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Home , Esophageal candidiasis, Herpes esophagitis

REVIEW

Herpes : a comprehensive review

Thievvy Ginkreau ’, Flove Roxenbey’, Olivier Bouchaud”, Claudie Mavche4 and Olivier Lovtholary”

‘Service de Mkdecine Interne, La Salpgtri&re,Paris, ’Service de Bactkriologie-Virologie-Hygi&ie, H6pital Saint-Vincent-de-Paul, Paris, 3Service des Maladies Infectieuses et Tropicales, Groupe Hospitalier Bichat-Claude-Bernard, Paris, 4Service d’Anatomopathologie, Groupe Hospitalier Bichat- Claude-Bernard, Paris, and 5Service de MCdecine Interne, H6pital Avicenne, Universiti. Paris Nord, Bobigny, France

Key words: , esophagitis, immunodepression

INTRODU CTl ON POPULATIONS AT RISK

Herpes esophagitis (HE) was first described by Pearce Several types of have been and Uagradi in 1943 [I]. For 30 years the diagnoses described as risk factors for HE (Table l), but cellular were made in post niortern studies of immuno- iniinunity is the key factor for the control of herpes compromised patients 12-41. Then, the developement simplex infection, while the role of antibodies and of endoscopy allowed an earlier diagnosis [5,6]. complement is less important [I 6,171. Thus, patients HE is a well-known complication of imniuno- with quantitative defects of T-lymphocytes are particu- depression, and the is the viscus most often larly prone to develop HSV infections. Indeed, we involved during the dissemination of herpes simplex recently reported such a complication during the late virus (HSV) infection 171. HE is observed in up to 5% stages of HIV infection [18]. Qualitative defects of T- of patients treated for malignant hematologic diseases lymphocytes also represent a risk factor; this is parti- [8], 1-6% of solid organ transplant recipients [9,10] and cularly true for liver and renal transplant patients [19]. 10-1 5% of bone marrow-transplanted patients [ll]. Furthermore, cellular immunodepression favors the HE is also an AIDS-defining condition [12] and a presence of HSV in the saliva [ZO], which may be a frequent site of disseminated neonatal HSV infection potential source of esophageal infection during swallow- [13,14]. Interestingly, HE has also been anecdotically ing [7,21]. described in imniunocoinpetent patients, in whom it is Corticosteroids and anticancer are a self-limited illness [15]. We give here an extensive also well-known risk factors for visceral HSV infection review of HE, including its pathophysiology, clinical [7]. Indeed, corticosteroids are able to inhibit the manifestations, treatment and outcome. activation, proliferation, differentiation and functions of virtually all cells involved in the immune response, but particularly T-cell proliferation [22-241. Anti- cancer chemotherapy and radiotherapy have imniuno- suppressive effects but are also associated with the Corresponding author and reprint requests: loss of normal esophageal mucosal integrity, which 0. Lortholary, Service de Medecine Interne, enhances the risk of HSV reactivation [25]. HBpital Avicenne, Universite Paris Nord, Previous upper digestive tract endoscopy or 125 Route de Stalingrad, 93009 Bobigny, France insertion of gastric tube are reported in 33-7 1% of cases Tel: 33 1 48 95 54 51 Fax: 33 1 48 95 54 50 during the weeks before HE [4,7,18,26]. Nasogastric e-mail: [email protected] intubation may favor the development of HE by Accepted 12 March 1997 trauma and/or viral autoinoculation 17,271. However,

