Editor—We were interested to see the article by Kallman et al,1 who have elegantly demonstrated the role that defective polymorphonuclear leucocyte (PMNL) function and reduced opsonic capacity have, in sepsis caused by group B streptococcus in preterm infants. They advocate the need for a vaccine or passive transfer of opsonic antibody. One vaccination strategy has recently been tried in an animal model.2

There are, however, other potential therapeutic strategies. One of us has previously shown that PMNL respiratory burst activity is reduced in preterm infants3 compared with term infants and adults, but can be increased (“primed”) by prior exposure to cytokines (rhGM-CSF). Therefore, an alternative approach in treatment is to enhance defective PMNL function with the administration of growth factors or cytokines, and we understand trials of this nature are currently in progress.

These observations highlight the need for further investigation of the mechanisms underlying the relative immunodeficiency of preterm infants as a basis for rational treatment. Even if a vaccine proves to be the most efficient treatment it can only work against the background of the child’s own immunological responsiveness.