Chronic Gastritis

Chronic gastritis is a persistent inflammatory condition of the gastric mucosa, characterized by histopathological evidence of inflammation lasting for weeks to months. It is a common cause of chronic vomiting in dogs and cats. The condition involves infiltration of the gastric lamina propria and epithelium by inflammatory cells, which may include lymphocytes, plasma cells, eosinophils, or neutrophils, depending on the underlying etiology. Chronic gastritis can be classified based on the predominant inflammatory cell type (lymphocytic-plasmacytic, eosinophilic, granulomatous, or suppurative) and the presence of atrophy, fibrosis, or metaplasia. The disease disrupts normal gastric acid secretion, mucosal barrier integrity, and gastric motility, leading to clinical signs such as intermittent vomiting, inappetence, and weight loss. Chronic gastritis may be a primary immune-mediated disorder or secondary to dietary intolerance, infectious agents, or other systemic diseases. It is distinct from acute gastritis, which is typically self-limiting and associated with dietary indiscretion or toxin exposure. Chronic gastritis requires thorough diagnostic evaluation, including histopathology, to differentiate it from gastric neoplasia and other chronic gastrointestinal disorders.

The etiology of chronic gastritis is multifactorial and often idiopathic. In dogs, the most common form is lymphocytic-plasmacytic gastritis, which is believed to be immune-mediated, possibly triggered by dietary antigens, bacterial overgrowth, or genetic predisposition. In cats, chronic gastritis is frequently associated with inflammatory bowel disease (IBD), which may involve the stomach as part of a panenteric inflammatory process. Specific infectious causes include Helicobacter spp. (e.g., H. pylori, H. felis, H. heilmannii), which colonize the gastric mucus layer and can induce chronic inflammation. Other bacterial agents such as Campylobacter and Salmonella may contribute. Parasitic infections, particularly Physaloptera spp. (stomach worms) in dogs and cats, can cause chronic gastritis. Fungal infections (e.g., Histoplasma capsulatum, Pythium insidiosum) are less common but can cause granulomatous gastritis. Eosinophilic gastritis may be due to dietary hypersensitivity, adverse food reactions, or parasitic migration. Chronic gastritis can also result from chronic use of non-steroidal anti-inflammatory drugs (NSAIDs), which impair mucosal prostaglandin synthesis, or from bile reflux (reflux gastritis). In rare cases, autoimmune gastritis with antibodies against parietal cells and intrinsic factor occurs, leading to atrophic gastritis and hypochlorhydria. Genetic factors may predispose certain breeds, such as the Basenji (with immunoproliferative enteropathy) and the Norwegian Lundehund (with protein-losing enteropathy and gastritis). Neoplastic infiltration (e.g., lymphoma) can mimic chronic gastritis clinically and histologically.

Chronic gastritis is a common diagnosis in small animal practice, particularly in middle-aged to older dogs and cats. No clear sex predilection is reported. In dogs, certain breeds may be overrepresented, including the Basenji, Norwegian Lundehund, and possibly the German Shepherd and Boxer, due to their predisposition to inflammatory bowel disease. In cats, chronic gastritis is often part of a generalized IBD, with no specific breed predilection, though Siamese and other purebred cats may be at higher risk. The exact incidence is unknown, but it is a frequent cause of chronic vomiting. The condition can occur at any age, but the median age at diagnosis is around 5-7 years. Environmental factors such as diet, stress, and concurrent diseases may influence the development and severity. There is no seasonal variation, but infectious causes like Physaloptera may be more common in certain geographic regions with high parasite prevalence. Chronic gastritis is more frequently diagnosed in animals with a history of dietary indiscretion or chronic NSAID use.

The pathophysiology of chronic gastritis involves a complex interplay of mucosal injury, immune dysregulation, and repair mechanisms. The gastric mucosa is protected by a mucus-bicarbonate barrier, tight junctions between epithelial cells, and rich submucosal blood flow. Chronic inflammation arises when these defenses are overwhelmed by persistent insults, such as infectious agents, dietary antigens, or drugs. In immune-mediated forms, T lymphocytes, particularly Th1 and Th17 subsets, are activated and release pro-inflammatory cytokines (e.g., TNF-α, IFN-γ, IL-17), which recruit additional inflammatory cells, including plasma cells and macrophages. This leads to infiltration of the lamina propria and epithelium, causing epithelial damage, increased apoptosis, and impaired regeneration. In eosinophilic gastritis, eosinophils infiltrate the mucosa and release cytotoxic granules, contributing to tissue damage. Chronic inflammation can lead to glandular atrophy, fibrosis, and intestinal metaplasia, reducing gastric acid secretion and mucosal function. Helicobacter spp. colonize the gastric mucus and adhere to epithelial cells, inducing a local immune response and production of urease, which generates ammonia and further damages the mucosa. The inflammatory process disrupts normal gastric motility, leading to delayed gastric emptying and distension, which contributes to vomiting. In severe cases, ulceration and bleeding may occur. The systemic inflammatory response can lead to anorexia, weight loss, and protein-losing enteropathy if concurrent intestinal involvement exists.

