In nature, individual ticks can be concomittently infected with more than one species of intracellular bacteria. Some may be important human pathogens acquired either from an infectious bloodmeal or transovarially. Others may be nonpathogenic symbionts acquired transovarially. The consequences and epidemiological significance of multiple bacterial infections in ticks are largely unexplored. We propose that the interactive effects between certain intracellular bacterial species within individual ticks may be of sufficient prevalence and magnitude to alter the vector competence of ticks. Ovaries of Dermacentor andersoni ticks harboring a particular nonpathogenic species of spotted fever group rickettsia, namely Rickettsia peacockii, have been shown to be refractory to subsequent co- infection with otherwise invasive R. rickettsii. Thus, ovarial infection of D. andersoni with R. peacockii rickettsiae interferes or blocks normal transovarial transmission of R. rickettsii. Infections with two or more closely-related rickettsial species may result either in interference (i.e., one species inhibits the development and/or transmission of the other), mutualism (i.e., enhanced transmission of both species), or phenotypic mixing (i.e., increased or decreased virulence). This proposal specifically addresses transovarial interference of the human pathogen, Rickettsia rickettsii, in the tick vector transovarially infected with nonpathogenic rickettsiae. We will investigate the phenomenon of transovarial interference in the context of its epidemiological significance and the mechanism(s) by which it occurs.
Two specific aims are proposed: 1) We will investigate the prevalence and relative efficiency of transovarial interference of R. rickettsii as medicated by other indigenous species of nonpathogenic spotted fever group rickettsiae within D. andersoni and D. variabilis. This will entail field collections of ticks and laboratory evaluation of the interference potential of these agents; and 2) We will initiate studies to examine the molecular mechanism (s) of transovarial interference of R. rickettsii by R. peacockii and other nonpathogenic spotted fever group rickettsiae.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Project (R01)
Project #
5R01AI043006-04
Application #
6362350
Study Section
Special Emphasis Panel (ZRG5-TMP (01))
Program Officer
Aultman, Kathryn S
Project Start
1998-03-01
Project End
2003-02-28
Budget Start
2001-03-01
Budget End
2002-02-28
Support Year
4
Fiscal Year
2001
Total Cost
$190,784
Indirect Cost
Name
University of Maryland Baltimore
Department
Microbiology/Immun/Virology
Type
Schools of Medicine
DUNS #
003255213
City
Baltimore
State
MD
Country
United States
Zip Code
21201
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Gillespie, Joseph J; Phan, Isabelle Q H; Scheib, Holger et al. (2015) Structural Insight into How Bacteria Prevent Interference between Multiple Divergent Type IV Secretion Systems. MBio 6:e01867-15
Pelc, Rebecca S; McClure, Jennifer C; Kaur, Simran J et al. (2015) Disrupting protein expression with Peptide Nucleic Acids reduces infection by obligate intracellular Rickettsia. PLoS One 10:e0119283
Smith, Todd A; Driscoll, Timothy; Gillespie, Joseph J et al. (2015) A Coxiella-like endosymbiont is a potential vitamin source for the Lone Star tick. Genome Biol Evol 7:831-8
Pelc, R S; McClure, J C; Sears, K T et al. (2014) Defending the fort: a role for defensin-2 in limiting Rickettsia montanensis infection of Dermacentor variabilis. Insect Mol Biol 23:457-65
Gillespie, Joseph J; Driscoll, Timothy P; Verhoeve, Victoria I et al. (2014) Genomic diversification in strains of Rickettsia felis Isolated from different arthropods. Genome Biol Evol 7:35-56
Petchampai, N; Sunyakumthorn, P; Guillotte, M L et al. (2014) Molecular and functional characterization of vacuolar-ATPase from the American dog tick Dermacentor variabilis. Insect Mol Biol 23:42-51
Rahman, M Sayeedur; Gillespie, Joseph J; Kaur, Simran Jeet et al. (2013) Rickettsia typhi possesses phospholipase A2 enzymes that are involved in infection of host cells. PLoS Pathog 9:e1003399

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