Fungal infections

Candida species are the most common agents of infectious esophagitis. Candida albicans is the most common pathogen, but C. tropicalis, C. parapsilosis and C. glabrata have occasionally been reported. These organisms are usually

Table 3.1 Causes of esophageal disease in HIV infection and AIDS

Common

Uncommon

Rare

Candida

Herpes simplex virus

Neoplasm

Cytomegalovirus

Gastroesophageal reflux disease

Mycobacteria

Idiopathic

Protozoa

present in the normal oral flora, where their growth is controlled by commensal organisms. Conditions predisposing to esophageal candidiasis in immunocompetent subjects are inhaled or ingested corticosteroids, prolonged antibiotic administration, acid suppressive therapy, disorders of esophageal motility, malnutrition, diabetes mellitus and neck or head radiotherapy because of malignancy. All abnormalities in cellular immunity lead to esophageal candidiasis, whereas improved management of immunosuppressive therapies and antifungal prophylaxis have reduced the occurrence of esophageal candidiasis in solid-organ transplant recipients.7

Esophageal candidiasis has the classical appearance of white or yellow plaques coating the esophageal mucosa (Figure 3.1). These plaques can extend up to the proximal esophagus, are usually thick and, characteristically, cannot be washed or brushed off, unlike food or milk residues overlying esophageal mucosa. They include desquamated esophageal epithelial cells intermingled with inflammatory cells, bacteria and mycelia and spores typical for Candida.8 The underlying squa-mous esophageal epithelium usually appears uninvolved, and ulcerations occur rarely.

Typical symptoms of esophageal candidiasis are painful swallowing (odynophagia) or dysphagia (difficulty in swallowing, described as food 'sticking') (Table 3.2).3,9 Any patient with risk factors for esophageal infection and complaining of dys-phagia should be suspected for esophageal candidiasis. The latter, however, can be detected by chance in asymptomatic subjects. When evaluating patients with esophageal complaints, an important part of the physical examination is a close inspection of the oropharynx. However, oral candidiasis is not predictive of esophageal involvement and the latter can occur in the absence of oral candidiasis even in the immunocompromised

Esophageal Burns With Alkaline
Figure 3.1 Esophageal candidiasis. White plaques coating the lower third of the esophageal mucosa.

subject. Complications from esophageal candidia-sis occur rarely. Hematemesis suggests underlying ulcerative esophagitis that occurs if the disease is severe and there is an associated coagulopathy.

Given that esophageal candidiasis is the most common of opportunistic infections of the esophagus in subjects with a predisposing condition (e.g. HIV infection, transplantation, immunosuppressive therapy), an empirical antifungal therapy has been proposed, with further diagnostic evaluation based on the clinical response (Figure 3.2). Interestingly, a prospective study comparing empirical fluconazole to endoscopy in HIV-infected adults has shown empirical fluconazole to be the best initial management strategy.3 Candida esophagitis usually responds rapidly to fluconazole.10

Before the advent of upper endoscopy, a barium esophagram was used as the initial diagnostic tool. However, a number of studies have shown the rela-

Table 3.2 Symptoms and clinical signs

in patients with esophageal infection

Candida

Viruses

Bacteria

Parasites

Dysphagia

tttt

t

t

t

Odynophagia

tt

tttt

ttt

tt

Heartburn

t

t

t

t

Chest pain

t

ttt

tt

t

Fever

-

t

ttt

-

Hematemesis

t

tt

t

t

(-), Not occurring; (+), rare; (++), occasional; (+++), common; (++++), always

present

Immunocompromised subject

Upper gastrointestinal endoscopy i

Biopsies

Pathogen identified and specific treatment given

Dysphagia or

odynophagia, chest pain

¿_

_w

Upper gastrointestinal endoscopy and biopsy

Pathogen identified and specific treatment given

Upper gastrointestinal endoscopy and biopsy

Refine diagnostic work-up and physical examination systemic symptoms no systemic symptoms

Consider empiric treatment (systemic fluconazole for 10-14 days)

no symptom improvement improvement of symptoms

Follow-up program: recurrent problems after therapy; therapy to correct immunosuppression

Figure 3.2 Algorithm for management of infectious esophagitis.

tive insensitivity and non-specificity of barium studies for evaluating esophageal mucosa infection. Commonly reported X-ray features in patients with esophageal candidiasis are plaque-like lesions in a linear configuration that, when severe, become confluent; a 'shaggy' aspect of the esophagus ensues.11,12 However, a normal barium esophagram does not exclude esophageal candidiasis. It should be remarked that a well-circumscribed ulceration should not indicate Candida infection of the esophagus.

