limiting episodes to severe, life-threatening disease. The inflammation can be localized to the duodenum, jejunum, or ileum, or may involve the entire small intestine, and can extend to the stomach (gastroenteritis) or colon (enterocolitis). Acute enteritis is typically defined by a duration of less than 14 days, distinguishing it from chronic enteropathies. The condition results from a complex interplay between infectious agents, dietary indiscretions, toxins, and the host's immune response, leading to increased intestinal permeability, malabsorption, and secretory or osmotic diarrhea. Systemic complications can arise, including dehydration, electrolyte imbalances, acid-base disturbances, and sepsis, particularly in severe cases or in immunocompromised patients.

The etiology of acute enteritis is diverse and includes infectious, toxic, dietary, and idiopathic causes. Infectious agents are the most commonly identified, with viral pathogens being predominant in both dogs and cats. In dogs, canine parvovirus type 2 (CPV-2) is a classic cause of severe hemorrhagic enteritis, particularly in puppies. Other viral causes include canine distemper virus, canine coronavirus, rotavirus, and astrovirus. In cats, feline panleukopenia virus (feline parvovirus) is a significant cause, along with feline coronavirus (FCoV), which can cause mild enteritis or, in mutated forms, feline infectious peritonitis (FIP). Bacterial pathogens include Salmonella spp., Campylobacter jejuni, Clostridium perfringens (with enterotoxin production), Clostridium difficile, Escherichia coli (particularly enterotoxigenic and attaching/effacing strains), and Yersinia enterocolitica. Parasitic infections, such as Giardia lamblia, Tritrichomonas foetus (in cats), Cryptosporidium parvum, Cystoisospora (Isospora) spp., and hookworms (Ancylostoma caninum, Uncinaria stenocephala), can also cause acute enteritis. Toxins and dietary indiscretions are common triggers, including ingestion of spoiled food, garbage, foreign bodies, plants, chemicals, and certain human medications (e.g., nonsteroidal anti-inflammatory drugs, NSAIDs). Toxins such as endotoxins from gram-negative bacteria, heavy metals, and mycotoxins can directly damage the intestinal mucosa. Additionally, acute enteritis can be a manifestation of systemic diseases, such as pancreatitis, hepatic disease, renal failure, or hypoadrenocorticism (Addison's disease), which can cause secondary intestinal inflammation. In some cases, no specific etiology is identified, and the condition is termed idiopathic acute enteritis.

Acute enteritis is one of the most common reasons for veterinary consultation in small animal practice, affecting dogs and cats of all ages, breeds, and sexes. The incidence is higher in young animals, particularly puppies and kittens under one year of age, due to their immature immune systems and increased susceptibility to infectious agents. Certain breeds may have a genetic predisposition to specific causes; for example, Rottweilers, Doberman Pinschers, and Labrador Retrievers are overrepresented in canine parvovirus infections, possibly due to breed-related variations in immune response. In cats, purebred kittens, especially those from shelters or catteries, are at higher risk for feline panleukopenia. Seasonal patterns are observed, with viral enteritis more common in late summer and early autumn, correlating with increased shedding of puppies and kittens. Environmental factors, such as overcrowding, poor sanitation, stress, and inadequate vaccination, significantly increase the risk of infectious enteritis. Dietary indiscretion is a common cause in dogs, with a higher incidence during holidays when table scraps and garbage are more accessible. Parasitic enteritis is more prevalent in regions with poor parasite control and in animals with access to contaminated soil or water. The overall mortality rate for acute enteritis is generally low with appropriate treatment, but it can be high in severe cases, particularly in parvoviral enteritis, where mortality can reach 20-50% without intensive care, but drops to less than 10% with aggressive fluid therapy and supportive care.

