Respiratory Syncytial Virus Infections in Infants: Detel1ninants of Clinical Severity

In 1955 a virus was isolated by Morris et al. from a chimpanzee with an upper respiratory tract infection. This apparently new virus was originally called chimpanzee coryza agent. Soon aftclwards, when it was isolated from children with respiratory disease, it became clear that this virus was a major human pathogen. The virus was from then onward called respiratory syncytial virus (RSV) because of its ability to caLise respiratory disease and to induce large syncytia in cell culture. RSV is now known as the single most common cause of severe respiratory tract infection in childhood. In fact up to 70% of hospital admissions of infants for respiratory infections during the winter season may be caused by RSV alone. Soon after RSV was found to be a significant cause of morbidity and 1ll00iaiity in childhood the search for a vaccine began. During the sixties a formalin inactivated RSV (FI-RSV) candidate vaccine, known as "lot 100", was developed and administered to children of two to seven years old. This vaccine, in stead of protecting vaccinees against RSV infection, predisposed for more severe disease upon natural infection in the following RSV season. Hospitalization rates were as high as 80% and two of the vaccinces died. At this moment, despite considerable research efforts, no licensed vaccine is available against this important pathogen. Development ofa vaccine against RSV is one of the priorities of the Global Program for Vaccines of the World Health Organization

G protein variation in respiratory syncytial virus group A does not correlate with clinical severity

Respiratory syncytial virus group A strain variations of 28 isolates from The Netherlands collected during three consecutive seasons were studied by ana

Patient-to-patient spread of a single strain of Corynebacterium striatum causing infections in a surgical intensive care unit

Over a 12-month period, Corynebacterium striatum strains were isolated from clinical specimens from 14 patients admitted to a surgical intensive care unit. These isolates were identical by morphology and biotype and displayed the same antibiogram. Ten isolates were found to be the sole possible pathogen. These 10 isolates were from six patients, three of whom had signs of infection at the time of positive culture. Further typing was performed by random amplification of polymorphic DNA analysis, by which all strains were identical and were found to differ to various degrees from reference strains and from isolates found in clinical samples from other wards. In a case-control study the only independent risk factor for acquiring the strain was intubation for longer than 24 h (odds ratio, 20.09; 95