Viral infections

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HSV and CMV are the most common viral agents involved in infectious esophagitis, although some cases have been ascribed to HIV infection of the esophagus. HSV (HSV I or, rarely, HSV II) esophagitis causes a self-limited disease in normal subjects, but it can be severe and prolonged in the compromised patients.

Table 3.3 Drugs for esophageal candidiasis





Ketoconazole (<80%)

7-14 days

5-10 mg/kg/per day

Liver disorders can occur during therapy. The occurrence of liver disorders while on ketoconazole could be fatal unless properly recognized. Liver function tests should be performed before treatment, after 2 weeks and at periodic intervals during treatment in patients who are expected to be on prolonged therapy

Fluconazole (>80%)

7-14 days

3 mg/kg/per day for superficial infections; 6-12 mg/kg/per day for systemic infections

Nausea, vomiting, diarrhea and allergic reactions are most common adverse events. May cause clinical hepatitis, cholestasis and fulminant hepatic failure with underlying clinical conditions (e.g. AIDS, malignancy)

Itraconazole (approximately


7-14 days

3-5 mg/kg/per day

Caution in liver insufficiencies; nausea, vomiting, diarrhea and abdominal discomfort may occur; high doses may produce hypertension, hypokalemia or edema

Amphotericin B


7 days

0.3-1.5 mg/kg/per day i.v. infused in 5% dextrose over 2-4 h

Infusion-related toxicity includes acute reactions occurring about 30-45 min after starting infusion; typically chills, fever and tachypnea may present; patients receiving any parenteral form of the drug must be monitored for renal and liver functions; normochromic normocytic anemia may develop, usually after 7-10 days of therapy

Amphotericin B, lipid formulations


7 days

ABLC (amphotericin B lipid complex): 5 mg/kg/per day i.v. for 1-2 h; ABCD (amphotericin B colloidal dispersion): 3-6 mg/kg/per day i.v. for 1-2 h; L-AMB (liposomal amphotericin B): 1-7 mg/kg per day i.v. for 1-2 h

Novel lipid formulations of amphotericin B delivering higher concentrations of the drug with a theoretical increase in the therapeutic potential and decreased nephrotoxicity

HSV esophagitis occurs as a primary infection or as a reactivation of previously latent HSV, especially in the compromised patient. It is particularly common in patients receiving immunosuppres-sion for solid organ or bone marrow transplantation,19 whereas it is infrequently reported in HIV-infected patients.4 HSV generally infects the squamous epithelium, where the earliest lesion is a vesicle. As vesicles enlarge and ulcerate, they tend to form larger lesions with a characteristic central ulceration and raised edges.

HSV esophagitis usually presents with a sudden onset of severe odynophagia, with inability to swallow liquids or solids. Herpes labialis and herpetic oropharyngeal ulcers can occur during the esophageal infection, whereas skin lesions are rarely present.20

A definite diagnosis of HSV esophagitis requires endoscopy and histology of the esophageal mucosa, even though contrast radiographic appearance of the esophagus may be suggestive by showing multiple vesicles and ulcers as stellate or volcano structures. Endoscopy usually reveals small, well-circumscribed ulcers (Figure 3.3), rarely vesicles, whereas deep ulcers, as seen with CMV, are rare.21,22 Brushing or biopsies should be taken from the edge or periphery of ulcerations, given that HSV infects squamous epithelial cells.23 Histology reveals intranuclear Cowdry type A inclusion bodies (eosinophilic material), ballooning degeneration cells, multinucleated giant cells, ground-glass-like nuclei and margination of chro-matin.24 Confirmation may require immunoperox-idase staining or positive viral culture.

