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Infectious esophagitis is the third most common cause of esophagitis after gastroesophageal reflux disease and eosinophilic esophagitis (EoE) and should always be considered in the differential of patients with dysphagia and odynophagia. The most common organisms causing disease are candida, Herpes simplex virus (HSV) and cytomegalovirus (CMV). It is well recognized that an impaired local or systemic immune system is a risk factor for disease; however, esophageal dysmotility and disruptions in esophageal homeostasis and the esophageal milieu are likely to represent additional risk factors in disease pathogenesis., Competing Interests: The authors report no conflicts of interest., (Copyright © 2022 by European Society for European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition.)

Objectives: Herpes simplex virus (HSV) and cytomegalovirus (CMV) immunohistochemical stains (IHC) are frequently applied on esophageal biopsies. Our aims were to identify IHC use patterns in viral esophagitis (VE), and clinicopathologic features of VE that could guide IHC use., Methods: We included 58 VE cases and 60 controls, defined as patients with negative HSV/CMV IHC between January 2006 and July 2017. Biopsies were reviewed and histologic features and clinical data recorded., Results: Thirteen cases required IHC for diagnosis. IHC was performed in 13 HSV and 5 CMV cases where diagnostic viral inclusions were present. VE patients were more likely to have endoscopic ulcer (P=0.002) and be immunocompromised (P<0.001). Pretest clinical concern for VE was common (P=0.006). Histologically, VE patients were more likely to have ulcer (P=0.004), ulcer exudate rich in neutrophils and histiocytes (P=0.001), neutrophils in squamous mucosa (P<0.001), histiocyte aggregates >15 (P<0.001) and spongiosis (P<0.001). Controls had frequent eosinophils, alone (P=0.008) or admixed with other inflammatory cells (P<0.0001)., Conclusions: IHC is used in VE biopsies despite definite viral inclusions on hematoxylin and eosin and in patients without concerning histology or clinical concern for VE. History, endoscopic findings, and histology can be used to better target IHC use in VE., Competing Interests: The authors declare no conflict of interest., (Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.)

Competing Interests: Declaration if interests We declare no competing interests.

Abstract: Herpes simplex virus esophagitis is a rare and not readily recognized condition which is often seen in immunocompromised individuals. This case highlights the rare complication of herpes simplex virus in an otherwise healthy male infant who presented with a possible seizure after listlessness, fever, and black stools for 1 day. The decedent died shortly after arrival to the hospital emergency department, and a complete autopsy was performed, which was remarkable for upper gastrointestinal bleeding due to esophageal ulcers secondary to viral infection (herpes simplex virus type 1). To our knowledge, this is the first reported case in which herpes simplex virus esophagitis resulted in ulcerations that extended through the esophagus and involved the adjacent wall of the aorta with subsequent upper gastrointestinal bleeding leading to the death of an infant., Competing Interests: The authors report no conflict of interest., (Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.)

Background: Herpes esophagitis is uncommon disease caused by Herpes simplex virus (HSV). While the disease most often occurs in immunocompromised patients, including post-chemotherapy, immunosuppression with organ transplants, and in AIDS, Herpes esophagitis can also occur in immunocompetent individuals., Case Presentation: We report a case of herpes esophagitis in a 72 year- old woman who was presumed to be immunocompromised following prolonged radiotherapy and chemotherapy for lymphoma. Her main symptom was epigastric pain. Upper endoscopy showed multiple rounded ulcers in lower esophagus. The diagnosis was confirmed histologically by multiple biopsies. The patient received Valacyclovir for 2 weeks and started to get better within 3 days of treatment., Conclusion: Although there are few published cases of Herpes esophagitis disease in the medical literature, we recommend that this disease should be considered as one of the differential diagnoses when assessing immuno-compromised patients presenting with non-specific abdominal symptoms.

Background: Herpetic esophagitis (EH) usually affects those who are immunocompromised and is uncommon in immunocompetent patients. In these cases, EH may occasionally present as an acute and self-limited illness. Such cases are rare and only a few have beenreported and limited published reviews exist making the benefits of antiviral therapy in immunocompetent patients unknown., Case Presentation: We report four cases of young patients who presented dysphagia, odynophagia and epigastric pain. Endoscopic findings revealed lesions in the distal esophagus and histopathological changes compatible with herpes virus infection confirmed by viral DNA in every case. After treatment, every patient showed significant improvement and tolerated oral intake after discharge., Conclusions: In this publication, we present four immunocompetent patients with EH, without relevant alterations in laboratory workup and with negative HIV status. This disease is infrequent in patients with such characteristics and there are few cases published. In order to better understand this pathology, we present the symptoms, the endoscopic alterations and the clinical evolution with treatment. In our series, 50% of patients had serology compatible with acute HVS type 1 infection, 25% had a subacute infection pattern (IgM and IgG positive antibodies) and in another 25% of patients, serology was not done. No patient presented leukocyte alterations, while all patients presented with anatomopathological findings compatible with acute herpetic esophagitis and responded to acyclovir therapy.

