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Updated: Jun 18, 2026

Tick Microbiome Characterization by Next-Generation 16S rRNA Amplicon Sequencing

Tick Microbiome Characterization by Next-Generation 16S rRNA Amplicon Sequencing

Published on: August 25, 2018

Persistence mechanisms in tick-borne diseases.

¹Department of Infectious Diseases & Pathology, College of Veterinary Medicine, University of Florida, Gainesville, Florida, USA.

The Onderstepoort Journal of Veterinary Research

|December 9, 2009

Summary

Persistent tick-borne diseases like babesiosis and anaplasmosis are common. Antigenic variation in pathogens, such as Babesia and Anaplasma, allows them to evade immunity and persist.

Area of Science:

Veterinary Parasitology
Molecular Biology
Immunology

Background:

Highly sensitive diagnostics reveal persistent infections are common in tick-borne diseases (babesiosis, anaplasmosis, heartwater).
Antigenic variation is a key mechanism enabling pathogen persistence by altering surface structures.
Previous research identified specific mechanisms in Babesia and Anaplasma, including cytoadhesion, ligand variation, and gene family diversity.

Purpose of the Study:

To investigate the role of antigenic variation in the persistence of tick-borne diseases.
To understand the mechanisms of immune evasion employed by Babesia, Anaplasma, and heartwater agents.
To explore the potential for genomic modification to study pathogen persistence and virulence.

Main Methods:

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Utilizing advanced diagnostic methods to detect persistent infections.

Analyzing gene families, such as pfam01617 in Anaplasma, associated with chronic infection and immune evasion.

Applying high-throughput sequencing for comprehensive analysis of pathogen genomes.

Considering genome modification techniques to assess effects on persistence and virulence.

Main Results:

Identified a polymorphic gene family in heartwater agents potentially involved in immune evasion.
Began characterizing the antigenic repertoires of these tick-borne pathogens.
Advanced understanding of mechanisms contributing to persistence, including cytoadhesion and genetic diversity in Babesia, and gene family variation in Anaplasma.

Conclusions:

Antigenic variation is a significant factor in the persistence of tick-borne diseases.
Further research is needed to address emerging infections (e.g., human Anaplasma) and the role of endothelial cell interaction in Anaplasma persistence.
Genomic approaches offer new possibilities for understanding and potentially manipulating pathogen persistence and virulence.