Predisposing factors for chronic gastritis include genetic susceptibility, as seen in certain breeds with a higher incidence of inflammatory bowel disease. Dietary factors, such as food allergies or intolerances to specific proteins, carbohydrates, or additives, can trigger or exacerbate inflammation. Chronic stress and environmental changes may influence the gut-brain axis and alter mucosal immunity. Concurrent diseases, such as chronic kidney disease, liver disease, or pancreatitis, can predispose to gastritis due to uremic toxins, bile reflux, or systemic inflammation. Medications, particularly NSAIDs and corticosteroids, can impair mucosal defenses and promote inflammation. Infectious agents, including Helicobacter spp., Physaloptera, and fungal pathogens, are direct causes. Immunosuppression, whether due to disease (e.g., feline leukemia virus, feline immunodeficiency virus) or drug therapy, can increase susceptibility to infectious gastritis. Age is a factor, as older animals may have reduced mucosal repair capacity. Finally, previous gastric surgery or trauma can lead to chronic gastritis due to altered anatomy and bile reflux.

Clinical signs of chronic gastritis are often intermittent and may progress over weeks to months. The most common sign is chronic vomiting, which may occur hours after eating and can contain bile, foam, or undigested food. Vomiting may be preceded by nausea, hypersalivation, lip-licking, or restlessness. Affected animals may have a decreased appetite (anorexia) or selective eating, leading to weight loss. Some animals may exhibit pica (eating non-food items) or polydipsia. In cases with concurrent esophagitis or reflux, signs of regurgitation or dysphagia may be present. Physical examination may reveal a thin body condition, mild dehydration, and possibly abdominal discomfort on palpation. In severe cases with ulceration, signs of hematemesis (vomiting blood) or melena (dark, tarry stools) may occur, leading to pallor and weakness. Cats may present with more subtle signs, such as chronic inappetence and weight loss, with less frequent vomiting. In advanced cases, signs of systemic illness, such as lethargy and fever, may be present if there is secondary bacterial infection or perforation. The clinical signs can be categorized by stage: early chronic gastritis may show only occasional vomiting, while advanced disease may have persistent vomiting, severe weight loss, and signs of protein-losing enteropathy if the intestines are also affected.

Differential diagnoses for chronic gastritis include: 1) Chronic enteropathy (inflammatory bowel disease) – often concurrent, but if vomiting is the primary sign, gastritis is more likely; diagnosis via intestinal biopsy. 2) Gastric neoplasia (e.g., adenocarcinoma, lymphoma) – can mimic chronic gastritis clinically; histopathology is essential. 3) Gastric ulceration – may be primary or secondary to NSAIDs, stress, or mast cell tumors; endoscopy and biopsy differentiate. 4) Helicobacter-associated gastritis – a specific infectious cause; diagnosed via biopsy, culture, or PCR. 5) Physaloptera infection – parasitic gastritis; diagnosed by fecal flotation or visualization on endoscopy. 6) Eosinophilic gastroenteritis – may involve the stomach; characterized by eosinophilic infiltration on biopsy. 7) Chronic pancreatitis – can cause vomiting and may be associated with gastritis; diagnosed via serum lipase (cPLI/fPLI) and imaging. 8) Chronic kidney disease – uremic gastritis; diagnosed via blood work (elevated creatinine, SDMA). 9) Liver disease – may cause vomiting due to hepatic encephalopathy or bile reflux; diagnosed via liver enzymes, bile acids, and ultrasound. 10) Gastric foreign body – can cause chronic intermittent vomiting; diagnosed via imaging or endoscopy. Each differential is ruled out by specific diagnostic tests: for example, abdominal ultrasound and endoscopy with biopsy are crucial to differentiate neoplasia and IBD; serum chemistry and urinalysis rule out renal disease; and fecal examination and PCR rule out parasitic and bacterial infections.

