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Shahid Karim - One of the best experts on this subject based on the ideXlab platform.
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The Tick endosymbiont Candidatus Midichloria mitochondrii and selenoproteins are essential for the growth of Rickettsia parkeri in the Gulf Coast Tick Vector
Microbiome, 2018Co-Authors: Khemraj Budachetri, Deepak Kumar, Gary Crispell, Christine Beck, Gregory A. Dasch, Shahid KarimAbstract:Background Pathogen colonization inside Tick tissues is a significant aspect of the overall competence of a Vector. Amblyomma maculatum is a competent Vector of the spotted fever group rickettsiae, Rickettsia parkeri. When R. parkeri colonizes its Tick host, it has the opportunity to dynamically interact with not just its host but with the endosymbionts living within it, and this enables it to modulate the Tick’s defenses by regulating Tick gene expression. The microbiome in A. maculatum is dominated by two endosymbiont microbes: a Francisella -like endosymbiont (FLE) and Candidatus Midichloria mitochondrii (CMM). A range of selenium-containing proteins (selenoproteins) in A. maculatum Ticks protects them from oxidative stress during blood feeding and pathogen infections. Here, we investigated rickettsial multiplication in the presence of Tick endosymbionts and characterized the functional significance of selenoproteins during R. parkeri replication in the Tick. Results FLE and CMM were quantified throughout the Tick life stages by quantitative PCR in R. parkeri -infected and uninfected Ticks. R. parkeri infection was found to decrease the FLE numbers but CMM thrived across the Tick life cycle. Our qRT-PCR analysis indicated that the transcripts of genes with functions related to redox (selenogenes) were upregulated in Ticks infected with R. parkeri . Three differentially expressed proteins, selenoprotein M, selenoprotein O, and selenoprotein S were silenced to examine their functional significance during rickettsial replication within the Tick tissues. Gene silencing of the target genes was found to impair R. parkeri colonization in the Tick Vector. Knockdown of the selenogenes triggered a compensatory response from other selenogenes, as observed by changes in gene expression, but oxidative stress levels and endoplasmic reticulum stress inside the Ticks were also found to have heightened. Conclusions This study illustrates the potential of this new research model for augmenting our understanding of the pathogen interactions occurring within Tick hosts and the important roles that symbionts and various Tick factors play in regulating pathogen growth.
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The Tick endosymbiont Candidatus Midichloria mitochondrii and selenoproteins are essential for the growth of Rickettsia parkeri in the Gulf Coast Tick Vector
Microbiome, 2018Co-Authors: Khemraj Budachetri, Deepak Kumar, Gary Crispell, Christine Beck, Gregory A. Dasch, Shahid KarimAbstract:Pathogen colonization inside Tick tissues is a significant aspect of the overall competence of a Vector. Amblyomma maculatum is a competent Vector of the spotted fever group rickettsiae, Rickettsia parkeri. When R. parkeri colonizes its Tick host, it has the opportunity to dynamically interact with not just its host but with the endosymbionts living within it, and this enables it to modulate the Tick’s defenses by regulating Tick gene expression. The microbiome in A. maculatum is dominated by two endosymbiont microbes: a Francisella-like endosymbiont (FLE) and Candidatus Midichloria mitochondrii (CMM). A range of selenium-containing proteins (selenoproteins) in A. maculatum Ticks protects them from oxidative stress during blood feeding and pathogen infections. Here, we investigated rickettsial multiplication in the presence of Tick endosymbionts and characterized the functional significance of selenoproteins during R. parkeri replication in the Tick. FLE and CMM were quantified throughout the Tick life stages by quantitative PCR in R. parkeri-infected and uninfected Ticks. R. parkeri infection was found to decrease the FLE numbers but CMM thrived across the Tick life cycle. Our qRT-PCR analysis indicated that the transcripts of genes with functions related to redox (selenogenes) were upregulated in Ticks infected with R. parkeri. Three differentially expressed proteins, selenoprotein M, selenoprotein O, and selenoprotein S were silenced to examine their functional significance during rickettsial replication within the Tick tissues. Gene silencing of the target genes was found to impair R. parkeri colonization in the Tick Vector. Knockdown of the selenogenes triggered a compensatory response from other selenogenes, as observed by changes in gene expression, but oxidative stress levels and endoplasmic reticulum stress inside the Ticks were also found to have heightened. This study illustrates the potential of this new research model for augmenting our understanding of the pathogen interactions occurring within Tick hosts and the important roles that symbionts and various Tick factors play in regulating pathogen growth.
