Dataset Information

Lyme carditis manifesting with sinoatrial exit block: a case report.

ABSTRACT:

Background

Lyme disease is the most common vector-borne disease in North America and Europe. Infection with the spirochete Borrelia burgdorferi complex can involve cardiac tissue causing Lyme carditis (LC). Due to the infection of conductive tissue, LC typically presents with varying degrees of atrioventricular conduction block. Here, we provide the first evidence that conductive tissue of the sinus node can be involved in LC resulting in higher degree sinoatrial (SA) block with concomitant syncope.

Case summary

We report the case of an otherwise healthy 31-year-old female presenting with LC manifesting with SA exit block causing asystole over 12 s with concomitant syncope. Signs of SA block completely resolved with antibiotic treatment with a third-generation cephalosporin. The patient did not require permanent pacemaker implantation and had no sinus pauses after 12 months of follow-up as confirmed via implantable loop recorder.

Conclusion

The possibility of LC in patients with sinus node dysfunction should be considered, as adequate antibiotic therapy can spare patients from potentially unnecessary pacemaker implantation.

SUBMITTER: Buscher A

PROVIDER: S-EPMC8801048 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:MicroRNAs have been shown to be important regulators of inflammatory and immune responses and are implicated in several immune disorders including systemic lupus erythematosus and rheumatoid arthritis, but their role in Lyme borreliosis remains unknown. We performed a microarray screen for expression of miRNAs in joint tissue from three mouse strains infected with Borrelia burgdorferi. This screen identified upregulation of miR-146a, a key negative regulator of NF-?B signaling, in all three strains, suggesting it plays an important role in the in vivo response to B. burgdorferi. Infection of B6 miR-146a-/- mice with B. burgdorferi revealed a critical nonredundant role of miR-146a in modulating Lyme arthritis without compromising host immune response or heart inflammation. The impact of miR-146a was specifically localized to the joint, and did not impact lesion development or inflammation in the heart. Furthermore, B6 miR-146a-/- mice had elevated levels of NF-?B-regulated products in joint tissue and serum late in infection. Flow cytometry analysis of various lineages isolated from infected joint tissue of mice showed that myeloid cell infiltration was significantly greater in B6 miR-146a-/- mice, compared to B6, during B. burgdorferi infection. Using bone marrow-derived macrophages, we found that TRAF6, a known target of miR-146a involved in NF-?B activation, was dysregulated in resting and B. burgdorferi-stimulated B6 miR-146a-/- macrophages, and corresponded to elevated IL-1?, IL-6 and CXCL1 production. This dysregulated protein production was also observed in macrophages treated with IL-10 prior to B. burgdorferi stimulation. Peritoneal macrophages from B6 miR-146a-/- mice also showed enhanced phagocytosis of B. burgdorferi. Together, these data show that miR-146a-mediated regulation of TRAF6 and NF-?B, and downstream targets such as IL-1?, IL-6 and CXCL1, are critical for modulation of Lyme arthritis during chronic infection with B. burgdorferi.