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The Trimeric Autotransporter Adhesin EmaA and Infective Endocarditis.

Keith P Mintz¹, David R Danforth¹, Teresa Ruiz²

¹Department of Microbiology and Molecular Genetics, University of Vermont, Burlington, VT 05405, USA.

Pathogens (Basel, Switzerland)

|February 23, 2024

Summary

Infective endocarditis (IE) can be caused by HACEK bacteria from the mouth. The adhesin EmaA from Aggregatibacter actinomycetemcomitans is a key factor in IE development.

Keywords:

3D structure bacterial adhesin biofilm collagen interactions electron tomography

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Area of Science:

Microbiology
Cardiology
Infectious Diseases

Background:

Infective endocarditis (IE) is a heart infection often linked to structural heart disease and Gram-positive bacteria.
The HACEK group, Gram-negative bacteria from the oral cavity, are less common causes of IE.
Aggregatibacter actinomycetemcomitans, a HACEK member, is associated with periodontitis and can spread to cause IE.

Purpose of the Study:

To explore the role of the bacterial adhesin EmaA in the pathogenesis of IE caused by Aggregatibacter actinomycetemcomitans.
To detail the biochemical, molecular, and structural properties of EmaA.
To understand how EmaA contributes to IE initiation and progression.

Main Methods:

Review of existing literature on EmaA, Aggregatibacter actinomycetemcomitans, and infective endocarditis.
Analysis of EmaA's sequence heterogeneity and its interaction with extracellular matrix components.
Discussion of EmaA's function as a virulence determinant.

Main Results:

EmaA, a nonfimbrial adhesin of A. actinomycetemcomitans, exhibits sequence variation based on serotype.
EmaA mediates bacterial adherence to host tissues by interacting with extracellular matrix components.
EmaA is identified as a critical virulence factor in the early stages of IE.

Conclusions:

The multifunctional adhesin EmaA plays a significant role in the pathogenicity of Aggregatibacter actinomycetemcomitans, particularly in the initiation of infective endocarditis.
Understanding EmaA's structure and function can provide insights into IE pathogenesis.
Targeting EmaA could be a potential strategy for preventing or treating IE caused by this bacterium.