John J. Hawkshead

SARS-CoV-2 has an impact on the nervous system as a result of pathological cellular and molecular events at the level of vascular and neural tissue. Severe neurologic manifestations including stroke, ataxia, seizure, and depressed level of consciousness are prevalent in patients with SARS-CoV-2 infection. Although the mechanism is still unclear, SARS-CoV-2 has been associated with the pathogenesis of intravascular coagulation and angiotensin-converting enzyme-I, both exacerbating systemic inflammation and contributing to hypercoagulation or blood–brain barrier leakage, resulting in ischemic or hemorrhagic stroke. On the other hand, the SARS-CoV-2 spike protein in neural tissue and within the cerebrospinal fluid may induce neural dysfunction, resulting in neuroinflammation, which is exacerbated by peripheral and neural hypercytokinemia that can lead to neuronal damage and subsequent neuroinflammation. A deeper understanding of the fundamental biological mechanisms of neurologic manifestations in SARS-CoV-2 infection can pave the way to identifying a single biomarker or network of biomarkers to help target neuroprotective therapy in patients at risk for developing neurological complications.

Staphylococcus aureus remains the most common etiology of hematogenous osteomyelitis in children. Recently emerged virulent strains of methicillin-resistant S. aureus (MRSA) strains now predominate. It remains uncertain whether these pathogens cause a measurably more severe illness than methicillin-sensitive strains. We reviewed records of 97 pediatric patients with hematogenous osteomyelitis of varying etiologies to determine whether there were significant differences among the groups in terms of predetermined measures of disease severity. These measures included degree and duration of elevated temperature, acute-phase reactants, length of hospitalization, the number of surgical procedures required, and long-term sequelae. Differences in the clinical course of illness were observed. Patients with MRSA had a significant increase in degree and duration of elevated temperature (P = 0.0001 for both), acute-phase reactant measures (white blood cell count, P = 0.0001; C-reactive protein, P = 0.0058; erythrocyte sedimentation rate, P = 0.0046), initial length of hospital stay (P = 0.0001), and surgical interventions (all procedures, P = 0.0001; therapeutic procedures, only P = 0.0002) as compared with patients with osteomyelitis caused by other bacterial pathogens and culture-negative osteomyelitis. A similar general pattern was observed when the analysis was restricted to culture-positive staphylococcal cases only. Our results support the hypothesis that MRSA produces more severe bone infection and is likely to require more aggressive surgical and medical management.