Multicystic Encephalomalacia: The Neuropathology of Systemic Neonatal Parechovirus Infection.

The Neuropathology of Human Parechovirus (HPeV) is not widely described due to the relatively recent discovery of the virus combined with a limited number of autopsy case reports. We report the case of an infant boy born at 38 weeks who, six days after birth, presented with fever and severe neurological dysfunction. Human Parechovirus Type 3 (HPeV3) RNA was detected in his cerebrospinal fluid (CSF) and blood. He died five days after his initial presentation. Neuropathologic examination demonstrated multicystic encephalomalacia (ME). This case report confirms that white matter pathology is dominant in HPeV3 infection. A unique feature, of HPeV encephalomalacia is absence of CSF pleocytosis and minimal inflammation in the meninges. The findings permit comment on the pathogenesis of brain injury by this virus.

Severe enteroviral encephalitis complicated by encephalomalacia--case presentation.

Enteroviral encephalitis is a rare neuroinfection more often diagnosed in children within the context of enteroviral epidemic outbreaks. It has pleomorphic clinical features, variable severity and a definite potential to cause neuropsychological sequelae especially in infants. Some subtypes are extremely severe with a mortality rate of up to 25% by affecting the brain stem. These subtypes usually come with highly specific findings on neuroimaging. We present a paediatric case of diffuse encephalitis most likely enteroviral in nature, with some particular features concerning the severe clinical form, the neuroimaging aspects and the neuropsychological sequelae due to the rarely described evolution towards encephalomalacia.

Persistence of herpes simplex virus DNA in cerebrospinal fluid of neonates with herpes simplex virus encephalitis.

OBJECTIVE: The significance of detecting herpes simplex virus (HSV) DNA in the cerebrospinal fluid (CSF) of infants with HSV encephalitis after receipt of prolonged therapy with high-dose (60 mg kg(-1) day(-1)) acyclovir is unknown. We report the clinical and laboratory characteristics, neuroimaging studies and outcomes of four neonates with HSV encephalitis who had persistence of CSF HSV DNA, by polymerase chain reaction (PCR) after 15 to 21 days of high-dose acyclovir therapy. STUDY DESIGN: Retrospective chart review. RESULTS: All four infants had abnormal neuroimaging studies and subsequently experienced severe developmental delay or death. CONCLUSION: A persistently positive CSF HSV PCR in neonates may be another risk factor for worse neurodevelopmental outcome. Prospective studies are needed to document how often HSV DNA persists in CSF, elucidate whether it represents an initially high CSF viral load, ongoing viral replication or viral resistance, and determine its possible association with neurodevelopmental impairment.

Brain lesions in pigs dually infected with porcine reproductive and respiratory syndrome virus and pseudorabies virus.

Four pigs were inoculated with an aerosol containing porcine reproductive and respiratory syndrome virus (PRRSV) followed 14 days later by inoculation with pseudorabies virus (PRV). The four dually infected pigs showed severe clinical signs, and one died on day 6 after infection with PRV. As demonstrated previously, the clinical disease was much more severe than that produced by either virus alone. All four dually infected pigs developed severe non-suppurative encephalitis, two had tonsillitis, two had necrotizing bronchiolitis, and one had lymphadenitis. The distribution of lesions corresponded closely with the detection of intranuclear inclusion bodies and PRV antigen. High numbers of TUNEL-positive cells detected in the thymus were associated with thymic atrophy.

Encephalomalacic lesions in pigs dually infected with porcine reproductive and respiratory syndrome virus and pseudorabies virus.

Four pigs (group 1) were infected with an aerosol containing porcine reproductive and respiratory syndrome virus (PRRSV) followed 7 days later by pseudorabies virus (PRV). Three further pigs (group 2) received PRRSV alone, two (group 3) received PRV alone, and two (group 4) remained as uninfected controls. Despite the admittedly small numbers of animals, the experiment appeared to throw light on aspects of synergy. Thus, the group 1 pigs showed severe neurological signs characterized by ataxia and muscular tremors. Total cell numbers in the bronchoalveolar lavage fluid were increased in all PRRSV-infected pigs, and PRRSV antigen was detected in the alveolar macrophages. Total cell numbers in the cerebrospinal fluid of group 1 pigs were considerably greater than those demonstrated in group 3, but no PRV antigen was found. Pigs of groups 1 and 2 showed pulmonary lesions, characterized by interstitial pneumonia and PRRSV antigen immunolabelling. Non-suppurative encephalitis was found in five of the six pigs of groups 1 and 3. In particular, one group 1 animal had severe necrotizing encephalitis with intranuclear inclusion bodies and associated immunolabelling of PRV antigen. The other three group 1 pigs had prominent malacic lesions, with macrophages. These neuropathological findings strongly suggested that PRRSV infection in pigs enhances the severity of brain lesions caused PRV.

Bilateral encephalomalacia in a pig related to latent Aujeszky's disease virus infection.

A case of bilateral encephalomalacia in a pig related to latent Aujeszky's disease virus infection is reported. The pig was experimentally inoculated with the NIA-3 strain and survived the infection after showing intense central nervous system disease. Abnormal behaviour was observed up to the date of death. The pig was demonstrated to be latently infected with the virus by polymerase chain reaction (PCR). The main microscopic lesion was a bilateral encephalomalacia which involved structures related to the limbic system. A complete description of lesions observed and their relation to abnormalities shown by the pig are exposed.