As the SARS-CoV-2 pandemic unfolds across the globe, consistent themes are emerging with regard to aspects of SARS-CoV-2 infection and its associated disease entities in children. Overall, children appear to be less frequently infected by, and affected by, SARS-CoV-2 virus and the clinical disease COVID-19. Large epidemiological studies have revealed children represent less than 2% of the total confirmed COVID-19 cases, of whom the majority experience minimal or mild disease that do not require hospitalisation. Children do not appear to be major drivers of SARS-CoV-2 transmission, with minimal secondary virus transmission demonstrated within families, schools and community settings. There are several postulated theories regarding the relatively low SARS-CoV-2 morbidity and mortality seen in children, which largely relate to differences in immune responses compared to adults, as well as differences in angiotensin converting enzyme 2 distribution that potentially limits viral entry and subsequent inflammation, hypoxia and tissue injury. The recent emergence of a multisystem inflammatory syndrome bearing temporal and serological plausibility for an immunemediated SARS-CoV-2-related disease entity is currently under investigation. This article summarises the current available data regarding SARS-CoV-2 and the paediatric population, including the spectrum of disease in children, the role of children in virus transmission, and host-virus factors that underpin the unique aspects of SARS-CoV-2 pathogenicity in children.

BACKGROUND AND OBJECTIVES: COVID-19 public health measures have altered respiratory syncytial virus (RSV) epidemiology, resulting in an unseasonal summer epidemic in Australia in 2020. We aimed to determine if the shifted RSV epidemic was more severe compared with previous years or if age-specific changes were associated with the resurgence. METHODS: Through this multicenter study, we analyzed routinely collected datasets from the Sydney Children’s Hospitals Network in southeast Australia. We examined overall trends in RSV-related disease in children aged <16 years in 2020 compared with 2014–2019. We compared observed and expected counts for RSV infections, RSV-related hospitalizations, and emergency department visits for acute respiratory illness. RESULTS: In 2020, there was a shift in the peak of RSV-related disease from autumn and winter to early summer. Compared with previous years, the overall frequency of RSV infections increased in children aged 2 to 4 years (83.91%; 95% confidence interval [CI], 34.21% to 192.07%; P < .01). There was also an increase in the peak case counts of RSV infections and RSV-coded hospitalizations for some age groups. There was an overall reduction of RSV-coded hospitalizations (−31.80%; 95% CI, −41.13% to −18.96%; P < .01) and ICU admissions (−44.63%; 95% CI, −60.76% to −5.96%; P < .05) in 2020 compared with previous years. CONCLUSIONS: Our observations provide evidence that the shifted 2020 RSV season was no more severe than previous years. Increased RSV infections in children aged 2 to 4 years may be explained by a buildup in age-specific population susceptibility and increased testing in older children.

Studies show children with asymptomatic congenital CMV are at increased risk of developing hearing loss but perform equally well on neurodevelopmental assessments when compared with healthy controls. There is no reliable virological marker to determine which infants will develop sequelae. Regular follow-up until school entry is supported by the literature.

Background A thorough understanding of local and contemporary invasive fungal infection (IFI) epidemiology in immunocompromised children is required to provide a rationale for targeted prevention and treatment strategies. Methods Retrospective data over 10 years from four tertiary pediatric oncology and hematopoietic stem cell transplant (HSCT) units across Australia were analyzed to report demographic, clinical, and mycological characteristics of IFI episodes, and crude IFI prevalence in select oncology/HSCT groups. Kaplan–Meier survival analyses were used to calculate 180‐day overall survival. Results A total of 337 IFI episodes occurred in 320 children, of which 149 (44.2%), 51 (15.1%), and 110 (32.6%) met a modified European Organization for Research and Treatment of Cancer (mEORTC) criteria for proven, probable, and possible IFI, respectively. There were a further 27 (8.0%) that met a “modified possible IFI” criteria. Median age at IFI diagnosis was 8.4 years. Crude mEORTC IFI prevalence in acute lymphoblastic leukemia, acute myeloid leukemia, solid tumor, and allogeneic HSCT cohorts was 10.6%, 28.2%, 4.4%, and 11.7%, respectively. Non‐Aspergillus species represented 48/102 (47.1%) molds identified, and non‐albicans Candida represented 66/93 (71.0%) yeasts identified. There were 56 deaths among 297 children who met mEORTC criteria, with 180‐day overall survival for proven, probable, and possible IFIs of 79.7%, 76.2%, and 84.4%, respectively. Conclusion Non‐Aspergillus molds and non‐albicans Candida contributed substantially to pediatric IFI in our study, with high IFI prevalence in leukemia and allogeneic HSCT cohorts. Inclusion of IFIs outside of European Organization for Research and Treatment of Cancer criteria revealed an IFI burden that would go otherwise unrecognized in published reports.

Background: Invasive fungal infections (IFI) are an important complication of acute lymphoblastic leukaemia (ALL) treatment. Our study describes the prevalence and outcomes of IFI in children with ALL. Methods: IFI episodes in children with primary or relapsed ALL, identified for The Epidemiology and Risk Factors for Invasive Fungal Infections in Immunocompromised Children study, were analysed. IFI were classified according to European Organization for Research and Treatment of Abbreviations: ALL, acute lymphoblastic leukaemia; CCG, Children'

Understanding the long-term maintenance of SARS-CoV-2 immunity is critical for predicting protection against reinfection. In an age and gender matched cohort of 24 participants, the association of disease severity and early immune responses on the maintenance of humoral immunity 12 months post-infection is examined. All severely affected participants maintain a stable subset of SARS-CoV-2 receptor-binding domain (RBD)-specific memory B cells (MBCs) and good neutralising antibody breadth against the majority of the variants of concern, including the Delta variant. Modelling these immune responses against vaccine efficacy data indicate 45-76% protection against symptomatic infection (variant dependent). Overall, these findings indicate durable humoral responses in most participants after infection, reasonable protection against reinfection, and implicate baseline antigen-specific CD4+ T cell responses as a predictor of maintenance of antibody neutralisation breadth and RBD-specific MBC levels at 12 months post-infection.

No abstract

The reality of climate change and biodiversity collapse is irrefutable in the 21st century, with urgent action required not only to conserve threatened species but also to protect human life and wellbeing. This existential threat forces us to recognise that our existence is completely dependent upon well‐functioning ecosystems that sustain the diversity of life on our planet, including that required for human health. By synthesising data on the ecology, epidemiology and evolutionary biology of various pathogens, we are gaining a better understanding of factors that underlie disease emergence and spread. However, our knowledge remains rudimentary with limited insight into the complex feedback loops that underlie ecological stability, which are at risk of rapidly unravelling once certain tipping points are breached. In this paper, we consider the impact of climate change and biodiversity collapse on the ever‐present risk of infectious disease emergence and spread. We review historical and contemporaneous infectious diseases that have been influenced by human environmental manipulation, including zoonoses and vector‐ and water‐borne diseases, alongside an evaluation of the impact of migration, urbanisation and human density on transmissible diseases. The current lack of urgency in political commitment to address climate change warrants enhanced understanding and action from paediatricians – to ensure that we safeguard the health and wellbeing of children in our care today, as well as those of future generations.