Herpes simplex virus (HSV) is a common cause of infectious esophagitis. The aim of this retrospective study is to identify comorbid and predisposing conditions and sequelae of HSV esophagitis in immunocompetent children. We reviewed 16 cases of HSV esophagitis diagnosed from January 1982 to March 2016. Five patients were immunosuppressed, 11 were immunocompetent and included in the study. Three (27%) had no other significant medical history. Five patients (45%) had repeat biopsies following their HSV infection, which showed eosinophilic infiltrate consistent with current diagnostic criteria of eosinophilic esophagitis (EoE), one of whom had known EoE. Environmental allergies and/or asthma were present in 4 of 5 of these patients. Among the immunocompetent patients, EoE was a comorbidity in almost half, although biopsies at the time of HSV esophagitis did not show diagnostic features of EoE. Clinical follow-up is therefore warranted for immunocompetent children presenting with HSV esophagitis, particularly those with atopic conditions.

We report a renal allograft transplant recipient with esophageal tuberculosis (TB) coinfected with herpes simplex virus (HSV) and Candida. The patient presented with oropharyngeal candidiasis and was started on fluconazole. Upper gastrointestinal endoscopy showed whitish patches with mucosal ulcers in the esophagus. Histopathological examination confirmed TB and HSV infection. The patient recovered after antiviral, antifungal, and anti-tubercular therapy with reduction in immunosuppression. In a TB-endemic zone, TB can coexist with opportunistic infections in an immunocompromised host., (© 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

The clinical observation of the patient at the age of 56 years, with lesions of the esophagus by the herpes simplex virus has been presented. The patient complained of odynophagia and dysphagia. Treatment with proton pump inhibitors in outpatient stage was not effective. On endoscopic examination revealed multiple ulcers in all parts of the esophagus. Herpes simplex virus has been detected in biopsy specimens of esophageal mucosa by the PCR method. Treatment with acyclovir led to rapid and complete clinical recovery. Analysis of the literature allowed making the conclusion about the importance and actuality this demonstration.

Background/aims: We investigated the utility of using histological changes to diagnose infectious oesophagitis when causative organisms cannot be seen., Materials and Methods: Sixty-seven endoscopic biopsy specimens (51 Candida, 9 herpes simplex virus, 4 tuberculosis, and 3 cytomegalovirus oesophagitis) collected from 2000-2010 that matched the investigative criteria were included in the study. Cases were re-evaluated for histological changes observed in oesophagitis, and the findings were statistically compared using nonparametric tests., Results: Thirty-nine cases occurred in male patients, and 28 occurred in female patients; the mean age of the patients was 51±20.1 years (range, 5-94 years). All cases showed lymphocytic and neutrophilic infiltration; while 27 (40.3%) showed eosinophilic infiltration. The density of lymphocytes and eosinophils were 8.43±6 and 1.07±1.62 per high power field, respectively, and these rates were higher in tuberculosis oesophagitis cases. Lamina propria infiltration was present in herpes simplex virus and Candida oesophagitis. Dense neutrophilic infiltration (>50/high power field) was noted in herpes simplex virus oesophagitis. Candida colonization was observed in 82% of cases with eosinophilic infiltration, and 80% of cases with erosion. Ulceration was present in all tuberculosis oesophagitis cases (p<0.001). Basal cell hyperplasia, papillary elongation, and dilated intercellular spaces were seen in all cases except for 2 Candida oesophagitis cases. Lamina propria fibrosis was especially noted in cytomegalovirus oesophagitis cases., Conclusion: It is not possible to distinguish infectious oesophagitis from other subtypes, especially reflux oesophagitis, if the causative organism is not detected. Clinicopathological correlation and control with repeat targeted biopsies are essential for diagnosis.

Herpes esophagitis due to infection with herpes simplex virus typically occurs in immunocompromised patients such as those with human immunodeficiency virus, malignancy, and those undergoing immunosuppressive therapy. Albeit rare, herpes esophagitis can occur in immunocompetent patients as a primary infection. We present a case of herpes esophagitis after corticosteroid treatment for back pain including epidural steroid injections. Corticosteroids, especially local injections, are a common treatment for chronic back pain, but they are not without risk. Epidural steroid injections can have systemic effects, which may go unrecognized and underappreciated. Although local infections have been reported after administering these injections, systemic immune suppression may allow for unexpected infections such as herpes esophagitis. Given the widespread use of epidural steroid injections, physicians should reevaluate the potential for harm when considering this treatment.

