Literature Review: Molecular Pathophysiology of Infection Esophagitis

Abstract

Infectious esophagitis refers to inflammation of the esophageal mucosa caused by various pathogenic microorganisms, including Helicobacter pylori, Candida albicans, and Herpes Simplex Virus type 1 (HSV-1). While commonly associated with gastroesophageal reflux disease (GERD) and other irritants, infections by these pathogens can exacerbate esophagitis and contribute to severe tissue damage. H. pylori, a Gram-negative bacterium, can affect the esophagus both directly through mucosal damage and indirectly by increasing gastric acid secretion, which worsens reflux conditions. Candida albicans, an opportunistic pathogen, is particularly prevalent in immunocompromised individuals and causes severe esophageal inflammation through its transition from yeast to invasive hyphal forms, secreting hydrolytic enzymes that damage tissues. HSV-1, known for its latent nature, can reactivate in immunocompromised individuals, leading to chronic esophagitis characterized by cytopathic lesions. The pathophysiological mechanisms of these infections involve complex interactions between pathogen virulence factors and the host immune response. Persistent inflammation and immune activation can result in serious complications such as esophageal strictures, dysphagia, and the need for more intensive therapeutic interventions. Understanding these mechanisms is crucial for developing effective treatment strategies for infectious esophagitis and improving clinical management, particularly in patients with underlying conditions such as HIV/AIDS and diabetes mellitus.