The diagnostic approach to chronic gastritis begins with a thorough history and physical examination. Initial laboratory tests include a complete blood count (CBC), serum biochemistry profile, urinalysis, and fecal examination (including flotation and direct smear) to rule out systemic diseases and parasitism. If vomiting is chronic and no obvious cause is found, abdominal radiographs and ultrasonography are recommended to assess gastric wall thickness, presence of masses, foreign bodies, or other organ abnormalities. Serum pancreatic lipase (cPLI or fPLI) and bile acids may be measured to rule out pancreatitis and liver disease. If these tests are unremarkable, upper gastrointestinal endoscopy is the next step, allowing direct visualization of the gastric mucosa and collection of multiple biopsy samples. Endoscopic findings may include erythema, erosions, ulcers, or a nodular appearance. Biopsies are essential for histopathological diagnosis and to differentiate chronic gastritis from neoplasia. In cases where endoscopy is not available or is inconclusive, full-thickness surgical biopsies may be obtained via laparotomy. Additional tests may include Helicobacter testing (rapid urease test, histopathology with special stains, PCR) and fecal PCR for infectious agents. If eosinophilic gastritis is suspected, dietary trials and allergy testing may be considered. The diagnostic algorithm should be stepwise, with non-invasive tests first, followed by more invasive procedures as needed.

Laboratory findings in chronic gastritis are often non-specific. The CBC may show mild anemia if there is chronic blood loss, or eosinophilia in cases of eosinophilic gastritis or parasitism. Serum biochemistry may reveal mild elevations in liver enzymes (ALT, ALP) due to concurrent hepatic disease or secondary to vomiting. Total protein and albumin may be decreased if there is protein-losing enteropathy or malnutrition. Electrolyte imbalances, particularly hypokalemia and hyponatremia, can occur due to vomiting. Blood gas analysis may show metabolic alkalosis due to loss of hydrogen ions in vomitus. Urinalysis is usually unremarkable but may show a low urine specific gravity if concurrent renal disease is present. Specific biomarkers such as cPLI (canine pancreatic lipase immunoreactivity) or fPLI (feline pancreatic lipase immunoreactivity) are useful to rule out pancreatitis. Serum gastrin levels may be elevated in cases of hypergastrinemia (e.g., gastrinoma), but this is rare. Fecal examination may reveal parasites (e.g., Physaloptera eggs) or occult blood. In cases of Helicobacter infection, a rapid urease test on gastric biopsy samples can be positive. PCR of gastric tissue or feces can detect Helicobacter DNA. Histopathology is the gold standard for diagnosis, revealing inflammatory infiltrates and architectural changes.

Imaging findings in chronic gastritis are often subtle. Abdominal radiographs may show a gas-filled stomach or evidence of gastric wall thickening, but this is not specific. Ultrasonography can reveal thickening of the gastric wall, loss of normal layering, and increased echogenicity of the mucosa. In cases of severe inflammation, the wall may appear hypoechoic. Doppler ultrasound may show increased blood flow in the gastric wall. Computed tomography (CT) can provide more detailed assessment of gastric wall thickness and detect masses, but it is not routinely used. Magnetic resonance imaging (MRI) is rarely indicated. Endoscopy is the most valuable imaging modality, allowing direct visualization of the gastric mucosa. Findings may include erythema, edema, erosions, ulcers, and a cobblestone appearance. Endoscopic biopsies are essential for histopathological confirmation. Fluoroscopy may be used to assess gastric emptying, which is often delayed in chronic gastritis. Echocardiography is not directly relevant but may be performed to rule out cardiac disease as a cause of vomiting.

Cytology of gastric brushings or fine-needle aspirates may reveal inflammatory cells, but histopathology is required for definitive diagnosis. On histopathology, chronic gastritis is characterized by infiltration of the lamina propria and epithelium by inflammatory cells. Lymphocytic-plasmacytic gastritis shows a predominance of lymphocytes and plasma cells, often with lymphoid follicle formation. Eosinophilic gastritis is characterized by eosinophilic infiltration, which may be diffuse or focal. Granulomatous gastritis shows aggregates of macrophages and multinucleated giant cells, often due to fungal infection. Suppurative gastritis is rare and shows neutrophilic infiltration, usually due to bacterial infection. Chronic changes include glandular atrophy, fibrosis, and intestinal metaplasia (gastric epithelium replaced by intestinal-type cells). Special stains, such as Warthin-Starry silver stain or Giemsa, can identify Helicobacter organisms. Biopsy samples should be taken from multiple sites, including the fundus, body, and antrum, as inflammation may be patchy. The severity of inflammation can be graded based on the density of infiltrates and the degree of architectural distortion.