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Catalase is a determinant of the colonization and transovarial transmission of Rickettsia parkeri in the Gulf Coast Tick Amblyomma maculatum
Insect molecular biology, 2017Co-Authors: Khemraj Budachetri, Deepak Kumar, Shahid KarimAbstract:The Gulf Coast Tick (Amblyomma maculatum) has evolved as a competent Vector of the spotted-fever group rickettsia, Rickettsia parkeri. In this study, the functional role of catalase, an enzyme responsible for the degradation of toxic hydrogen peroxide, in the colonization of the Tick Vector by R. parkeri and transovarial transmission of this pathogen to the next Tick generation, was investigated. Catalase gene (CAT) expression in midgut, salivary glands and ovarian tissues exhibited a 2–11-fold increase in transcription level upon R. parkeri infection. Depletion of CAT transcripts using an RNA-interference approach significantly reduced R. parkeri infection levels in midgut and salivary gland tissues by 53–63%. The role of CAT in transovarial transmission of R. parkeri was confirmed by simultaneously blocking the transcript and the enzyme by injecting double-stranded RNA for CAT and a catalase inhibitor (3-amino-1,2,4-triazole) into gravid females. Simultaneous inhibition of the CAT transcript and the enzyme significantly reduced the egg conversion ratio with a 44% reduction of R. parkeri transovarial transmission. These data suggest that catalase is required for rickettsial colonization of the Tick Vector and transovarial transmission to the next generation.
Jose De La Fuente - One of the best experts on this subject based on the ideXlab platform.
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anaplasma phagocytophilum infection subverts carbohydrate metabolic pathways in the Tick Vector ixodes scapularis
Frontiers in Cellular and Infection Microbiology, 2017Co-Authors: Alejandro Cabezascruz, Jose De La Fuente, Pilar Alberdi, James J Valdes, Margarita VillarAbstract:The obligate intracellular pathogen, Anaplasma phagocytophilum, is the causative agent of human, equine and canine granulocytic anaplasmosis and Tick-borne fever in ruminants. A. phagocytophilum has become an emerging Tick-borne pathogen in the United States, Europe, Africa and Asia, with increasing numbers of infected people and animals every year. It has been recognized that intracellular pathogens manipulate host cell metabolic pathways to increase infection and transmission in both vertebrate and invertebrate hosts. However, our current knowledge on how A. phagocytophilum affect these processes in the Tick Vector, Ixodes scapularis is limited. In this study, a genome-wide search for components of major carbohydrate metabolic pathways was performed in I. scapularis Ticks for which the genome was recently published. The enzymes involved in the seven major carbohydrate metabolic pathways glycolysis, gluconeogenesis, pentose phosphate, tricarboxylic acid cycle, glyceroneogenesis, and mitochondrial oxidative phosphorylation and β-oxidation were identified. Then, the available transcriptomics and proteomics data was used to characterize the mRNA and protein levels of I. scapularis major carbohydrate metabolic pathway components in response to A. phagocytophilum infection of Tick tissues and cultured cells. The results showed that major carbohydrate metabolic pathways are conserved in Ticks. A. phagocytophilum infection inhibits gluconeogenesis and mitochondrial metabolism, but increases the expression of glycolytic genes. A model was proposed to explain how A. phagocytophilum could simultaneously control Tick cell glucose metabolism and cytoskeleton organization, which may be achieved in part by up-regulating and stabilizing hypoxia inducible factor 1 alpha in a hypoxia-independent manner. The present work provides a more comprehensive view of the major carbohydrate metabolic pathways involved in the response to A. phagocytophilum infection in Ticks, and provides the basis for further studies to develop novel strategies for the control of granulocytic anaplasmosis.
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Tick Genome Assembled: New Opportunities for Research on Tick-Host-Pathogen Interactions.
