Related Experiment Video
Updated: Aug 7, 2026
07:43
Mouse Models Of Helicobacter Infection And Gastric Pathologies
Published on: October 18, 2018
[Gastric histoplasmosis simulating a malignant gastric ulcer]
Alonso Ricardo Soto Tarazona1, José Luis Meza Flores, Doris Garrido Rivadeneyra
1Hospital Nacional Hipólito Unanue.
Summary
Chronic disseminated histoplasmosis can mimic gastric cancer in endemic areas. This case highlights the importance of considering fungal infections in patients with gastrointestinal symptoms and risk factors.
Area of Science:
- Medical Mycology
- Gastroenterology
- Infectious Diseases
Background:
- Histoplasmosis is a fungal infection endemic to specific regions.
- Gastrointestinal involvement in histoplasmosis can present with diverse symptoms.
- Chronic alcoholic liver disease can be an immunocompromising factor.
Observation:
- A young patient from a histoplasmosis-endemic area presented with chronic abdominal pain.
- Gastric endoscopy revealed ulcerous damage mimicking gastric carcinoma.
- The patient had a history of chronic alcoholic hepatopathy.
Findings:
- The final diagnosis was chronic disseminated histoplasmosis with gastric compromise.
- The gastric lesions were characteristic of fungal infiltration rather than malignancy.
- Underlying alcoholic liver disease may have contributed to disease dissemination.
Implications:
- Histoplasmosis should be considered in the differential diagnosis of gastrointestinal ulcerations and infiltrative lesions.
- Early recognition is crucial for appropriate treatment and management of disseminated histoplasmosis.
- This case underscores the importance of geographical and immunocompromise status in diagnosing gastrointestinal pathologies.
More Related Videos
Related Concept Videos
01:22Pathophysiology of Peptic Ulcer Disease: Injurious Factors
Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...
01:17Gastritis-II: Pathophysiology
Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
01:28Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies
Peptic ulcer disease (PUD) presents with diverse symptoms depending on the location and severity of the ulcer. Clinical manifestations of peptic ulcer include dull pain and a burning sensation in the mid-epigastric region.
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.
01:27Peptic Ulcer
Peptic ulcers are erosive lesions of the gastric or duodenal lining, most commonly caused by Helicobacter pylori infection. This Gram-negative, helical bacterium has adapted to survive the stomach’s acidic environment by producing urease, which converts urea into ammonia and carbon dioxide. The ammonia neutralizes gastric acid in the bacterium’s immediate environment, allowing colonization of the gastric mucosa. H. pylori attaches to mucus-secreting epithelial cells, penetrates the mucus...
01:26Gastritis II: Pathophysiology
The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
01:24Peptic Ulcer Disease II: Pathophysiology
Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...