Undetected respiratory infections may adversely affect the intrapulmonary resistance after Stage 2 or Stage 3 Fontan palliation. A few studies describe a higher risk for viral pneumonia during respiratory virus season, but none of them have focused on the effect of symptomatic viral pneumonia on in-hospital clinical course after bidirectional Glenn shunt. We analysed 77 patients who underwent bidirectional Glenn shunt surgery. Six patients were detected with pneumonia and proof of viral ribonucleic acid in tracheal mucus in the very early postoperative time. We compared them retrospectively to the remaining 71 patients regarding preoperative inflammatory signs, mortality, paediatric ICU length of stay, and ventilation time. The infection rate was not seasonal dependent. Ventilation time was significantly elongated in the pneumonia group (558 h ± 634 vs. 8.7 h ± 1.9; p < 0.0001) and so was the paediatric ICU length of stay (29 days ± 26 vs. 3 days±1; p = 0.007). Significantly more patients in the pneumonia group required extracorporeal cardiac life support postoperatively. The mortality was significantly increased in patients with pneumonia. Even subclinical viral pneumonia may cause ventilation-to-perfusion mismatch by raising intrapulmonary resistance. Recorded parameters of postoperative paediatric ICU therapy showed a significant impact of a viral pneumonia on patients after bidirectional Glenn shunt. The respiratory syncytial virus vaccination does not protect these patients from infection with other respiratory viruses. The focus should be put on preoperative diagnosis of pulmonary infections in the vulnerable group of patients with univentricular hearts.

The COVID-19 pandemic modified the epidemiology and the transmission of respiratory syncytial virus (RSV). We collected data on RSV positivity and incidence from children hospitalized in the largest tertiary paediatric hospital in Greece before (2018–2020, period A), during (2020–2021, period B), and after (2021–2023, period C) the COVID-19 lockdown. A total of 9,508 children were tested for RSV. RSV positivity (%) was 17.6% (552/3,134) for period A, 2.1% (13/629) for period B, and 13.4% (772/5,745) for period C (p < 0.001). The mean age (±SD) of RSV-positive children among the three periods was A: 5.9(±9.3), B: 13.6 (±25.3), and C: 16.7 (±28.6) months (p < 0.001). The peak of RSV epidemiology was shifted from January–March (period A) to October–December (period C). RSV in-hospital incidence per 1,000 hospitalizations in paediatric departments was A:16.7, B:1.0, and C:28.1 (p < 0.001), and the incidence in the intensive care unit was A: 17.3, B: 0.6, and C: 26.6 (p < 0.001). A decrease in RSV incidence was observed during the COVID-19 lockdown period, whereas a significant increase was observed after the lockdown. A change in epidemiological patterns was identified after the end of the lockdown, with an earlier seasonal peak and an age shift of increased RSV incidence in older children.

We examined the associations of middle childhood infectious morbidity and inflammatory biomarkers with adolescent internalizing and externalizing behavior problems. We recruited 1018 Colombian schoolchildren aged 5–12 years into a cohort. We quantified white blood cell (WBC) counts and C-reactive protein at enrollment and prospectively recorded incidence of gastrointestinal, respiratory, and fever-associated morbidity during the first follow-up year. After a median 6 years, we assessed adolescent internalizing and externalizing behavior problems using child behavior checklist (CBCL) and youth self-report (YSR) questionnaires. Behavior problem scores were compared over biomarker and morbidity categories using mean differences and 95% confidence intervals (CI) from multivariable linear regression. Compared with children without symptoms, CBCL internalizing problem scores were an adjusted 2.5 (95% CI: 0.1, 4.9; p = .04) and 3.1 (95% CI: 1.1, 5.2; p = .003) units higher among children with moderate diarrhea with vomiting and high cough with fever rates, respectively. High cough with fever and high fever rates were associated with increased CBCL somatic complaints and anxious/depressed scores, respectively. WBC >10,000/mm3 was associated with both internalizing problem and YSR withdrawn/depressed scores. There were no associations with externalizing behavior problems. Whether or not decreasing the burden of common infections results in improved neurobehavioral outcomes warrants further investigation.

