Nosocomial infection and spread of SARS-CoV-2 infection among hospital staff,patients and caregivers

BACKGROUND There are difficulties in diagnosing nosocomial transmission of severe acute respiratory syndrome coronavirus 2(SARS-CoV-2) infection in hospital settings. Furthermore, mortality of cases of nosocomial infection(NI) with SARS-CoV-2 is higher than that of the general infected population. In the early stage of the pandemic in Taiwan, as patients were not tested for SARS-CoV-2 at admission, NIs often go undetected. Strictly applying the systematic polymerase chain reaction(PCR) screening, as a standard infection control measure was subsequently implemented to reduce NI incidence. However, evidence on risk factors for SARS-CoV-2 NIs among healthcare workers(HCWs) and caregivers is limited.AIM To assess NI incidence of SARS-CoV-2 among hospital staff, hospitalized patients, and caregivers, and the transmission routes of clusters of infection.METHODS This descriptive retrospective analysis at our hospital from May 15 to August 15, 2021 included data on 132 SARS-CoV-2 NIs cases among hospital staff, inpatients, and caregivers who previously tested negative but subsequently identified with a positive SARS-CoV-2 reverse transcriptase-PCR(RT-PCR) test results, or a hospital staff who tested positive following routine SARS-CoV-2 RT-PCR test. Chi-square tests were performed to compare the differences between hospital staff and private caregivers, and between clusters and sporadic infections.RESULTS Overall, 9149 patients and 2005 hospital staff members underwent routine SARS-CoV-2 RT-PCR testing, resulting in 12 confirmed cluster and 23 sporadic infections. Among the index cases of the clusters, three(25%) cases were among hospital staff and nine(75%) cases were among other contacts. Among sporadic infections, 21(91%) cases were among hospital staff and two(9%) cases were among other contacts(P < 0.001). There was an average of 8.08 infections per cluster. The secondary cases of cluster infection were inpatients(45%), hospital staff(30%), and caregivers(25%). Private caregivers constituted 27% and 4% of the clusters and sporadic infections, respectively(P = 0.024);92.3% of them were infected in the clusters. The mortality rate was 0.0%.CONCLUSION The incidence of SARS-CoV-2 infection was relatively high among private caregivers, indicating a need for infection control education in this group, such as social distancing, frequent handwashing, and wearing PPE.

Amyloid,tau,pathogen infection and antimicrobial protection in Alzheimer’s disease-conformist,nonconformist,and realistic prospects for AD pathogenesis

Background:Alzheimer’s disease(AD)is a fatal disease that threatens the quality of life of an aging population at a global scale.Various hypotheses on the etiology of AD have been developed over the years to guide efforts in search of therapeutic strategies.Main body:In this review,we focus on four AD hypotheses currently relevant to AD onset:the prevailing amyloid cascade hypothesis,the well-recognized tau hypothesis,the increasingly popular pathogen(viral infection)hypothesis,and the infection-related antimicrobial protection hypothesis.In briefly reviewing the main evidence supporting each hypothesis and discussing the questions that need to be addressed,we hope to gain a better understanding of the complicated multi-layered interactions in potential causal and/or risk factors in AD pathogenesis.As a defining feature of AD,the existence of amyloid deposits is likely fundamental to AD onset but is insufficient to wholly reproduce many complexities of the disorder.A similar belief is currently also applied to hyperphosphorylated tau aggregates within neurons,where tau has been postulated to drive neurodegeneration in the presence of pre-existing Aβplaques in the brain.Although infection of the central nerve system by pathogens such as viruses may increase AD risk,it is yet to be determined whether this phenomenon is applicable to all cases of sporadic AD and whether it is a primary trigger for AD onset.Lastly,the antimicrobial protection hypothesis provides insight into a potential physiological role for Aβpeptides,but how Aβ/microbial interactions affect AD pathogenesis during aging awaits further validation.Nevertheless,this hypothesis cautions potential adverse effects in Aβ-targeting therapies by hindering potential roles for Aβin anti-viral protection.Conclusion:AD is a multi-factor complex disorder,which likely requires a combinatorial therapeutic approach to successfully slow or reduce symptomatic memory decline.A better understanding of how various causal and/or risk factors affecting disease onset and progression will enhance the likelihood of conceiving effective treatment paradigms,which may involve personalized treatment strategies for individual patients at varying stages of disease progression.