Health Questions and Answers

Esophageal Infections

Which organisms are most commonly identified in esophageal infections?
The most common etiologies are Candida albicans, herpes simplex virus (HSV), and cytomegalovirus (CMV). C. albicans and HSV can be seen in individuals with normal immunity, whereas CMV esophagitis is found in immunocompromised hosts.

What are the typical presenting symptoms in patients with infectious esophagitis?
Odynophagia and, to a lesser degree, dysphagia are the most common complaints. Heartburn, chest pain, nausea, dysgeusia, and bleeding can also be symptoms/signs.

What is the most common cause of infectious esophagitis in the general population?
Candida albicans. This yeast is virtually ubiquitous and is considered normal oral flora. Esophageal infection occurs by a two-step process.

  • The first step is colonization, which involves adherence to the mucosal surface and proliferation. It is estimated that 20% of asymptomatic people have esophageal colonization with Candida, and this becomes more common with advanced age.
  • The second step is often associated with impaired host defenses and is identified by mucosal invasion of budding yeast and the presence of mycelial forms on microscopic examination. Adherent creamy white plaques or exudates are the common appearance on endoscopic examination.

What commonly used drugs are associated with fungal esophagitis?
Antibiotics that affect normal oral flora change the competitive milieu, increasing colonization and the likelihood of fungal infection. Both systemic and inhaled topical corticosteroids increase risk of infection due to effects on mucosal immunity. Acid suppressive therapies, most significantly proton pump inhibitors but also H2-receptor blockers, increase mucosal colonization with C. albicans, probably as a result of the loss of the cleansing effect of spontaneous gastroesophageal reflux events.

How is Candida esophagitis treated?
The most commonly prescribed therapy for candidal esophagitis is fluconazole, 100-200 mg orally for 10-14 days. Other options for therapy include topical agents. Nystatin can be given as a liquid “swish-and-swallow” or as a dissolvable oral troche. Dosing of nystatin ranges from 200,000 to 500,000 units four or five times daily for 7-14 days. Clotrimazole, a nonabsorbable azole, can be given as a buccal troche, 10 mg five times daily for 1 week, or as a vaginal tablet, 100 mg dissolved in the mouth and swallowed five times daily. Oral suspensions of amphotericin B are also available but are usually reserved for azole-resistant infections. Topical agents have the advantage of being well tolerated, having no significant adverse effects or drug interactions. Topical therapy should be reserved for less severe infections in immunocompetent individuals. Other oral imidazole agents are itraconazole and voriconazole. Ketoconazole is no longer recommended for treatment of monilial esophagitis.

How is candidal esophagitis treated in granulocytopenic patients?
Granulocytopenic patients should be treated with intravenous amphotericin B due to the high risk of fungal dissemination. Dose and duration of therapy are based on severity of infection; febrile patients with extensive esophagitis or evidence of systemic infection should receive 0.5 mg/kg/day, whereas milder cases may be treated with 0.3 mg/kg/day. Newer liposomal formulations of amphotericin B that are less nephrotoxic and have fewer systemic side effects are available and are dosed at 3-5 mg/kg/day.

Should empiric therapy for candidal esophagitis be considered in an at-risk patient presenting with typical symptoms of esophageal infection?
Yes. A therapeutic trial of fluconazole for patients with presumed esophageal candidiasis is a cost-effective alternative to endoscopy. Patients not demonstrating symptomatic improvement within 3-5 days should undergo endoscopic evaluation.

What other fungal organisms should be considered in esophageal infections? Non-albicans species of Candida and other noncandidal fungi can be seen in severely immunocompromised patients. Candida glabrata and Candida krusei have been identified more frequently in recent years. Non-albicans Candida species are more resistant to imidazole antifungals, requiring intravenous amphotericin B therapy. Histoplasma, Cryptococcus, Blastomyces, and Aspergillus species may also cause fungal esophagitis.

What is the most common viral pathogen-causing esophagitis?
CMV is the most common cause of viral esophagitis. This is because viral esophagitis occurs more frequently in immunocompromised patients, and CMV is identified as the pathogen in most cases. Other viral pathogens, including HSV, varicella-zoster virus (VZV), and Epstein-Barr virus (EBV), can also cause esophageal infections in patients with immune dysfunction.

What is the most common cause of viral esophagitis in patients with normal immunity?
HSV esophagitis, although rare, may cause viral esophagitis in an immunocompetent patient. The infection can be primary or due to reactivation of a latent infection. The finding of orolabial HSV may suggest the diagnosis in patients with acute esophageal symptoms but is present in only about 20% of cases. HSV esophagitis tends to be seen more commonly in males (male to female ratio >3:1).

How is viral esophagitis diagnosed?

In patients with esophageal ulcers presenting with symptoms of infectious esophagitis, multiple biopsies (10 biopsies are recommended to maximize diagnostic yield) of each ulcer should be obtained. Biopsies from the ulcer base and ulcer margins are evaluated for typical cytopathic changes microscopically. Tissue also needs to be sent in medium for viral cultures. Cultures are more sensitive than microscopic examination, and immunohistochemistry can increase the diagnostic sensitivity as well.

Differentiate herpes simplex virus (HSV) and cytomegalovirus (CMV) esophagitis endoscopically.
Early in HSV esophagitis, the typical small vesicles can be seen in the middle-distal esophagus. The vesicles may coalesce, forming well-circumscribed ulcers that have raised yellowish edges: the classic “volcano ulcers.” HSV esophagitis can cause a diffusely ulcerated mucosa devoid of squamous epithelium in severe infections. CMV ulcers are more often linear, serpiginous lesions in the middle and/or distal esophagus. These ulcers may unite, forming giant ulcers, and may produce stricturing of the esophageal lumen. Concomitant infections with both organisms have been reported, and, in candidal esophagitis, a viral coinfection can be present in 20-50% of cases. Candidal plaques often obscure viral ulcers.