Frontiers in Cellular and Infection Microbiology, 2016Co-Authors: Jose De La Fuente, Robert M Waterhouse, Daniel E. Sonenshine, Jose M C Ribeiro, R. Michael Roe, David B. Sattelle, Catherine A. HillAbstract:As Tick-borne diseases are on the rise, an international effort resulted in the sequence and assembly of the first genome of a Tick Vector. This result promotes research on comparative, functional and evolutionary genomics and the study of Tick-host-pathogen interactions to improve human, animal and ecosystem health on a global scale.
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anaplasma phagocytophilum increases the levels of histone modifying enzymes to inhibit cell apoptosis and facilitate pathogen infection in the Tick Vector ixodes scapularis
Epigenetics, 2016Co-Authors: Alejandro Cabezascruz, Pilar Alberdi, Nieves Ayllon, James J Valdes, Margarita Villar, Raymond J Pierce, Jose De La FuenteAbstract:Epigenetic mechanisms have not been characterized in Ticks despite their importance as Vectors of human and animal diseases worldwide. The objective of this study was to characterize the histones and histone modifying enzymes (HMEs) of the Tick Vector Ixodes scapularis and their role during Anaplasma phagocytophilum infection. We first identified 5 histones and 34 HMEs in I. scapularis in comparison with similar proteins in model organisms. Then, we used transcriptomic and proteomic data to analyze the mRNA and protein levels of I. scapularis histones and HMEs in response to A. phagocytophilum infection of Tick tissues and cultured cells. Finally, selected HMEs were functionally characterized by pharmacological studies in cultured Tick cells. The results suggest that A. phagocytophilum manipulates Tick cell epigenetics to increase I. scapularis p300/CBP, histone deacetylase, and Sirtuin levels, resulting in an inhibition of cell apoptosis that in turn facilitates pathogen infection and multiplication. These results also suggest that a compensatory mechanism might exist by which A. phagocytophilum manipulates Tick HMEs to regulate transcription and apoptosis in a tissue-specific manner to facilitate infection, but preserving Tick fitness to guarantee survival of both pathogens and Ticks. Our study also indicates that the pathogen manipulates arthropod and vertebrate cell epigenetics in similar ways to inhibit the host response to infection. Epigenetic regulation of Tick biological processes is an essential element of the infection by A. phagocytophilum and the study of the mechanisms and principal actors involved is likely to provide clues for the development of anti-Tick drugs and vaccines.
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Genomic insights into the Ixodes scapularis Tick Vector of Lyme disease
Nature Communications, 2016Co-Authors: Monika Gulia-nuss, Andrew B. Nuss, Karyn Megy, Jose De La Fuente, Robert M Waterhouse, Jason M Meyer, Daniel E. Sonenshine, Jose M C Ribeiro, Jyothi ThimmapuramAbstract:Ticks transmit more pathogens to humans and animals than any other arthropod. We describe the 2.1 Gbp nuclear genome of the Tick, Ixodes scapularis (Say), which Vectors pathogens that cause Lyme disease, human granulocytic anaplasmosis, babesiosis and other diseases. The large genome reflects accumulation of repetitive DNA, new lineages of retro-transposons, and gene architecture patterns resembling ancient metazoans rather than pancrustaceans. Annotation of scaffolds representing ∼57% of the genome, reveals 20,486 protein-coding genes and expansions of gene families associated with Tick–host interactions. We report insights from genome analyses into parasitic processes unique to Ticks, including host ‘questing’, prolonged feeding, cuticle synthesis, blood meal concentration, novel methods of haemoglobin digestion, haem detoxification, vitellogenesis and prolonged off-host survival. We identify proteins associated with the agent of human granulocytic anaplasmosis, an emerging disease, and the encephalitis-causing Langat virus, and a population structure correlated to life-history traits and transmission of the Lyme disease agent. Ticks transmit a large number of pathogens that cause human diseases. Here, the authors sequence the genome of the Tick Ixodes scapularis and uncover expansion of genes associated with parasitic processes unique to Ticks and Tick-host interactions.