Eosinophilic and herpetic esophagitis are listed as independent causes of dysphagia, especially in young adult males. However, herpetic esophagitis rarely affects immunocompetent individuals. We report the case of a young, not immunocompromised patient, admitted because of severe dysphagia secondary to herpes simplex virus esophagitis. After complete resolution, an endoscopic and histologic reevaluation established the diagnosis of eosinophilic esophagitis. The potential association between the two conditions is discussed.

Herpes simplex virus esophagitis has rarely been reported in immunocompetent children. We describe 2 immunocompetent wrestlers on the same team who presented with fever, odynophagia, and dysphagia. Histologic examination of the esophagus showed ulceration and exudate, herpes simplex virus was detected by polymerase chain reaction. We propose that wrestling may be a mode of transmission for this disease.

Herpes simplex virus is a common cause of ulcerative esophagitis in the immunocompromised or debilitated host. Despite a high prevalence of primary and recurrent Herpes simplex virus infection in the general population, Herpes simplex virus esophagitis (HSVE) appears to be rare in the immunocompetent host. We report three cases of endoscopically-diagnosed HSVE in apparently immunocompetent children; the presentation was characterized by acute onset of fever, odynophagia, and dysphagia. In two cases, the diagnosis was confirmed histologically by identification of herpes viral inclusions and culture of the virus in the presence of inflammation. The third case was considered to have probable HSVE based on the presence of typical cold sore on his lip, typical endoscopic finding, histopathological evidence of inflammation in esophageal biopsies and positive serologic evidence of acute Herpes simplex virus infection. Two cases received an intravenous course of acyclovir and one had self-limited recovery. All three cases had normal immunological workup and excellent health on long-term follow-up.

A 52-year-old woman with a 6-year history of systemic lupus erythematosus (SLE) developed acute abdominal pain, nausea, vomiting, and diarrhea accompanied by hypocomplementemia. Herpes simplex virus (HSV) esophagitis and lupus enteritis were diagnosed on the basis of the results of endoscopic and histological examinations and abdominal computed tomography (CT) findings. Treatment with acyclovir followed by high-dose intravenous steroids improved her symptoms. To our knowledge, this is the first case of simultaneous HSV esophagitis and lupus enteritis.

Concomitant herpetic and candidal esophagitis is a very rare disease that had not been reported in uremic patients. A 57-year-old woman receiving continuous ambulatory peritoneal dialysis (CAPD) therapy for 3 years was admitted due to CAPD-related peritonitis. Endoscopic examination was performed due to severe epigastralgia and upper gastrointestinal bleeding, and combined herpetic and candidal esophagitis was diagnosed. Intravenous acyclovir and fluconazole were prescribed and symptoms improved. The patient subsequently died due to progressive sepsis and respiratory failure. This is the first report of a dual infectious esophagitis in a uremic patient. Since infectious esophagitis may cause severe complications, early diagnosis and aggressive treatment are important.

Background and Aims: The aim of the present study was to clarify relationship between macroscopic and microscopic features of herpes simplex esophagitis (HSE), and localization of herpes simplex virus type 1 (HSV-1)-infected cells in esophageal lesions from autopsy cases of histopathologically proven HSE., Methods: The study comprised morphological, immunohistochemical, cultural and electron microscopic investigations for 24 HSE patients collected from 1307 serial autopsy cases in the past 10 years., Results: Macroscopic characteristics of HSE were divided into three types. Types I and II showed small punched-out lesions with and without raised margins, respectively. Type III revealed that multiple ulcers became confluent like a map. Microscopic findings showed that the HSV infection process seemed to begin in squamous epithelium and to induce vertical cellular change into the intact epithelial layer. Intranuclear inclusion bodies were observed at the centers of lesions, and ballooning changes of squamous cells at the margins. Both localization of HSV-1-infected cells and presence of HSV-1 in the esophageal lesions were confirmed with immunohistochemical staining, viral culture and electron microscopy., Conclusion: The present results suggest that the macroscopic and microscopic postmortem features of HSE may provide useful information for clinical diagnosis of HSE.