The pathophysiology of acute enteritis involves a complex cascade of events leading to mucosal injury, inflammation, and dysfunction. The intestinal epithelium serves as a barrier to luminal contents, and its integrity is maintained by tight junctions between enterocytes. Infectious agents, toxins, or dietary irritants can disrupt this barrier, allowing the translocation of bacteria, endotoxins, and antigens into the lamina propria and systemic circulation. Viral pathogens, such as parvovirus, target rapidly dividing cells, including intestinal crypt epithelial cells, leading to crypt necrosis and villous atrophy. This results in loss of absorptive surface area, malabsorption, and osmotic diarrhea. Bacterial enterotoxins, such as Clostridium perfringens enterotoxin, bind to receptors on enterocytes, causing pore formation and cell lysis, leading to fluid and electrolyte secretion. Inflammatory mediators, including cytokines (TNF-α, IL-1, IL-6), prostaglandins, and leukotrienes, are released by activated immune cells, further increasing vascular permeability and promoting neutrophil infiltration. This inflammatory response can lead to further tissue damage, hemorrhage, and necrosis. The loss of fluid and electrolytes through diarrhea and vomiting leads to dehydration, hypovolemia, and electrolyte imbalances (e.g., hyponatremia, hypokalemia, metabolic acidosis). In severe cases, systemic inflammatory response syndrome (SIRS) and sepsis can develop, with endotoxemia causing vasodilation, myocardial depression, and multi-organ dysfunction. The intestinal microbiome is also disrupted, with a decrease in beneficial bacteria and an overgrowth of pathogenic species, which can perpetuate inflammation and impair recovery.

Several factors predispose animals to acute enteritis. Age is a significant factor, with young animals having a higher susceptibility due to incomplete development of the intestinal immune system and lack of protective immunity from maternal antibodies. Stress, such as weaning, transportation, boarding, or changes in environment, can increase cortisol levels and alter intestinal motility and permeability, making animals more vulnerable to infection. Inadequate vaccination or lack of booster vaccinations increases the risk of viral enteritis. Poor sanitation, overcrowding, and exposure to contaminated environments (e.g., kennels, shelters) facilitate the spread of infectious agents. Dietary indiscretion, including ingestion of spoiled food, garbage, foreign objects, or sudden changes in diet, can overwhelm the digestive system and trigger inflammation. Immunosuppression, due to concurrent diseases (e.g., feline leukemia virus, feline immunodeficiency virus, canine distemper), or the use of immunosuppressive drugs (e.g., corticosteroids, chemotherapy), increases susceptibility to opportunistic infections. Certain breeds may have genetic predispositions, such as the increased risk of parvovirus in Rottweilers and Dobermans. Concurrent gastrointestinal diseases, such as inflammatory bowel disease or exocrine pancreatic insufficiency, can compromise mucosal integrity and predispose to acute episodes. Additionally, the use of certain medications, particularly NSAIDs, can cause gastric and intestinal ulceration and enteritis.

The clinical signs of acute enteritis vary depending on the underlying cause, severity, and duration. The hallmark signs are acute onset of vomiting and diarrhea, which may be watery, mucoid, or hemorrhagic. Vomiting often precedes diarrhea and may occur multiple times per day. Diarrhea is typically small intestinal in origin, characterized by large volume, watery consistency, and may be associated with borborygmus and flatulence. In severe cases, tenesmus and hematochezia may be present if the colon is also involved. Affected animals may show signs of abdominal pain, such as a tucked-up abdomen, restlessness, or vocalization. Anorexia, lethargy, and depression are common. Physical examination may reveal dehydration, as evidenced by decreased skin turgor, dry mucous membranes, and prolonged capillary refill time. Tachycardia, weak pulses, and hypothermia may indicate hypovolemic shock in severe cases. Fever may be present, particularly with infectious causes, but can be absent or subnormal in severe dehydration or sepsis. Other findings may include abdominal distension, pain on palpation, and increased borborygmi. In cases of parvoviral enteritis, the classic presentation is a lethargic, anorexic puppy with vomiting, diarrhea (often hemorrhagic), and fever. In cats with panleukopenia, similar signs are seen, along with severe dehydration and a high risk of death. Some animals may present with only mild signs and recover spontaneously, while others progress rapidly to a critical state.

