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...

Full description

Saved in:
Bibliographic Details
Published inCurrent Issues in Molecular Biology Vol. 42; pp. 473 - 518
Main Authors Coburn, Jenifer, Garcia, Brandon, Hu, Linden T., Jewett, Mollie W., Kraiczy, Peter, Norris, Steven J., Skare, Jon
Format Journal Article
LanguageEnglish
Published Switzerland 2021
Subjects
Online AccessGet full text
ISSN1467-3037
1467-3045
1467-3045
DOI10.21775/cimb.042.473

Cover

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.
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
BackLink https://www.ncbi.nlm.nih.gov/pubmed/33353871$$D View this record in MEDLINE/PubMed
BookMark eNp1kM1LwzAYh4NM3Jw7evAiO3rpzGeTXgSZnzDQw-4hTd9ugbaZTSfsv1_m5lDBUwJ58vu973OOeo1vAKFLgieUSCluravzCeZ0wiU7QQPCU5kwzEXveGeyj0YhuBzzyLBMiTPUZ4wJpiQZoKvZpobxgwtgAozfTbf0C2gguHCBTktTBRgdziGaPz3Opy_J7O35dXo_S2xM6BJVCp6DBcFKwzlWQmSWKsvTMiVAMyysoiojRWF4xpkhvKBUMFNKKkCmkg3R3T52tc5rKCw0XWsqvWpdbdqN9sbp3y-NW-qF_9QK85RIHANuDgGt_1hD6HTtgoWqMg34ddA0rs1xSjIS0eufXceSbx0RSPaAbX0ILZRHhGD9ZVzvjOtoXO9sDhH7w1vXmc753aiu-ufXFrCXg0A
CitedBy_id crossref_primary_10_1128_iai_00306_22
crossref_primary_10_3389_fimmu_2024_1390468
crossref_primary_10_1111_zph_13073
crossref_primary_10_1128_spectrum_02221_24
crossref_primary_10_3390_ijms24065594
crossref_primary_10_1007_s10096_024_04836_5
crossref_primary_10_1128_aem_01555_21
crossref_primary_10_1021_acsinfecdis_2c00346
crossref_primary_10_3389_fmicb_2022_998365
crossref_primary_10_3389_fmed_2023_1183344
crossref_primary_10_7874_jao_2023_00129
crossref_primary_10_33084_jmd_v2i1_3407
crossref_primary_10_1128_spectrum_01675_23
crossref_primary_10_1128_iai_00227_23
crossref_primary_10_3389_fcimb_2022_884171
crossref_primary_10_1128_iai_00090_24
crossref_primary_10_7759_cureus_64987
crossref_primary_10_1007_s00436_022_07445_3
crossref_primary_10_1080_21505594_2023_2265015
crossref_primary_10_1128_spectrum_01254_23
crossref_primary_10_3389_fmicb_2024_1469411
crossref_primary_10_1021_acs_analchem_3c04501
crossref_primary_10_1055_a_2215_0830
crossref_primary_10_3390_microorganisms10122509
crossref_primary_10_1007_s12326_023_00592_z
crossref_primary_10_7554_eLife_90135
crossref_primary_10_7554_eLife_90135_3
ContentType Journal Article
DBID AAYXX
CITATION
CGR
CUY
CVF
ECM
EIF
NPM
7X8
5PM
DOI 10.21775/cimb.042.473
DatabaseName CrossRef
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
MEDLINE - Academic
PubMed Central (Full Participant titles)
DatabaseTitle CrossRef
MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
MEDLINE - Academic
DatabaseTitleList
MEDLINE - Academic
MEDLINE
Database_xml – sequence: 1
  dbid: NPM
  name: PubMed
  url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 2
  dbid: EIF
  name: MEDLINE
  url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search
  sourceTypes: Index Database
DeliveryMethod fulltext_linktorsrc
Discipline Biology
EISSN 1467-3045
EndPage 518
ExternalDocumentID PMC8046170
33353871
10_21775_cimb_042_473
Genre Journal Article
Review
GrantInformation_xml – fundername: NIAID NIH HHS
  grantid: R01 AI037277
– fundername: NIAID NIH HHS
  grantid: R21 AI133367
– fundername: NIAID NIH HHS
  grantid: R21 AI140510
– fundername: NIAID NIH HHS
  grantid: R01 AI118799
– fundername: NIAID NIH HHS
  grantid: R01 AI121217
– fundername: NIAID NIH HHS
  grantid: R21 AI111317
– fundername: NIAID NIH HHS
  grantid: R01 AI099094
– fundername: NINDS NIH HHS
  grantid: R21 NS102766
– fundername: NIAID NIH HHS