397 398 Clinical Microbiology and Infection, Volume 3 Number 4, August 1997

Table 1 Populations at risk for HE associated with an increased frequency of HSV reacti- vation, including HE [32]. Hematologic malignancies, with or without neutropenia [6-8,27,62,65,75,79,82,87,95,97,102,107.109,117,118] Solid tumors [3,7,27,57,62,65,68,78,87,88,97,102,107,116, during bone marrow transplantation 119,120] There is no significant difference in HE incidence Systemic or inflanimatory diseases [24]: systemic lupus between autologous and allografted bone marrow erytheniatosus [62,120,121], recipients [33].Prior to the prophylactic use of acyclovir, Wegener’s granulomatosis [7,62], polyarteritis nodosa [7], giant cell arteritis [27], rheumatoid arthritis [27,68.75,102], 80% of seropositive patients excreted HSV during the polymyositis [102], Crohn’s disease [7,62], ulcerative first SO days after bone marrow transplantation, with a [57], rapidly progressive glomerulonephritis [7], tuberculosis [2] peak excretion during the second or third week 1331. HIV infection [18,27,38-44,62,55,92,102,107,109,120] By contrast, fewer than 2% of seronegative patients Extensive burns (271-Recent trauma (71 excrete HSV after transplantation, suggesting that Alcoholism [102,120] Diabetes mellitus [27,57,102,120,122] HSV infection after transplantation is mostly due to Cystic fibrosis [lZO] reactivation [33,34]. During a prospective study of 44 Heart insufficiency [57] episodes of unexplained and vomiting after Renal insufficiency 1781 allogeneic bone marrow transplantation, Spencer et a1 Gastro-esophageal acid reflux [29,78,120] [31] documented HE in five cases occurring 1-4 Mental retardation [123] Iatrogenic factors months after transplantation. HSV infection was less Radiation therapy (particularly for mediastinal tumors) common than (CMV) infection in [6,27,75,87,102,119] two series [11,31], probably because of the frequent Solid organ transplantation-cyclosporin [ 19,Z7,62,107,124-127] use of prophylactic acyclovir. Among 39 bone marrow Bone marrow transplantation [80,95,102,109] transplant recipients, 21 had infectious esophagitis, Anti-CD3 monoclonal antibodies [32] Immunosuppressive agents: cyclophosphamide, azathioprine including six isolated HE cases and four co-infections [68,120] with CMV or sp. HE occurred mostly in non- Systemic steroid therapy [27,57,68,75,87,102,120,12 11 neutropenic patients within a mean of 72 days after Inhaled steroids [128] transplantation and earlier than fungal esophagitis [ 111. Recent surgery [129]-trigeminal nerve surgery [21] Surveillance cultures of the oropharynx obtained 1-7 days before the endoscopy were not useful in predicting the organism causing esophagitis [l 11. Three of six patients with HE died without resolution of their no definitive conclusion concerning its role in favoring esophagitis. The same authors reported postmortem HE can be drawn in the absence of case-control data showing evidence of esophageal infection in 25/59 studies in immunocompromised patients. Endotracheal patients, including six due to HSV [ll]. In the intubation and nasogastric tubes should be avoided in neutropenic population, herpetic ulcerations have been such patients in case of patent labial or buccal herpetic reported to be a portal of entry for various bacterial and infection [28]. Gastroesophageal reflux has also been fungal infections [35]. cited as a possible risk factor for HE [29]. Herpes esophagitis in AIDS patients Herpes esophagitis in solid organ transplant recipients [281 During HIV infection, HSV seroprevalence is 80-95% HSV reactivation is mostly observed during the first for type 1 and 20-30% for type 2 [36]. HIV and HSV- month post-transplantation, and HSV infections occur 1 enhance reciprocally their replication in macrophages within the first 2 months after transplantation [30]. In and keratinocytes [37]. During HIV-1 infection, HE a prospective study of infectious esophagitis following has been considered to be relatively uncommon and liver and renal transplantation, the authors discovered classically less frequent than esophagitis due to CMV HE in 3/47 