C. Mel Wilcox University of Alabama at Birmingham, Birmingham, AL, USA While the acquired immunodeficiency syndrome (AIDS) epidemic was the major contributor to the witnessed upsurge in esophageal infections observed in the 1980s and 1990s, more recently, with the widespread availability of highly active antiretroviral therapy, these infections are becoming much less common. In addition, the adoption of antimicrobial prophylaxis for high‐risk immunocompromised patients and the development of more targeted immunomodulators, such as those post organ transplantation, have also led to an overall fall in the incidence of infections, including those involving the esophagus. Despite these advancements, however, esophageal infections will remain important complications of immunodeficiency states. Esophageal infections can be categorized by the infecting organism. Candida spp. are the most common fungal pathogens, with aspergillosis, histoplasmosis, and blastomycosis being very rare. Following fungi, viruses (herpes simplex virus [HSV] and cytomegalovirus [CMV]) are the most common cause of infection. Rare additional causes of esophagitis include bacteria, mycobacteria, and parasites. Odynophagia is the most common symptom of esophageal infection with dysphagia being reported less frequently. Although barium esophagography is helpful in suggesting the presence of infectious esophagitis, these studies are not definitive. Endoscopy provides the highest diagnostic accuracy. Candida albicans is the most common pathogen causing esophageal infection. Classically, barium radiographs of esophageal candidiasis reveal a “shaggy” appearance resulting from diffuse plaque material that coats the esophageal mucosa, mimicking ulceration (Figure 12.1). The endoscopic appearance of Candida is well recognized and is essentially pathognomonic (Figures 12.2 and 12.3). Candida rarely causes true ulceration; thus, the presence of esophageal ulcer associated with Candida esophagitis suggests an additional esophageal process (Figures 12.4 and 12.5). Esophageal brushings have the highest diagnostic yield for candidal infection. Mucosal biopsies will be diagnostic when more severe disease is present, and should be performed in the presence of ulceration. Fungal cultures are not widely available and provide no additional information over the endoscopic and histological findings unless fungi other than Candida are suspected. Other fungi rarely cause esophageal disease. Histoplasma is the most frequent fungal pathogen reported to involve the esophagus, usually from mediastinal involvement (Figure 12.6). In contrast to Candida esophagitis, barium radiographs of viral esophagitis demonstrate ulceration. The ulcers are usually well circumscribed but may coalesce to form a superficial esophagitis. Ulcers associated with HSV infection typically are small and well circumscribed, whereas those associated with CMV have a greater propensity to form larger, well‐circumscribed longitudinal or linear lesions. A diffuse viral esophagitis may result in a cobblestone or shaggy mucosal appearance, similar to that observed in esophageal candidiasis (Figure 12.7). Endoscopically, HSV ulcers correspond to the radiographic features. appearing as well‐circumscribed small volcano‐like lesions, likely the site of a vesicle (Figure 12.8), or shallow ulcers (Figure 12.9); occasionally when multiple and small, the lesions may mimic esophageal candidiasis (Figure 12.10). Although esophageal ulcers caused by CMV may resemble HSV (Figure 12.11), in general, CMV causes larger or more extensive lesions, which are often very deep in patients with AIDS (Figures 12.12–12.14), leading to bleeding, stricture, or, rarely, perforation. Multiple biopsies of the ulcer edge (for HSV) and ulcer base (for CMV) with careful histological examination of biopsy material should reveal the intranuclear (Cowdry type A) or cytoplasmic inclusions characteristic of HSV (Figure 12.15) or CMV infection (Figure 12.16), respectively. Radiographic findings in esophageal tuberculosis are nonspecific but may show ulceration, stricture, or fistulas extending from the esophagus to the trachea, bronchi, or mediastinal lymph nodes (Figures 12.17 and 12.18). An interesting disorder whose pathogenesis is not well defined is the HIV‐associated idiopathic esophageal ulcer. Characteristically, these lesions become manifest when immunodeficiency is severe (CD4 lymphocyte count <100/mm3). The clinical, radiographic, and endoscopic manifestations are indistinguishable from CMV (Figures 12.19–12.21). These ulcers may be deep and result in esophagoesophageal fistula. Other esophageal diseases seen in AIDS patients include parasites and, rarely, neoplasms such as Kaposi sarcoma or non‐Hodgkin lymphoma (Figure 12.22).
CHAPTER 12
Esophageal infections and disorders associated with acquired immunodeficiency syndrome
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