Perinatal viral infections

Prober, Charles G.; Arvin, Ann M.

doi:10.1007/bf02017608

Cited by 14 publications

(6 citation statements)

References 152 publications

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“…This technique detects HSV within 16 to 48 h after inoculation (49,114,120,154). Serologic examination is of no assistance is diagnosing neonatal infection due to HSV (6,119).…”

Section: Serologymentioning

confidence: 99%

Role of the virology laboratory in diagnosis and management of patients with central nervous system disease

1989

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A number of viruses cause acute central nervous system disease. The two major clinical presentations are aseptic meningitis and the less common meningoencephalitis. Clinical virology laboratories are now more widely available than a decade ago; they can be operated on a modest scale and can be tailored to the needs of the patients they serve. Most laboratories can provide diagnostic information on diseases caused by enteroviruses, herpesviruses, and human immunodeficiency virus. Antiviral therapy for herpes simplex virus is now available. By providing a rapid diagnostic test or isolation of the virus or both, the virology laboratory plays a direct role in guiding antiviral therapy for patients with herpes simplex encephalitis. Although there is no specific drug available for enteroviruses, attention needs to be paid to these viruses since they are the most common cause of nonbacterial meningitis and the most common pathogens causing hospitalization for suspected sepsis in young infants in the United States during the warm months of the year. When the virology laboratory maximizes the speed of viral detection or isolation, it can make a significant impact on management of these patients. Early viral diagnosis benefits patients with enteroviral meningitis, most of whom are hospitalized and treated for bacterial sepsis or meningitis or both; these patients have the advantage of early withdrawal of antibiotics and intravenous therapy, early hospital discharge, and avoidance of the risks and costs of unnecessary tests and treatment. Enteroviral infection in young infants also is a risk factor for possible long-term sequelae. For compromised patients, the diagnostic information helps in selecting specific immunoglobulin therapy. Good communication between the physician and the laboratory will result in the most benefit to patients with central nervous system viral infection.

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“…This technique detects HSV within 16 to 48 h after inoculation (49,114,120,154). Serologic examination is of no assistance is diagnosing neonatal infection due to HSV (6,119).…”

Section: Serologymentioning

confidence: 99%

Role of the virology laboratory in diagnosis and management of patients with central nervous system disease

1989

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“…It has been hypothesized that a viral insult during embryogenesis or development may be involved in the etiology of these disorders. Supporting this hypothesis are epidemiological studies (Deykin and MacMahon, 1979;Kirch, 1993) and the known teratogenic potential of viruses (Prober and Arvin, 1987) that can preferentially infect dividing neuroblasts (Margolis and Kilham, 1975), disrupt neural cell migration (Stoltenburg et al, 1991), or inhibit developmentally regulated hormone production (Oldstone et al, 1984). The complex inter-relationship between neuronal circuitry and neuron degeneration (Houser, 1990;Olney et al, 1991) suggests that viruses can induce neuronal death through an indirect mechanism, for example, by interrupting inhibitory control over a potentially excitotoxic synapse.…”

mentioning

confidence: 99%

Persistent dentate granule cell hyperexcitability after neonatal infection with lymphocytic choriomeningitis virus

et al. 1996

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Infection of neonatal Lewis rats with lymphocytic choriomeningitis virus (LCMV) produces distinct retinal, cerebellar, and hippocampal neuropathology. To understand the neurophysiological consequences of LCMV-induced hippocampal pathology, we studied evoked monosynaptic potentials and electro-encephalographic (EEG) activity in the dentate gyrus and CA1 and CA3 subfields of the hippocampus in vivo. Lewis rats were inoculated intracerebrally with LCMV at postnatal day 4. In rats studied 84-107 d postinfection, virus was cleared from the dentate gyrus and the number of dentate granule cells was decreased by 70%. No viral antigen or cell loss was apparent in CA1 or CA3. The hippocampal EEG of LCMV-infected rats 84-102 d postinfection was dominated by continuous theta. Although evoked potentials elicited in CA1 and CA3 by monosynaptic afferent stimulation revealed no differences between sham- and LCMV-infected rats, there was a site-specific dissociation of synaptic [population excitatory postsynaptic potential (pEPSP)] and cellular (population spike) responses and a suppression of GABA-mediated recurrent inhibition in the dentate gyrus of LCMV-infected rats. These findings indicate that GABA-mediated inhibition was markedly decreased in LCMV-infected rats. In support of this, parvalbumin-immunoreactive cell bodies and neuronal processes were decreased in LCMV-infected rats, suggesting that a subpopulation of GABA interneurons was affected. These findings indicate that abnormalities in synaptic function persist after clearance of infectious virus from the central nervous system and suggest that decreased inhibition subsequent to pathological sequence in a subpopulation of GABA interneurons may be implicated in the hyperexcitability of dentate granule cells.

