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Published on: September 11, 2020
Host-to-Host Transmission of Streptococcus pneumoniae Is Driven by Its Inflammatory Toxin, Pneumolysin
M Ammar Zafar1, Yang Wang2, Shigeto Hamaguchi1
1Department of Microbiology, New York University, New York, NY 10016, USA.
Insights
Streptococcus pneumoniae transmission relies on inflammation and bacterial shedding. Pneumolysin toxin drives inflammation, increasing shedding and environmental survival for new host transmission.
Area of Science:
- Microbiology
- Infectious Diseases
- Pathogenesis
Background:
- Host-to-host transmission is essential for pathogen propagation.
- Streptococcus pneumoniae is an opportunistic pathogen requiring effective transmission strategies.
Purpose of the Study:
- To investigate the mechanisms of Streptococcus pneumoniae transmission in a mouse model.
- To elucidate the role of pneumolysin in transmission and host-pathogen interaction.
Main Methods:
- Utilized an infant mouse model for studying Streptococcus pneumoniae transmission.
- Quantified bacterial shedding in nasal secretions and assessed inflammatory responses.
- Investigated the necessity and sufficiency of pneumolysin in promoting transmission.
Main Results:
- High bacterial shedding and acute inflammatory response were critical for transmission.
- Pneumolysin was essential and sufficient to induce inflammation, increase shedding, and enable transmission.
- Transmission occurred without direct contact, suggesting an environmental reservoir.
- Pneumolysin enhanced bacterial survival outside the host.
Conclusions:
- Pneumolysin-induced inflammation facilitates Streptococcus pneumoniae transmission by increasing shedding and environmental survival.
- This study reveals a microbial strategy for host transit, explaining the expression of damaging toxins.
Abstract:
Host-to-host transmission is a critical step for infection. Here we studied transmission of the opportunistic pathogen Streptococcus pneumoniae in an infant mouse model. Transmission from nasally colonized pups required high levels of bacterial shedding in nasal secretions and was temporally correlated with, and dependent upon, the acute inflammatory response. Pneumolysin, a pore-forming cytotoxin and major virulence determinant, was both necessary and sufficient to promote inflammation, which increased shedding and allowed for intralitter transmission. Direct contact between pups was not required for transmission indicating the importance of an environmental reservoir. An additional in vivo effect of pneumolysin was to enhance bacterial survival outside of the host. Our findings provide experimental evidence of a microbial strategy for transit to new hosts and explain why an organism expresses a toxin that damages the host upon which it depends.
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