Chorioretinitis

A 46-year-old man presented to the University of California, Davis Medical Center with severe electrical burns. The patient had been trimming trees and came into contact with some high-voltage power lines. The patient suffered third and fourth degree burns of 46% of his total body surface area. He was admitted to the intensive care unit for management of his burns. Subsequently, the patient developed stridor. The patient underwent bronchos-copy and laryngoscopy. Approximately 3 to 4 cm below the glottis an area of tracheal stenosis was noted; biopsy material was obtained for both frozen section and regular processing to rule out a potential neoplasm. The frozen section diagnosis was acute inflammation, granulation tissue, and necrosis; no malignancy. Hematoxylin-eosin stains showed acute inflammation, granulation tissue, and necrosis. No neoplastic cells were seen. Numerous scattered enlarged cells with abnormal nuclei were noted (Figure 1, hematoxylin-eosin, original magnification ×200). Higher magnification revealed nuclear inclusions (Figure 2, hematoxylin-eosin, original magnification ×400). An immunohistochemical stain for cytomegalovirus (CMV) antigen was performed and was noted to stain the nuclei of the abnormal cells (Figure 3, arrows indicate cells positive for CMV, original magnification X400). The cells staining in Figure 3 were presumed to be histiocytes or macrophages infected by CMV The stain for CMV antigen was a monoclonal mouse immunoglobulin (Ig) G antibody purchased from BioGenex (San Ramon, Calif). Staining was performed according to the manufacturer's instructions on formalin-fixed, paraffin-embedded tissue sections. Enzyme predigestion with pepsin was performed as recommended by the manufacturer. This antibody does not cross-react with other herpes viruses. Silver and periodic acid-Schiff stains were negative for fungal organisms. The patient had no other conditions that would cause tracheal stenosis, thus the CMV was presumed to be the cause.

Cytomegalovirus infection is caused by a member of the family Herpesviridae. Infectious particles are composed of an electron-dense core of double-stranded DNA, a capsid with icosahedral configuration, and a surrounding envelope. A variety of cells can be infected by the virus, including endothelial cells, alveolar pneumocytes, fibroblasts, histiocytes, and exocrine and endocrine glandular epithelial cells. Viral replication occurs within the nucleus of the host cell. Actively infected cells exhibit cytomegaly with both nuclear and cytoplasmic enlargement. Typically, one sees the characteristic intranuclear and intracytoplasmic inclusion bodies that are amphophilic to deeply basophilic. The single nuclear inclusion is characteristically round to oval with a smooth border. Often, the nucleolus is retained within the inclusion body. There is a clear zone, or halo, around the inclusion, as well as margination and condensation of chromatin on the inner aspect of the nuclear membrane. The inclusion may be eosinophilic in some stages of development.

Clinical and laboratory manifestations of active infection may be extremely variable, ranging from a mild self-limited illness to severe infection with jaundice, hepatosplenomegaly, encephalitis, and chorioretinitis. We found no other reports of trachéal stenosis associated with cytomegalovirus in the literature. A study of 120 burn patients performed in 1990 showed no evidence that CMV contributed either directly or indirectly to the morbidity or mortality of the patients.1 Another study performed in 1985 on 52 burn patients found that CMV infection was associated with longer duration of hospitalization and full-thickness burn areas, but found no significant association of CMV infections with mortality.2

References

1. Bale JF, Kealey GP, Massanari RM, Strauss RG. The epidemiology of cytomegalovirus infection among patients with burns. Infect Contra! Hasp Epidcmiol. 1990:11:17-22.

2. Kagan RJ, Naraqi S, Matsuda T, Jonasson OM. Herpes simplex virus and cytomegalovirus infections in burned patients. J Trauma. 1985;25:40-45.

Amanda Ashton-Sager, MD; Thomas Konia, MD

Accepted for publication April 29, 2004.

From the Department of Pathology, University of California, Davis Medical Center, Sacramento.

The authors have no relevant financial interest in the products or companies described in this article.

Reprints: Amanda Ashton-Sager, MD, Department of Pathology, University of California, Davis Medical Center, 4400 V St, Sacramento, CA 95817 (e-mail: amanda.ashton@ucdmc.ucdavis.edu).

Copyright College of American Pathologists Sep 2004
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