liver transplants post-transplantation (6%) [38-401, in contrast to results reported in other studies and in 1/21 renal transplants post-transplantation (5%). [41-431. In HIV-1 patients, HE was the cause of4-16% These data showed a lower prevalence of HE than that of esophageal symptoms [38,39,41-431 and occurred in observed after marrow transplantation [11,31]. In the four out of 154 patients (2.5%) followed prospectively latter paper [31], no association between HE and [43]. We recently reported 34 AIDS patients with HE administration of prednisone or blood level of cyclo- [18]. In that paper, the mean CD4 cell count was sporin A was found. HE has also been reported after 15/mm3 and recent predisposing factors (nasogastric cardiac transplantation, but no clear data on the pre- procedures, steroid therapy, anticancer therapy) were valence were reported [lo]. Mter transplantation, the noted in 47% of patients. Only 15% of our patients use of anti-CD3 monoclonal antibodies has also been relapsed, most of them having an iatrogenic pre- Genereau et al: Herpes esophagitis 399 disposing factor (steroids, anticancer therapy). HE has mented in adults, and does not represent a significant also been reported during HIV primary infection [44]. route of viral replication. However, viremia occurs in neonates infected at birth with HSV-2 [69], and has Herpes esophagitis during disseminated neonatal HSV been reported in HSV-1-infected children receiving infection immunosuppressive therapy [70]. Therefore, esophageal In neonates, the esophagus is frequently involved in infection is most often secondary to a viral recurrence, the dissemination of HSV infection 1141. The exact most of the time by regional extension of buccal or prevalence has not been precisely described, but histo- pulmonary localization 1711. It is now well established logic changes consistent with HE were demonstrated that after infection of the oral epithelium, viral particles in up to 75% of fatal cases [45]. In the absence of skin are taken up by the peripheral nerve endings of sensory vesicles (20%), the clinical signs of disseminated HSV neurons that innervate the primary site of infection, infection are often non-specific, mimicking those of and are transported by retroaxonal axoplasniic flow to neonatal bacterial sepsis 1141. HE by itself may be the neuronal bodies, located in the sensory ganglia. responsible for feeding difficulties, deglution disorders, Latent virus has been detected in the nodose ganglia hypersalivation, glottic edema and vomiting 1461. innervating the [72]. Experimental niurine models have clearly shown that oral HSV-1 Herpes esophagitis in immunocompetent patients inoculation in the esophageal lumen leads to latency in HE may occur in immunocompetent patients [15,29, the sensory ganglion of the tenth cranial nerve [73]. 47-68]. I11 such cases, HE is similar to that occurring Furthermore, HSV-1 was shown to spread considerably in ininiunocomproniised patients, but is rarely diffuse through all levels of the enteric nervous system, infect- and necrotic [55]. It spontaneously disappears within a ing niucosal nerve fibers directly in contact with the few days or weeks, but esophageal recurrence has been epithelium 1741. These findings might explain why described [55]. Because HE occurring in immuno- HSV is a frequent cause of recurrent competent patients may be paucisymptomatic, it is in humans. probably underdiagnosed 155,601. The respective roles of HSV-1 and HSV-2, primary infection and recurrence, and the main mechanisms explaining the esophageal localization, are summarized PATHOGENIC MECHANISMS OF ESOPHAGEAL in Table 2. In adults, HE is niostly caused by HSV-1 INVOLVEMENT [15,55,57,75], but HSV-2 may also seldom be incrimi- nated [ 761. The factors that determine HSV-1 virulence in humans are not known, although experimental models have CLINICAL FEATURES helped in deciphering host genetic and immune factors, as well as viral genes conferring increased HE symptomatology is protean [62]. Major symptoms virulence. Herpes simplex viremia has not been docu- are and esophageal pain. The main clinical

