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Scientists reveal how a deadly infant pathogen thrives without oxygen

A stealthy bacterium linked to fatal newborn infections just got deadlier. Scientists discovered its secret weapon: hijacking metabolism to outsmart both oxygen starvation and our defenses.

The image shows a paper with text written on it and a stamp on the left side. The text reads "New...
The image shows a paper with text written on it and a stamp on the left side. The text reads "New Process for Keeping Probiotics Perfectly Fresh".

Scientists reveal how a deadly infant pathogen thrives without oxygen

Scientists have uncovered a key mechanism that boosts the infectious power of Cronobacter sakazakii, a dangerous bacterium linked to severe neonatal infections. Their findings reveal how small RNA molecules (sRNAs) trigger nitrate respiration, helping the pathogen thrive in low-oxygen environments like the infant gut.

The study shows that sRNAs bind to mRNA encoding nitrate reductase, stabilising these transcripts and enhancing their translation. This process activates nitrate respiration, allowing the bacteria to use nitrogen oxides for energy when oxygen is scarce. As a result, the pathogen can form resilient biofilms, which resist both immune defences and antibiotic treatment.

Genetic experiments confirmed the link between sRNA-controlled nitrate respiration and increased virulence. In cell cultures and animal models, the bacteria exhibited stronger adhesion, invasion, and immune evasion when this mechanism was active. The sRNAs also suppress host immune responses by reducing bacterial surface antigens, making the pathogen harder to detect.

This discovery challenges the idea that virulence factors act separately from metabolism. Instead, the research suggests that bacterial energy production and infection strategies are tightly connected through RNA-based regulation.

The findings could lead to new diagnostic tools for detecting C. sakazakii infections in newborns. Targeting the nitrate respiration pathway might also offer therapeutic options by disrupting the bacterium's survival in oxygen-poor environments. The study highlights a direct link between metabolic flexibility and the pathogen's ability to cause severe disease.

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