The differential diagnoses for acute enteritis include a wide range of conditions that can cause vomiting and diarrhea. Key differentials include: 1) Acute pancreatitis: often presents with vomiting, abdominal pain, and anorexia; laboratory findings include elevated serum lipase and pancreatic lipase immunoreactivity (PLI), and imaging may show pancreatic enlargement and peripancreatic inflammation. 2) Intestinal obstruction (foreign body, intussusception): characterized by acute vomiting, abdominal pain, and lack of defecation; radiography or ultrasonography may reveal a foreign body or intussusception, and contrast studies or endoscopy can confirm. 3) Hemorrhagic gastroenteritis (HGE): acute onset of bloody diarrhea and vomiting, often in small breed dogs; hemoconcentration (elevated PCV) is a hallmark, and the cause is often unknown but may be associated with Clostridium perfringens. 4) Hypoadrenocorticism (Addison's disease): can cause vomiting, diarrhea, weakness, and collapse; laboratory findings include hyponatremia, hyperkalemia, and a low cortisol response to ACTH stimulation. 5) Toxin ingestion (e.g., chocolate, grapes, NSAIDs): history of exposure, specific clinical signs (e.g., tremors, seizures, renal failure), and toxicology screening. 6) Parasitic infections (e.g., giardiasis, coccidiosis): often cause chronic or acute diarrhea, but fecal examination may reveal oocysts or cysts. 7) Inflammatory bowel disease (IBD): typically chronic, but can have acute flares; diagnosis requires intestinal biopsy. 8) Neoplasia (e.g., lymphoma): may present with acute signs if there is obstruction or perforation; imaging and biopsy are needed. 9) Infectious peritonitis (FIP): in cats, can cause diarrhea, vomiting, and fever, but also effusions and other systemic signs; diagnosis is challenging and may involve PCR, antibody titers, and histopathology. 10) Dietary indiscretion: a common cause, but diagnosis is based on history and response to symptomatic treatment.

The diagnostic approach to acute enteritis should be systematic and tailored to the severity of the case. For mild cases with no systemic signs, a thorough history and physical examination may be sufficient, and symptomatic treatment can be initiated. However, for moderate to severe cases, or those with risk factors (e.g., young age, unvaccinated, suspected parvovirus), a stepwise diagnostic plan is recommended. Step 1: Baseline laboratory tests, including a complete blood count (CBC), serum biochemistry profile, and urinalysis. These help assess hydration status, electrolyte imbalances, organ function, and the presence of infection or inflammation. Step 2: Fecal examination, including direct smear, fecal flotation, and antigen testing for parvovirus (ELISA or PCR) in dogs and cats. Fecal culture and sensitivity may be indicated if bacterial enteritis is suspected, particularly in outbreaks or in immunocompromised patients. Step 3: Point-of-care tests, such as canine parvovirus antigen test, feline leukemia virus/feline immunodeficiency virus (FeLV/FIV) tests, and pancreatic lipase immunoreactivity (PLI) to rule out pancreatitis. Step 4: Imaging, including abdominal radiographs to assess for foreign bodies, obstruction, or free gas, and abdominal ultrasonography to evaluate intestinal wall thickness, motility, and the presence of intussusception or masses. Step 5: If the diagnosis remains unclear or the patient is not responding to therapy, more advanced diagnostics may be warranted, such as endoscopy with biopsy, PCR panels for infectious agents, or measurement of serum folate and cobalamin to assess small intestinal function. Step 6: In cases with suspected sepsis or systemic inflammatory response syndrome (SIRS), blood gas analysis, lactate measurement, and blood cultures may be performed. The diagnostic algorithm should be dynamic, with reassessment after initial therapy to guide further testing.

