Infection with Candida species is the most common type of infectious esophagitis. Major predisposing factors include antibiotic use, radiation therapy or chemotherapy, hematologic malignancies, and acquired immunodeficiency syndrome (AIDS). A compromised immune system may be the most important risk factor for the development of infectious esophagitis, and HIV or AIDS and solid organ transplant patients are particularly at risk.  Other conditions associated with an increased incidence of Candida esophagitis include esophageal stasis, alcoholism, malnutrition, and advanced age. Occasionally, Candida esophagitis can occur in otherwise healthy individuals with no underlying esophageal or systemic disease. [2, 3, 4, 5, 6, 7, 8]
In one study, the prevalence of Candida esophagitis was 11.2% in HIV-infected patients and 2.9% in non-HIV-infected patients. 
Because Candida esophagitis is primarily a mucosal disease, it often is difficult to recognize with single-contrast esophagography. In contrast, double-contrast esophagography has a sensitivity of 90% in detecting the condition. On double-contrast studies, Candida esophagitis initially is manifested by discrete plaquelike lesions in the esophagus. Usually, the plaques are oriented longitudinally, appearing en face as linear or irregular filling defects with normal intervening mucosa (see the image below). The plaques may be localized or diffuse and usually are located in the upper or mid esophagus. Some patients may have multiple tiny plaques, which produce a finely granular or nodular appearance of the mucosa.
Diagnosis of infectious esophagitis often hinges on endoscopic visualization and histopathologic analysis. 
In advanced Candida esophagitis, the esophagus may have a grossly irregular or shaggy appearance as a result of innumerable plaques and pseudomembranes, with trapping of barium between the lesions (see the image below). This appearance is most commonly seen in patients with AIDS; therefore, the presence of a shaggy esophagus should suggest the possibility of AIDS in patients who are not yet known to be positive for the human immunodeficiency virus (HIV). Some of the plaques and pseudomembranes may eventually be sloughed off, producing 1 or more areas of ulceration on a background of diffuse plaque formation. Occasionally, barium may also dissect beneath the pseudomembranes, resulting in an intramural dissection tract or double-barrel esophagus.
Candida esophagitis is usually self-limiting, and most patients have a marked response to treatment with antifungal agents. However, necrotic mucosal debris and fungal mycelia in the esophagus occasionally form a mycetoma (ie, fungus ball) that causes obstruction. In other patients, severe Candida esophagitis may lead to development of strictures, which are typically long, smooth, tapered areas of narrowing.
In patients with chronic stasis, such as those with advanced achalasia or scleroderma involving the esophagus, superimposed Candida esophagitis may manifest as tiny nodules, polypoid folds, or a lacy appearance in the esophagus. Other patients with scleroderma or achalasia may have a foamy esophagus with innumerable bubbles layering out in the barium column as a result of a yeast form of the infection (see the image below). Other rare complications of esophageal candidiasis include perforation, tracheobronchial fistulas, and aortoesophageal fistulas.
Glycogenic acanthosis, reflux esophagitis, herpes esophagitis, and superficial spreading carcinoma may produce findings similar to those seen in Candida esophagitis. However, patients with glycogenic acanthosis are almost always older individuals who have no esophageal symptoms, and the mucosal nodules of glycogenic acanthosis tend to have a more rounded appearance, whereas the plaques of candidiasis are more linear. Reflux esophagitis may also manifest as a nodular mucosa, but the nodules tend to be more poorly defined than those in candidiasis, and they are always contiguous with the gastroesophageal junction.
Occasionally, herpes esophagitis manifests as multiple plaquelike lesions in the esophagus, but this infection is more commonly associated with small, superficial ulcers (see Herpes Esophagitis, below). Superficial, spreading carcinoma may also manifest as a nodular mucosa, but the nodules tend to have poorly defined borders, producing a confluent area of disease. Undissolved, effervescent particles and debris in the esophagus can be mistaken for the plaques of candidiasis. Thus, if infectious esophagitis is suggested clinically, a double-contrast study should initially be performed without the use of effervescent granules.
Herpes simplex virus type I is the second most common cause of infectious esophagitis, after Candida. Herpes esophagitis is most commonly seen in immunocompromised patients with AIDS, an underlying malignancy, or a debilitating illness, or in patients who have been treated with radiation, steroids, or chemotherapy. However, herpes esophagitis occasionally occurs as an acute, self-limiting disease in otherwise healthy patients who have no underlying immunologic problems. Although obtaining accurate figures regarding the prevalence of herpes esophagitis is difficult, this infection has been reported in approximately 1% of patients who are immunocompromised and in as many as 43% of patients at autopsy. [11, 12, 13, 14, 15, 16]
On double-contrast esophagrams, herpes esophagitis usually manifests as multiple, small, superficial ulcers in the upper esophagus or midesophagus on an otherwise normal background mucosa (see the image below).