Treatment of chronic gastritis is multimodal and aimed at controlling inflammation, managing clinical signs, and addressing underlying causes. Dietary management is crucial: a highly digestible, low-fat, and hypoallergenic diet (e.g., novel protein or hydrolyzed protein) is recommended. In cases of food allergy, a strict elimination diet trial for 8-12 weeks is necessary. For Helicobacter-associated gastritis, a combination of antimicrobials and acid suppressants is used: amoxicillin (20 mg/kg PO q12h) and clarithromycin (7.5 mg/kg PO q12h) or metronidazole (10-15 mg/kg PO q12h) for 14 days, along with a proton pump inhibitor such as omeprazole (0.7-1.0 mg/kg PO q12h) or a histamine-2 blocker like famotidine (0.5-1.0 mg/kg PO q12h). For immune-mediated lymphocytic-plasmacytic gastritis, immunosuppressive therapy may be required: prednisolone (1-2 mg/kg PO q24h, then tapered) or budesonide (0.1-0.2 mg/kg PO q24h) for dogs; in cats, prednisolone (1-2 mg/kg PO q24h) or chlorambucil (0.1-0.2 mg/kg PO q48h) if refractory. Antiemetics such as maropitant (1 mg/kg SC q24h or 2 mg/kg PO q24h) or metoclopramide (0.2-0.5 mg/kg PO q8h) can control vomiting. Gastroprotectants like sucralfate (0.5-1 g PO q8h) may be used if ulceration is present. In cases of eosinophilic gastritis, a hypoallergenic diet and corticosteroids are the mainstay. For parasitic gastritis, appropriate anthelmintics (e.g., fenbendazole 50 mg/kg PO q24h for 3 days) are used. Supportive care includes fluid therapy for dehydration and electrolyte imbalances, and nutritional support if anorexia is severe. In rare cases of gastric outflow obstruction or neoplasia, surgery may be indicated.

The prognosis for chronic gastritis is generally good with appropriate management, but it depends on the underlying cause and severity. For lymphocytic-plasmacytic gastritis, many animals respond well to dietary modification and immunosuppressive therapy, with resolution of clinical signs within weeks to months. However, some cases may require long-term therapy and can have relapses. Eosinophilic gastritis also has a favorable prognosis if dietary triggers are identified and avoided. Helicobacter-associated gastritis typically responds to antimicrobial therapy, but reinfection can occur. Chronic gastritis due to NSAIDs or other drugs may resolve after discontinuation of the offending agent. The prognosis is guarded for granulomatous gastritis due to fungal infection, which is often difficult to treat. Negative prognostic indicators include severe weight loss, hypoalbuminemia, concurrent inflammatory bowel disease, and lack of response to initial therapy. The mortality rate is low, but chronic gastritis can significantly impact quality of life if not managed properly. Long-term monitoring is essential to adjust therapy and detect complications such as gastric ulceration or neoplasia.

Follow-up for chronic gastritis involves regular re-evaluations to monitor clinical response and adjust therapy. Initially, re-check appointments may be scheduled every 2-4 weeks until clinical signs are controlled. At each visit, a thorough history and physical examination should be performed, and body weight should be monitored. Serial laboratory tests, including CBC, serum biochemistry, and urinalysis, may be repeated every 3-6 months to assess for drug side effects (e.g., steroid-induced changes) and systemic health. If the animal is on immunosuppressive therapy, blood pressure and urine protein-to-creatinine ratio should be monitored periodically. Repeat endoscopy with biopsy may be indicated if there is poor response to therapy or if clinical signs recur, to reassess the degree of inflammation and rule out neoplasia. Dietary management should be continued long-term, and any dietary indiscretions should be avoided. Owners should be educated on the importance of compliance with medication and dietary recommendations. In cases of Helicobacter infection, a follow-up test (e.g., fecal PCR or urease test) may be performed after treatment to confirm eradication. The long-term prognosis is good with appropriate management, but some animals may require lifelong therapy.

