Lyme Disease Pathogenesis
Lyme disease are obligately parasitic, tick- transmitted, invasive, persistent bacterial pathogens that cause disease in humans and non-reservoir vertebrates primarily through the induction of inflammation. During transmission from the infected tick, the bacteria undergo significant changes in gene...
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Published in | Current Issues in Molecular Biology Vol. 42; pp. 473 - 518 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
2021
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Subjects | |
Online Access | Get full text |
ISSN | 1467-3037 1467-3045 1467-3045 |
DOI | 10.21775/cimb.042.473 |
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Abstract | Lyme disease
are obligately parasitic, tick- transmitted, invasive, persistent bacterial pathogens that cause disease in humans and non-reservoir vertebrates primarily through the induction of inflammation. During transmission from the infected tick, the bacteria undergo significant changes in gene expression, resulting in adaptation to the mammalian environment. The organisms multiply and spread locally and induce inflammatory responses that, in humans, result in clinical signs and symptoms.
virulence involves a multiplicity of mechanisms for dissemination and colonization of multiple tissues and evasion of host immune responses. Most of the tissue damage, which is seen in non-reservoir hosts, appears to result from host inflammatory reactions, despite the low numbers of bacteria in affected sites. This host response to the Lyme disease
can cause neurologic, cardiovascular, arthritic, and dermatologic manifestations during the disseminated and persistent stages of infection. The mechanisms by which a paucity of organisms (in comparison to many other infectious diseases) can cause varied and in some cases profound inflammation and symptoms remains mysterious but are the subjects of diverse ongoing investigations. In this review, we provide an overview of virulence mechanisms and determinants for which roles have been demonstrated
, primarily in mouse models of infection. |
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AbstractList | Lyme disease
Borrelia
are obligately parasitic,
tick-transmitted, invasive, persistent bacterial pathogens that cause disease in
humans and non-reservoir vertebrates primarily through the induction of
inflammation. During transmission from the infected tick, the bacteria undergo
significant changes in gene expression, resulting in adaptation to the mammalian
environment. The organisms multiply and spread locally and induce inflammatory
responses that, in humans, result in clinical signs and symptoms.
Borrelia
virulence involves a multiplicity of mechanisms
for dissemination and colonization of multiple tissues and evasion of host
immune responses. Most of the tissue damage, which is seen in non-reservoir
hosts, appears to result from host inflammatory reactions, despite the low
numbers of bacteria in affected sites. This host response to the Lyme disease
Borrelia
can cause neurologic, cardiovascular, arthritic,
and dermatologic manifestations during the disseminated and persistent stages of
infection. The mechanisms by which a paucity of organisms (in comparison to many
other infectious diseases) can cause varied and in some cases profound
inflammation and symptoms remains mysterious but are the subjects of diverse
ongoing investigations. In this review, we provide an overview of virulence
mechanisms and determinants for which roles have been demonstrated
in
vivo
, primarily in mouse models of infection. Lyme disease Borrelia are obligately parasitic, tick- transmitted, invasive, persistent bacterial pathogens that cause disease in humans and non-reservoir vertebrates primarily through the induction of inflammation. During transmission from the infected tick, the bacteria undergo significant changes in gene expression, resulting in adaptation to the mammalian environment. The organisms multiply and spread locally and induce inflammatory responses that, in humans, result in clinical signs and symptoms. Borrelia virulence involves a multiplicity of mechanisms for dissemination and colonization of multiple tissues and evasion of host immune responses. Most of the tissue damage, which is seen in non-reservoir hosts, appears to result from host inflammatory reactions, despite the low numbers of bacteria in affected sites. This host response to the Lyme disease Borrelia can cause neurologic, cardiovascular, arthritic, and dermatologic manifestations during the disseminated and persistent stages of infection. The mechanisms by which a paucity of organisms (in comparison to many other infectious diseases) can cause varied and in some cases profound inflammation and symptoms remains mysterious but are the subjects of diverse ongoing investigations. In this review, we provide an overview of virulence mechanisms and determinants for which roles have been demonstrated in vivo, primarily in mouse models of infection.Lyme disease Borrelia are obligately parasitic, tick- transmitted, invasive, persistent bacterial pathogens that cause disease in humans and non-reservoir vertebrates primarily through the induction of inflammation. During transmission from the infected tick, the bacteria undergo significant changes in gene expression, resulting in adaptation to the mammalian environment. The organisms multiply and spread locally and induce inflammatory responses that, in humans, result in clinical signs and symptoms. Borrelia virulence involves a multiplicity of mechanisms for dissemination and colonization of multiple tissues and evasion of host immune responses. Most of the tissue damage, which is seen in non-reservoir hosts, appears to result