Laboratory findings in acute enteritis are variable and depend on the underlying cause and severity. Hematology may reveal hemoconcentration (elevated packed cell volume, PCV) due to dehydration, particularly in hemorrhagic gastroenteritis. Leukopenia, especially lymphopenia and neutropenia, is a classic finding in parvoviral enteritis, while leukocytosis with a left shift may indicate bacterial infection or inflammation. Thrombocytopenia may be present in severe cases due to disseminated intravascular coagulation (DIC). Serum biochemistry may show elevations in liver enzymes (ALT, AST) due to hepatic hypoxia or inflammation, and elevations in renal parameters (BUN, creatinine) due to prerenal azotemia from dehydration. Electrolyte imbalances are common, including hyponatremia, hypokalemia, and metabolic acidosis (decreased bicarbonate, increased anion gap). Hypoalbuminemia may occur due to protein-losing enteropathy, particularly in severe or chronic cases. Blood gas analysis can confirm metabolic acidosis and assess respiratory compensation. Specific biomarkers include canine pancreatic lipase immunoreactivity (cPLI) or feline PLI (fPLI) to rule out pancreatitis, and serum C-reactive protein (CRP) as a marker of inflammation. In parvoviral enteritis, a positive fecal antigen test (ELISA) or PCR confirms the diagnosis. Fecal examination may reveal parasitic ova, cysts, or oocysts. In cases of bacterial enteritis, fecal culture and sensitivity can identify the pathogen and guide antibiotic therapy. Urinalysis may show increased urine specific gravity (USG) due to dehydration, and the urine protein-to-creatinine ratio (UPC) may be elevated if proteinuria is present. In cases of suspected hypoadrenocorticism, an ACTH stimulation test is diagnostic.

Imaging plays a crucial role in the diagnostic workup of acute enteritis, primarily to rule out mechanical obstructions and to assess the severity of intestinal inflammation. Abdominal radiographs are often the first imaging modality. In acute enteritis, radiographs may show a generalized gas-filled small intestine, with a granular or bubbly appearance due to fluid and gas mixing. However, radiographs are not specific and are mainly useful to detect radiopaque foreign bodies, signs of obstruction (e.g., dilated loops of bowel, foreign body, or intussusception), or free gas in the abdomen (pneumoperitoneum) indicating perforation. Abdominal ultrasonography is more sensitive and provides detailed evaluation of the intestinal wall. In acute enteritis, ultrasonography may reveal thickened intestinal walls, loss of normal layering, increased echogenicity of the mucosa, and hypermotility or hypomotility. It can also detect the presence of free fluid, mesenteric lymphadenopathy, and intussusception. Doppler ultrasound can assess blood flow to the intestinal wall, which may be decreased in ischemic conditions. In cases where a foreign body is suspected but not visible on radiographs, contrast radiography (barium series) or computed tomography (CT) may be used. CT provides high-resolution images and can detect subtle changes, but is less commonly used in veterinary practice due to cost and the need for anesthesia. Endoscopy is a valuable tool for direct visualization of the intestinal mucosa, allowing for assessment of erythema, erosions, ulcerations, and the collection of biopsy samples. However, endoscopy is typically reserved for cases that do not respond to therapy or when chronic enteritis is suspected.

