Infectious Esophagitis

• Infection of the esophagus
• Rare in children, most often seen in immunocompromised patients
• may be incidental finding in asymptomatic patients being treated with topical corticosteroids for EoE
• HSV most common infection in immunocompetent host
  
• Three main causative agents: Fungal, Viral, Bacterial (parasites much less common)
  
• Esophageal infection, like all inflammatory processes can lead to stricture
  

• Candida 95% other players include: Torulopsos glabrata, C tropicalis, C krusei, C stellatoidea
• Cryptococcus - similar clinical course with Candida - seen w/ AIDS Dx w/ Cx or Bx
• Histoplasmosis - immunocompromised patient w/ disseminated histoplasma. Severe systemic Dz: fever, bone marrow failure, Hepatosplenomegaly (HSM)
  
• Blastomycosis and Aspergillosis are very rare
  
• May or may not have concommitant oral candidiasis
• Oncology patients: thrush and esophageal candidiasis typically coexist
• Predisposing factors
• mucositis
• leukopenia
• steroid use including inhaled steroids
• immunocompromised
• Stasis, Abnormal motility: scleroderma, achalasia
• Severe Malnutrition - typically leading to immune compromise
• Broad spectrum Abx Rx
• underlying esophageal Dz (EoE, GERD -prolonged PPI use)
• Clinical Manifestations
• dysphagia, odynophagia, substernal chest pain, and emesis
• Diagnosis
• Endoscopy with Biopsy
• Endoscopy shows white plaques
• Bx shows tangles hyphae with unicellular forms invading surface epithelium
• Tissue invasion distinguishes esophagitis from mere colonization
• Culture is not sensitive as Candida is normally present in Oral/ GI tract
• Radiology - Air Contrast Barium esophagram - may reveal ulcerations and exudates
• Therapy
• May be self-limited in healthy individual
• Candida - treat with fluconazole (PO or IV) or itraconazole (PO) for 14-21 days after clinical improvement . Duration depends on severity of illness
• If esophageal Bx was not possible, empiric Tx for Candida may be necessary
• Histoplasmosis - Tx with Amphotericin B followed by itraconazole
  
• Complication
• stricture
• fungal ball

• HSV
• Background
• Occurs in immunocompetent host
• HSV1 most common , HSV2 less common
• Typically seen as superinfection after physical or chemical injury
• May not have typical oral herpetic lesions
• Presentation
• odynophagia +/- dysphagia, squeezing chest pain with swallowing -similar to pill esophagitis
  
• often with Fever, Malaise
• dehydration, ketosis, weight loss from patient avoiding intake 2/2 pain
• Diagnosis
• Endoscopy
• Days 1-2: Herpetic vesicles
  
• Days 2-3+: Volcano ulcers: round lesions, yellow borders
  
• Histology
• multinucleated giant cells with intranuclear Cowdry type A (eosinophilic) and type B (ground glass appearance) inclusions
• mononuclear cell infiltrate
• Culture
• viral culture
• immunohistochemical stains
• Test for HIV
• Tx
• self limited in immunocompetent host
• Acyclovir for severe cases or immunocompromised host
• Foscarnet if acyclovir resistance
• CMV
• Background
• seen in AIDS patients or organ transplant patients
• rare in immunocompetent host
• Endoscopy
• ulcerations similar to HSV, but typically a single deep ulcer (more linear/deeper)
• Histology
• intranuclear and intracytoplasmic inclusions producing Owl's Eye appearance
  
• Labs: PCR, Tissue-Viral Cx, immunocytochemistry
• Tx
• Valganciclovir, Ganciclovir, Foscarnet
• treatment dictated by response - high recurrence risk
• HIV
• Ideopathic Esophageal Ulceration (IEU)
• giant ulcers seen in primary HIV infection, chronic AIDS, and CD4 <100
• clinically similar to CMV
• seen in up to 40% of pts

• Mycobacterium Tuberculosum
• assoc w/ systemic infection, pulmonary or mediastinal infection
• UGI Series may reveal displaced esophagus due to extensive lymphadenopathy

• Peptic Esophagitis - typically presents with less severe pain
• EoE
• Pill Esophagitis
• Foreign body
  

1. Kliegman, Robert. Nelson Textbook of Pediatrics. Edition 21. Philadelphia, PA: Elsevier, 2020.
2. Tortora, Gerard J. Principles of Anatomy and Physiology. 15th ed. Hoboken, NJ: J. Wiley, 2009. Print.
3. Moore, Keith L.,, Arthur F. Dalley, II, and Keith L Moore. Clinically Oriented Anatomy. Fifth edition. Baltimore: Wolters Kluwer Health, 2009. Print.
4. Kleinman RE, Goulet O, Mieli-Vergani G, et al, eds. Pediatric Gastrointestinal Disease: Pathophysiology, Diagnosis, and Management. 5th ed. Hamilton, Ontario: BC Decker; 2008.
5. The NASPGHAN fellows concise review of pediatric gastroenterology, hepatology, and nutrition. 1st edition (2011)
6. Wyllie, Robert & Hyams, J.S.. (2011). Pediatric Gastrointestinal and Liver Disease. 10.1016/C2009-0-53242-4.  (Accessed online Feb 2020)