The Different Clinical Courses of Legionnaires’ Disease in Newborns from the Same Maternity Hospital

Abstract

In children, the incidence of Legionnaires’ disease (LD) is unknown, hospital-acquired LD is associated with clinical risk factors and environmental risk, and children with cell-mediated immune deficiency are at high risk of infection. Both newborns were born in the same delivery room; stayed in the same hospital room where they were cared for, bathed, and breastfed; were male; were born on time, with normal birth weight, and with high Apgar score at birth; and survived this severe infection (L. pneumophila, serogroup 2-15) but with different clinical courses. In neonate 1, bleeding in the brain, thrombosis of deep pelvic veins, and necrosis of the lungs, which left behind cystic and cavernous changes in the lungs, were found, while neonate 2 suffered from pneumonia alone. The only difference in risk factors for LD between these two newborns is the number of days of illness until the start of azithromycin treatment (sixth versus the third day of illness). We suggest that a change in the guidelines for diagnosing and treating community-acquired pneumonia and hospital-acquired pneumonia in newborns is needed in terms of mandatory routine testing for Legionella pneumophila. Early initiation of macrolide therapy is crucial for the outcome of LD in the newborn.

A nutritional immunity blockade controls extracellular bacterial replication inLegionella pneumophilainfections

“…Under those conditions, extracellular replication can sustain bacterial growth despite IFNg production further aggravating inflammation, eliciting the severe symptomatology associated with Legionnaires' disease and causing pulmonary failure without a timely antibiotic administration. [120][121][122] Such a model places an emphasis on extracellular survival and replication as important determinants of disease progression, assertion strongly supported by the dominance of clinical strains with the capacity to evade host defenses targeting extracellular bacteria. Majority of serogroup-1 clinical isolates unlike environmental isolates (80% vs 30%) express the lag-1 gene encoding a LPS O-acetyltransferase, which confers resistance to complement killing and neutrophil internalization.…”