Herpes esophagitis is an infectious inflammation of esophagus caused by two members of herpesvirus family, herpes simplex virus HSV-1 or HSV-2. It rarely affects immunocompetent hosts, thus it is an opportunistic infection for with the esophagus being the most frequent visceral target.
Initial presentation for herpes esophagitis (HE) is non-specific. The prodromal stage may mimic the common flu and includes a fever of about 39°C, malaise, reduction in weight, as well as pulmonary symptoms and sore throat. After flu-like symptoms, patients develop esophageal signs specifically, acute odynophagia, dysphagia for both fluids and solid foods, retrosternal pain, nausea and subsequent vomiting  . Symptoms for immunocompetent subjects can be self-limiting thus hindering the process of diagnosis. Furthermore, prodromal symptoms of herpes esophagitis in immunocompetent patients may be absent and manifest as acute odynophagia and dysphagia. In some cases, the infection is mild in character or even asymptomatic .
HSV-specific signs such as oropharyngeal (herpes labialis) and genital lesions are not commonly concurrent with esophagitis but are described in about 20% of cases . Herpes lesions may herald esophagitis, or may arise after esophagitis or may be absent   .
Specifics of history data are important to exclude collateral immunological conditions and possible HIV infection. On the grounds that herpes esophagitis is an opportunistic infection, subjects prone to developing it are either immunocompromised or are taking immunosuppressive medications. For example, a patient with a chronic autoimmune disease takes systemic corticosteroids that act on suppressing the immune system   . Gastro-esophageal reflux disease (GERD) patients and radiation therapy participants should be considered at risk of developing HE. Those receiving chemotherapy and transplant recipients are also at high risk. Cases of patients with HE and prior nasogastric intubation are reported, So, history of surgical procedures and previous inpatient care should be obtained .
When evaluating herpes esophagitis, radiological examination is inferior to endoscopy as HE findings are not specific for this type of disorder. Misdiagnosis as fungal esophagitis is a common error because this condition also presents with large lesions.
Endoscopy is necessary for both the examination of the esophagus and obtaining a biopsy specimen to confirm the diagnosis. In the early stage of HE, the macroscopic examination may reveal diffuse ulcerations with central depressions (volcano-like) that are yellow-white in color and variable in size. Edematous halo and white exudate can also be present. Subsequently, lesions may consolidate . Most common site of ulcerations in infectious esophagitis is the lower third of the esophagus, although cases of the middle third and ulcerations throughout the esophagus are also present. Occurrence in upper third is less likely  . The tendency to form superficial ulcers may be the characteristic feature distinguishing HE from esophagitis caused by cytomegalovirus (CMV), which in contrast is associated with deep ulcerations.
Biopsy analysis is imperative for correct diagnosis. The histological specimen of mucosa must be collected from margins of the ulcer. Microscopy will reveal a unique picture of herpes infection like acute inflammation, multinucleated giant cells with ground glass nuclei, as well as eosinophilic inclusions in the nuclei  . Immunohistochemistry is also necessary to confirm the presence of HSV antigens .
Virus isolation and cell culture along with polymerase chain reaction (PCR) are also beneficial in confirming the diagnosis .