The ulcers can have a punctate, linear, stellate, or volcano-like appearance, often with a thin halo of edema at the margins. The ulcers may be clustered together or widely separated with normal intervening mucosa. Severe herpes esophagitis may produce extensive ulceration and plaque formation, mimicking the appearance of Candida esophagitis.
In the appropriate clinical setting, discrete, superficial ulcers in the upper esophagus or midesophagus, without associated plaques, should be highly suggestive of herpes esophagitis. In contrast, ulceration in Candida esophagitis almost invariably occurs on a background of extensive plaque formation. Candida and herpes esophagitis can often be diagnosed on double-contrast studies, obviating endoscopy. However, if radiographic findings are equivocal or if response to treatment is inadequate, endoscopy should be performed for a more definitive diagnosis. Other causes of small, superficial ulcers in the upper esophagus or midesophagus include drug-induced esophagitis and Crohn disease. However, these entities usually can be differentiated from infectious esophagitis on the basis of the clinical history.
Asymptomatic cytomegalovirus (CMV) infection is common worldwide, with a large percentage of the world's population having been exposed to CMV. Before the AIDS epidemic, CMV infections of the esophagus were primarily found on postmortem examinations. The first clinical case of CMV esophagitis was not reported until 1985. Unlike herpes esophagitis, CMV esophagitis almost never occurs in immunocompetent patients, and the vast majority of affected individuals are found to have AIDS. The incidence of CMV esophagitis—along with that of other forms of infectious esophagitis—has declined among patients with AIDS since the widespread use of highly active antiretroviral therapy.  However, CMV esophagitis has increased among patients with solid organ transplants.  Delayed-onset disease is typical in this population because of increasing routine use of early CMV prophylaxis. 
On double-contrast esophagrams, CMV esophagitis is typically manifested by 1 or more giant and relatively flat ulcers, sometimes associated with small satellite ulcers (see the image below).
These ulcers may be ovoid, elongated, or diamond shaped, and they are frequently surrounded by a radiolucent rim of edematous mucosa. Less commonly, CMV esophagitis appears as small, superficial ulcers that are indistinguishable from the ulcers of herpes esophagitis on barium studies.
Because herpetic ulcers rarely become as large as those of infectious esophagitis, the presence of 1 or more giant ulcers suggests the possibility of CMV esophagitis in patients with AIDS.
However, giant esophageal ulcers can also be caused by HIV (see the HIV Esophagitis section, below). Moreover, CMV esophagitis cannot be reliably differentiated from HIV esophagitis on the basis of clinical and radiographic findings, so endoscopy is required for a definitive diagnosis before patients are treated.
Other causes of giant esophageal ulcers include the following:
Oral medications (including nonsteroidal anti-inflammatory drugs, potassium chloride, and quinidine)
Giant esophageal ulcers have been described in the esophagus in patients with AIDS in whom no other infectious etiology for the ulcers can be found. These ulcers have been termed idiopathic or HIV ulcers, because they are believed to be caused by HIV. In fact, results of electron microscopy confirm the presence of HIV-like viral particles in these lesions. Although some patients with HIV ulcers may have undergone recent seroconversion, most are found to have chronic AIDS and to have a CD4 count of less than 100 cells per cubic millimeter. HIV ulcers are more common than is generally recognized, accounting for as many as 40% of all esophageal ulcers in patients with AIDS. [6, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29]
Ulcers usually appear on double-contrast esophagrams as 1 or more giant, flat ulcers (>1 cm in diameter) of the esophagus (see the image below). This finding is sometimes associated with a cluster of small satellite ulcers. The ulcers are often surrounded by a radiolucent rim of edema.
As previously mentioned, most HIV ulcers are indistinguishable from CMV ulcers on the basis of clinical and radiographic criteria. Therefore, CMV esophagitis must be excluded by means of endoscopy before a diagnosis of HIV esophagitis can be established.
Tuberculosis esophagitis occurs primarily in patients with advanced pulmonary or mediastinal tuberculosis or in immunocompromised patients who have disseminated tuberculosis or another mycobacterial disease. The esophagus is usually involved by erosion of the involved mediastinal lymph nodes abutting the esophagus. Barium studies or computed tomography (CT) scans may reveal extrinsic compression or displacement of the esophagus due to enlarged collections of nodes in the adjacent mediastinum. In some patients, traction diverticula may develop in the upper esophagus or midesophagus.