The Policy Research Programme, Department of Health, UK.

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Defining the causal relationship between a microbe and encephalitis is complex. Over 100 different infectious agents may cause encephalitis, often as one of the rarer manifestations of infection. The gold-standard techniques to detect causative infectious agents in encephalitis in life depend on the study of brain biopsy material; however, in most cases this is not possible. We present the UK perspective on aetiological case definitions for acute encephalitis and extend them to include immune-mediated causes. Expert opinion was primarily used and was supplemented by literature-based methods. Wide usage of these definitions will facilitate comparison between studies and result in a better understanding of the causes of this devastating condition. They provide a framework for regular review and updating as the knowledge base increases both clinically and through improvements in diagnostic methods. The importance of new and emerging pathogens as causes of encephalitis can be assessed against the principles laid out here.

BackgroundOur intention was to compare the rate of immunological progression prior to antiretroviral therapy (ART) and the virological response to ART in patients infected with subtype B and four non-B HIV-1 subtypes (A, C, D and the circulating recombinant form, CRF02-AG) in an ethnically diverse population of HIV-1-infected patients in south London.MethodsA random sample of 861 HIV-1-infected patients attending HIV clinics at King's and St Thomas' hospitals' were subtyped using an in-house enzyme-linked immunoassay and env sequencing. Subtypes were compared on the rate of CD4 cell decline using a multi-level random effects model. Virological response to ART was compared using the time to virological suppression (< 400 copies/ml) and rate of virological rebound (> 400 copies/ml) following initial suppression.ResultsComplete subtype and epidemiological data were available for 679 patients, of whom 357 (52.6%) were white and 230 (33.9%) were black African. Subtype B (n = 394) accounted for the majority of infections, followed by subtypes C (n = 125), A (n = 84), D (n = 51) and CRF02-AG (n = 25). There were no significant differences in rate of CD4 cell decline, initial response to highly active antiretroviral therapy and subsequent rate of virological rebound for subtypes B, A, C and CRF02-AG. However, a statistically significant four-fold faster rate of CD4 decline (after adjustment for gender, ethnicity and baseline CD4 count) was observed for subtype D. In addition, subtype D infections showed a higher rate of virological rebound at six months (70%) compared with subtypes B (45%, p = 0.02), A (35%, p = 0.004) and C (34%, p = 0.01)ConclusionsThis is the first study from an industrialized country to show a faster CD4 cell decline and higher rate of subsequent virological failure with subtype D infection. Further studies are needed to identify the molecular mechanisms responsible for the greater virulence of subtype D.

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Background: A study was undertaken to determine the impact of respiratory syncytial virus (RSV) infection, both in hospital and the community, on healthcare utilisation and respiratory morbidity in prematurely born infants and to identify risk factors for symptomatic RSV infection. Methods: A hospital and community follow up study was undertaken of 126 infants born before 32 weeks of gestational age. Healthcare utilisation (hospital admissions and general practitioner attendances) in the first year, respiratory morbidity at follow up (wheeze and cough documented by parent completed diary cards), and RSV positive lower respiratory tract infections (LRTIs) were documented. Nasopharyngeal aspirates were obtained for immunofluorescence and culture for RSV whenever the infants had an LRTI, either in the community or in hospital. Results: Forty two infants had an RSV positive LRTI (RSV group), 50 had an RSV negative LRTI (RSV negative LRTI group), and 32 infants had no LRTI (no LRTI group). Compared with the RSV negative LRTI and the no LRTI groups, the RSV group required more admissions (p = 0.392, p,0.001) and days in hospital (p = 0.049, p = 0.006) and had more cough (p = 0.05, p = 0.038) and wheeze (p = 0.003, p = 0.003) at follow up. Significant risk factors for symptomatic RSV LRTI were number of siblings (p = 0.035) and maternal smoking in pregnancy (p = 0.005), for cough were number of siblings (p = 0.002) and RSV LRTI (p = 0.02), and for wheeze was RSV LRTI (p = 0.019). Conclusion: RSV infection, even if hospital admission is not required, is associated with increased subsequent respiratory morbidity in prematurely born infants.