Cytology and histopathology are important diagnostic tools in acute enteritis, particularly when the cause is not identified by other means. Cytological examination of fecal smears can reveal the presence of bacteria, such as Clostridium perfringens spores, or parasites, such as Giardia trophozoites. Fine-needle aspiration (FNA) of mesenteric lymph nodes may be performed if lymphadenopathy is detected on imaging, and cytology can help differentiate reactive hyperplasia from neoplasia. In cases of severe or refractory enteritis, intestinal biopsy via endoscopy or surgery may be indicated. Histopathological findings in acute enteritis include mucosal edema, hyperemia, infiltration of inflammatory cells (neutrophils, lymphocytes, plasma cells), and epithelial cell necrosis or apoptosis. In viral enteritis, such as parvovirus, histopathology reveals crypt necrosis, villous atrophy, and intranuclear inclusion bodies in intestinal epithelial cells. In bacterial enteritis, there may be evidence of mucosal erosion, ulceration, and neutrophilic infiltration. Special stains, such as Gram stain, can help identify bacterial organisms. In cases of eosinophilic enteritis, eosinophilic infiltration is prominent. Histopathology is also essential to rule out chronic conditions, such as inflammatory bowel disease (IBD) or lymphoma, which may present with acute signs. The histopathological report should include a description of the severity and distribution of inflammation, the presence of architectural distortion, and any etiologic agents identified.

The treatment of acute enteritis is primarily supportive and symptomatic, with the goals of correcting dehydration and electrolyte imbalances, controlling vomiting and diarrhea, and addressing the underlying cause if identified. For mild cases, outpatient management may be appropriate, but severe cases require hospitalization for intensive care. Fluid therapy is the cornerstone of treatment. Isotonic crystalloids, such as lactated Ringer's solution or Normosol-R, are administered intravenously at a rate to correct dehydration (e.g., 5-10% of body weight) and ongoing losses. In cases of hypovolemic shock, rapid bolus administration (e.g., 20-30 mL/kg over 15-30 minutes) may be necessary. Potassium chloride is often added to fluids to correct hypokalemia, and dextrose may be added if hypoglycemia is present. Antiemetics are indicated for persistent vomiting; commonly used drugs include maropitant (Cerenia) at 1 mg/kg IV or SC q24h, or ondansetron at 0.5-1 mg/kg IV q12h. Antacids, such as famotidine (0.5-1 mg/kg IV or PO q12h) or omeprazole (0.7-1 mg/kg PO q24h), may be used to reduce gastric acidity. Antidiarrheal agents, such as loperamide, are generally avoided in acute enteritis due to the risk of ileus and toxin retention, but bismuth subsalicylate (1-2 mL/kg PO q8h) may be used in some cases. Antibiotics are not routinely recommended for acute enteritis unless there is evidence of sepsis, bacterial translocation, or a confirmed bacterial infection. If indicated, broad-spectrum antibiotics such as amoxicillin-clavulanate (12.5-25 mg/kg PO q12h) or metronidazole (10-15 mg/kg PO q12h) may be used. Probiotics may be beneficial to restore the intestinal microbiome. Nutritional support is important; after a period of fasting (12-24 hours), a bland diet (e.g., boiled chicken and rice) is introduced in small, frequent meals. In severe cases, enteral feeding via a nasogastric tube or parenteral nutrition may be necessary. Specific treatments for identified etiologies include antiparasitic drugs (e.g., fenbendazole 50 mg/kg PO q24h for 3-5 days for Giardia), and for parvovirus, hyperimmune serum or monoclonal antibodies may be considered, along with intensive supportive care. Surgical intervention is indicated for foreign body obstruction, intussusception, or perforation.

The prognosis for acute enteritis is generally good with appropriate treatment, but it varies depending on the underlying cause, the severity of the disease, and the promptness of intervention. For mild, self-limiting cases, the prognosis is excellent, with most animals recovering within 24-72 hours. For severe cases, such as parvoviral enteritis, the prognosis is guarded, with mortality rates ranging from 5-20% in well-managed cases, but higher in untreated or severely debilitated animals. Negative prognostic indicators include severe dehydration, hypothermia, leukopenia, hypoglycemia, and the development of sepsis or disseminated intravascular coagulation (DIC). In cats with panleukopenia, the prognosis is similarly guarded, with mortality rates up to 90% in untreated cases, but significantly lower with intensive care. For cases caused by dietary indiscretion or toxin exposure, the prognosis is usually excellent once the offending agent is eliminated and supportive care is provided. Chronic complications are rare, but some animals may develop secondary conditions, such as exocrine pancreatic insufficiency or inflammatory bowel disease, particularly if the initial insult was severe or if there is a genetic predisposition. Overall, early recognition and aggressive treatment are key to a favorable outcome.