Pneumonia is a respiratory condition with complex etiology. Host genetic variation is thought to contribute to individual differences in susceptibility and symptom manifestation. Here, we analyze pneumonia data from the UK Biobank (14,780 cases and 439,096 controls) and FinnGen (9980 cases and 86,519 controls) and perform a genomewide association study meta-analysis. We use gene-based tests, colocalization, genetic correlation, latent causal variable (LCV) and polygenic prediction in an independent Australian sample (N = 5595) to draw insights into the etiology of pneumonia risk. We identify two independent loci on chromosome 15 (lead single-nucleotide polymorphisms rs2009746 and rs76474922) to be associated with pneumonia (p < 5e−8). Gene-based tests revealed 18 genes in chromosomes 15, 16 and 9, including IL127, PBX3, ApoB receptor (APOBR) and smoking related genes CHRNA3/5, statistically associated with pneumonia. We observed genetic correlations between pneumonia and cardiorespiratory, psychiatric and inflammatory related traits. LCV analysis suggests a strong genetic causal relationship with cardiovascular health phenotypes. Polygenic risk scores for pneumonia significantly predicted self-reported pneumonia in an independent sample, albeit with a small effect size (OR = 1.11 95% CI [1.04, 1.19], p < .05). Sensitivity analyses suggested the associations in chromosome 15 are mediated by smoking history, but the associations in chromosomes 16 and 9, and polygenic prediction were robust to adjustment for smoking. Altogether, our results highlight common genetic variants, genes and potential pathways that contribute to individual differences in susceptibility to pneumonia, and advance our understanding of the genetic factors underlying heterogeneity in respiratory medical outcomes.

Five of the 13 known species of Mammomonogamus have been described in members of the family Felidae, including domestic cats, making felids the most frequent hosts of Mammomonogamus. The occurrence of Mammomonogamus in felids is geographically scattered and information on the life cycle and other aspects of infections is lacking. The paucity of data opens the questions on possible conspecificity of some of the described species of Mammomonogamus and on the existence of possible reservoirs for infections in domestic cats in geographically isolated endemic foci of infection. To test such hypotheses, we compared sequences of mitochondrial and nuclear markers obtained from Mammomonogamus adults or eggs collected from domestic cats in three geographically distant localities. Based on morphology, geographic origin and site of infection, the worms examined can be referred to as Mammomonogamus ierei and Mammomonogamus auris. Phylogenetic analyses of both mitochondrial and ribosomal DNA markers showed monophyly of the genus Mammomonogamus and suggested the existence of at least two species in cats. Review of the literature, the existence of several species and the discontinuous geographic distribution of Mammomonogamus infections in domestic cats suggest an historical spillover of infection from wild reservoirs, presumably wild felids.

Respiratory infections among infants constitute a major burden to health care systems in developed nations, yet the course and risk factors leading to these conditions are poorly understood. We examine the longitudinal patterns of respiratory infection hospitalisation (RIH) and how these patterns are influenced by neonatal pulmonary morbidities. We included all live births (n = 429 058) occurring in the Australian state of Queensland between January 2009 and December 2015. Data were structured so that each participant had a record (present/absent) of RIH for each month from birth to 12 months. Initially, latent class growth analysis was used to identify the trajectories of RIH adjusted for spatial–temporal factors; using the identified trajectories of RIH as outcomes, we built a multinomial logistic regression model to identify neonatal predictors of RIH trajectories. Our results indicated that a four-class solution was the best fit to the data, comprising a ‘no-risk’ trajectory, a ‘low-risk’ trajectory, an ‘early-risk’ trajectory and a ‘chronic-risk’ trajectory. Compared with the no-risk trajectory, membership in the other trajectories was predicted by a range of neonatal pulmonary morbidities, with transient tachypnoea of newborn showing a specific relationship with the early-risk group and sleep apnoea showing a specific and strong risk with the chronic-risk group. Our findings suggest the possibility of identifying neonates at risk of recurrent RIH and implementing effective intervention strategies prior to neonatal discharge.

