Herpes simplex virus (HSV) esophagitis is a well-recognized infection of immunocompromised hosts but has rarely been described in immunocompetent children. Fever, odynophagia, and retrosternal pain of acute onset are the most common signs and symptoms at presentation.1,2 Esophagoscopy with biopsy and collection of tissue for culture or polymerase chain reaction (PCR) are required to make a definitive diagnosis. We present 2 patients with herpetic esophagitis who share a possible risk factor.
CASE 1
A 17-year-old previously healthy male, member of a wrestling team, presented with 3-day history of progressive retrosternal chest pain, odynophagia, and fever. He had no previous hospitalizations, surgeries, or history of prior HSV infection, recurrent infections, or other findings suggestive of immunodeficiency. His only medication was methylphenidate for attention deficit hyperactivity disorder.
On examination, the patient was mildly uncomfortable, complaining of midsternal chest pain. Vital signs were normal. Physical examination was remarkable for mild epigastric tenderness. He had normal serum electrolytes, amylase, and lipase values. The white blood cell count was 8000/mm3; hematocrit, 46.4 g/dL; and platelet count, 221,000/mm3. Serum troponin was normal. Electrocardiogram and chest radiograph were unremarkable. Endoscopy revealed multiple ulcerations, several white patches, and exudates throughout the mid and lower esophagus with extremely friable mucosa (Fig., Supplemental Digital Content 1, https://links.lww.com/INF/A864). Microscopic evaluation of the esophageal biopsies showed moderate-to-severe acute and chronic inflammation, basal cell hyperplasia, and rare intraepithelial eosinophils. No viral inclusions or fungal elements were recognized.
HSV type I was detected through PCR; PCR for cytomegalovirus (CMV) was negative.
Oral esomeprazole and sucralfate were started to treat the esophagitis. Antiviral therapy was not initiated as the results of PCR were not available at that time and a definitive diagnosis could not be made. The patient was discharged home the same day because he was able to tolerate oral liquids. He was completely asymptomatic at the 2-week follow-up visit and medications were discontinued.
CASE 2
A 16-year-old previously healthy male, member of the same wrestling team as previous patient, presented with 2-day history of dysphagia, odynophagia, and fever to 39.4°C. He had no previous hospitalizations, surgeries or history of previous HSV infection, recurrent infections, or other findings suggestive of immunodeficiency. He had been taking Maalox for 2 days without improvement in symptoms.
On admission, he had normal vital signs and unremarkable physical examination findings. Serum electrolyte values were normal, as were amylase and lipase values. The white blood cell count was 11,500/mm3 with 12% lymphocytes and 75% neutrophils, hematocrit was 43.5 g/dL, and platelet count was 171,000/mm3. Electrocardiogram and chest radiograph were unremarkable. Endoscopy demonstrated multiple white patches, several areas of ulceration, and exudates in the mid and distal esophagus with friable mucosa (Fig., Supplemental Digital Content 2, https://links.lww.com/INF/A865). Microscopic evaluation of the esophageal biopsy demonstrated highly reactive appearing squamous epithelium with acute inflammatory cells and a maximum of 5 eosinophils per high power field. No viral inclusions or fungal organisms were observed.
HSV type 1 was detected by PCR; PCR for CMV was negative.
The patient was treated with oral esomeprazole and sucralfate. Antiviral therapy was not initiated because the results of PCR were not available at that time and a definitive diagnosis could not be made. Because he was tolerating oral liquids, he was discharged home the same day with close follow-up. He was asymptomatic at the 2-week visit. Repeat upper endoscopy in 1 month demonstrated healing esophageal ulcerations. Repeat PCR did not detect HSV.
DISCUSSION
HSV is well known to cause infection of the esophagus and is usually observed in patients who are immunocompromised. Those receiving immunosuppressive agents, such as solid organ and bone marrow transplant recipients are particularly susceptible. However, it has also been described in otherwise healthy immunocompetent hosts.1,2 The majority of patients present with acute onset of fever, chest pain, and dysphagia.2 Endoscopy typically shows erythema, ulcerations, and exudates mainly in the mid to distal esophagus.1 Clinical evidence of HSV infection elsewhere is usually lacking.
It has been well documented that HSV skin infection (herpes gladiatorum) is endemic among high school and college wrestlers. In 1989, there was a large outbreak of herpes gladiatorum among high school wrestlers attending a 4-week intensive-training camp.3 Mode of transmission was attributed to skin-to-skin contact with likely contribution from contact with the wrestling mat.3 To our knowledge, there have been no reports to date of HSV esophagitis being transmitted among wrestlers.
The disease commonly affects the mid and distal esophagus and less frequently the proximal esophagus1; this pattern was observed in our patients. Esophagoscopy is the diagnostic procedure of choice. The gross appearance of the esophagus is characteristic, with friable mucosa, multiple superficial ulcerations with exudate. The endoscopic appearance can be confused with esophagitis secondary to Candida, CMV, or eosinophilic disease. Thus, a biopsy specimen is essential to make a definitive diagnosis. Histologic evaluation reveals inflammation and in about half of the cases intranuclear inclusions are visualized.4 It has been found that there is higher frequency of detection of HSV DNA by PCR as compared with virus isolation or histologic evaluation.5 Our 2 cases had positive PCR for HSV despite the absence of intranuclear inclusions on histologic evaluation.
Clinical and laboratory assessment of immunocompetence was normal in our patients, and it has been suggested that immunologic investigation is not indicated for patients who promptly recover because their recovery implies intact immunity.2
The benefit of acyclovir therapy for HSV esophagitis is established in immunocompromised hosts.6 In immunocompetent patients, however, HSV esophagitis appears to be a self-limited disease. Previous reports suggest that therapy with acyclovir in immunocompetent patients may shorten the duration of symptoms although a controlled study has not been done.7 Our patients recovered promptly without antiviral therapy.
CONCLUSIONS
These cases demonstrate that herpetic esophagitis in the immunocompetent patient is self-limited and that supportive care without antiviral medication is usually sufficient for treatment. HSV is already known to be transmitted among wrestlers in the form of herpes gladiatorum. On the basis of our 2 cases, we postulate that transmission of herpetic esophagitis among wrestlers is also possible.
REFERENCES
1. Ramanathan J, Rammouni M, Baran J, et al. Herpes simplex virus esophagitis in the immunocompetent host: an overview.
Am J Gastroenterol. 2000;95:2171–2176.
2. Rodrigues F, Brandao N, Duque V, et al. Herpes simplex virus esophagitis in immunocompetent children.
J Pediatr Gastroenterol Nutr. 2004;39:560–563.
3. Belongia E, Goodman J, Holland E, et al. An outbreak of herpes gladiatorum at a high-school wrestling camp.
N Engl J Med. 1991;325:906–910.
4. Galbraith J, Shafran S. Herpes simplex esophagitis in the immunocompetent patient: report of four cases and reviews.
Clin Infect Dis. 1992;14:894–901.
5. Wald A, Huang Mee-Li, Carrell D, et al. Polymerase chain reaction for detection of Herpes Simplex Virus (HSV) DNA on mucosal surfaces: comparison with HSV isolation in cell culture.
J Infect Dis. 2003;188:1345–1351.
6. Jenkins D, Wicks AC. Herpes simplex esophagitis in a renal transplant patient: the need for antiviral therapy.
Am J Gastroenterol. 1988;83:331–332.
7. Kurahara K, Aoyagi K, Nakamura S, et al. Treatment of herpes simplex esophagitis in an immunocompetent patient with intravenous acyclovir: a case report and review of the literature.
Am J Gastroenterol. 1998;93:2239–2240.
