Disseminated neonatal herpes simplex virus infection acquired from the father

A disseminated herpes virus type 1 infection in a baby was acquired from the father, who had herpes labialis. This was shown by virus strain typing using restriction endo-nuclease DNA analysis. Labial herpes, a common infection in adults, must be recognised as a potential threat to newborn babies.Abbreviations HSV herpes simplex virus - CSF cerebrospinal fluid - IFA immunofluorescent assay     

INTRAVASCULAR COAGULATION IN GENERALIZED HERPES SIMPLEX INFECTION OF THE NEWBORN

A case of disseminated herpes simplex virus infection in a newborn associated with a fatal bleeding diathesis is reported. The presence of intravascular coagulation was suggested by thrombocytopenia, fibrinogenopenia, and reduced Factor V level. At necropsy localized fibrin and platelet deposition was found in liver and lung. It is postulated that intravascular coagulation resulted from local tissue necrosis and the subsequent release of thrombo-plastin-like substances into the general circulation. Heparin therapy did not alter the fatal outcome.     

Disseminated neonatal herpes simplex virus (HSV) type 2 infection diagnosed by HSV DNA detection in blood and successfully managed by liver transplantation

We report a case of neonatal herpes presenting with liver failure and disseminated coagulopathy which followed unrecognised maternal primary genital herpes and was diagnosed by herpes simplex virus DNA detection in blood by polymerase chain reaction 2 weeks after initiation of empiric intravenous aciclovir. The child underwent liver transplantation while receiving suppressive antiviral therapy and remains well after 10 months of follow-up. Conclusion:our case highlights potential pitfalls in the diagnosis of neonatal herpes and indicates a role for blood herpes simplex virus polymerase chain reaction as a sensitive diagnostic tool in disseminated infection. It is one of very few reports where liver transplantation has been successfully carried out in a neonate with herpes simplex virus-induced liver failure.Abbreviations HSV herpes simplex virus - PCR polymerase chain reaction     

Neonatal herpes infection: diagnosis,treatment and prevention

Approximately 2000 neonates contract infection due to herpes simplex virus each year in the United States. Although herpes simplex virus type 2 is responsible for most neonatal infections, approximately 30% of infections are caused by herpes simplex virus type 1. Infections are categorized by extent of disease into skin/eye/mouth, central nervous system and disseminated disease categories. Each disease category is responsible for roughly one third of neonatal infections. Mortality is highest in disseminated disease. Morbidity is highest for survivors of central nervous system infection. Treatment with high dose parenteral acyclovir (60 mg/kg/day) for 14–21 days improves outcome. Since most neonatal infections are acquired from contact with infected maternal genital tract secretions, potential preventative strategies include: Caesarean delivery, serologic screening of pregnant women, prophylactic acyclovir and vaccination. The two strategies currently accepted by most obstetricians are Caesarean delivery for women with active lesions or prodromal symptoms and prophylactic acyclovir for women with gestational herpes.     

Development of acyclovir-resistant herpes simplex virus early during the treatment of herpes neonatorum.

Genotypic analysis of herpes simplex virus (HSV) DNA extracted from clinical specimens from a case of fatal disseminated neonatal HSV demonstrated that an infant developed an acyclovir-resistant HSV containing a mutation in the HSV thymidine kinase gene during the first seven days of acyclovir therapy.     

Neonatal herpes simplex infection possibly acquired via maternal breast milk.

A newborn infant with disseminated herpes simplex virus type 1 (HSV-1) infection was determined serologically to have acquired the infection postnatally; his mother was found to have HSV-1 in her breast milk but had no history of genital lesions and negative viral cultures of cervix, vagina, and throat. We suggest that HSV-infected maternal breast milk may be a source of this infection for susceptible infants.     

Herpes simplex type 1 infections in group day care.

To characterize patterns of herpes simplex virus type 1 infection, illness and transmission among children in group day care, the data for 115 children who had been followed longitudinally from early infancy in a research day care center were examined. By 5 years of age 37% of study children had evidence of herpes simplex virus type 1 infection as demonstrated by virus isolation and/or seroconversion. The incidence of infection was highest among children 1 to 2 years old. Four small clusters of primary infections were observed over the 12-year study period but no cluster involved more than 6 children. Fifty-five percent of primary infections occurred during these small outbreaks; the remainder were sporadic. Gingivostomatitis was observed in 26% of children with primary culture-proved infections; no child with infection identified solely by serologic means had a history of gingivostomatitis. The occurrence of gingivostomatitis did not appear to be associated with increased transmission of herpes simplex virus type 1 infection in this day-care setting.     