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The intracellular bacterium Anaplasma phagocytophilum selectively manipulates the levels of vertebrate host proteins in the Tick Vector Ixodes scapularis
Parasites and Vectors, 2016Co-Authors: Margarita Villar, Pilar Alberdi, Nieves Ayllon, Alejandro Cabezas Cruz, Juan A. Lopez, Jesus Vazquez, Vladimir López, Jose De La FuenteAbstract:Background: The intracellular bacteria Anaplasma phagocytophilum are emerging zoonotic pathogens affecting human and animal health, and a good model for the study of Tick-host-pathogen interactions. This Tick-borne pathogen is transmitted by Ixodes scapularis in the United States where it causes human granulocytic anaplasmosis. Tick midguts and salivary glands play a major role during Tick feeding and development, and in pathogen acquisition, multiplication and transmission. Vertebrate host proteins are found in Tick midguts after feeding and have been described in the salivary glands of fed and unfed Ticks, suggesting a role for these proteins during Tick feeding and development. Furthermore, recent results suggested the hypothesis that pathogen infection affects Tick metabolic processes to modify host protein digestion and persistence in the Tick with possible implications for Tick physiology and pathogen life-cycle. Methods: To address this hypothesis, herein we used I. scapularis female Ticks fed on uninfected and A. phagocytophilum-infected sheep to characterize host protein content in midguts and salivary glands by proteomic analysis of Tick tissues. Results: The results evidenced a clear difference in the host protein content between Tick midguts and salivary glands in response to infection suggesting that A. phagocytophilum selectively manipulates the levels of vertebrate host proteins in Ticks in a tissue-specific manner to facilitate pathogen infection, multiplication and transmission while preserving Tick feeding and development. The mechanisms by which A. phagocytophilum manipulates the levels of vertebrate host proteins are not known, but the results obtained here suggested that it might include the modification of proteolytic pathways. Conclusions: The results of this study provided evidence to support that A. phagocytophilum affect Tick proteolytic pathways to selectively manipulate the levels of vertebrate host proteins in a tissue-specific manner to increase Tick Vector capacity. Investigating the biological relevance of host proteins in Tick biology and pathogen infection and the mechanisms used by A. phagocytophilum to manipulate host protein content is essential to advance our knowledge of Tick-host-pathogen molecular interactions. These results have implications for the identification of new targets for the development of vaccines for the control of Tick-borne diseases.
Khemraj Budachetri - One of the best experts on this subject based on the ideXlab platform.
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The Tick endosymbiont Candidatus Midichloria mitochondrii and selenoproteins are essential for the growth of Rickettsia parkeri in the Gulf Coast Tick Vector
Microbiome, 2018Co-Authors: Khemraj Budachetri, Deepak Kumar, Gary Crispell, Christine Beck, Gregory A. Dasch, Shahid KarimAbstract:Background Pathogen colonization inside Tick tissues is a significant aspect of the overall competence of a Vector. Amblyomma maculatum is a competent Vector of the spotted fever group rickettsiae, Rickettsia parkeri. When R. parkeri colonizes its Tick host, it has the opportunity to dynamically interact with not just its host but with the endosymbionts living within it, and this enables it to modulate the Tick’s defenses by regulating Tick gene expression. The microbiome in A. maculatum is dominated by two endosymbiont microbes: a Francisella -like endosymbiont (FLE) and Candidatus Midichloria mitochondrii (CMM). A range of selenium-containing proteins (selenoproteins) in A. maculatum Ticks protects them from oxidative stress during blood feeding and pathogen infections. Here, we investigated rickettsial multiplication in the presence of Tick endosymbionts and characterized the functional significance of selenoproteins during R. parkeri replication in the Tick. Results FLE and CMM were quantified throughout the Tick life stages by quantitative PCR in R. parkeri -infected and uninfected Ticks. R. parkeri infection was found to decrease the FLE numbers but CMM thrived across the Tick life cycle. Our qRT-PCR analysis indicated that the transcripts of genes with functions related to redox (selenogenes) were upregulated in Ticks infected with R. parkeri . Three differentially expressed proteins, selenoprotein M, selenoprotein O, and selenoprotein S were silenced to examine their functional significance during rickettsial replication within the Tick tissues. Gene silencing of the target genes was found to impair R. parkeri colonization in the Tick Vector. Knockdown of the selenogenes triggered a compensatory response from other selenogenes, as observed by changes in gene expression, but oxidative stress levels and endoplasmic reticulum stress inside the Ticks were also found to have heightened. Conclusions This study illustrates the potential of this new research model for augmenting our understanding of the pathogen interactions occurring within Tick hosts and the important roles that symbionts and various Tick factors play in regulating pathogen growth.