  grantid: R21 AI103905
– fundername: NIAID NIH HHS
  grantid: R56 AI146930
GroupedDBID AAYXX
ALMA_UNASSIGNED_HOLDINGS
CITATION
M~E
---
0VX
36B
53G
5GY
A8Z
ADBBV
AENEX
AFZYC
BAWUL
C1A
CGR
CUY
CVF
DIK
E3Z
ECM
EIF
EMB
EMOBN
F5P
FRP
GROUPED_DOAJ
GX1
IAO
IGS
IHR
INH
ITC
MM.
MODMG
NPM
OK1
PGMZT
RNS
RPM
SV3
TR2
7X8
5PM
ID FETCH-LOGICAL-c387t-8f54bece53fa4408559c28c46f61e2905c82891dda4943a14d2253af725e7673
ISSN 1467-3037
1467-3045
IngestDate Thu Aug 21 18:18:31 EDT 2025
Fri Jul 11 13:32:33 EDT 2025
Wed Feb 19 02:27:24 EST 2025
Thu Apr 24 23:02:05 EDT 2025
Tue Jul 01 01:03:09 EDT 2025
IsDoiOpenAccess false
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Language English
LinkModel OpenURL
MergedId FETCHMERGED-LOGICAL-c387t-8f54bece53fa4408559c28c46f61e2905c82891dda4943a14d2253af725e7673
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
content type line 23
OpenAccessLink https://www.caister.com/cimb/v/v42/473.pdf
PMID 33353871
PQID 2473406191
PQPubID 23479
PageCount 46
ParticipantIDs pubmedcentral_primary_oai_pubmedcentral_nih_gov_8046170
proquest_miscellaneous_2473406191
pubmed_primary_33353871
crossref_primary_10_21775_cimb_042_473
crossref_citationtrail_10_21775_cimb_042_473
ProviderPackageCode CITATION
AAYXX
PublicationCentury 2000
PublicationDate 2021-00-00
PublicationDateYYYYMMDD 2021-01-01
PublicationDate_xml – year: 2021
  text: 2021-00-00
PublicationDecade 2020
PublicationPlace Switzerland
PublicationPlace_xml – name: Switzerland
PublicationTitle Current Issues in Molecular Biology
PublicationTitleAlternate Curr Issues Mol Biol
PublicationYear 2021
SSID ssib044733985
ssj0057871
Score 2.5237744
SecondaryResourceType review_article
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...
SourceID pubmedcentral
proquest
pubmed
crossref
SourceType Open Access Repository
Aggregation Database
Index Database
Enrichment Source
StartPage 473
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
URI https://www.ncbi.nlm.nih.gov/pubmed/33353871
https://www.proquest.com/docview/2473406191
https://pubmed.ncbi.nlm.nih.gov/PMC8046170
Volume 42
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1RT9swELZYJ6S9TGzAKGOoSIgXSFfHdpw8IlRUoRZegtQ3K3EcqERTtLZC5YHfvrvYSVvGJLYXq7ItN71LP9_Zd98RcgwAmCaBSD0TZcbjkQ69VEjtge2ueYfnkRSYjTy4Dnq3_GoohsvCkGV2ySxt6-c380r-R6vQB3rFLNl_0Gy9KHTAZ9AvtKBhaN-l4_5ibJA_E69YkGz_fnKH0DWarpqcFQNTKeEy-nVclcQ9dRRM9UXEBERcuKAXjHmpo3Ow4pAt0gx7W7a8uu_NK8feFMt46yvz5MJ_B8j5bWwUX3W4YHOVHRIiguI1qt0o3uhz8GnJsRz-cVuX5DUug98jkcNCj8ZpG2Ci7eat819f36jL235fxd1h_IF89GUQ-NX5i91bEV6ozRezD2JZU8vlf64uvm5l_OE6vI6AXTEp4i3y2fkCrXOr2C9kwxRfyaatDrrYJk1Ub8upt7Wq3h0SX3bji57nKll4moVy5oW54PBnMYLlCZb4BjdO-6HmQR5Q40cdodHxpVmW8IizhPIMYJYlufSFkYFku6RRTAqzR1oJFaGJaE59TblMdRhlidQs436W5mDdN8lZ9cOVdizvWGzkQYG3V8pJoZwUyEmBnJrkpJ7-aOlN_jbxqJKiAgDCW6WkMJP5VPkwilZhRJvkm5VqvRRjDDZUCSNyTd71BCQ3Xx8pRvclyXmIlQBkZ_8d3_udfMJ31x6MHZDG7Nfc_ABTcZYelkcs0A5euoflm_QbTPtrwg
linkProvider National Library of Medicine
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Lyme+Disease+Pathogenesis&rft.jtitle=Current+issues+in+molecular+biology&rft.au=Coburn%2C+Jenifer&rft.au=Garcia%2C+Brandon&rft.au=Hu%2C+Linden+T&rft.au=Jewett%2C+Mollie+W&rft.date=2021&rft.issn=1467-3045&rft.eissn=1467-3045&rft.volume=42&rft.spage=473&rft_id=info:doi/10.21775%2Fcimb.042.473&rft.externalDBID=NO_FULL_TEXT
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1467-3037&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1467-3037&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1467-3037&client=summon