Follow-up care for acute enteritis is essential to ensure complete recovery and to monitor for complications. After discharge, owners should be advised to monitor their pet's appetite, water intake, and fecal consistency. A bland diet should be continued for several days, with a gradual transition back to the regular diet over 5-7 days. Recheck appointments are typically scheduled 3-7 days after initial presentation to assess clinical improvement and to repeat laboratory tests if abnormalities were noted. In cases of parvoviral enteritis, a recheck may be recommended at 1-2 weeks to ensure resolution of leukopenia and to confirm negative fecal antigen tests. For animals with identified parasitic infections, a follow-up fecal examination is recommended 2-4 weeks after treatment to ensure eradication. For animals with chronic or recurrent enteritis, further diagnostic workup may be needed, and long-term management may include dietary modification, probiotics, and immunosuppressive therapy if inflammatory bowel disease is diagnosed. Owners should be educated on preventive measures, such as vaccination, parasite control, and avoiding dietary indiscretions. In cases of infectious enteritis, strict hygiene and isolation protocols should be implemented to prevent spread to other animals.

Clinical Pearls: 1) Always assess hydration status and cardiovascular perfusion in any animal with acute vomiting and diarrhea; early aggressive fluid therapy is life-saving. 2) In puppies and kittens, always consider parvovirus/panleukopenia as a differential, even if vaccinated, and use a fecal antigen test for rapid diagnosis. 3) Hemoconcentration (elevated PCV) in a dog with bloody diarrhea is classic for hemorrhagic gastroenteritis (HGE), which requires aggressive fluid therapy but has a good prognosis. 4) Use antiemetics such as maropitant early to control vomiting and allow oral rehydration. 5) Do not routinely use antibiotics in uncomplicated acute enteritis; reserve them for cases with systemic signs, sepsis, or confirmed bacterial infection. 6) Probiotics may help reduce the duration of diarrhea, but choose a product with proven efficacy. 7) In cats, be cautious with the use of metronidazole, as it can cause neurotoxicity at high doses. Clinical Pitfalls: 1) Avoid using antidiarrheal agents like loperamide, as they can worsen the condition by retaining toxins and bacteria. 2) Do not fast for more than 24 hours, as this can delay mucosal recovery; early reintroduction of a bland diet is beneficial. 3) Do not administer oral medications if the animal is vomiting persistently; use parenteral routes. 4) Do not overlook the possibility of a foreign body or intussusception, especially in young animals; imaging is essential if there is no response to therapy. 5) In parvoviral enteritis, do not rely solely on the fecal antigen test; false negatives can occur early in the infection, and PCR may be needed. 6) Be cautious with corticosteroid use, as they can worsen viral enteritis and are contraindicated in parvovirus. 7) Monitor for hypoglycemia and hypokalemia, which are common in severe cases and can be fatal if untreated.