Non-invasive methods to diagnose esophageal infections without endoscopy are cytology brush and balloon devices. The latter consists of a tube with a ridged cytology balloon on the distal end: when inflated, it can be withdrawn from the esophagus and the brushings removed and submitted for cytological evaluation as well as viral culture. Whereas these methods are useful to identify Candida, they are less sensitive for viral disease and have no real advantage over empirical antifungal therapy.13

Endoscopy with biopsy is the gold standard for diagnosing esophageal candidiasis because mucosal biopsies can be performed. Despite the fact that gross endoscopic features can suggest a diagnosis of esophageal candidiasis, this is confirmed by the presence of hyphae in biopsies. Cytological specimens, which can be obtained at the time of endoscopy, are also a sensitive tool for the diagnosis, especially when organisms are washed off the tissue surface in mild superficial candidiasis after processing of bioptic specimens. When endoscopy is performed in patients with esophageal candidiasis, removal of plaque material by scraping with the endoscope is important to evaluate the underlying mucosa for ulcers.6 In general, Candida should not be considered a cause of esophageal ulcers in HIV-infected patients.

Both oral and intravenous drugs are available for treating esophageal candidiasis. Oral medications are generally administered first, whereas intravenous therapy is reserved for refractory cases or when oral administration is contraindicated. Non-systemic locally acting agents such as nystatin or clotrimazole are not very effective and must be reserved for the treatment of oropharyngeal disease. In patients with mild disease, with minimal or reversible immunodeficiency, a short course of therapy with a systemically absorbed agent can be given, whereas in patients with HIV infection or with transplantation immunodeficiency, longer courses of azoles are best given. Patients with granulocytopenia, at risk for systemic Candida infection, require the use of systemically acting intravenous agents such as azoles or amphotericin B. All available oral agents (ketoconazole, fluconazole and itraconazole) are efficacious for the treatment of esophageal candidiasis (Table 3.3). Ketoconazole and itracona-zole should be avoided in patients requiring anti-

acid therapy, as an alkaline pH limits their bioavailability. Fluconazole appears to be more efficacious than itraconazole; a poor response to fluconazole suggests non-compliance, drug resistance or other causes for esophageal symptoms.14 Randomized trials suggest that fluconazole is significantly more effective for the treatment of esophageal candidiasis in HIV-infected patients than ketoconazole and itraconazole.14 Fluconazole is available in oral and intravenous preparations, is minimally metabolized, is highly water soluble and is slightly protein bound. The new oral suspension formulations of fluconazole and itra-conazole may have superior efficacy over pills due to an additional local antifungal effect and improved absorption.15 The adverse effects of keto-conazole, fluconazole and itraconazole are dose dependent and include nausea, hepatotoxicity, inhibition of steroid production and cyclosporin metabolism.16 The latter effect is more pronounced with ketoconazole.17 Minor increases in amino-transferases are commonly found in patients treated with oral azoles and do not require drug discontinuation.

Amphotericin B represents the other family of antifungal agents (polyene antibiotics), which bind irreversibly to sterol in fungal cell membranes, causing cell death. This drug has a limited use for the treatment of esophageal candidiasis, owing to its severe side-effects (nephro- and hepatotoxic-ity). This drug is now available in an oral formulation. Patients with esophageal candidiasis that is resistant to treatment with fluconazole or other azoles can be treated effectively with lower doses of intravenous amphotericin B.

The prophylaxis of esophageal candidiasis in malignancy and transplant patients has yielded controversial results.18

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