Actinomyces-Induced Esophageal Stricture in an Immunocompetent Host

Abstract

Actinomyces is an anaerobic organism that resides in the GI tract and is a rare cause of esophageal stricture, usually in immunocompromised patients. We present an immunocompetent patient with chronic dysphagia whom we found to have an esophageal stricture growing Actinomyces. A 44 year-old Haitian woman with no past medical history was admitted for 6 months of dysphagia to both solids and liquids that later progressed to odynophagia. She also complained of fatigue, weakness, and 15 lb weight loss. She denied having nausea, vomiting, abdominal pain, or substernal burning. Our initial EGD showed an esophageal stricture 15 cm from the incisors that was too narrow for the scope to pass (Fig. 1). Biopsies at the site showed ulceration with granulation tissue and clusters of Actinomyces. Brush cytology was negative for malignancy. Dilation was deferred due to extensive edema and friability. A follow-up barium esophagram confirmed the stricture was 2cm long (Fig. 2). She was started on IV penicillin G. Our repeat EGD six weeks later showed resolution of the swelling (Fig. 3) and subsequent video fluoroscopy showed 50% luminal narrowing over a 5-6 cm segment. We then scheduled the patient for balloon dilatation, which was successful, and six more months of antibiotics, which are ongoing.1726_A Figure 1. Initial EGD Finding1726_B Figure 2. Esophagram Findings1726_C Figure 3. Post-Treatment EGD FindingsActinomyces typically resides in the GI and genitourinary tracts, but can become pathogenic upon breaching the mucosal barrier. Commonly affected groups include men, diabetics, and the immunosuppressed. It will generally present with odynophagia, dysphagia, and weight loss. Initial work-up includes neck CT and barium studies, but definitive diagnosis is via tissue biopsy. Fewer than 30 cases of esophageal Actinomyces have been reported and only 9 involved immunocompetent hosts. Factors such as trauma, surgery, malignancy, chemotherapy, and radiation therapy may increase risk of pathogenesis. Esophageal dysmotility from hiatal hernias is another potential mechanism for infection in immunocompetent hosts since acid reflux can damage the mucosa and lead to invasion. Strictures causing dysphagia can be treated with mechanical dilatation, and any infection must be treated with beta-lactam antibiotics. There have been no reported incidents of recurrent symptoms in immunocompetent hosts following treatment.