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The Tick endosymbiont Candidatus Midichloria mitochondrii and selenoproteins are essential for the growth of Rickettsia parkeri in the Gulf Coast Tick Vector
Microbiome, 2018Co-Authors: Khemraj Budachetri, Deepak Kumar, Gary Crispell, Christine Beck, Gregory A. Dasch, Shahid KarimAbstract:Pathogen colonization inside Tick tissues is a significant aspect of the overall competence of a Vector. Amblyomma maculatum is a competent Vector of the spotted fever group rickettsiae, Rickettsia parkeri. When R. parkeri colonizes its Tick host, it has the opportunity to dynamically interact with not just its host but with the endosymbionts living within it, and this enables it to modulate the Tick’s defenses by regulating Tick gene expression. The microbiome in A. maculatum is dominated by two endosymbiont microbes: a Francisella-like endosymbiont (FLE) and Candidatus Midichloria mitochondrii (CMM). A range of selenium-containing proteins (selenoproteins) in A. maculatum Ticks protects them from oxidative stress during blood feeding and pathogen infections. Here, we investigated rickettsial multiplication in the presence of Tick endosymbionts and characterized the functional significance of selenoproteins during R. parkeri replication in the Tick. FLE and CMM were quantified throughout the Tick life stages by quantitative PCR in R. parkeri-infected and uninfected Ticks. R. parkeri infection was found to decrease the FLE numbers but CMM thrived across the Tick life cycle. Our qRT-PCR analysis indicated that the transcripts of genes with functions related to redox (selenogenes) were upregulated in Ticks infected with R. parkeri. Three differentially expressed proteins, selenoprotein M, selenoprotein O, and selenoprotein S were silenced to examine their functional significance during rickettsial replication within the Tick tissues. Gene silencing of the target genes was found to impair R. parkeri colonization in the Tick Vector. Knockdown of the selenogenes triggered a compensatory response from other selenogenes, as observed by changes in gene expression, but oxidative stress levels and endoplasmic reticulum stress inside the Ticks were also found to have heightened. This study illustrates the potential of this new research model for augmenting our understanding of the pathogen interactions occurring within Tick hosts and the important roles that symbionts and various Tick factors play in regulating pathogen growth.
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Catalase is a determinant of the colonization and transovarial transmission of Rickettsia parkeri in the Gulf Coast Tick Amblyomma maculatum
Insect molecular biology, 2017Co-Authors: Khemraj Budachetri, Deepak Kumar, Shahid KarimAbstract:The Gulf Coast Tick (Amblyomma maculatum) has evolved as a competent Vector of the spotted-fever group rickettsia, Rickettsia parkeri. In this study, the functional role of catalase, an enzyme responsible for the degradation of toxic hydrogen peroxide, in the colonization of the Tick Vector by R. parkeri and transovarial transmission of this pathogen to the next Tick generation, was investigated. Catalase gene (CAT) expression in midgut, salivary glands and ovarian tissues exhibited a 2–11-fold increase in transcription level upon R. parkeri infection. Depletion of CAT transcripts using an RNA-interference approach significantly reduced R. parkeri infection levels in midgut and salivary gland tissues by 53–63%. The role of CAT in transovarial transmission of R. parkeri was confirmed by simultaneously blocking the transcript and the enzyme by injecting double-stranded RNA for CAT and a catalase inhibitor (3-amino-1,2,4-triazole) into gravid females. Simultaneous inhibition of the CAT transcript and the enzyme significantly reduced the egg conversion ratio with a 44% reduction of R. parkeri transovarial transmission. These data suggest that catalase is required for rickettsial colonization of the Tick Vector and transovarial transmission to the next generation.
Deepak Kumar - One of the best experts on this subject based on the ideXlab platform.
