SARS-CoV-2 infection induces a wide spectrum of neurologic dysfunction. Here we show that a particularly vulnerable population with neurologic manifestations of COVID-19 harbor an influx of inflammatory cytokines within the cerebrospinal fluid in the absence of viral neuro-invasion. The majority of these inflammatory mediators are driven by type 2 interferon and are known to induce neuronal injury in other disease models. Levels of matrix metalloproteinase-10 within the spinal fluid correlate with the degree of neurologic dysfunction. Furthermore, this neuroinflammatory process persists weeks following convalescence from the acute respiratory infection. These prolonged neurologic sequelae following a systemic cytokine release syndrome lead to long-term neurocognitive dysfunction with a wide range of phenotypes.

Identifying extrapulmonary legionellosis is difficult due to the lack of clinical suspicion and limitations of conventional microbiologic methods. We present a case series of hematopoietic cell transplant recipients with extrapulmonary legionellosis diagnosed via molecular diagnostics: 16S ribosomal ribonucleic acid gene Sanger sequencing and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry.