A hypervirulent Acinetobacter baumannii strain has robust anti-phagocytosis ability.

Area of Science:

• Microbiology
• Infectious Diseases
• Pathogenesis

Background:

• Acinetobacter baumannii (A. baumannii) is a significant cause of hospital-acquired infections (HAP) and community-acquired pneumonia (CAP).
• This study focuses on a novel CAP-associated A. baumannii (CAP-AB) strain, YC128, isolated from a severe CAP case in an otherwise healthy individual.

Observation:

• The YC128 strain induced severe pneumonia and high mortality (60%) in a mouse model, significantly exceeding the mortality caused by a hospital-acquired strain (HAP-AB, YC156).
• Pathological analysis revealed more severe lung inflammation and higher bacterial burden in mice infected with YC128 compared to YC156.
• YC128 exhibited enhanced resistance to phagocytosis by macrophages and induced a more rapid and severe pro-inflammatory cytokine response.

Findings:

• Whole Genome Sequencing (WGS) identified a complete Type VI Secretion System (T6SS) gene cluster in YC128, which was largely absent in the less virulent YC156 strain.
• The presence of T6SS in YC128 is strongly correlated with its hypervirulence and potent anti-phagocytic capabilities.
• Minimal differences in other virulence-related genes were observed between the two strains.

Implications:

• This research highlights a novel hypervirulent CAP-AB strain with the potential to cause severe community-acquired pneumonia.
• The findings suggest that T6SS is a key factor contributing to the increased pathogenicity of this A. baumannii strain.
• Understanding the role of T6SS in A. baumannii virulence could lead to new therapeutic strategies for combating severe bacterial pneumonia.