Infective esophagitis is a rare disease, affecting mostly immunocompromised patients. Very few cases of a multiple viral infection have been reported. We present a case of combined cytomegalovirus (CMV) and herpes simplex virus (HSV) esophagitis in an 81-year-old female with extracapillary sclerosing glomerulonephritis treated for five months with steroids and chemotherapy. She died of septic shock. At autopsy, erosive and ulcerative esophagitis was found in the distal half of the esophagus. Slides were stained by HE, and the immunohistochemical avidin-biotin method was used to detect HSV and CMV infection. On histological examination of the esophagus, epithelial giant cells with intranuclear viral inclusions showing HSV immunopositivity were found at the margin of the ulcerations. Giant cells with intranuclear inclusions with CMV immunopositivity were also found in the mesenchymal cells obtained from the ulcer bed. Long-term immunosuppressive therapy provoked an immune deficiency, evidenced by grave leukopenia and depletion of all bone marrow elements. Diagnosis of HSV and CMV esophagitis is important to evaluate the risk of hemorrhage and esophageal perforation in esophagitis.

Background: Establishing a diagnosis of viral esophagitis in patients with human immunodeficiency virus (HIV) infection has important clinical relevance. However, the number of biopsies required to diagnose viral esophagitis is currently unknown., Methods: Over a 34-month period, all HIV-infected patients with esophageal ulcer underwent 10 biopsies of the largest and/or most accessible lesion, primarily from the ulcer base. The first 3 specimens were placed in one formalin container, the second 3 in another, and 4 additional specimens in the third. Standard histopathologic methods were employed, as well as in situ hybridization or immunohistochemical studies in most patients, and viral cytopathic effect was defined using previously proposed criteria. Patients were then treated on the basis of the results of the initial biopsy specimens with both clinical and endoscopic follow-up., Results: One hundred HIV-infected patients with esophageal ulcer were studied. Cytomegalovirus (CMV) was considered etiologic in 50 patients. Of these 50 patients, the first three biopsy specimens were sufficient to diagnosis CMV in 40 (80%). In 5 patients (10%), the first two sets were negative with only the third set of biopsies positive. Similarly, of the 4 patients with simultaneous CMV and herpes simplex virus (HSV) esophagitis, three sets of biopsy specimens were required for diagnosis of both agents in 3 patients. HSV esophagitis alone was found in 2 patients; diagnostic viral inclusions were present in the first 3 biopsies in each patient. Thirty-five patients had HIV-associated idiopathic esophageal ulcer; only one of these patients was misdiagnosed., Conclusions: At least 10 biopsies may be required to exclude viral esophagitis in HIV-infected patients. If biopsy specimens are adequate and no evidence of viral cytopathic effect has been found, the patient may be treated on the basis of the results of the initial clinical, endoscopic, and pathologic findings with close clinical follow-up rather than repeat endoscopy.

Frequency of herpes simplex virus(HSV)-induced esophagitis was reported to range from 0.5% to 6% in non-selected patients according to autopsy and clinical studies. In case of gastrointestinal involvement, affinity of herpes simplex virus to squamous epithelia predisposes the esophagus to be affected. Typically, patients complain about acute onset of odynophagia, retrosternal pain, or symptoms of gastrointestinal blood loss, while systemic signs of inflammation are often absent. Endoscopic examination usually reveals disseminated, roundish mucosal defects with distinct borders preferably in the distal part of the esophagus. If suspected clinically and by endoscopy, a histological and/or cytological diagnosis should be achieved by carefully taking multiple biopsies from the edge of the suspicious lesions. Antiviral therapy is not obligatory, since HSV esophagitis often resolves spontaneously. In the presence of preexisting immunodeficiency, marked clinical symptoms, or complicated course, however, the guanosine analogue aciclovir is the treatment of choice. In view of a comparably low sensitivity of macroscopic assessment and an expected increase in incidence of this viral infection, a high index of suspicion for this disorder appears to be necessary for all clinicians working in the field of endoscopy. Based on 15 personal observations recorded from 1983 to 1995, epidemiological, pathogenetic, morphological, and clinical features of HSV esophagitis will be summarized and discussed in the light of the pending literature on this subject.

This paper describes five renal transplant recipients, out of a series of 221 consecutive patients, who developed herpes simplex esophagitis. This opportunistic infection presented as odyno- and/or dysphagia. It occurred during or shortly after treatment of acute cellular rejection episodes with high doses of steroids and, in four cases, of anti-lymphocyte globulins. The infection responded to acyclovir in all patients. We conclude from these observations that herpes esophagitis occurs during periods of intensive immunosuppression. Because its endoscopic manifestations are variable, biopsies and cultures are essential to reach the diagnosis. Prevention may be possible by avoiding transplantation from a seropositive donor to a negative recipient and by prophylactic oral acyclovir.