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The Tick endosymbiont Candidatus Midichloria mitochondrii and selenoproteins are essential for the growth of Rickettsia parkeri in the Gulf Coast Tick Vector
Microbiome, 2018Co-Authors: Khemraj Budachetri, Deepak Kumar, Gary Crispell, Christine Beck, Gregory A. Dasch, Shahid KarimAbstract:Background Pathogen colonization inside Tick tissues is a significant aspect of the overall competence of a Vector. Amblyomma maculatum is a competent Vector of the spotted fever group rickettsiae, Rickettsia parkeri. When R. parkeri colonizes its Tick host, it has the opportunity to dynamically interact with not just its host but with the endosymbionts living within it, and this enables it to modulate the Tick’s defenses by regulating Tick gene expression. The microbiome in A. maculatum is dominated by two endosymbiont microbes: a Francisella -like endosymbiont (FLE) and Candidatus Midichloria mitochondrii (CMM). A range of selenium-containing proteins (selenoproteins) in A. maculatum Ticks protects them from oxidative stress during blood feeding and pathogen infections. Here, we investigated rickettsial multiplication in the presence of Tick endosymbionts and characterized the functional significance of selenoproteins during R. parkeri replication in the Tick. Results FLE and CMM were quantified throughout the Tick life stages by quantitative PCR in R. parkeri -infected and uninfected Ticks. R. parkeri infection was found to decrease the FLE numbers but CMM thrived across the Tick life cycle. Our qRT-PCR analysis indicated that the transcripts of genes with functions related to redox (selenogenes) were upregulated in Ticks infected with R. parkeri . Three differentially expressed proteins, selenoprotein M, selenoprotein O, and selenoprotein S were silenced to examine their functional significance during rickettsial replication within the Tick tissues. Gene silencing of the target genes was found to impair R. parkeri colonization in the Tick Vector. Knockdown of the selenogenes triggered a compensatory response from other selenogenes, as observed by changes in gene expression, but oxidative stress levels and endoplasmic reticulum stress inside the Ticks were also found to have heightened. Conclusions This study illustrates the potential of this new research model for augmenting our understanding of the pathogen interactions occurring within Tick hosts and the important roles that symbionts and various Tick factors play in regulating pathogen growth.
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The Tick endosymbiont Candidatus Midichloria mitochondrii and selenoproteins are essential for the growth of Rickettsia parkeri in the Gulf Coast Tick Vector
Microbiome, 2018Co-Authors: Khemraj Budachetri, Deepak Kumar, Gary Crispell, Christine Beck, Gregory A. Dasch, Shahid KarimAbstract:Pathogen colonization inside Tick tissues is a significant aspect of the overall competence of a Vector. Amblyomma maculatum is a competent Vector of the spotted fever group rickettsiae, Rickettsia parkeri. When R. parkeri colonizes its Tick host, it has the opportunity to dynamically interact with not just its host but with the endosymbionts living within it, and this enables it to modulate the Tick’s defenses by regulating Tick gene expression. The microbiome in A. maculatum is dominated by two endosymbiont microbes: a Francisella-like endosymbiont (FLE) and Candidatus Midichloria mitochondrii (CMM). A range of selenium-containing proteins (selenoproteins) in A. maculatum Ticks protects them from oxidative stress during blood feeding and pathogen infections. Here, we investigated rickettsial multiplication in the presence of Tick endosymbionts and characterized the functional significance of selenoproteins during R. parkeri replication in the Tick. FLE and CMM were quantified throughout the Tick life stages by quantitative PCR in R. parkeri-infected and uninfected Ticks. R. parkeri infection was found to decrease the FLE numbers but CMM thrived across the Tick life cycle. Our qRT-PCR analysis indicated that the transcripts of genes with functions related to redox (selenogenes) were upregulated in Ticks infected with R. parkeri. Three differentially expressed proteins, selenoprotein M, selenoprotein O, and selenoprotein S were silenced to examine their functional significance during rickettsial replication within the Tick tissues. Gene silencing of the target genes was found to impair R. parkeri colonization in the Tick Vector. Knockdown of the selenogenes triggered a compensatory response from other selenogenes, as observed by changes in gene expression, but oxidative stress levels and endoplasmic reticulum stress inside the Ticks were also found to have heightened. This study illustrates the potential of this new research model for augmenting our understanding of the pathogen interactions occurring within Tick hosts and the important roles that symbionts and various Tick factors play in regulating pathogen growth.