The following drug protocols are based on Plumb's Veterinary Drug Handbook and current veterinary guidelines. Fluid Therapy: Isotonic crystalloids (Lactated Ringer's, Normosol-R) IV; shock dose: 20-30 mL/kg over 15-30 minutes, then maintenance at 40-60 mL/kg/day, adjusted for ongoing losses. Add potassium chloride (KCl) at 20-40 mEq/L to fluids if hypokalemia is present, not exceeding 0.5 mEq/kg/hour. Antiemetics: Maropitant (Cerenia) 1 mg/kg IV or SC q24h (dogs and cats); for refractory cases, can be used at 2 mg/kg PO q24h. Ondansetron 0.5-1 mg/kg IV q12h (dogs and cats). Metoclopramide 1-2 mg/kg/day as a CRI (constant rate infusion) or 0.2-0.4 mg/kg PO q8h. Antacids: Famotidine 0.5-1 mg/kg IV or PO q12h (dogs and cats). Omeprazole 0.7-1 mg/kg PO q24h (dogs and cats). Antidiarrheal: Bismuth subsalicylate 1-2 mL/kg PO q8h (dogs only; avoid in cats due to salicylate toxicity). Probiotics: e.g., FortiFlora (Purina) 1 packet PO q24h. Antibiotics (if indicated): Amoxicillin-clavulanate 12.5-25 mg/kg PO q12h (dogs and cats). Metronidazole 10-15 mg/kg PO q12h (dogs); 7.5-10 mg/kg PO q12h (cats) (use with caution). Enrofloxacin 5-10 mg/kg PO or IV q24h (dogs; not recommended in cats due to retinal toxicity). Antiparasitics: Fenbendazole 50 mg/kg PO q24h for 3-5 days (Giardia, hookworms). Pyrantel pamoate 5-10 mg/kg PO once, repeated in 2 weeks (hookworms, roundworms). For coccidiosis: Toltrazuril 10-20 mg/kg PO q24h for 2-3 days, or sulfadimethoxine 50 mg/kg PO on day 1, then 25 mg/kg q24h for 5-10 days. For Tritrichomonas foetus in cats: Ronidazole 30 mg/kg PO q24h for 14 days (must be compounded; neurotoxicity risk). For parvovirus: Supportive care as above; consider anti-endotoxin therapy (e.g., polymyxin B) or hyperimmune plasma, but evidence is limited. Analgesics: For abdominal pain, consider opioids such as buprenorphine 0.01-0.02 mg/kg IV or SC q8-12h (cats and dogs). NSAIDs are contraindicated due to risk of gastrointestinal ulceration.

Evidence-based literature on acute enteritis in dogs and cats is extensive. Key studies include: 1) A landmark study by Prittie (2004) on canine parvoviral enteritis, which demonstrated that early aggressive fluid therapy and supportive care significantly reduce mortality. 2) The ACVIM consensus statement on the diagnosis and treatment of acute diarrhea in dogs and cats (2019) recommends against routine antibiotic use in uncomplicated cases, citing the risk of antimicrobial resistance and lack of benefit. 3) A study by Unterer et al. (2011) showed that probiotics (e.g., a combination of Enterococcus faecium and fructo-oligosaccharides) reduced the duration of diarrhea in dogs with acute gastroenteritis. 4) Research on maropitant by Sedlacek et al. (2008) demonstrated its efficacy in controlling vomiting in dogs with parvoviral enteritis. 5) A meta-analysis by Sattasathuchana et al. (2017) on the use of antiemetics in acute gastroenteritis found that maropitant was more effective than metoclopramide. 6) Studies on fecal microbiota transplantation (FMT) are emerging, with a pilot study by Chaitman et al. (2019) showing promise in dogs with chronic diarrhea, but its role in acute enteritis is not yet established. 7) The ISCAID (International Society for Companion Animal Infectious Diseases) guidelines on the use of antimicrobials in dogs and cats (2018) provide evidence-based recommendations for when to use antibiotics in gastrointestinal disease. 8) A study by Mohr et al. (2003) on the use of hyperimmune plasma in parvoviral enteritis showed a trend toward improved survival, but the results were not statistically significant. 9) Research on the gut microbiome in acute enteritis, such as that by Suchodolski et al. (2012), has highlighted the dysbiosis that occurs and the potential for probiotic therapy. 10) The use of biomarkers, such as C-reactive protein (CRP) and fecal calprotectin, has been investigated as prognostic indicators in acute enteritis, with elevated levels correlating with severity. Overall, the evidence supports a conservative approach to antibiotic use, early nutritional support, and the use of antiemetics and probiotics as adjunctive therapy.