Helicobacter Suis and Gastric Microbiota in Porcine Gastric Ulceration

The development of gastric ulcers in pigs is influenced by multiple interacting factors, and the gastric microbiota has emerged as an important component of this process. Among the microorganisms associated with porcine gastric health, Helicobacter suis has received particular attention because of its ability to colonize the gastric mucosa and alter the stomach environment. Although gastric ulceration cannot be attributed to a single infectious agent, changes in gastric acid secretion and microbial populations may contribute to lesion development and progression¹. Understanding these microbial interactions enables veterinarians to interpret gastric lesions more comprehensively while considering other contributing nutritional and management factors. 

Helicobacter suis Colonization in the Pig Stomach 

Helicobacter suis is a zoonotic bacterium that colonizes the gastric mucosa of pigs worldwide¹. Infection becomes increasingly common with age. Colonization has been reported at low levels in suckling pigs, increasing progressively in weaned pigs, slaughter-age pigs, and adult animals. High prevalence in adult pigs suggests that the host immune response does not readily eliminate the organism^1,2. 

Colonization patterns also appear to change over time. In younger pigs, H. suis is predominantly found within the pyloric gland region, whereas prolonged infection is associated with greater bacterial numbers in the fundal gland region^1,2. These findings indicate that bacterial distribution within the stomach may evolve as infection persists. 

How Microbial Changes May Influence Ulcer Development 

The precise mechanism by which H. suis contributes to gastric ulceration remains incompletely understood, but alterations in gastric acid secretion appear to play an important role. During the earlier stages of infection, reduced gastric acid secretion may alter the microbial composition of the pars esophagea, creating conditions that favour the establishment of other bacterial populations^2,3. 

One organism receiving increasing attention is Fusobacterium gastrosuis. A higher number of this bacterium has been identified in stomachs affected by H. suis, suggesting that changes induced by H. suis may facilitate its proliferation¹. Colonization of the pars esophagea by F. gastrosuis has been associated with lesion development, and metabolites produced by this organism may contribute to epithelial cell death and gastric ulcer formation⁴. 

As infection progresses into the chronic phase, gastric acid secretion may increase, potentially worsening lesions in the pars esophagea. Because this non-glandular region lacks a protective mucus layer, it remains particularly susceptible to acid-induced injury^2,3. These observations support the concept that microbial alterations and acid secretion changes may act together during ulcer development. 

The Role of Gastric Microbiota 

The composition of the gastric microbiota may also influence mucosal health. A reduction in beneficial Lactobacillus populations has been associated with increased erosion and ulceration⁴. Lower numbers of these bacteria may reduce the production of antimicrobial substances such as lactic acid and bacteriocins while increasing gastric pH, creating a more favourable environment for pathogenic organisms¹. 

Other microorganisms, including Arcobacter spp., Bacillus spp., Candida spp., and additional bacterial species, have occasionally been detected in pigs with gastric lesions. However, these organisms have not been consistently recognised as highly specific risk factors for gastric ulceration¹. 

Although the direct effect of probiotic supplementation on gastric ulcer prevention has not yet been established, the recognised role of gastric microflora suggests that maintaining a balanced microbial environment may warrant further consideration in future herd health strategies¹. 

Practical Clinical Insights 

When gastric ulcers are identified in a herd, veterinarians should recognise that microbial factors represent only one component of a multifactorial disease process. 

Practical considerations include: 

• Consider H. suis as a potential contributor when evaluating gastric ulceration, particularly in older pigs.

• Interpret microbial findings alongside nutritional, housing, and management factors rather than in isolation.

• Recognise that age-related changes in bacterial colonization may influence lesion development.

• Be aware that disruption of beneficial gastric microflora, particularly Lactobacillus spp., may accompany ulcer progression.

• Remember that current evidence does not support attributing gastric ulceration to a single infectious organism.

A practical clinical approach integrates microbial findings with the overall herd picture, recognising that interactions between gastric bacteria, acid secretion, and environmental factors collectively influence the development and severity of gastric ulcers in pigs. 

References 

1. Krepelková Z, Novotný J, Bárdová K, Link R, Csörgö A. Gastric ulcers in pigs–a review. Folia veterinaria. 2024 Jun 27;68(2):33-42. https://sciendo.com/pdf/10.2478/fv-2024-0015 

2. De Witte C, Devriendt B, Flahou B, Bosschem I, Ducatelle R, Smet A, Haesebrouck F. Helicobacter suis induces changes in gastric inflammation and acid secretion markers in pigs of different ages. Veterinary research. 2017 Jun 15;48(1):34. https://link.springer.com/content/pdf/10.1186/s13567-017-0441-6.pdf 

3. Ziegler A, Gonzalez L, Blikslager A. Large animal models: the key to translational discovery in digestive disease research. Cellular and molecular gastroenterology and hepatology. 2016 Nov 1;2(6):716-24. https://www.sciencedirect.com/science/article/pii/S2352345X16301047 

4. Taillieu E, Taelman S, De Bruyckere S, Goossens E, Chantziaras I, Van Steenkiste C, Yde P, Hanssens S, De Meyer D, Van Criekinge W, Stock M. The role of Helicobacter suis, Fusobacterium gastrosuis, and the pars oesophageal microbiota in gastric ulceration in slaughter pigs receiving meal or pelleted feed. Veterinary Research. 2024 Feb 5;55(1):15. https://link.springer.com/content/pdf/10.1186/s13567-024-01274-1.pdf