Two cases of rotavirus gastroenteritis associated with neurological involvement, one with encephalitis (defined by abnormal neurological signs, cerebrospinal fluid (CSF) pleocytosis and detection of rotavirus genomic nucleic acid in the CSF) and one with a non-inflammatory encephalopathy (defined by abnormal neurological signs, an entirely normal CSF and detection of rotavirus genomic nucleic acid in the CSF), are presented and used as a basis to review and explore potential pathogenetic mechanisms, including direct viral replication within neurons and indirect effects of the newly described rotavirus 'enterotoxin'.

A rapid method for detection of respiratory syncytial virus (RSV) in nasopharyngeal aspirates, involving a combination of reverse transcription and polymerase chain reaction amplification (RT-PCR), has been developed. The RT-PCR assay employs oligonucleotide primers specific for the region of the RSV genome which encodes the Fl subunit of the fusion (F) glycoprotein. Other respiratory viruses do not give a positive reaction. The RT-PCR assay was tested on 202 nasopharyngeal aspirates collected from children with clinical signs of respiratory infection, and the results from RT-PCR were compared with those obtained from virus culture and direct detection by enzyme immunoassay (EIA). RT-PCR results were positive in 118 of 125 samples from which RSV was cultured, as well as in 4 of 7 samples which were culture negative but EIA positive. RT-PCR results were negative in 68 of 70 culture-negative, EIA-negative samples, which included 11 samples from which other respiratory viruses were isolated. The speed, sensitivity (94.6%), and specificity (>97%) of the RT-PCR assay suggest that this technique could be useful for rapid detection of RSV in clinical samples.

Objective  To investigate the role of fetal viral infection in the development of a range of adverse pregnancy outcomes (APOs), including pregnancy‐induced hypertensive disorders (PIHD), antepartum haemorrhage (APH), birthweight <10th percentile (small for gestational age, SGA) and preterm birth (PTB). Design  Population‐based case–control study. Setting  Laboratory‐based study. Population  The newborn screening cards of 717 adverse pregnancy cases and 609 controls. Methods  Newborn screening cards were tested for RNA from enteroviruses and DNA from herpesviruses using polymerase chain reaction (PCR). The herpesviruses were detected using two PCRs, one detecting nucleic acids from herpes simplex virus (HSV)‐1, HSV‐2, Epstein–Barr virus (EBV), cytomegalovirus (CMV) and human herpesvirus (HHV)‐8, hereafter designated Herpes PCR group A viruses, and the other detecting nucleic acids from varicella‐zoster virus (VZV), HHV‐6 and HHV‐7, hereafter designated Herpes PCR group B viruses. Main outcome measure  Odds ratios and 95% CIs for specific APOs. Results  For both term and PTBs, the risk of developing PIHD was increased in the presence of DNA from Herpes PCR group B viruses (OR 3.57, 95% CI 1.10–11.70), CMV (OR 3.89, 95% CI 1.67–9.06), any herpesvirus (OR 5.70, 95% CI 1.85–17.57) and any virus (OR 5.17, 95% CI 1.68–15.94). The presence of CMV was associated with PTB (OR 1.61, 95% CI 1.14–2.27). No significant association was observed between SGA or APH and exposure to viral infection. Conclusions  Fetal exposure to herpesvirus infection was associated with PIHD for both term and PTBs in this exploratory study. Exposure to CMV may also be associated with PTB. These findings need confirmation in future studies.

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Routine microbiological testing in cases presenting as SIDS did not reveal occult sepsis in most instances. Such testing did, however, add support to the diagnosis of SIDS where no pathogens were isolated and, if not undertaken, would have resulted in a small percentage of cases of sudden infant death due to infections remaining undiagnosed.

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