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Year : 2011  |  Volume : 54  |  Issue : 1  |  Page : 219-220
Esophageal ulcer in a HIV-seropositive patient co-infected by herpes simplex and cytomegalovirus

1 Department of Pathology, Melaka Manipal Medical College (Manipal campus), Manipal University, Karnataka, India
2 Department of Gastroenterology, Kasturba Hospital, Manipal, Karnataka, India

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Date of Web Publication7-Mar-2011

How to cite this article:
Srilatha P S, Suvarna N, Gupta A, Bhat G. Esophageal ulcer in a HIV-seropositive patient co-infected by herpes simplex and cytomegalovirus. Indian J Pathol Microbiol 2011;54:219-20

How to cite this URL:
Srilatha P S, Suvarna N, Gupta A, Bhat G. Esophageal ulcer in a HIV-seropositive patient co-infected by herpes simplex and cytomegalovirus. Indian J Pathol Microbiol [serial online] 2011 [cited 2022 Aug 11];54:219-20. Available from: https://www.ijpmonline.org/text.asp?2011/54/1/219/77420

A 38-year-old married male, known human immunodeficiency virus (HIV)-seropositive, presented with low grade fever, loss of appetite and weight, productive cough, vomiting, and loose stools of 3 months duration. He also had persistent dysphagia and odynophagia of 3 weeks duration. He had pulmonary tuberculosis 10 years back.

On general physical examination, he was thin built and had oral thrush. A routine hemogram, echocardiography, and ultrasound abdomen were normal. A plain x-ray of chest showed a non-homogenous opacity in the upper lobe of right lung. Biochemical parameters revealed hypokalaemia and mild derangement of liver function tests. On stool culture, no intestinal pathogen was isolated. Serum ELISA was reactive for HIV infection. His CD4+ T-lymphocyte count was 37 cells per microliter. Sputum samples were negative for acid fast bacilli.

Upper gastro-esophageal endoscopy showed ulcerated friable mucosa involving lower 2/3 of esophagus without normal intervening mucosa up to gastro- esophageal junction [Figure 1]. A biopsy of the ulcer was done and histologic examination with hematoxylin and eosin stain revealed an ulcerated stratified squamous epithelium covered by dense neutrophilic and fibrinous exudate, proliferating blood vessels, fibroblasts, and red cell exudate. Few of the endothelial and stromal cells showed features of cytomegalovirus (CMV) infection such as cytomegaly, nucleomegaly with thick marginated chromatin, and a large ovoid eosinophilic intranuclear inclusion surrounded by a clear halo [Figure 2] and [Figure 3]. Few squamous cells showed 'ground glass' homogenized nuclear chromatin and multinucleation with molding of nuclei, which are suggestive of herpes simplex virus (HSV) infection [Figure 3]. Periodic acid Schiff and silver methenamine stains showed no fungal organisms. Ziehl-Neelsen stain was done and it showed no acid fast bacilli. A diagnosis of esophageal ulcer co-infected by HSV and CMV was made.
Figure 1: Endoscopy showed ulcerated mucosa of lower end of esophagus up to the gastro-esophageal junction.

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Figure 2: Histological section showing enlarged stromal cell with large eosinophilic intranuclear inclusion surrounded by a clear halo, suggestive of CMV infection (H and E stain, ×400).

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Figure 3: Histological section showing squamous cells with 'ground glass' homogenized nuclear chromatin and multinucleation with molding of nuclei, which are suggestive of HSV infection (small bold arrow) and one CMV-infected cell (thin long arrow) (H and E stain, ×200).

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He was started on oral acyclovir. The patient and his family members were not willing for further management and the patient was discharged against the medical advice.