Although HSV esophagitis has a spontaneous resolution in a normal host, antiviral therapy is commonly used both in immunocompetent and immunocompromised subjects. Several uncontrolled trials and clinical experience indicate the efficacy of acyclovir, a nucleoside analog, for the treatment of HSV esophagitis.25 Parenteral acyclovir should be initiated until the patient can be converted to oral therapy (when dysphagia or odynophagia is resolved). Generally, patients are treated with acyclovir for 7-10 days. Because resistance to acyclovir has been reported, therapy with foscarnet should be considered in case of clinical failure with acyclovir.25 Acyclovir is efficacious in prophylaxis for patients undergoing transplantation and those who are HSV-antibody-positive. Table 3.4 lists the available antiviral agents for treating viral esophagitis.

CMV is the most frequent infectious complication of organ transplantation, occurring in 60-70% of these patients. Esophagitis is one of the most common manifestations in this setting. CMV is by far the most frequent cause of esophageal ulcer in patients with advanced HIV infection and a CD4 count lower than 100mm3 (see reference 26). In contrast to HSV esophagitis, CMV esophagitis has rarely been detected in an immunocompetent host;27 however, CMV and HSV are equally common organisms in transplant patients who do not receive antiviral prophylaxis.28 Odynophagia is a constant feature and is typically severe; chest pain of esophageal origin, mainly occurring upon deglutition, is also described. Prior or co-existent

Hsv Esophageal Ulcers
Figure 3.3 Herpes simplex virus esophagitis. Small, well-circumscribed ulcers (short arrows) and two small vesicles (long arrows) in the lower third of the esophageal mucosa.

CMV infection in other regions (e.g. retinitis, colitis) is not uncommonly found.29

As with HSV, a definite diagnosis of CMV esophagitis requires endoscopy and biopsy. Contrast X-ray examination of the esophagus reveals either focal or diffuse images of mucosal ulcerations. Ulcers may be vertical or linear with central umbilication, or may be diffuse and super-ficial;30 they are usually deep and large in patients with advanced HIV infection. Endoscopy remains the definitive diagnostic tool for CMV esophagitis. The endoscopic appearance is variable and may include multiple shallow ulcers, solitary ulcers or diffuse superficial esophagitis (Figure 3.4). In contrast to Candida and HSV, brushing cytology has a poor sensitivity and multiple biopsies should be taken. Since the cytopathic effect of CMV occurs at the level of endothelial and mesenchy-mal cells in the granulation tissue, endoscopic biopsies must be taken from the base of the ulcer.31 Histology typically shows large cells with intranuclear and intracytoplasmic inclusions having an eosinophilic appearance. Immunohistochemical stains can reveal more infected cells than routinely appreciated with hematoxylin and eosin staining. Mucosal biopsy is also more specific than viral culture as with other esophageal infections.32

The drugs available for treating CMV disease include ganciclovir, an acyclovir derivative, foscarnet and cidofovir. CMV esophagitis responds clinically and endoscopically to ganciclovir in approximately 75-80% of patients (Table 3.4).29 Duration of treatment should be based on clinical and endoscopic variables, but there is wide agreement that a 2-4-week period is usually effective. Oral ganciclovir is not effective for treating active infection, owing to its low bioavailability (< 10%).33 If an acute CMV infection occurs in transplant patients, ganciclovir should be given for about 1-2 months, until immunosuppressive drugs are reduced or discontinued. In patients receiving a protracted course of therapy, clinical and virological resistance to ganciclovir may occur.34 In this condition foscarnet, a pyrophosphate analog inhibiting DNA polymerase and reverse transcriptase, is usually effective.35 The relapse rate of CMV esophagitis in HIV-infected patients is approximately 50%,29 but long-term ganciclovir maintenance therapy is not routinely recommended unless there is a co-existent retini-tis.33

Ganciclovir and high-dose acyclovir have been used with moderate success for the prophylaxis of CMV infection in transplant patients. However, in

Cmv Ulcers
Figure 3.4 Cytomegalovirus esophagitis. A round, solitary deep ulcer is evident in the distal esophageal mucosa (arrow).

this setting ganciclovir prophylaxis is limited to high-risk patients, i.e. CMV-seropositive patients, CMV-seronegative patients receiving CMV-seropositive organ or blood products, and patients treated with immunosuppressive drugs because of episodes of rejection.36

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