Pearls: 1) Chronic gastritis is a histopathological diagnosis; always obtain gastric biopsies during endoscopy, even if the mucosa appears normal. 2) In cats, chronic gastritis is often part of IBD; evaluate the entire gastrointestinal tract. 3) Dietary trials are essential for food-responsive gastritis; use a novel protein or hydrolyzed diet for at least 8 weeks. 4) Helicobacter infection is common in healthy animals; treat only if clinical signs are present and other causes are ruled out. 5) Eosinophilic gastritis may be associated with hypereosinophilic syndrome; check peripheral eosinophil count. Pitfalls: 1) Do not rely solely on clinical signs or imaging to diagnose chronic gastritis; histopathology is mandatory. 2) Avoid using corticosteroids without a definitive diagnosis, as they can mask signs of lymphoma. 3) Do not forget to rule out systemic diseases like chronic kidney disease and pancreatitis, which can cause gastritis. 4) In cases of vomiting, always consider gastric foreign bodies or neoplasia; endoscopy is crucial. 5) When treating with NSAIDs, always use gastroprotectants if the animal has a history of gastritis.

Based on Plumb's Veterinary Drug Handbook, the following drug protocols are recommended for chronic gastritis: 1) Antiemetics: Maropitant (Cerenia) – dogs: 1 mg/kg SC q24h for up to 5 days, or 2 mg/kg PO q24h for up to 14 days; cats: 1 mg/kg SC q24h for up to 5 days. Metoclopramide – dogs and cats: 0.2-0.5 mg/kg PO q8h, or 1-2 mg/kg/day as a CRI. 2) Gastroprotectants: Sucralfate – dogs: 0.5-1 g PO q8h; cats: 0.25-0.5 g PO q8h. 3) Acid suppressants: Omeprazole – dogs: 0.7-1.0 mg/kg PO q12h; cats: 0.7-1.0 mg/kg PO q12h. Famotidine – dogs: 0.5-1.0 mg/kg PO q12h; cats: 0.5-1.0 mg/kg PO q12h. 4) Corticosteroids: Prednisolone – dogs: 1-2 mg/kg PO q24h, then taper over 3-6 months; cats: 1-2 mg/kg PO q24h, then taper. Budesonide – dogs: 0.1-0.2 mg/kg PO q24h; cats: 0.1-0.2 mg/kg PO q24h. 5) Immunosuppressants: Chlorambucil – cats: 0.1-0.2 mg/kg PO q48h; dogs: 0.1-0.2 mg/kg PO q48h. 6) Antimicrobials for Helicobacter: Amoxicillin – dogs and cats: 20 mg/kg PO q12h; Clarithromycin – dogs and cats: 7.5 mg/kg PO q12h; Metronidazole – dogs and cats: 10-15 mg/kg PO q12h. These are typically combined with a proton pump inhibitor for 14 days. 7) Anthelmintics: Fenbendazole – dogs and cats: 50 mg/kg PO q24h for 3 days. Dosages should be adjusted for renal or hepatic impairment, and drug interactions should be considered (e.g., corticosteroids with NSAIDs increase ulcer risk).

Evidence-based literature on chronic gastritis in dogs and cats is limited, but several key studies and consensus statements provide guidance. The ACVIM consensus statement on chronic inflammatory bowel disease in dogs and cats (2010) includes recommendations for diagnosis and treatment of gastritis as part of IBD. Studies have shown that dietary modification is effective in a significant proportion of dogs with chronic gastritis, with response rates of 50-60% for novel protein diets. Immunosuppressive therapy with corticosteroids is effective in many cases, but the evidence is largely based on retrospective studies. A study by Jergens et al. (1992) reported that 70% of dogs with lymphocytic-plasmacytic gastritis responded to a combination of dietary and medical therapy. For Helicobacter-associated gastritis, a study by Neiger and Simpson (2000) demonstrated that a triple therapy protocol (amoxicillin, metronidazole, and omeprazole) was effective in eliminating the organism in 80% of dogs. However, the clinical significance of Helicobacter in chronic gastritis remains controversial, as many healthy dogs harbor the organism. Eosinophilic gastritis is less common, but a study by Lecoindre et al. (2002) found that a hypoallergenic diet and corticosteroids were effective in managing clinical signs. Overall, the evidence supports a stepwise approach to diagnosis and treatment, with histopathology being the gold standard. More research is needed to establish standardized treatment protocols and long-term outcomes.