from host inflammatory reactions, despite the low numbers of bacteria in affected sites. This host response to the Lyme disease Borrelia can cause neurologic, cardiovascular, arthritic, and dermatologic manifestations during the disseminated and persistent stages of infection. The mechanisms by which a paucity of organisms (in comparison to many other infectious diseases) can cause varied and in some cases profound inflammation and symptoms remains mysterious but are the subjects of diverse ongoing investigations. In this review, we provide an overview of virulence mechanisms and determinants for which roles have been demonstrated in vivo, primarily in mouse models of infection. Lyme disease are obligately parasitic, tick- transmitted, invasive, persistent bacterial pathogens that cause disease in humans and non-reservoir vertebrates primarily through the induction of inflammation. During transmission from the infected tick, the bacteria undergo significant changes in gene expression, resulting in adaptation to the mammalian environment. The organisms multiply and spread locally and induce inflammatory responses that, in humans, result in clinical signs and symptoms. virulence involves a multiplicity of mechanisms for dissemination and colonization of multiple tissues and evasion of host immune responses. Most of the tissue damage, which is seen in non-reservoir hosts, appears to result from host inflammatory reactions, despite the low numbers of bacteria in affected sites. This host response to the Lyme disease can cause neurologic, cardiovascular, arthritic, and dermatologic manifestations during the disseminated and persistent stages of infection. The mechanisms by which a paucity of organisms (in comparison to many other infectious diseases) can cause varied and in some cases profound inflammation and symptoms remains mysterious but are the subjects of diverse ongoing investigations. In this review, we provide an overview of virulence mechanisms and determinants for which roles have been demonstrated , primarily in mouse models of infection. |
Author | Kraiczy, Peter Jewett, Mollie W. Norris, Steven J. Garcia, Brandon Hu, Linden T. Coburn, Jenifer Skare, Jon |
AuthorAffiliation | 2 Department of Microbiology and Immunology, East Carolina University, Brody School of Medicine, Greenville, NC 27858, USA 6 Department of Pathology and Laboratory Medicine, University of Texas Medical School at Houston, P.O. Box 20708, Houston, TX 77225, USA 5 Institute of Medical Microbiology and Infection Control, University Hospital Frankfurt, Goethe University Frankfurt, Paul-Ehrlich-Str. 40, 60596 Frankfurt, Germany 4 Immunity and Pathogenesis Division Head, Burnett School of Biomedical Sciences, University of Central Florida College of Medicine, 6900 Lake Nona Blvd. Orlando, FL 32827, USA 3 Department of Molecular Biology and Microbiology, Vice Dean of Research, Tufts University School of Medicine, 136 Harrison Ave., Boston, MA 02111, USA 1 Center For Infectious Disease Research, Medical College of Wisconsin, 8701 Watertown Plank Rd., TBRC C3980, Milwaukee, WI 53226, USA 7 Professor and Associate Head, Texas A&M University, 8447 Riverside Pkwy, Bryan, TX 77807, USA |
AuthorAffiliation_xml | – name: 3 Department of Molecular Biology and Microbiology, Vice Dean of Research, Tufts University School of Medicine, 136 Harrison Ave., Boston, MA 02111, USA – name: 7 Professor and Associate Head, Texas A&M University, 8447 Riverside Pkwy, Bryan, TX 77807, USA – name: 6 Department of Pathology and Laboratory Medicine, University of Texas Medical School at Houston, P.O. Box 20708, Houston, TX 77225, USA – name: 1 Center For Infectious Disease Research, Medical College of Wisconsin, 8701 Watertown Plank Rd., TBRC C3980, Milwaukee, WI 53226, USA – name: 5 Institute of Medical Microbiology and Infection Control, University Hospital Frankfurt, Goethe University Frankfurt, Paul-Ehrlich-Str. 40, 60596 Frankfurt, Germany – name: 4 Immunity and Pathogenesis Division Head, Burnett School of Biomedical Sciences, University of Central Florida College of Medicine, 6900 Lake Nona Blvd. Orlando, FL 32827, USA – name: 2 Department of Microbiology and Immunology, East Carolina University, Brody School of Medicine, Greenville, NC 27858, USA |
Author_xml | – sequence: 1 givenname: Jenifer surname: Coburn fullname: Coburn, Jenifer – sequence: 2 givenname: Brandon surname: Garcia fullname: Garcia, Brandon – sequence: 3 givenname: Linden T. surname: Hu fullname: Hu, Linden T. – sequence: 4 givenname: Mollie W. surname: Jewett fullname: Jewett, Mollie W. – sequence: 5 givenname: Peter surname: Kraiczy fullname: Kraiczy, Peter – sequence: 6 givenname: Steven J. surname: Norris fullname: Norris, Steven J. – sequence: 7 givenname: Jon surname: Skare fullname: Skare, Jon |
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Snippet | Lyme disease
are obligately parasitic, tick- transmitted, invasive, persistent bacterial pathogens that cause disease in humans and non-reservoir vertebrates... Lyme disease Borrelia are obligately parasitic, tick- transmitted, invasive, persistent bacterial pathogens that cause disease in humans and non-reservoir... Lyme disease Borrelia are obligately parasitic, tick-transmitted, invasive, persistent bacterial pathogens that cause disease in humans and non-reservoir... |
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SubjectTerms | Animals Arthropod Vectors - microbiology Borrelia - genetics Disease Models, Animal Disease Susceptibility Gene Expression Regulation, Bacterial Host-Pathogen Interactions Humans Lyme Disease - microbiology Lyme Disease - transmission Ticks - microbiology Virulence Virulence Factors - genetics |
Title | Lyme Disease Pathogenesis |
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