Table 2 Pathophysiology of herpes esophagitis

Main Mcchanisiiis of pathogenic e~ophageal Populatioii Virus mechanism localization

Neonates [14] HSV-2 Primary infection Vireniia Multi-organ extension IIniiiunocoiiipetent children and adults HSV-1 Primary infection Regional extemion Iinniuiioc-oiiipromised patients [I 1 I] Hematologic malignancies or solid organ transplantation HSV-la Kecurrence" Regional extension Multi-organ extciision AIDS 1181 HSV-la Recurrence Regional extension

'HSV-2 anecdotally hMay occationally be a primary infection, transmitted by direct person-to-person contact or via the allograft [I 301 400 Clinical Microbiology and Infection, Volume 3 Number 4, August 1997 symptoms reported during large series of HE [18, empirical systemic anticandidiasis treatment, as recently 62,771 are mentioned in Table 3. Chest pain or upper proposed for AIDS patients [90]. digestive tract hemorrhage may reveal HE [78,79], the The classic predominance of lesions in the lower latter being reported in 11-25% of the cases [18,62]. half of the esophagus in inimunocompromised patients Chronic is rarely described during HE [18,80]. [75] was confirmed in AIDS patients [18]; indeed, the Postmortem and endoscopic series clearly denion- lower third was affected in 50% of the cases, the median strated that HE may be asymptomatic [3,4,18]. Ulcer- third in 12% and the upper third in only one case. In ative oropharyngeal mucosal lesions are inconstantly one-third of these cases, lesions were spread throughout present (12-38% of cases) [18,77] but may contribute the entire esophagus. to the diagnosis in patients with esophageal symptoms. The most typical macroscopic appearance is only Therefore, the absence of mucocutaneous herpes does seen during early HE, with vesicles and/or volcano not in any way rule out the diagnosis of HE. HE may ulcers whose size varies from a few millimeters up to be associated with other HSV visceral localizations in 2 cni. Later in the evolution, they may coalesce, and patients with hematologic malignancies 171, in neonates the mucosa becomes friable with diffuse erosions [7,62] and in patients who have undergone solid organ and/or superficial potentially hemorrhagic ulcers [l 1, transplantation [81], but, interestingly, not in AIDS 62,75,77]. [18l. Diffuse superficial ulcers encountered in the majority of HE cases help to distinguish HE from RADIOLOGY CMV, which causes deeper ulcerations [87,91]. Non- ulcerated erytheniatous esophagitis is nonetheless Barium esophagography should include simple and possible but rare; it was found in 9% of our AIDS double contrasted films [65,82,83]. Small ulcerations patients [ 181. The presence of pseudomembranes which predominate in the distal part of the esophagus without esophageal , and bullous esophagitis, are the most typical radiologic features [65,84-861. has also been described with HSV [11,18,62]. Anec- However, radiologic aspects are often less specific dotically, ulcerated exophytic stenosis [18], tracheo- [27,55,87]. Indeed, large ulcers indistinguishable from esophageal fistula 1921, spontaneous esophageal per- those observed in fungal esophagitis have also been foration [93] and aspects mimicking a lye burn in a reported [86,88]. child [61] have been reported in isolated case reports. Margins of esophageal ulcers and islands of ENDOSCOPY squamous epithelium have to be biopsied and brushed [77,94]. Indeed, of the ulcer’s base are usually Since confirmation of diagnosis is obtained by histology non-diagnostic [77]. Interestingly, HE may be un- or culture of esophageal specimens, endoscopic exami- suspected eiidoscopically in several patients [ 18,771, nation must be carried out [55,87,89]. It can be done confirming the need for biopsies and brushing in first when a patient complains of suggestive inimunocompromised patients with esophageal synip- of ulcerated esophageal lesions, or after the failure of an toms [62]. The association of HE with herpetic

Table 3 Clinical symptoms of herpes esophagitis

GCnCreau [ 181 McBane 1621 Baehr [771 (n=34) (n=23) (n=48)

Underlying AIDS (100) Malignancies (52) Inimunodepression (100) conditions (96) Innnunodepression (48) Dysphagia 84% 52% 79% Odynophagia 7 2% 52% 79% Chest pain 72% 56% Fever 39% 35% 4% Extraesophdgeal herpes 33% 35% 29% Nausea/vomiting 30% 39% 15% Digestive hemorrhage 9% 34% Hypersalivation 6% Chronic hiccups 3% Asymptomatic 6%) 0% Genereau et al: Herpes esophagitis 40 1

