Hospital-treated serious and invasive aspergillosis and candidiasis infections during the COVID-19 pandemic: a retrospective analysis of Hospital Episode Statistics data from England.

OBJECTIVES: To investigate the impact of COVID-19 on the burden of hospital-treated Aspergillus and Candida infections in England. DESIGN: A retrospective study using Hospital Episodes Statistics data to estimate the burden of serious and invasive fungal infections (SIFIs) in all patients admitted in England during March 2018-February 2020 (pre-COVID-19) and during March 2020-October 2021 (the COVID-19 period). SETTING: Hospitals in England. POPULATION: All patients with codes corresponding to serious and invasive aspergillosis and candidiasis in any diagnosis position during their admission pre-COVID-19 and during the COVID-19 period. OUTCOME MEASURES: Age, spells, patient counts, mean length of stay, admission to critical care unit (CCU), length of stay in CCU, 30-day readmissions, failed discharges (readmission within 7 days) and comorbidities. RESULTS: During the COVID-19 period, hospitalisation spells with an invasive candidiasis code fell by 3.2% and spells with an aspergillosis code by 24.8%. Mean length of stay was higher for patients with aspergillosis with or without COVID-19 and candidiasis with or without COVID-19 during the pandemic than before the pandemic. During the pandemic, mean length of stay was higher for patients with aspergillosis with COVID-19 than those with aspergillosis alone but slightly lower for patients with candidiasis with COVID-19 than for those with candidiasis alone. Of patients with a diagnosis of COVID-19, 52.5% with aspergillosis and 60.0% with candidiasis were treated in CCU compared with 13.2% and 37.1%, respectively, without a COVID-19 diagnosis. The percentage of 30-day readmissions and failed discharges for patients with SIFI was higher for those with COVID-19 than for those without. CONCLUSIONS: The burden of aspergillosis and candidiasis has been affected by COVID-19. Aspergillosis diagnoses fell among hospitalised patients during the pandemic, while candidiasis continued to fluctuate in patterns similar to pre-COVID-19. A higher burden for patients with SIFI was observed, whether or not they also had a diagnosis of COVID-19. Our findings highlight extra considerations and burden on management of serious SIFI as a result of the COVID-19 pandemic.

Headache as the Presenting Symptom in 2 Patients With COVID-19 and a History of Migraine: 2 Case Reports.

The coronavirus disease 2019 (COVID-19) pandemic has now affected more than 5 million people globally. Typical symptoms include fever, cough, and shortness of breath. Patients with underlying medical comorbidities such as cardiovascular disease and diabetes are more likely to become severely ill. To date there is limited information on how COVID-19 affects patients with a history migraine. Here, we present the cases of 2 women with a history of migraine whose first symptom of COVID-19 was a severe persistent headache.

Lack of Cyclin B1 in zebrafish causes lengthening of G2 and M phases.

An essential part of the Mitosis Promoting Factor, Cyclin B1 is indispensable for cells to enter mitosis. We report here that the zebrafish early arrest mutant specter is a loss-of-function mutation in the сyclin B1 gene. cyclin B1 is maternally transcribed in zebrafish, and the zygotic phenotype is apparent by early segmentation. Lack of zygotic Cyclin B1 does not stop cells from dividing, rather it causes an abnormal and elongated progression through the G2 and M phases of the cell cycle. Many mutant cells show signs of chromosomal instability or enter apoptosis. Using CRISPR-mediated gene editing, we produced a more severe gain-of-function mutation confirming that specter is the result of nonfunctional Cyclin B1. Although also a recessive phenotype, this new mutation produces an alternative splice-form of cyclin B1 mRNA, whose product lacks several key components for Cyclin B1, but not the Cdk1-binding domain. This mutant form of Cyclin B1 completely prevents cell division. We conclude that, although Cyclin B1 is critical for cells to enter mitosis, another cell cycle protein may be cooperating with Cdk1 at the G2/M checkpoint to sustain a partly functional Mitosis Promoting Factor.