The unexpected diagnosis of herpetic esophagitis in a patient with nausea led us to review our experience with this disease. Review of our records from 1979 to 1989 produced 23 cases proven by endoscopic culture or microscopic examination (Cowdry-type A inclusions), the largest such series reported to date. Twenty-two of the 23 patients were immunocompromised. Odynophagia and chest pain were each present in half of the cases, but 26% of patients had neither. Gastrointestinal bleeding was attributable to herpetic esophagitis in 30%. Thirty percent of patients had disseminated herpes simplex infection and 70% had simultaneous infections with other organisms. Endoscopic findings included nonspecific inflammation, discrete ulcers, coalescent ulcers, and pseudomembranous esophagitis. Herpes virus was not suspected endoscopically as the cause of esophagitis in 30% of cases. Culture was slightly more sensitive than microscopic examination for diagnosis (89% vs. 76%), but both methods should be employed in any immunocompromised patient with esophagitis.

Herpetic esophagitis is an infrequent ulcerative infection of the esophagus caused by Herpes Virus type I. It is usually seen in immunocompromised patients though it may present in immunocompetent ones. Odynophagia and/or dysphagia associated with chest pain are the most frequent clinical symptoms. Radiology, endoscopy, biopsy and serological markers are the basis for diagnosis. We report 3 patients with herpetic esophagitis diagnosed between 1984-1989 and evaluated the clinical, endoscopic and biopsy characteristics. Certain clinical and endoscopic findings common to our patients tend to identify the disease, with biopsy and or serological markers the diagnosis may be established.

A patient is described with oesophageal ulceration due to herpes simplex virus type I. The endoscopic, light, electron microscopic, and immunohistochemical appearances are described and the literature of this under-diagnosed entity is reviewed.

Autopsy cases were reviewed in order to determine the incidence and underlying diseases of herpes esophagitis. Review of both autopsy records and the preserved viscera of 145 cases disclosed 9 cases (6%) of herpes esophagitis. Herpes simplex virus type I specific antigen was detected in all of these nine cases by immunohistochemical method. Eight of nine cases had malignant diseases. Review only of autopsy records of other 254 cases disclosed 5 cases (2%) of herpes esophagitis. Thus, herpes esophagitis is thought to be more common than has previously been appreciated and may be overlooked at autopsy. Although antemortem diagnosis of this condition has been very rare, clinicians should have an accurate knowledge of this disease because herpetic esophageal ulcer may act as a portal of entry for generalized dissemination of virus and other pathogens, and effective antiviral agents are becoming available.

Ultra-thin sections obtained from routine biopsy specimens and cytological smears of 3 cases, together with one autopsy case suggestive of herpes oesophagitis, clearly demonstrate herpes viruses. The infected epithelial cells reveal different stages of virus replication and propagation. Cowdry A type inclusion bodies, however, representing early alterations in the course of infection are less frequent. Ground-glass looking nuclei of light microscopical balloon cells and infected multinuclear giant cells of epithelial origin are characteristic changes of the late ulcerative stage of herpes oesophagitis usually seen at the time of detection. These typical virus induced cell changes are mostly to be found at the ulcers edge.

A case of relapsing ulcerative esophagitis presumably due to herpes virus infection in temporary association with two relapses of an idiopathic inflammatory bowel disease is reported.

A 20-year old white male developed a self-limited ulcerative esophagitis followed by a transient vesicular skin eruption due to infection by herpes simplex virus Type I (HSV-I). While herpetic esophagitis has been described previously, this case appears to be unique in that there was no concomitant serious delibitating illness or pharmacological immunosuppression. Herpes simplex Type I should be included in the differential diagnosis of unusual esophageal ulceration in otherwise healthy patients.

In two patients with non-specific lesions of oesophagitis, malpighian cells infected with type I herpes simplex virus were collected by brush cytology. The cytological appearance was typical of herpes infection. Within a specimen comprising many highly necrotic areas, giant multi-nucleated malpighian cells were seen, with marginate nuclear chromatin and characteristic inclusion bodies in the nuclei. The discovery of herpes lesions in the oesophagus raises important disease questions, both from the point of view of opportunistic infection and the development of cancer.

Herpes simplex virus may cause esophagitis, usually in patients with malignant neoplasms or immunocompromise. We have reported three cases of herpes simplex esophagitis in healthy young men, all of whom had positive mucosal biopsy culture for herpes simplex virus. All three patients recovered quickly without specific therapy.

Two cases of herpes simplex virus esophagitis diagnosed in vivo by cytologic examination and biopsy of the lesion are reported. The importance of and the criteria for the diagnosis of herpes esophagitis in vivo are discussed. An awareness by the clinician and pathologist of this lesion would probably result in a more frequent diagnosis of herpes esophagitis.