is rare [95], as viral ulcers are most often located only Histolog allowed a definitive diagnosis in 40-67‘%1 of in the Malphigian epithelium and thus above the the cases [11,18,94]. esophagogastric junction. Iiiiiiiunohistocheniistry [09,103], immunofluor- In iiiirnunoconiproniised patients, HE may be escence [104], in situ hybridization (ISH) 1103, 1051, associated with various opportunistic diseases such as or in situ polynierase chain reaction may be warranted candidiasis, CMV and Kaposi’s sarconia [18,57,62,87]. when the herpetic nature of ulcerated esophagitis has Finally, HE can disappear with fibrous scarring and not been demonstrated by standard techniques [ 1031. subsequent esophageal stenosis that may necessitate ISH (using biotinylated .probes) and immunohisto- dilatation [ 13I. cheiiiistry are used to rapidly detect viral nucleic acids in formalin-fixed, paraffin-embedded tissues [ 1031. These two methods appear equally effective for the HISTOLOGY diagnosis of HE, and their results are better correlated with the presence of viral inclusions than with culture Brush cytology is very useful for HE diagnosis 196-981, results [103]. ISH stains are more difficult to inter- and niay also help in the diagnosis of esophageal pret; thus immunohistocheniistry, which is also less candidiasis [97]. Cytologic preparations have better expensive than ISH, may be preferable for routine cell preservation, and inay provide a more definitive clinical practice work [103]. Furthermore, the presence diagnosis [97]. The most typical cytologic aspects are of the HSV genome within a cell without viral ground-glass nuclei and inultinuclear giant cells [96]. inclusions or iiiiniuriohistoclieiiiical or histologic Brushing allows the sampling of larger areas than changes should be interpreted with caution [I Oh]. biopsies 1971, and was sometimes reported to be more Iminunohistocheniistry results may disclose granular to useful than histology [87], with a definitive diagnosis in homogeneous reaction product within the nuclei and 20-100%1 of cases. the cytoplasm of squamous cells infected by HSV 1991. Histologic studies should be performed on The normal esophageal squanious epithelium at some formaldehyde-fixed, paraffin-embedded samples distance from the ulcer, as well as inflammatory and stained with hematoxylin-eosin and Gienisa. Grocott’s niesenchynial cells, does not stain with anti-HSV 1991. methenaiiiine silver and periodic acid-Schiff are neces- In some cases, histologic and ultrastructural studies sary to eliminate the diagnosis of fungal esophagitis. may disclose mixed viral and fungal esophageal infect- Typical HE pathologic changes are mostly found only ions [loo]. at the edge of ulcers [99]. Characteristic histopathologic aspects found by VIROLOGY light microscopy include ballooning degeneration, ground-glass nuclei with marginated chromatin and The most sensitive and specific diagnostic niethod for eosinophilic nuclear inclusions (Cowdry type A confirming HSV infection remains isolation of the inclusions) of squamous epithelial cells as well as virus from tissue cultures [10,81]. Indeed, it allowed a niultinuclear giant cells [99]. Typical Cowdry A in- definitive diagnosis in 70-100% of the cases [l 1,18, clusions are rarely encountered when samples are riot 62,941. Specimens must be transported to the labora- fixed in Zencker’s acetic acid or Bouin’s solution [99]. tory in virus-stabilizing media [81] and cultured by By electron microscopy, they appear to be para- inoculation onto human embryonic lung fibroblasts or crystalline viral structures [94,100,101]. Giant cells and rabbit kidney cells. are identified by typical sinall coniplexes of squamous cells are niostly seen on cytopathic changes, in most samples within 48-96 h the epithelial border of the ulcer [99]. after inoculation. HSV can be identified rapidly by lntranuclear inclusions cannot differentiate between imiiiunohistochemical staining of a centrifuged culture HSV and varicella-zoster infections, but in the absence suspension after 24-36 h [77]. Virus isolation also of disseminated pox, these inclusions are highly allows subtyping, gene sequence mapping and antiviral suggestive of HE [97]. Ground-glass nuclei can also be sensitivity testing [81]. observed during CMV esophagitis; however, during the latter they also involve mesenchymal and glandular DIAGNOSTIC STRATEGY epithelial cells [99]. The floor of the ulcer contains inflammatory cells, fibrin and necrotic debris 1991. The diagnostic evaluation of an initnunodepressed When typical herpetic changes are not seen, aggregates patient with esophageal symptoms should involve both of large mononuclear cells (mostly CDh8-positive histology and viral esophageal cultures, whose conibina- macrophages and activated T-cells) [lo21 with con- tion gives the better diagnostic value. However, the voluted nuclei are also characteristic of HE [102]. exact sensitivity and specificity of all these methods are 402 Clinical Microbiology and Infection, Volume 3 Number 4, August 1997

