Odynophagia in HIV: Localising the Cause from Endoscopy

A 30-year-old male recently diagnosed with HIV presents with odynophagia. Upper GI endoscopy shows serpiginous (linear, snake-like) ulcers set in otherwise normal-appearing surrounding mucosa in the distal oesophagus. In an HIV-positive patient, the endoscopic morphology of oesophageal ulcers is the key that distinguishes among the infectious causes of odynophagia — and this pattern is classic for Cytomegalovirus (CMV) esophagitis.

Why CMV Esophagitis Fits

• Ulcer morphology: CMV characteristically produces one or few large, shallow, linear or serpiginous ulcers with relatively normal-looking intervening mucosa — exactly as described here. This reflects CMV's tropism for endothelial cells and fibroblasts in the submucosa rather than the squamous epithelium itself.
• Host context: CMV disease, including CMV esophagitis, is an AIDS-defining opportunistic infection that classically occurs in patients with advanced immunosuppression (typically CD4 <50–100 cells/µL), consistent with a newly diagnosed, likely untreated HIV patient.
• Diagnosis: Confirmed on biopsy from the base of the ulcer (not the edge), showing large cells with characteristic intranuclear "owl's eye" inclusions and perinuclear halos.
• Treatment: IV ganciclovir (or valganciclovir/foscarnet) rather than acyclovir or antifungals, underscoring why correct identification matters clinically.

Why the Other Options Are Incorrect

• Herpes simplex (HSV) esophagitis: HSV typically produces multiple small, discrete, "volcano-like" or punched-out vesiculo-ulcerative lesions, often with a raised, inflamed edge, rather than large serpiginous ulcers in normal mucosa. Biopsy from the ulcer edge shows multinucleated giant cells with Cowdry type A intranuclear inclusions — a distinctly different endoscopic and histologic picture from what is described.
• Candida esophagitis: Presents with white-yellow adherent plaques/pseudomembranes on an inflamed, friable mucosa — not discrete ulcers with normal surrounding mucosa. It is also the most common cause of odynophagia in HIV overall, but the endoscopic picture here does not match plaque-forming candidiasis.
• Gastro-esophageal reflux disease (GERD): Causes erosive esophagitis typically at the gastro-esophageal junction with mucosal erythema/erosions related to acid exposure, not serpiginous ulcers in an otherwise normal mucosa, and is not specifically linked to HIV immunosuppression. The patient was already empirically started on a PPI, which would be expected to improve reflux-related changes, not serpiginous ulceration.

Conclusion

The combination of HIV-related immunosuppression with large, serpiginous distal esophageal ulcers in normal surrounding mucosa is the classic description of Cytomegalovirus (CMV) esophagitis, making it the most likely diagnosis.