Esophageal disease is one of the common causes for morbidity in a HIV infected patient. The presenting complaints are usually dysphagia, odynophagia, and retro-sternal pain. Odynophagia can cause weight loss due to disinclination to eat. [1] Varied etiologies for esophagitis and esophageal ulcers have been observed in HIV patients which include opportunistic infections like candidiasis, CMV, HSV, mycobacterium and protozoa, aphthous ulcer, peptic ulcer, gastro-intestinal reflux disease (GERD), and idiopathic ulcers related to HIV disease. [1],[2],[3] Candidiasis, CMV, and HSV infection are the common causes. Various combinations of co-infection of esophageal ulcers have been noted in HIV infected patients. Our patient had simultaneous infection of HSV and CMV, which is observed to be rare.

The diagnostic modalities include endoscopy, histopathology, cytology, barium swallow, and viral cultures. Endoscopic biopsies are of great help in the diagnosis of the common pathogens. Three or more biopsies are required to rule out viral esophagitis. [2] CMV infects the endothelial, stromal, and epithelial cells causing cytomegaly with round to oval intranuclear basophilic or eosinophilic inclusion surrounded by a clear halo and thickened nuclear membrane. This gives the characteristic "owl's eye" appearance to the infected cell. The cytoplasm can be granular to foamy. Occasional binucleated cells, reminiscent of  Reed-Sternberg cells More Details with abundant cytoplasm, and prominent nucleoli can be observed. Surrounding areas show chronic inflammatory infiltrate and vasculitis. Ulcers are thought to be secondary to vasculitis. [4] HSV infects mostly the epithelial cells. They cause ballooning degeneration, ground glass appearance of nuclei, intranuclear inclusions, and multinucleated giant cells. [3] If the viral cytopathic effect is either infrequent in number or atypical, an in-situ DNA hybridization or other immunohistochemical techniques was useful in diagnosing viral esophagitis. [2]

Bonacini et al.[3] and Connolly et al.[1] have reported one case each of co-infection with HSV and CMV in their independent studies on 19 and 10 HIV sero-positive patients with esophageal ulcer, respectively.

The pathogenesis of co-infection is unknown. The presence of these two viruses in the ulcers can be coincidental, representing a synergistic effect, or may indicate viral codependence for these particular ulcers. [5]

In HIV infected patients, concomitant infection with HSV and CMV have also been documented in other organs like central nervous system, retina, skin, and oral cavity. [4],[5]

In conclusion, opportunistic infections are the most frequent causes for esophageal ulcers in patients with HIV infection. The possibility of co-infections with two or more organisms must be kept in mind and multiple biopsies should be studied so that appropriate therapy is instituted to improve the quality of life by alleviating the painful symptoms.

   References Top

1.Connolly GM, Hawkins D, Harcourt-Webster JN, Parsons PA, Husain OA, Gazzard BG. Oesophageal symptoms, their causes, treatment, and prognosis in patients with the acquired immunodeficiency syndrome. Gut 1989;30:1033-9.  Back to cited text no. 1
2.Wilcox CM, Schwartz DA, Clark WS. Esophageal ulceration in human immunodeficiency virus infection. Causes, response to therapy and long-term outcome. Ann Intern Med 1995;122:143-9.   Back to cited text no. 2
3.Bonacini M, Young T, Laine L. The causes of esophageal symptoms in human immunodeficiency virus infection: A prospective study of 110 patients. Arch Intern Med 1991;151:1567-72.  Back to cited text no. 3
4.Heinic GS, Northfelt DW, Greenspan JS, MacPhail LA, Greenspan D. Concurrent oral cytomegalovirus and herpes simplex virus infection in association with HIV infection. Oral Surg Oral Med Oral Pathol 1993;75:488-94.  Back to cited text no. 4
5.Regezi JA, Eversole LR, Barker BF, Rick GM, Silverman S Jr. Herpes simplex and cytomegalovirus coinfected oral ulcers in HIV-positive patients. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1996;81:55-62.  Back to cited text no. 5

Correspondence Address:
P S Srilatha
Department of Pathology, Melaka Manipal Medical College (Manipal campus), Manipal, Karnataka - 576 104
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0377-4929.77420

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  [Figure 1], [Figure 2], [Figure 3]

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