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Abstract
PLATE V
GROUP-B streptococci were recognised first as animal pathogens (Stableforth, 1932; Lancefield, 1934). However, Colebrook and Purdie (1937) related group-B streptococci to human disease, and there have since been reports linking group-B streptococci with human infections including septic abortion, puerperal sepsis, bacteraemia, neonatal sepsis, mastitis, meningitis, arthritis, osteomyelitis and inflammation of the urogenital tract (Duma et al., 1969, Eickhoff et al., 1964; Jelinkova, Neubauer and Duben, 1970; Bayer et al., 1976); the most fully documented of these are neonatal sepsis and meningitis. The first published account of neonatal meningitis caused by this organism in Great Britain was given by Jones and Howells (1968). Since then reports from all over the world have implicated group-B streptococci as neonatal pathogens (Jelinkova, 1977). It has been suggested that the newborn acquire the organism during passage through the birth canal (Hood, Janney and Dameron, 1961; Eickhoff et al., 1964; Baker and Barrett, 1973; Franciosi, Knostman and Zimmerman, 1973; Finch, French and Phillips, 1976). Group-B streptococcal infections in neonates appear to be of two types: one, an "early-onset" disease in the first week of life which may be septicaemic or meningitic, the other a "late-onset" disease which is almost always meningitic. There is little doubt that early-onset infections are the result of maternal carriage of the organism, but the source of the infecting streptococcus in late-onset disease is still unknown (Paredes et al., 1977).
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