Chlamydiatrachomatis and placental inflammation in early preterm delivery

Chlamydiatrachomatis may infect the placenta and subsequently lead to preterm delivery. Our aim was to evaluate the relationship between the presence of Chlamydiatrachomatis and signs of placental inflammation in women who delivered at 32 weeks gestation or less. Setting: placental histology and clinical data were prospectively obtained from 304 women and newborns at the Erasmus MC-Sophia, Rotterdam, the Netherlands. C.trachomatis testing of placentas was done retrospectively using PCR. C.trachomatis was detected in 76 (25%) placentas. Histological evidence of placental inflammation was present in 123 (40%) placentas: in 41/76 (54%) placentas with C.trachomatis versus 82/228 (36%) placentas without C.trachomatis infection (OR 2.1, 95% CI 1.2–3.5). C.trachomatis infection correlated with the progression (P = 0.009) and intensity (P = 0.007) of materno-fetal placental inflammation. C.trachomatis DNA was frequently detected in the placenta of women with early preterm delivery, and was associated with histopathological signs of placental inflammation

Fatal necrotizing pneumonia caused by group A streptococcus

Group A streptococcus (GAS) causes invasive, non-invasive and non-suppurative diseases. Pneumonia is one of the invasive infections caused by GAS. Although GAS is a significant and serious cause of childhood pneumonia, it is often overlooked clinically. Similarly, the recent literature is surprisingly scant on reports of GAS pneumonia and concentrates mainly on varicella-associated invasive GAS diseases. In this case report, we present a previously healthy 7-year-old child with community-acquired pneumonia that progressed rapidly and resulted in sepsis, respiratory failure and death. In both blood and pleural fluid cultures, Streptococcus pyogenes were isolated. On autopsy, macroscopic examination revealed that the lung tissue appeared to have lost its normal architecture. Necrosis was present and the lung had a spongy appearance with some solid areas. The light microscopy revealed massive oedema, haemorrhages, intense inflammatory cell infiltration and necrosis. This case report highlights the need for consideration of invasive GAS infection in the event of severe, rapidly progressing pneumonia in children