Molecular epidemiology and clinical impact of human rhinovirus (HRV) are not well documented in tropical regions. This study compared the clinical characteristics of HRV to other common viral infections and investigated the molecular epidemiology of HRV in hospitalized children with acute respiratory infections (ARIs) in Vietnam. From April 2010 to May 2011, 1082 nasopharyngeal swabs were screened for respiratory viruses by PCR. VP4/VP2 sequences of HRV were further characterized. HRV was the most commonly detected virus (30%), in which 70% were diagnosed as either pneumonia or bronchiolitis. Children with single HRV infections presented with significantly higher rate of hypoxia than those infected with respiratory syncytial virus or parainfluenza virus (PIV)-3 (12·4% vs. 3·8% and 0%, respectively, P < 0·05), higher rate of chest retraction than PIV-1 (57·3% vs. 34·5%, P = 0·028), higher rate of wheezing than influenza A (63·2% vs. 42·3%, P = 0·038). HRV-C did not differ to HRV-A clinically. The genetic diversity and changes of types over time were observed and may explain the year-round circulation of HRV. One novel HRV-A type was discovered which circulated locally for several years. In conclusion, HRV showed high genetic diversity and was associated with significant morbidity and severe ARIs in hospitalized children.

Acute respiratory infections (ARI) are the leading cause of death worldwide in children aged <5 years, and understanding contributing factors to their seasonality is important for targeting and implementing prevention strategies. In tropical climates, ARI typically peak during the pre-rainy and rainy seasons. One hypothesis is that rainfall leads to more time spent indoors, thus increasing exposure to other people and in turn increasing the risk of ARI. A case-crossover study design in 718 Bangladeshi children aged <5 years was used to evaluate this hypothesis. During a 3-month period with variable rainfall, rainfall was associated with ARI [odds ratio (OR) 2·97, 95% confidence interval (CI) 1·87–4·70]; some evidence of an increased strength of association as household crowding increased was found (⩾3 people/room, OR 3·31, 95% CI 2·03–5·38), but there was a lack of association in some of the most crowded households (⩾5 to <6 people/room, OR 1·55, 95% CI 0·54–4·47). These findings suggest that rainfall may be increasing exposure to crowded conditions, thus leading to an increased risk of ARI, but that additional factors not captured by this analysis may also play a role.

The measurement and analysis of common recurrent conditions such as diarrhoea, respiratory infections or fever pose methodological challenges with regard to case definition, disease surveillance and statistical analysis. In this paper we describe a flexible and robust model that can generate simulated longitudinal datasets for a range of recurrent infections, reflecting the stochastic processes that underpin the data collected in the field. It can be used to evaluate and compare alternative disease definitions, surveillance strategies and statistical methods under ‘controlled conditions’. Parameters in the model include: characterizing the distributions of the individual disease incidence and the duration of disease episodes; allowing the average disease duration to depend on an individual's number of episodes (simulating a correlation between incidence and duration); making the individual risk of disease depend on the occurrence of previous episodes (simulating autocorrelation of successive episodes); finally, incorporating seasonal variation of disease.

Previous control studies carried out in children showed that respiratory infection alters riboflavin metabolism and leads to excessive urinary losses of the vitamin. In order to understand the nature of biochemical changes in riboflavin metabolism during respiratory infection, a study was carried out using the mouse as the experimental model, and Klebsiella pneumonjue as the infective organism. Mice were fed on either a low(0·5 mg/kg)- or high(13·3 mg/kg)-riboflavin semi-synthetic diet. Infection resulted in a 5–6-fold higher excretion of riboflavin in the urine of mice fed on the low-riboflavin diet. Higher erythrocyte FAD levels and lower liver FAD levels were also observed during infection. Of the four enzymes involved in the synthesis and breakdownof the flavin coenzymes studied, the activity of hepatic flavokinase (ATP: riboflavin 5'-phosphotransferase; EC 2.7.1.26) was significantly lower, and that of FAD synthetase (ATP: FMN adenylyltransferase; EC 2.7.7.2) was higher during riboflavin restriction and infection. The activity of FMN (acid) phosphatase (EC 3.1.3.2) was unchanged, whereas FAD (nucleotide) pyrophosphatase (EC 3.6.1.9) activity was significantly higher both with the low-riboflavin diet and during infection. Thyroid hormone is known to modulate flavokinase activity and, hence, thyroid status was assessed. Plasma triiodothyronine (T3) levels were not affected, but thyroxine levels were lower in the mice fed on the low-riboflavin diet. However, plasma T3 was significantly lower during infection, suggesting a mechanistic role for the hormone in the reduction of flavokinase activity.