Virulence studies of <it>Enterobacter sakazakii </it>isolates associated with a neonatal intensive care unit outbreak

<p>Abstract</p> <p>Background</p> <p>In 1994, an outbreak of <it>Enterobacter sakazakii </it>infections in France occurred in a neonatal intensive care unit during which 17 neonates were infected. More than half of the infected neonates had severe clinical symptoms; 7 cases of necrotising enterocolitis (one with abdominal perforation), one case of septicemia, and one case of meningitis. The other 8 neonates were shown to be colonized but remained asymptomatic. There were three deaths. Four distinguishable pulsotypes of <it>E. sakazakii </it>were isolated during the outbreak, and the deaths were attributable to one pulsotype. This paper compares strains, from the four pulsotypes, for attachment and invasion of mammalian intestinal cells, macrophage survival and blood-brain barrier invasion. A fourth death from septic shock also occurred during the <it>E. sakazakii </it>outbreak. This was due to <it>E. cloacae </it>which at the time of the outbreak had been misidentified as <it>E. sakazakii</it>. This isolate has been included in this study.</p> <p>Results</p> <p>All <it>E. sakazakii </it>strains attached and invaded Caco-2 human epithelial cells, and invaded rat brain capillary endothelial cells. The majority of strains persisted in macrophage cells for 48 h. Two strains from fatal NEC and meningitis cases showed the highest invasion rate of Caco-2 intestinal cells. Their invasion of brain capillary endothelial cells was equivalent or greater than that of the neonatal <it>E. coli </it>meningitis strain K1. These strains also had extended spectrum β-lactamase activities. <it>E. cloacae </it>differed from <it>E. sakazakii </it>due to the greater attachment and less invasion of epithelial cells, no survival in macrophages, and less invasion of capillary endothelial brain cells.</p> <p>Conclusion</p> <p>While variables such as host factors and treatment strategies determine the outcome of infection, our <it>in vitro </it>studies evaluated the virulence of the isolates associated with this outbreak. It was not possible to directly correlate clinical symptoms and outcomes with <it>in vitro </it>studies. Nevertheless, we have shown the variation in invasive potential of <it>E. sakazakii </it>with intestinal and blood-brain barrier cells between and within pulsotypes from a neonatal intensive care unit outbreak. <it>E. sakazakii </it>strains were able to persist and even replicate for a period within macrophage cells. These traits appear to facilitate host immune evasion and dissemination.</p>

Abstract licence: CC BY-NC-ND

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