Unusual concurrence of heterotopic glial nodule of the scalp and congenital herpes simplex virus type‐2 infection

Heterotopic glial nodules are rare congenital cutaneous lesions; only 13 cases of scalp localized lesions of this kind are reported in the English medical literature. Herpes simplex virus is a rare cause of neonatal morbidity and mortality and is a rare cause of intrauterine infection. We report the first case of concurrent presence of a heterotopic glial nodule of the scalp and neonatal, in utero‐acquired, fatal herpes simplex virus type‐2 infection.     

Neonatal herpes simplex: clinical findings and outcome in relation to type of maternal infection

In 39 mothers of children with neonatal herpes simplex virus infection, maternal infection was serologically characterized retrospectively and was related to maternal clinical symptoms and to the clinical findings and outcome in the child. Thirteen mothers had a primary infection (six type 1, seven type 2), mostly with clinical symptoms. The mean age of onset of the disease of the infants was 7 days and a disseminated disease was most commonly found. Most of the type 1-infected children recovered completely, whereas all but one of the type 2-infected children died. Twenty mothers had a recurrent (2 type 1, 18 type 2) and 4 an intermediate infection (primary type 2, prior infection with type 1), mostly asymptomatic. Their children had a localized disease (of the skin-eye-mouth or the central nervous system) with onset at a mean age of 14 or 13 days, respectively. The frequency of neurological sequelae was high. Two mothers had no serological signs of herpes infection.     

Procalcitonin may help differentiate disseminated herpes simplex viral infection from bacterial sepsis in neonates

Disseminated herpes simplex virus infection is a potentially fatal condition which may be difficult to differentiate from bacterial sepsis. We report the case of a neonate with overwhelming herpes simplex (type 2) viraemia who presented with `septic shock'. Conclusion A low procalcitonin level (1.6 ng/ml), inconsistent with bacteraemia, suggests an alternative aetiology and may strengthen the case for antiviral therapy. Received: 28 March 1999 / Accepted: 10 August 1999     

Herpes Simplex Virus Infection in the Newborn

Fourteen cases of neonatal herpes simplex virus infection in 10 boys and 4 girls are described. The disease was disseminated in 9 cases. In 5 cases skin symptoms predominated, and 1 had only central nervous system symptoms. Two had a vesicular eruption when born. Six of the children with disseminated disease died.EEG recordings were made on 7 patients: 5 had clinical symptoms compatible with encephalitis, and in these the EEG showed periodic complexes, consisting of triangular or sharp waves, a pattern described in adult cases of herpetic encephalitis.The diagnosis was made by virus isolation and antibody titration. Herpes virus type 2 was the causative agent in all 8 cases where the type was determined. In 5 patients herpes virus antigen was demonstrated using immunofluorescence either in vesicles or throat swabs, in the early phase of the disease.Two children with generalized disease were treated with intravenous iododeoxyuridine (IDU). The first died, but the other, treated early in his disease, recovered completely.The clinical picture, complemented by the immunofluorescent technique for virus detection and repeated EEG recordings, should lead to the early diagnosis of herpetic encephalitis in the newborn, and warrant the use of systemic IDU treatment.     

Nosocomial and maternally acquired herpesvirus hominis infections. A report of four fatal cases in neonates.

Four fatal cases of neonatal herpes simplex infection occurred during a two-month period in the perinatal intensive care unit of a hospital. Virus isolation or serologic studies, or both, implicated herpesvirus hominis type 2 in all four cases. Three of the infants developed symptoms in the first week of life and were probably infected in utero or at delivery. The fourth infant did not develop signs of illness until age 6 weeks, an interval much longer than that expected with disease acquired at birth. An epidemiologic investigation indicated that the most likely source of this fourth infant's herpes infection was by indirect contact with one of the other three infected neonates. Nosocomial spread of herpes simplex virus within a hospital nursery, although uncommon, may pose an added risk to the newborn infant if nursery techniques among infants are compromised.     

Herpes simplex viral pneumonitis in childhood

We report two cases of herpes simplex pneumonia in children. One patient had Down syndrome, and the other was immunosuppressed by cancer therapy. Both had interstitial pneumonitis with nonspecific physical, radiographic, and laboratory findings, and both died. The diagnosis of herpes simplex pneumonia was made by isolation of herpes simplex virus from autopsy lung cultures as well as by demonstration of antigen in the tissue with an immunoperoxidase procedure. Inasmuch as herpes simplex pneumonia is a potentially treatable infection, early virologic studies are recommended in immunocompromised children with progressive pneumonitis of undetermined cause.     

Parietal pseudofracture and spontaneous intracranial hemorrhage suggesting nonaccidental trauma: report of 2 cases

Massive intracranial hemorrhage, no history of trauma and radiographic findings that were initially interpreted as linear parietal fractures raised the possibility of nonaccidental trauma in 2 infants. Both had severe coagulopathy, 1 due to hemorrhagic disease of the newborn (vitamin K deficiency) and the other due to disseminated herpes simplex virus infection. Both infants died. At autopsy, the parietal bone abnormalities were not fractures, but proved to be an anomalous suture in 1 and a connective tissue fissure in the other.     

