No abstract

No abstract

We report a case of new-onset postural orthostatic tachycardia syndrome in a healthy 46-year-old female after a single dose of the BNT162b2 (Pfizer-BioNTech) SARS-CoV-2 vaccine. There have been three prior reports of new-onset postural orthostatic tachycardia syndrome after COVID-19 vaccination. Predominant symptoms noted included fatigue, brain fog, headache, sinus tachycardia, and dizziness. Management includes noninvasive therapies, behavioral approaches, and pharmacologic regimens. Here, the patient presented with fatigue, palpitations, dizziness, and presyncope, with symptoms beginning 7 days after vaccination. Presenting vitals included temperature within normal limits, inappropriate tachycardia, up to 120 beats per minute, blood pressure of 128/87 mm of mercury, and 100% saturation in room air. Her management included lifestyle changes, dietary supplements, and ivabradine. Further studies are needed to evaluate prevalence, etiology, and optimal management.

Chlamydia pneumoniae causes respiratory infection in adults and children. Previous studies in our laboratory identified significantly higher in vitro T lymphocyte responses to C. pneumoniae in children with asthma compared to healthy controls which may indicate the presence of T effector memory (TEM) lymphocytes. In the present study, we screened healthy subjects for the presence of TEM cells and their cytokines. CCR7 negative effector TEMs may indicate persistent infection with C. pneumoniae. METHODS: Peripheral blood mononuclear cells (PBMC) (1310 6 /mL) from adult non-asthmatic subjects (N55) were infected or mock-infected for 1h +/-C. pneumoniae TW-183 at a multiplicity of infection (MOI) 5 0.1 or 0.01 and cultured for 48 hrs. Distributions of lymphocytes (CD4+, CD8+) and TEM cells (CD4+CCR7+CD45RA+CD154+, CD8+CCR7+CD45RA+CD154+) were determined. Levels of intracellular Interleukin (IL)-2, IL-4, and Interferon (IFN)-gamma were measured (flow microfluorimetry). RESULTS: C. pneumoniae infection (48 hr) led to a decrease in numbers of CD8+ TEM and CD8+CD154+ cells (50%, 33%, respectively); numbers of CD4+TEM and CD4+CD154+ cells did not change. In addition, numbers of TEM cells (CD4+IL-2+, CD8+ IL-2+) decreased (;27%, 50%, respectively). However, number of TEM cells (CD4+IL4-+, CD8+ IL-4+) and (CD4+ IFN-gamma+, CD8+IFN-gamma+) did not change significantly (P<0.05). CONCLUSIONS: C. pneumoniae infection decreased CD4+ and CD8+ IL-2+ TEM cells in this study population. These findings may provide more understanding of the mechanisms of persistent C. pneumoniae infection.

No abstract