Herpetic eye infections
HSV infection of the eye is the most frequent cause of corneal blindness in the United States. HSV keratitis presents with acute onset of pain, blurring of vision, chemosis, conjunctivitis, and characteristic dendritic lesions of the cornea. Use of topical corticosteroids may exacerbate symptoms and lead to involvement of deep structures of the eye. Debridement, topical antiviral, and/or interferon therapy hasten healing. However, recurrences are common and immunopathologic injury of the deeper structures of the eye may occur. Chorioretinitis, usually as a manifestation of disseminated HSV infection, may occur in neonates or those with AIDS. Acute necrotizing retinitis due to HSV is also an uncommon but severe manifestation of HSV infection.
Central and peripheral nervous system infections with HSV-1 and HSV-2 HSV encephalitis is the most common identified cause of acute, sporadic viral encephalitis in the United States, comprising 10 to 20 percent of all cases. The estimated incidence is about 2.3 cases per million persons per year. Cases are distributed throughout the year, and the age distribution appears biphasic with peaks at between 5 and 30 and greater-than-50 years of age. HSV-1 accounts for more than 95 percent of cases. The pathogenesis of HSV encephalitis is varied. In children and young adults primary HSV infection may result in encephalitis; presumably exogenously acquired virus enters the CNS by neurotropic spread from the periphery via the olfactory bulb. However, most adults with HSV encephalitis have clinical or serologic evidence of mucocutaneous HSV-1 infection prior to the onset of the CNS symptoms. In about 25 percent of the cases examined, the HSV-1 strains from the oropharynx and brain tissue from the same patient differ, suggesting that some cases may result from reinfection with another strain of HSV-1 that reached the CNS. Two theories have been proposed to explain the development of actively replicating HSV in localized areas of the CNS in persons from whom the ganglionic and CNS isolates are similar. Reactivation of latent trigeminal or autonomic nerve root HSV-1 infection may be associated with extension of virus into the CNS via nerves innervating the middle cranial fossa. HSV DNA has been demonstrated by DNA hybridization in human autopsy brain tissue. As such, reactivation of long-standing latent CNS infection may be another potential mechanism for the development of HSV encephalitis.
The clinical hallmark of HSV encephalitis has been the acute onset of fever and focal neurologic, especially temporal lobe, symptoms. To date no reliable noninvasive radiologic or virologic technique has been developed to diagnose HSV encephalitis during its early clinical stages, and differentiation of HSV encephalitis from other viral encephalitides and other focal infections and noninfectious processes is difficult. An increase in CSF and serum antibodies to HSV does occur with most cases of HSV encephalitis. However, these antibody rises rarely are present prior to 10 days into the illness and, while useful retrospectively, are not helpful in establishing the clinical diagnosis early in the course of disease. Brain biopsy because of its high sensitivity, low complication rate, and ability to establish alternative potentially treatable diagnoses has been felt by many to be the most expeditious method to diagnose HSV encephalitis. Antiviral chemotherapy reduces the mortality of HSV encephalitis, and intravenous acyclovir appears to be more effective than vidarabine. Even with therapy, however, neurologic sequelae are frequent.
HSV has been isolated from the cerebrospinal fluid from 0.5 to 3 percent of patients presenting to the hospital with aseptic meningitis. HSV meningitis is usually seen in association with primary genital HSV infection. HSV meningitis is an acute self-limited disease manifested by headache, fever, and mild photophobia, which lasts from 2 to 7 days. A lymphocytic pleocytosis in the CSF is characteristic. Neurologic sequelae are rare. Recurrent bouts of aseptic meningitis related to reactivation of HSV have been reported.
Autonomic nervous system (ANS) dysfunction, especially of the sacral region, has been reported in association with both HSV and varicella-zoster infections. Numbness, tingling of the buttock or perineal areas, urinary retention, constipation, cerebrospinal fluid pleocytosis, and impotence in males may occur. Symptoms appear to resolve slowly over a period of days to weeks. Occasionally hypesthesia and/or weakness of the lower extremities may persist for many months. Rarely transverse myelitis manifested by a rapidly progressive symmetric paralysis of the lower extremities or a Guillain-Barre syndrome may occur after HSV infection. Similarly, peripheral nervous system involvement [idiopathic facial paralysis (Bell’s palsy)] or cranial polyneuritis may also be related to reactivation of HSV-1 infection. Transitory hypesthesia of the area of skin innervated by the trigeminal nerve and vestibular system dysfunction as measured by electronystagmography are the predominant signs of disease. Studies to determine if antiviral chemotherapy may abort or alleviate the frequency and severity of these signs are unavailable.