Generalized Herpes Simplex and Hypoadrenocorticism

Abstract

THIS REPORT presents the evaluation of a prematurely born male infant who was infected with herpes simplex virus (HSV) near or at term and who developed generalized infection with central nervous system involvement and chorioretinitis. At 4 months of age he was recognized to have adrenocortical insufficiency. His unique clinical presentation, together with the prospective accumulation of relevant ophthalmologic, virologic, and metabolic findings prompted this report.The isolation of HSV from CSF served to help establish the pathogenesis of his eye lesions. Although the adrenal cortices of infants having generalized herpes simplex infection have been judged to be infected,1-3 functional impairment of this organ has not been recorded previously. Report of a CaseThe patient was born on March 17, 1964, after a 34-week gestation of a 21-year-old woman who had developed extensive genital herpes simplex infection, first noted 20 days prior to delivery. After meconium-stained amniotic fluid was noted per vaginum, an irregular fetal heart rate prompted an emergency cesarean section. A small, limp infant was delivered (Apgar score: 4 at one minute). En¬ dotracheal intubation and positive pressure resuscita-Adelbert Rd, Cleveland 44106 (Dr. Teree). tion were necessary. Penicillin and chloramphenicol were given and he was transferred to the Isolation Nursery where his color and respirations improved. No mucocutaneous lesions or organomegaly were noted. Although his cry and suck were weak, his muscular tone and Moro reflex were normal. Hemoglobin concentration was 20 gm/100 ml; hematocrit, 75%; and WBC count 18,650/cu mm, including 19 nucleated RBC per 100 WBC. Urine was normal. Bacterial cultures of skin, throat, urine, blood, and amniotic fluid were nega¬ tive.The infant appeared well until facial papulovesicular lesions were noted at the age of 7 days. Two days later similar lesions appeared on buccal mu¬ cosa. HSV was isolated from a forehead lesion.Lumbar punctures were performed on the seventh and ninth day of life; on both occasions mononu¬ clear pleocytosis was noted (98 and 47 cells/cu mm, respectively). HSV was isolated from both specimens. Beginning on the 11th day, focal motor seizures were noted and phénobarbital and diphenyl¬ hydantoin were administered. Idoxuridine was ap¬ plied to the cutaneous lesions. On the 13th day of life, the liver was noted to be enlarged, although tests of liver function remained normal. The sei¬ zures stopped on the 17th day but régurgitation and vomiting necessitated tube feedings. At 27 days of age the CSF contained 272 mg protein/100 ml, and frontal transillumination was first noted.During the early part of his course, a complete eye examination was not done, but the external appearance of the eyes showed no pertinent dis¬ orders. It was not until 30 days of age that the first ophthalmoscopic examination was made. Bi¬ lateral lenticular fluid clefts, most dense centrally, and marked vitreous clouding were observed. These abnormalities prevented accurate visualization of the eye gro...

Herpes simplex virus type 1 and 2 in the adrenal glands: Replication and histopathology

“…The question therefore arises, whether HSV not only produces pathogenic effects in the acute situation of the disease but also late after infection during life. And indeed, one ease of adrenal gland failure after HSV-infection has been proven (1). There are still unexplained eases of failures of the adrenM glands during later life, which could be the consequence of earlier infections of the adrenal glands by HSV, for example in eases of Herpes-sepsis.…”

Infection of the Adrenal Gland as a Route to the Central Nervous System after Viraemia with Herpes Simplex Virus in the Mouse

“…Although in many human infections with HSV viraemia is not important, in neonatal infection (Bahrani et al, 1966;Arvin et al, 1982) and in immunosuppressed people (Montgomerie et al, 1969) it probably plays a significant role in the disease. Involvement of the adrenal gland and the possibility of damage in the cord should be borne in mind when considering explanations of nervous system dysfunction associated with HSV infections (Klastersky et aL, 1972;Craig & Nahmias, 1973;Shturman-Ellstein et al, 1976;Caplan et al, 1977;Oates & Greenhouse, 1978;White et al, 1984).…”

Analysis by RNA-PCR of latency and reactivation of herpes simplex virus in multiple neuronal tissues

“…Following reactivation from latently infected ganglia, HSV spreads through efferent nerves and induces recurrent infection at regions near the site of primary infection. In addition, HSV has been reported to cause primary infections of the central and/or peripheral nervous system including encephalitis, myelitis and adrenocorticitis (Bahrani et al, 1966;Blyth & Hill, 1984). Infection by HSV of the nervous systems, induced by viral recurrence from latency, can also cause severe and sometimes fatal diseases in clinical cases (Whitley, 1990).…”