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Catalase is a determinant of the colonization and transovarial transmission of Rickettsia parkeri in the Gulf Coast Tick Amblyomma maculatum
Insect molecular biology, 2017Co-Authors: Khemraj Budachetri, Deepak Kumar, Shahid KarimAbstract:The Gulf Coast Tick (Amblyomma maculatum) has evolved as a competent Vector of the spotted-fever group rickettsia, Rickettsia parkeri. In this study, the functional role of catalase, an enzyme responsible for the degradation of toxic hydrogen peroxide, in the colonization of the Tick Vector by R. parkeri and transovarial transmission of this pathogen to the next Tick generation, was investigated. Catalase gene (CAT) expression in midgut, salivary glands and ovarian tissues exhibited a 2–11-fold increase in transcription level upon R. parkeri infection. Depletion of CAT transcripts using an RNA-interference approach significantly reduced R. parkeri infection levels in midgut and salivary gland tissues by 53–63%. The role of CAT in transovarial transmission of R. parkeri was confirmed by simultaneously blocking the transcript and the enzyme by injecting double-stranded RNA for CAT and a catalase inhibitor (3-amino-1,2,4-triazole) into gravid females. Simultaneous inhibition of the CAT transcript and the enzyme significantly reduced the egg conversion ratio with a 44% reduction of R. parkeri transovarial transmission. These data suggest that catalase is required for rickettsial colonization of the Tick Vector and transovarial transmission to the next generation.
Tom G. Schwan - One of the best experts on this subject based on the ideXlab platform.
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ecological niche modeling and distribution of ornithodoros hermsi associated with Tick borne relapsing fever in western north america
PLOS Neglected Tropical Diseases, 2017Co-Authors: Kylie Sage, Mike B. Teglas, Tammi L Johnson, Nathan C Nieto, Tom G. SchwanAbstract:Tick-borne relapsing fever in western North America is a zoonosis caused by the spirochete bacterium, Borrelia hermsii, which is transmitted by the bite of infected Ornithodoros hermsi Ticks. The pathogen is maintained in natural cycles involving small rodent hosts such as chipmunks and tree squirrels, as well as the Tick Vector. In order for these Ticks to establish sustained and viable populations, a narrow set of environmental parameters must exist, primarily moderate temperatures and moderate to high amounts of precipitation. Maximum Entropy Species Distribution Modeling (Maxent) was used to predict the species distribution of O. hermsi and B. hermsii through time and space based on current climatic trends and future projected climate changes. From this modeling process, we found that the projected current distributions of both the Tick and spirochete align with known endemic foci for the disease. Further, global climate models predict a shift in the distribution of suitable habitat for the Tick Vector to higher elevations. Our predictions are useful for targeting surveillance efforts in areas of high risk in western North America, increasing the efficiency and accuracy of public health investigations and Vector control efforts.
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cotransmission of divergent relapsing fever spirochetes by artificially infected ornithodoros hermsi
Applied and Environmental Microbiology, 2011Co-Authors: Paul F. Policastro, Sandra J Raffel, Tom G. SchwanAbstract:The soft Tick Ornithodoros hermsi, which ranges in specific arboreal zones of western North America, acts as a Vector for the relapsing fever spirochete Borrelia hermsii. Two genomic groups (genomic group I [GGI] and GGII) of B. hermsii are differentiated by multilocus sequence typing yet are codistributed in much of the Vector's range. To test whether the Tick Vector can be infected via immersion, noninfected, colony-derived O. hermsi larvae were exposed to reduced-humidity conditions before immersion in culture suspensions of several GGI and GGII isolates. We tested for spirochetes in Ticks by immunofluorescence microscopy and in mouse blood by quantitative PCR of the vtp locus to differentiate spirochete genotypes. The immersed larval Ticks were capable of spirochete transmission to mice at the first nymphal feeding. Tick infection with mixed cultures of isolates DAH (vtp-6) (GGI) and MTW-2 (vtp-5) (GGII) resulted in Ticks that caused spirochetemias in mice consisting of MTW-2 or both DAH and MTW-2. These findings show that this soft Tick species can acquire B. hermsii by immersion in spirochete suspensions, that GGI and GGII isolates can coinfect the Tick Vector by this method, and that these spirochetes can be cotransmitted to a rodent host.
