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Updated: Feb 28, 2026
Extraction of Saliva, Haemolymph, Salivary Glands, and Midgut from Individual Ticks (Acari: Ixodidae)
Published on: October 31, 2025
Rickettsia parkeri genetic diversity from three different hard tick species (family: Ixodidae)
Madeleine Meyer Torelli1,2, Lídia Gual-Gonzalez1,2,3, Kristy Baus1
1Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC, 29208, USA.
Background:
Rickettsia parkeri sensu stricto, a causative agent of spotted fever rickettsiosis, is spread via the bite of infected ticks within the Amblyomma maculatum complex group. In the United States of America (USA), Am. maculatum Koch, 1844 is the primary vector for R. parkeri; however, Amblyomma americanum (Linnaeus, 1758) and Dermacentor variabilis (Say, 1821) have demonstrated potential to transmit R. parkeri under laboratory conditions. In this study, we investigate the genetic differences between R. parkeri detected in Am. maculatum, the primary enzootic vector, and potential secondary vectors - Am. americanum and De. variabilis.
Methods:
Using Nanopore long-read amplicon sequencing, we compared four R. parkeri genes amplified from naturally infected Am. maculatum, Am. americanum, and De. variabilis collected in the USA. Three R. parkeri genes associated with potential virulence factors were sequenced: outer membrane protein A (OmpA/sca0), outer membrane protein B (OmpB/sca5), and surface cell antigen 4 (gene D/sca4). One species-level gene target was used for species confirmation: 16S ribosomal RNA gene (16S).
Results:
Differences in cellular-entry and pathogen chromosomal genes (OmpA, OmpB, and 16S) were detected within the different tick species. No differences were noted in the cell-to-cell mediated transfer gene (gene D) between tick species.
Conclusions:
This preliminary study suggests that infection in Am. americanum may lead to changes in R. parkeri genes responsible for pathogen-host cell attachment and replication processes, but once established in a host cell, R. parkeri transfer between cells is unlikely to be impacted.
Insights
Genetic differences in Rickettsia parkeri were found between the primary vector tick, Amblyomma maculatum, and potential secondary vectors like Amblyomma americanum. These changes affect pathogen genes involved in host cell entry and replication.
Area of Science:
- Microbiology
- Vector-borne diseases
- Genomics
Background:
- Rickettsia parkeri causes spotted fever rickettsiosis, transmitted by ticks.
- Amblyomma maculatum is the primary US vector, but Amblyomma americanum and Dermacentor variabilis can also transmit R. parkeri.
Purpose of the Study:
- Investigate genetic variations of R. parkeri in different tick species.
- Compare R. parkeri genes between the primary vector (Am. maculatum) and potential secondary vectors (Am. americanum, De. variabilis).
Main Methods:
- Nanopore long-read amplicon sequencing used to analyze R. parkeri genes.
- Sequenced virulence factor genes (OmpA, OmpB, gene D) and a species confirmation gene (16S rRNA).
- Analyzed genes from R. parkeri in naturally infected Am. maculatum, Am. americanum, and De. variabilis.
Main Results:
- Detected genetic differences in R. parkeri genes related to cellular entry and chromosomal functions (OmpA, OmpB, 16S) across tick species.
- No genetic variations were observed in the cell-to-cell transfer gene (gene D).
Conclusions:
- R. parkeri infection in Am. americanum may alter genes involved in host cell attachment and replication.
- R. parkeri's cell-to-cell transfer mechanism is unlikely to be affected once established within a host cell.