Differentiate HSV and CMV microscopically.
HSV infects squamous epithelium. Biopsies from the ulcer margins demonstrate multinucleated giant cells with ballooning degeneration of squamous cells, margination of chromatin, and characteristic ground-glass nuclei. Cowdry type A intranuclear inclusions are pathognomonic for HSV infections. The classic histologic features of CMV infection are large cells with both intracytoplasmic inclusions and amphophilic intranuclear inclusions. Biopsies should be placed in viral transport media; culture remains the standard for diagnosis.

Does HIV cause esophageal ulceration?

Idiopathic esophageal ulcers (IEUs) have been reported in HIV-infected patients. HIV can be isolated from esophageal ulcers without evidence of other pathogens. It is thought that the mucosal injury is immunologically mediated and not a direct result of cytotoxic effects of HIV. IEUs do not respond to antiviral or antifungal treatment, but healing can be accomplished in approximately 90% of cases with corticosteroids or thalidomide. Because steroid use predisposes to candidiasis, prophylaxis with fluconazole is suggested. Recommended therapies include prednisone, 40 mg orally for 4 weeks, then tapering by 10 mg/week, or thalidomide, 200 mg/day for 4 weeks.

Are immunocompromised patients at risk for bacterial esophagitis?
In HIV/AIDS patients, the risk of bacterial esophagitis is low due to preserved granulocyte function. Patients receiving chemotherapy for malignancy are at greatest risk. The use of acid suppressive medications is also considered a risk factor.

How is the diagnosis of bacterial esophagitis established?
Gram stain of mucosal biopsies demonstrates invasion of the esophageal mucosa. Fungal/viral pathogens must be excluded to make a diagnosis of bacterial esophagitis. Cultures of biopsy material are not helpful because of the unavoidable contamination with oral flora. Infections are usually polymicrobial, typically with gram-positive organisms found in the normal oral flora, but gram-negative species may also be seen.

Does it make sense to stain for acid-fast organisms in evaluating esophageal ulcers?
Yes. A shallow linear ulcer with smooth edges and a necrotic base, usually in the middle third of the esophagus, is suggestive of Mycobacterium tuberculosis (TB). TB is seldom a primary infection in the esophagus, but cases have been reported. It more often results from direct extension of adjacent mediastinal lymph nodes in patients with pulmonary tuberculosis. Mycobacterium-avium complex is commonly reported in patients with AIDS and tends to be widely disseminated at the time of diagnosis. Esophageal involvement is rare but should be considered in the differential diagnosis; appropriate tissue stains and culture should be obtained. As is the case with TB, treatment is difficult, requiring multidrug regimens over months.

Can the diagnosis of Chagas’ disease be based on classic manometric findings and confirmed by histologic evaluation of deep mucosal biopsies from the distal esophagus?
Chagas disease is caused by infection with Trypanosoma cruzi, which is endemic in South America. The organism destroys ganglion cells, and multiple organs are involved. The esophageal abnormalities resemble achalasia, but the lower esophageal sphincter pressure is not elevated and, in fact, may be low. Symptoms occur typically years to decades after the acute infection. Diagnosis requires typical manometric findings, positive serologic tests for the parasite, and evidence of other organ involvement. Mucosal biopsies are of no value in the diagnosis. The esophagus in Chagas’ disease is more responsive to nitrates and calcium channel antagonists, which improve esophageal emptying. Unlike primary achalasia, Chagas’ disease is often associated with cardiac, renal, intestinal, and biliary abnormalities.

Date last updated: March 28, 2010

References

WEBSITES
http://www.gastroatlas.com/
http://www-medlib.med.utah.edu/WebPath/webpath.html

BIBLIOGRAPHY

  • Dietrich DT, Wilcox CM: Diagnosis and treatment of esophageal diseases associated with HIV infection. Am J Gastroenterol 91:2265, 1996.
  • Grim SA, Smith KM, Romanelli F, Ofotokun I: Treatment of azole-resistant candidiasis with topical amphotericin B. Ann Pharmacother 36:1383, 2002.
  • Kearney DJ, McDonald GB: Esophageal disorders caused by infection, systemic illness, medications, radiation and trauma. In Feldman M, Friedman LS, Sleisenger MH (eds): Gastrointestinal and Liver Disease, 7th ed. Philadelphia, W.B. Saunders, 2002, p 623.
  • Monkemuller KE, Wilcox CM: Diagnosis of esophageal ulcers in acquired immunodeficiency syndrome. Semin Gastrointest Dis 10:85, 1999.
  • Perez RA, Early DS: Endoscopy in patients receiving radiation therapy to the thorax. Dig Dis Sci 47:79, 2002.
  • Ramanathan J, Rammouni M, Baran J, Khatis R: Herpes simplex virus esophagitis in the immunocompetent host: An overview. Am J Gastroenterol 95:2171, 2000.
  • Rex JH, Walsh TJ, Sosel JD, et al: Practice guidelines for the treatment of candidiasis. Clin Infect Dis 30:662, 2000.
  • Vasquez JA: Options for the management of mucosal candidiasis in patients with AIDS and HIV infection. Pharmacotherapy 19:76, 1999.

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