In children, the incidence of complicated pneumonias (including empyemas an
d lung abscesses) associated with Streptococcus pneumonia infection has inc
reased in recent years. Ire many cases, these complicated pneumonias follow
ed flu-like illnesses. To determine mechanisms behind this association, a m
urine model of sequential pulmonary infection has been developed. BALB/cJ m
ice infected with influenza A had mild pulmonary inflammation that resolved
within 5-7 days. Seven days following their initial 'treatment' (mock infe
ction or influenza exposure), mice were challenged with 10(6) cfu of S. pne
umoniae, and their lungs were harvested at intervals fur analysis. Lungs of
influenza-exposed mice demonstrated greater colony counts 24 and 48 h foll
owing S. pneumoniae exposure compared to control mice. In addition, neutrop
hil numbers were significantly increased in the influenza/S. pneumoniae seq
uentially-infected animals compared to S. pneumoniae infection alone (1.4 /- 0.6 x 10(6) vs. 0.06 +/- 0.07 x 10(6) cells, P < 0.05, 24 h). Influenza-
exposed animals had greater levels of IL-1 beta and TNF-alpha in lung homog
enates following S. pnemoniae inoculation. These data demonstrate that mice
exposed to influenza have enhanced inflammatory responses and increased ba
cterial burden following S. pneumoniae exposure than do control mice. This
model will be useful in defining mechanisms behind the enhanced susceptibil
ity to S. pneumoniae that occurs after influenza exposure. (C) 2001 Elsevie
r Science B.V. All rights reserved.