Impaired phagocytosis and opsonisation towards group B streptococci in preterm neonates
a Department of Infectious Diseases, b Department of Paediatrics, c Department of Clinical Microbiology,
Medical Centre Hospital, Örebro, Sweden, d Department of Clinical Microbiology, University
Hospital, Lund, Sweden, e Clinical Microbiology, Faculty of Health Sciences,
Linköping, Sweden
Correspondence to: Dr Jan Källman Department of Infectious Diseases, Medical Centre Hospital, Örebro S-701 85 Örebro, Sweden.
Accepted 21 July 1997
AIMS
To study the chemiluminescence response in
polymorphonuclear leucocytes (PMNL) at different stages of maturity and
the opsonic capacity of sera with defined titres of anti-capsular type
III antibodies, after exposure to serotype III group B streptococci (GBS). The influence of GBS type III capsule expression on PMNL chemiluminescence response was also investigated.
METHODSTwo clinical isolates of serotype III GBS
and two serotype III reference strains which form isogenic variants
with high and low amounts of capsule substance, respectively, were
used. PMNL and sera were obtained from adult healthy blood donors, full
term neonates, and preterm neonates.
RESULTSPMNL from premature infants showed a
significantly lower chemiluminescence response (p<0.0001) than the
PMNL from adults and neonates, while the chemiluminescence response
with adult, neonatal, and preterm sera gradually diminished. In the
presence of a serum pool with a standardised complement value, raised
(>10 mg/l), rather than low (<1.0 mg/l) anti-III antibody titres
induced a higher chemiluminescence response to the capsule expressing
variant. When GBS were cultured at pH 5.0, the bacteria had a higher
buoyant density, reflecting decreased expression of capsule substance compared with bacteria grown at pH 7.4. Concomitantly, there was a
substantial increase in chemiluminescence response for all isolates cultured at the lower pH, except for the capsule deficient mutant.
CONCLUSIONSPMNL function and opsonic capacity are
significantly impaired in neonates and correlate with maturation of the
newborn child. The combined defect in cellular and humoral defences in
preterm neonates may contribute to their increased susceptibility to
GBS infection. Growth conditions for GBS, simulating different in vivo
environments, greatly affect capsule expression and resistance to phagocytosis.
© 1998 by Archives of Disease in Childhood
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