Table 4 Major differential diagnoses of herpes esophagitis odynophagia and vomiting. Intravenous administration (15 mg/kg/day or 250 mg/m2/day) is usually rapidly Esophageal infections [77,131] Common infections effective in solid organ transplant recipients [28], Caridida albicanr [91,132] AIDS patients [18] or marrow transplant recipients Cytomegalovirus [91,132-1341 [33].In immunodepressed patients, treatment failure Uncommon infections may be explained by esophageal co-infections or other Human virus [135-1371 esophageal disease [18,31]. Epstein-Barr virus [138] Herpes zoster [139] Some HE may be due to acyclovir-resistant viral Papilloma virus [14OJ strains [109,110], more frequently in patients who have Mycobacterium tnberrulosis [141-1431 been repeatedly exposed to this drug [lll]. Such cases M. avium intracellulare complex [43] should be treated with foscarnet [112], which is Bacteria from the oral flora (1441 superior to vidarabine for acyclovir-resistant muco- Nocardia asteroidex [145] Eeponema pallidm (tertiary syphilis) [1461 cutaneous herpes infections in AIDS [113]. Helicobacter pylori [ 1471 Primary prophylactic acyclovir treatment can be sp. [148] considered in high-risk immunodepressed patients, but Histoplasma capsztlatum [149] not in AIDS patients. Indeed, when given 3 days before Tomloppsis Qlabrata [15O] bone marrow transplantation, it prevented HSV Cryptosporidium [151] Pnenmocystir rarinii [152] reactivation and reduced the incidence of HSV Leishmania donovani [153] infections from 50-80% to less than 10% [114,115]. AIDS-related idiopathic ulcers 1154,1551 In AIDS, HE recurrences are uncommon [18] and Malignancies suppressive therapy should not be systematically pre- Kaposi’s sarcoma [91] scribed. However, in cases of frequent or severe Malignant lymphoma [91] Carcinoma-sarcoma recurrences, a preventive regimen (600-1000 mg in Peptic esophagitis 3-5 divided oral doses per day) may be administered Medications [156] [116]. Common: tetracyclines, potassium, quinidine, aspirin and non-steroidal anti-inflammatory drugs Uncommon: zidovudine [157], iron, clindamycin, captopril, CONCLUSION theophyllin, ascorbic acid, alendronate [I581 HE is common in immunocompromised patients and should be systematically suspected in cases of odyno- phagia, chest pain, unexplained nausea or upper digestive tract bleeding. Most of the time, HE results still questionable, as they have not been studied with from HSV-1 reactivation and the regional extension of adequate methodology. As all of the above described an oral or pulmonary infection. Diagnosis is suggested diagnostic methods may be falsely negative, suspected through endoscopy, which usually displays ulcerated HE may be finally confirmed by the efficacy of the esophagitis predominantly in the lower third. The acyclovir therapeutic test [18,107]. combination of brush cytology, histology and viral Finally, it has to be noted that the detection of anti- cultures allows the best diagnostic sensitivity. Empirical HSV antibodies does not have any clinical utility for the acyclovir treatment also allows a presumptive diagnosis diagnosis of HE in immunocompromised individuals when it is rapidly effective. Finally, HE most often [108]. Major differential diagnoses of HE are described presents as a benign condition when it is diagnosed in Table 4. early and treated.

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