Background
Nosocomial spread of COVID-19 causes clusters of infection among high-risk individuals. Controlling this spread is critical to reducing COVID-19 morbidity and mortality. We describe an outbreak of COVID-19 in Keio University Hospital, Japan, and its control, and propose effective control measures.
Methods
When an outbreak was suspected, immediate isolation and thorough polymerase chain reaction (PCR) testing of patients and healthcare workers (HCWs) using an in-house system, together with extensive contact tracing and social distancing measures, were conducted. Nosocomial infections (NIs) were defined as having an onset or positive test after the fifth day of admission for patients, and having high-risk contacts in our hospital for HCWs. We performed descriptive analyses for this outbreak.
Results
Between March 24 and April 24, 2020, 27 of 562 tested patients were confirmed positive, of whom 5 (18.5%) were suspected as NIs. For HCWs, 52 of 697 tested positive, and 40 (76.9%) were considered NIs. Among transmissions, 95.5% were suspected of having occurred during the asymptomatic period. Large-scale isolation and testing at the first sign of outbreak terminated NIs. The number of secondary cases directly generated by a single primary case found before March 31 was 1.74, compared to 0 after April 1. Only 4 of 28 primary cases generated definite secondary infection, which were all asymptomatic.
Conclusions
Viral shedding from asymptomatic cases played a major role in NIs. PCR screening of asymptomatic individuals helped clarify the pattern of spread. Immediate large-scale isolation, contact tracing, and social distancing measures were essential to containing outbreaks.
Using duplex ultrasonography (US), the authors showed compression of the extracranial vertebral artery (ECVA) during neck rotation in 5.0% of 1,108 patients. Age (per 10-year increase, OR 0.80, 95% CI 0.67 to 0.96), vessel diameters (per 0.5-mm diameter increase, OR 0.63, 95% CI 0.51 to 0.79), and symptoms upon neck rotation (OR 4.01, 95% CI 1.35 to 11.9) were associated with vessel compression. In one case, SPECT revealed decreased cerebral perfusion of the hindbrain during rotation. ECVA US is useful in identifying vessel compression, especially in patients with symptoms on neck rotation.
In the subgranular zone (SGZ) of the hippocampus, neurogenesis persists throughout life and is upregulated following ischemia. Accumulating evidence suggests that enhanced neurogenesis stimulated by ischemic injury contributes to recovery after stroke. However, the mechanisms underlying the upregulation of neurogenesis are unclear. We have demonstrated that a neuropeptide, pituitary adenylate cyclase-activating polypeptide (PACAP), exerts a wide range of effects on neural stem cells (NSCs) during neural development. Here, we examined the effects of endogenous and exogenous PACAP in adult NSCs of the SGZ. Immunostaining showed expression of the PACAP receptor PAC1R in nestin-positive NSCs of adult naive mice. PACAP injection into the lateral ventricle increased bromodeoxyuridine (BrdU)-positive proliferative cells in the SGZ. These data suggest that PACAP promoted the proliferation of NSCs. In global ischemia model mice, the number of BrdU-positive cells was increased in wild-type mice but not in PACAP heterozygous knockout mice. The BrdU-positive cells that increased in number after ischemia were immunopositive for SOX2, a marker of NSCs, and differentiated into NeuN-positive mature neurons at 4 weeks after ischemia. These findings suggest that PACAP contributes to the proliferation of NSCs and may be associated with recovery after brain injury.
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