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Outer surface protein A protects Lyme disease spirochetes from acquired host immunity in the Tick Vector.
Infection and immunity, 2008Co-Authors: James M. Battisti, Patricia A. Rosa, Tom G. Schwan, James L. Bono, Merry E. Schrumpf, Paul F. PolicastroAbstract:The Lyme disease spirochete Borrelia burgdorferi alters the expression of outer surface protein (osp) genes as the bacterium cycles between Ticks and mammals. OspA is produced as borreliae enter the Tick Vector and remains a major surface antigen during midgut colonization. To elucidate the role of OspA in the Vector, we created an insertional deletion of ospA in strain B31-A3. The ospA mutant infects mice when it is injected intradermally and is acquired by larval Ticks fed on these mice, where it persists through the molt to the nymph stage. Bacterial survival rates in artificially infected Tick larvae fed on naive mice were compared with those in the Vector fed on immune mice. The ospA mutant proliferates in larvae if it is exposed to blood from naive mice, but it declines in density after larval feeding if the blood is from immune mice. When uninfected larvae are fed on B-cell-deficient mice infected with the ospA mutant, larvae show borrelial densities and persistence that are significantly greater than those fed on infected, immunocompetent mice. We conclude that OspA serves a critical antibody-shielding role during Vector blood meal uptake from immune hosts and is not required for persistence in the Tick Vector.
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Defining plasmids required by Borrelia burgdorferi for colonization of Tick Vector Ixodes scapularis (Acari: Ixodidae).
Journal of medical entomology, 2005Co-Authors: Dorothee Grimm, Kit Tilly, Tom G. Schwan, Dawn M. Bueschel, Mark A. Fisher, Paul F. Policastro, Frank C. Gherardini, Patricia A. RosaAbstract:Maintenance in nature of Borrelia burgdorferi, the pathogenic bacterium that causes Lyme disease, requires transmission through an infectious cycle that includes a Tick Vector and a mammalian host. The genetic requirements for persistence in these disparate environments have not been well defined. B. burgdorferi has a complex genome composed of a chromosome and >20 plasmids. Previous work has demonstrated that B. burgdorferi requires two plasmids, lp25 and lp28-1, in the mammalian host. To investigate the requirement for these same two plasmids during Tick infection, we experimentally infected larval Ticks with B. burgdorferi lacking either lp25 or lp28-1 and then assessed the spirochete load in Ticks at different points of the infection. Whereas plasmid lp28-1 was dispensable in Ticks, plasmid lp25 was essential for Tick infection. Furthermore, we investigated the requirement in Ticks for the lp25 gene bbe22, which encodes a nicotinamidase that is necessary and sufficient for mammalian infection by B. burgdorferi clones lacking lp25. This gene was also sufficient in Ticks to restore survival of spirochetes lacking lp25. This is the first study to investigate the requirement for specific plasmids by B. burgdorferi within the Tick Vector, and it begins to establish the genomic components required for persistence of this pathogen throughout its natural infectious cycle.
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lethal effect of rickettsia rickettsii on its Tick Vector dermacentor andersoni
Applied and Environmental Microbiology, 1999Co-Authors: Mark L Niebylski, Mort G Peacock, Tom G. SchwanAbstract:Rickettsia rickettsii, the causative agent of Rocky Mountain spotted fever, was lethal for the majority of experimentally and transovarially infected Rocky Mountain wood Ticks (Dermacentor andersoni). Overall, 94.1% of nymphs infected as larvae by feeding on rickettsemic guinea pigs died during the molt into adults and 88.3% of adult female Ticks infected as nymphs died prior to feeding. In contrast, only 2.8% of uninfected larvae failed to develop into adults over two generations. Infected female Ticks incubated at 4°C had a lower mortality (80.9%) than did those held at 21°C (96.8%). Rickettsiae were vertically transmitted to 39.0% of offspring, and significantly fewer larvae developed from infected Ticks. The lethal effect of R. rickettsii may explain the low prevalence of infected Ticks in nature and affect its enzootic maintenance.
