Keith Berndtson
Park Ridge MultiMed, Park Ridge, IL, USA
Abstract:
Is chronic illness in patients with Lyme disease caused by persistent infection? Three decades of basic and clinical research have yet to produce a definitive answer to this question. This review describes known and suspected mechanisms by which spirochetes of the Borrelia genus evade host immune defenses and survive antibiotic challenge. Accumulating evidence indicates that Lyme disease spirochetes are adapted to persist in immune competent hosts, and that they are able to remain infective despite aggressive antibiotic challenge. Advancing understanding of the survival mechanisms of the Lyme disease spirochete carry noteworthy implications for ongoing research and clinical practice.
Introduction
Lyme disease (LD) is a tick-borne illness caused by the spirochete Borrelia burgdorferi (Bb). In North America, virulent strains of Bb are transmitted to humans and other animals by the deer tick, Ixodes scapularis. In addition to transmitting Bb into various animal hosts, during a feeding session deer ticks can also transmit strains of Anaplasma, Bartonella, Ehrlichia, or Babesia in combination with Bb.1,2
The illnesses resulting from such transmissions can produce polymicrobial infections whose interaction effects pose serious challenges for researchers investigating the etiopathogenesis of tick-borne illnesses, and for clinicians who would diagnose and treat the illness dynamics caused by them. Some aspects of the morbidity seen in posttreatment Lyme cases are likely caused by postinfectious immune processes, but this line of research is not the subject of this review. This paper reviews the known and suspected mechanisms by which Bb evades the immune systems of animal hosts. The review sections cover notable capabilities of the Bb genome, which encodes Bb’s ability to:
• Exploit tick salivary proteins to delay early host immune responses.
• Deceive alternative complement pathways by masking surface antigens.
• Usurp the host’s plasminogen activating system.
• Continuously vary its surface antigens to frustrate humoral immune responses.
• Translocate using uniquely agile motility skills.
• Use chemotactic and niche-seeking traits to evade host immune traffic.
• Engage in quorum sensing and in biofilm-like behavior.
• Upgrade its genetic code through horizontal gene transfer (HGT).
• Assume atypical morphologies that differ from its spirochetal form.
Park Ridge MultiMed, Park Ridge, IL, USA
Abstract:
Is chronic illness in patients with Lyme disease caused by persistent infection? Three decades of basic and clinical research have yet to produce a definitive answer to this question. This review describes known and suspected mechanisms by which spirochetes of the Borrelia genus evade host immune defenses and survive antibiotic challenge. Accumulating evidence indicates that Lyme disease spirochetes are adapted to persist in immune competent hosts, and that they are able to remain infective despite aggressive antibiotic challenge. Advancing understanding of the survival mechanisms of the Lyme disease spirochete carry noteworthy implications for ongoing research and clinical practice.
Introduction
Lyme disease (LD) is a tick-borne illness caused by the spirochete Borrelia burgdorferi (Bb). In North America, virulent strains of Bb are transmitted to humans and other animals by the deer tick, Ixodes scapularis. In addition to transmitting Bb into various animal hosts, during a feeding session deer ticks can also transmit strains of Anaplasma, Bartonella, Ehrlichia, or Babesia in combination with Bb.1,2
The illnesses resulting from such transmissions can produce polymicrobial infections whose interaction effects pose serious challenges for researchers investigating the etiopathogenesis of tick-borne illnesses, and for clinicians who would diagnose and treat the illness dynamics caused by them. Some aspects of the morbidity seen in posttreatment Lyme cases are likely caused by postinfectious immune processes, but this line of research is not the subject of this review. This paper reviews the known and suspected mechanisms by which Bb evades the immune systems of animal hosts. The review sections cover notable capabilities of the Bb genome, which encodes Bb’s ability to:
• Exploit tick salivary proteins to delay early host immune responses.
• Deceive alternative complement pathways by masking surface antigens.
• Usurp the host’s plasminogen activating system.
• Continuously vary its surface antigens to frustrate humoral immune responses.
• Translocate using uniquely agile motility skills.
• Use chemotactic and niche-seeking traits to evade host immune traffic.
• Engage in quorum sensing and in biofilm-like behavior.
• Upgrade its genetic code through horizontal gene transfer (HGT).
• Assume atypical morphologies that differ from its spirochetal form.
Источник Dovepress Journal