Herpes simplex virus colitis in a neonate

Involvement of the gastrointestinal tract in neonates with congenital herpes simplex virus (HSV) infection is rarely described. We report a case of a newborn with disseminated HSV infection associated with profuse hematochezia and late sigmoid colon perforation. Histologic examination showed patchy areas of ulceration with multinucleated giant cells and HSV nucleic acid was detected by polymerase chain reaction in colonic tissue. No clinically apparent episodes of recurrent colitis occurred in the first year of life.     

Neonatal herpes simplex virus infection: follow-up evaluation of vidarabine therapy

An open study of vidarabine (adenine arabinoside) therapy was performed to verify the mortality from neonatal herpes simplex virus infection and to define further long-term morbidity. A total of 39 babies not previously reported were treated with either 15 mg/kg/d (16 newborns) or 30 mg/kg/d (23 newborns) of vidarabine administered intravenously for ten to 14 days. Outcome was compared with that from 56 newborns evaluated in a prior trial. Irrespective of the dose of medication, therapy decreased the mortality in babies with disseminated and CNS disease to 40%. The extent of organ involvement and, in particular, pulmonary herpes simplex infection were predictive of mortality (P = .001, for both). For these babies, 32% achieved normal developmental milestones 2 years after therapy. Disease localized to the skin, eye, and/or mouth was not associated with death. However, neurologic impairment occurred in 12% of this treated group of newborns. These findings underscore the value of vidarabine therapy of neonatal herpes simplex virus infection. However, an increase in dosage did not appear to result in significant improvement in either mortality or morbidity. Further improvement in the mode of therapy and the utilization of more potent antiviral drugs are currently being tested.     

Cystic encephalomalacia and intrauterine herpes simplex virus infection

Cystic encephalomalacia occurred in two preterm infants who had proven intrauterine herpes simplex virus type 2 infection. Calcification was evident in the basal ganglia. Follow-up scans indicated that the cysts had resolved over a period of two months in one infant, while in the case of the other, the cysts became progressively larger with significant ventricular dilatation developing. While cystic changes in the brain of preterm infants are usually due to periventricular leukomalacia intrauterine infection needs to be considered as a possible cause. Antiviral treatment may be of benefit to infants with herpes simplex virus infection.     

Herpes simplex virus-stimulated gamma-interferon production by newborn mononuclear cells

Blood mononuclear cells from newborns and from adults, immune or nonimmune to herpes simplex virus, were cultured with IL 2 and herpes simplex virus and the amount of gamma-interferon in the supernatant measured after 3 days. The newborn and nonimmune adult cells made equivalent trace amounts of gamma-interferon in cultures containing either herpes simplex virus or IL 2 alone and there was a 5- to 10-fold increase in cultures containing both. Experiments in which the Leu 11+ cells were either depleted or enriched suggest that this subset of natural killer cells is both necessary and sufficient for gamma-interferon production in the absence of immune T cells.     

Use of aciclovir in herpes simplex virus infections

Herpes simplex virus type 1 and type 2 cause a wide range of illnesses ranging from minor cold sores to severe necrotising encephalitis or disseminated systemic infections seen in immunocompromised patients including neonates. Following primary infection, the virus is not eradicated from the body but is latent in sensory nerve ganglia where it can reactivate and cause recurrent disease. Aciclovir is the most studied and used antiviral agent with activity against herpes simplex virus infections. In most situations the use of aciclovir shortens the duration of clinical illness and viral shedding and reduces morbidity and mortality. All life- or sight-threatening infections should be managed in an inpatient hospital setting with intravenous therapy. The use of oral aciclovir is recommended in patients with non-life-threatening illness who may still have significant symptoms.     

Hemophagocytic lymphohistiocytosis caused by systemic herpes simplex virus type 1 infection: Successful treatment with dexamethasone palmitate

Hemophagocytic lymphohistiocytosis (HLH) is a hyperinflammatory condition resulting from an uncontrolled and ineffective immune response. Here, we report a case of HLH caused by disseminated herpes simplex virus (HSV)‐1 infection. The patient was initially treated with prednisolone and high‐dose acyclovir. Although liver enzymes, coagulation abnormalities, and inflammatory markers were remarkably improved, the platelet count remained low. Prednisolone was therefore switched to dexamethasone palmitate. Thereafter, the platelet count normalized. Inflammatory markers normalized 30 days after admission and serum HSV‐DNA became undetectable on day 41. The patient was discharged on day 91 and no developmental delay was evident at 7 months of age. These findings suggest that dexamethasone palmitate is effective for neonatal HLH.