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“…On the other hand, symptomatic congenital CMV infection occurs exclusively in infants born to seronegative women who contracted primary CMV infection during pregnancy (10,12,15,17). The milk-borne CMV infection may increase the seropositivity of women at the childbearing age and therefore decrease the risk of symptomatic congenital CMV infection of their children.…”

Section: Discussionmentioning

confidence: 99%

Role of Breast Milk in Acquisition of Cytomegalovirus Infection

Minamishima

Ueda

Minematsu

et al. 1994

Microbiology and Immunology

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The prevalence of IgG antibody against cytomegalovirus (CMV) was compared between the age-matched (0 month to 2 years of age) groups of 212 breast-fed children and 223 bottle-fed children to examine the role of breast milk for acquisition of CMV. Mothers of both groups of children were also examined for CMV IgG antibodies. Both the breast-fed and bottle-fed children groups showed high seropositivity for CMV at 0 to 2 months of age, which gradually decreased and bottomed at 6 to 8 months of age. Thereafter, in the breast-fed children group, the seropositivity rate increased up to 70% by 1 year of age. In contrast, in the bottle-fed children group, the seropositivity rate remained at the bottom level of lower than 30%, without showing any apparent increases. The serological data of the children whose mothers were confirmed to be seropositive, revealed that mother-to-child transmission of CMV occurred in 11 of 17 (64.7%) of the breast-fed children and in 24 of 87 (27.6%) of the bottle-fed children. All the bottle-fed children born to seronegative mothers remained seronegative for CMV up to 1 year of age. The bottle-fed children showed significantly lower seropositivity than the breast-fed children, although most of both groups of children were born to seropositive mothers. The results strongly suggested that about 40% of the breast-fed children acquire CMV via breast milk and breast-feeding has certain protective effects on congenital CMV disease in the offspring. CMV is known to be one of the most common viruses which are transmitted transplacentally. In fact, congenital CMV infection occurs at incidences ranging from 0.2 to 2.2% among all live births, as reviewed by Stagno and Whitley (15). Although most of these congenitally infected newborns show no clinical signs of CMV infection, approximately 10% of them will develop congenital cytomegalic inclusion disease with sequelae (1, 11).Moreover, CMV infection which occurs during or after delivery is much more common than congenital infection. Such perinatal CMV infection is usually acquired through contact with breast milk and/or cervical secretions. In fact, Numazaki et al reported that approximately 30% of the pregnant women excreted CMV in the cervical excretions and more than 60% of newborn infants in Japan were vertically infected by CMV via the birth canal (8). On the other hand, CMV was isolated from breast milk, and CMV infection via breast milk was also reported (2, 5, 9, 13). Breast milk has then also been considered as an important route of mother-to-child transmission of CMV (9). In the present study, we compared the prevalence of CMV antibodies between the age-matched groups of breast-fed children and bottle-fed children. The serological status of mothers of both the breast-fed and bottle-fed children was also examined. An evidence that the seropositivity is apparent higher in the breast-fed children than in the bottle-fed children suggests an important role of breast milk

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Perinatal viral infections

Cited by 14 publications

References 152 publications

Role of the virology laboratory in diagnosis and management of patients with central nervous system disease

Role of the virology laboratory in diagnosis and management of patients with central nervous system disease

Persistent dentate granule cell hyperexcitability after neonatal infection with lymphocytic choriomeningitis virus

Role of Breast Milk in Acquisition of Cytomegalovirus Infection

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