Chickenpox in Mid‐Trimester Pregnancy: Always Innocent?

Wheatley, Robert E.; Morton, Richard E.; Nicholson, Jan M.

doi:10.1111/j.1469-8749.1996.tb15105.x

Cited by 9 publications

(3 citation statements)

References 15 publications

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“…Usually, CVS is considered to be a multi-systemic disorder characterized by skin lesions and accompanied by neurological defects, eye diseases, and/or limb hypoplasia (Sauerbrei and Wutzler 2000). To date, manifestations of CVS limited to the brain have rarely been described in the literature (Scheffer et al 1991, Wheatley et al 1996, Dimova and Karparov 2001. In our patient the disease was manifest as generalized clonic seizures first apparent 4 months after birth.…”

Section: Discussionmentioning

confidence: 74%

“…microphthalmia, chorioretinitis, cataracts), and limb hypoplasia, mostly accompanied by cicatricial alterations of the skin. Only in a few patients has CVS been associated with isolated manifestations in the brain (Scheffer et al 1991, Wheatley et al 1996, Dimova and Karparov 2001 or the eye (Cotlier 1978, Palmer and Pauli 1988, Andreou et al 1995. On the basis of the segmental distribution of some of the clinical signs, in particular the skin lesions, it has been postulated that CVS is not the immediate consequence of intrauterine varicella, but is caused by intrauterine VZV reactivations with accompanying encephalitis (Higa et al 1987).…”

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confidence: 99%

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Intracerebral varicella‐zoster virus reactivation in congenital varicella syndrome

Sauerbrei

Pawlak²,

Luger

et al. 2003

Develop Med Child Neuro

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Patients with congenital varicella syndrome (CVS) typically present with clinical symptoms consisting of skin lesions, neurological defects, eye diseases, and/or limb hypoplasia. In rare cases, isolated manifestations in the brain or eye have been reported. The varicella‐zoster virus (VZV), as the causative agent of CVS, could only be detected in a few infants with CVS. In addition, there is little in the literature on antiviral treatment of infants born with signs of CVS. We report a case of CVS in a male infant who presented with generalized clonic cerebral seizures at age 4 months. An endogenous intracerebral viral reactivation following intrauterine VZV infection was assumed. After the diagnosis was confirmed virologically, acyclovir was administered intravenously for 10 days and afterwards orally for 3 weeks. This antiviral treatment was aimed at preventing progression of the disease. We concluded from this case that infants with intrauterine VZV infection can suffer intracerebral VZV reactivations that require antiviral treatment.

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Section: Discussionmentioning

confidence: 74%

mentioning

confidence: 99%

Intracerebral varicella‐zoster virus reactivation in congenital varicella syndrome

Sauerbrei

Pawlak²,

Luger

et al. 2003

Develop Med Child Neuro

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“…Ocular manifestations include microphthalmia, chorioretinitis, cataract, opaque cornea, optic nerve atrophy or hypoplasia and Horner syndrome. [21][22][23][24][25] Brain lesions include cerebral dysgenesis or atrophy, 26,27 porenchephaly, 28 and microcephaly. 29 Diffuse spinal cord scarring has been described.…”

Section: Signs and Symptomsmentioning

confidence: 99%

Fetal varicella – diagnosis, management, and outcome

Mandelbrot

2012

Prenatal Diagnosis

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Fetal varicella syndrome (FVS) is due to transplacental infection by the Varicella zoster virus following maternal infection. The risks for the fetus and neonate depend on the timing. When varicella occurs around delivery, it often leads to disseminated neonatal varicella. When varicella occurs during pregnancy, transmission can occur, but is usually asymptomatic; some infants develop zoster postnatally and a few have FVS. Before 20 weeks' gestation, FVS can occur, with an incidence of about 1%. The lesions can affect the skin, limbs, central and autonomous nervous systems, eyes, cause calcifications, and growth retardation; mortality is high. Lesions typically follow one or several nerve territories, suggesting that damage results from in utero zoster following primary fetal infection. There has been little study of prenatal diagnosis of FVS. Serial ultrasound examination can detect various anomalies, magnetic resonance imaging can be of use to investigate for microphthamia and cerebral lesions, and amniocentesis can diagnose viral transmission. Prevention strategies include vaccination and post-exposure prophylaxis with immune globulin and/or antivirals. Perspectives for treating infected fetuses in utero require further research.

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Hints of intracerebral varicella-zoster virus reactivation in congenital varicella syndrome

et al. 2003

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Infants with intrauterine varicella-zoster virus (VZV) infection can suffer intracerebral VZV reactivations that require antiviral treatment.We report a 4-month-old boy whose mother had clinically confirmed mild varicella at 17 weeks' gestation, acquired from her first infant who had typical childhood chickenpox at the age of 5 years. At the age of 3 months, the infant developed typical dermatomal zoster rash within the ophthalmic division of the trigeminal nerve. On admission to hospital 1 day after onset of symptoms, the boy demonstrated right-accentuated clonic attacks. The EEG revealed delta waves with high amplitude and occasionally inserted spikes over the left occipito-parietal and temporal regions. MRI showed a signal alteration in the left region of the putamen interpreted as a post-ischaemic lesion (Fig. 1). Additionally, the ventricles were slightly enlarged. For laboratory studies, CSF and blood samples were taken 1 day after seizure onset. In the CSF, the number of cells (26 cells/ll) showing a lymphocytic cell picture was slightly elevated. Using the polymerase chain reaction, VZV DNA could be identified in the CSF. In a serum sample, specific IgM was negative and specific IgG concentration was elevated (enzyme-linked immunosorbent assay; Virotech, Ru¨sselsheim, Germany), indicating a past VZV infection. In the CSF, VZV-specific IgG class antibodies could be measured in titres of 1:64 with an indirect fluorescence antibody test. The boy was treated with phenobarbital, primarily 10 mg/kg as a single dose, followed by 5 mg/kg er day divided in two doses. For antiviral treatment, acyclovir was given intravenously at a dose of 10 mg/kg every 8 h for 10 days. Afterwards, the treatment with acyclovir was continued orally as suppressive therapy at a reduced dose for a period of 3 weeks. The drug was well tolerated and no signs of toxicity, in particular no signs of neutropenia, were seen. At the age of 6 months, VZV DNA could not be detected in the CSF and the titre of intrathecally measured VZV-specific IgG class antibodies decreased from 1:64 to 1:16. EEG findings did improve markedly at the age of 7 months and seizures did not occur.According to previous recommendations [4], diagnosis of congenital varicella syndrome (CVS) in our case was based on (1) the positive history of maternal varicella infection, (2) the presence of neurological defects, and (3) the proof of intrauterine VZV infection by the appearance of zoster during early infancy. Normally, CVS has been considered a multi-systemic disorder characterised by skin lesions accompanied with neurological defects, eye disease and/or limb hypoplasia [4]. In our case, the disease presented as generalised clonic seizures and the cerebral damage could be verified by both EEG and MRI findings. To date, manifestations of CVS limited to the brain have rarely been described in the literature [1,5,6]. In none of these reported cases was intracerebral infection proven by the detection of viral DNA and/or antibodies in the CSF. We could verify an intracerebral...

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Chickenpox in Mid‐Trimester Pregnancy: Always Innocent?

Cited by 9 publications

References 15 publications

Intracerebral varicella‐zoster virus reactivation in congenital varicella syndrome

Intracerebral varicella‐zoster virus reactivation in congenital varicella syndrome

Fetal varicella – diagnosis, management, and outcome

Hints of intracerebral varicella-zoster virus reactivation in congenital varicella syndrome

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