COVID-19 in Neonates and Infants: Progression and Recovery.

Between March 10, 2020 and April 17, 2020, of 8/70 (11.4%) SARS-CoV-2 positive infants that presented, 5/8 (63%) developed fever, 4/8 (50%) had lower respiratory tract involvement, 2/8 (25%) had neutropenia and thrombocytosis, and 4/8 infants (50%) were treated for suspected sepsis with broad-spectrum antibiotics. Only 1/8 (13%) required pediatric intensive care. All patients were eventually discharged home well.

Association between secondary thrombocytosis and viral respiratory tract infections in children.

Secondary thrombocytosis (ST) is frequently observed in children with a variety of clinical conditions. The leading cause of ST is respiratory tract infection (RTI) in children. Nasopharyngeal aspirate samples were collected and assessed for common respiratory viruses. The relationships between virus infections and secondary thrombocytosis were analyzed retrospectively. The blood platelet count and the presence of respiratory viruses were determined for 3156 RTI patients, and 817 (25.9%) cases with platelet ≥500 × 10(9)/L were considered as the thrombocytosis group. Compared with the normal group, the detection rates of respiratory syncytial virus (RSV) and human rhinovirus (HRV) were significantly higher in the thrombocytosis group (P = 0.017 and 0.042, respectively). HRV single infection was a risk factor associated with thrombocytosis [odds ratio (OR) = 1.560, 95% confidence interval (CI) = 1.108-2.197]. Furthermore, ST was more likely to occur in younger patients who had clinical manifestations of wheezing and dyspnea and who had been diagnosed with bronchiolitis. Furthermore, the course of disease lasted longer in these patients. ST is associated with viral respiratory tract infections, especially RSV and HRV infections. HRV single infection is a risk factor associated with thrombocytosis.

Reactive thrombocytosis in children with viral respiratory tract infections.

AIM: Secondary thrombocytosis occurs commonly in children and is associated with a variety of lower respiratory tract infections, bacterial most often than viral. Aim of the study was to have an insight into the incidence and the clinical significance of thrombocytosis in children with lower respiratory tract infection caused by viral pathogens. METHODS: Clinical data of 92 children, aged 10 days to 8 years, hospitalized with viral lower respiratory tract infection were studied retrospectively for presence of thrombocytosis (platelet count >500×109/l). RESULTS: Thrombocytosis was detected in 59.78% of patients. When children with and without thrombocytosis were compared a significant difference was found for age (P=0.002). We have found no differences among the two groups in sex, SaO2, clinical severity score and CRP levels at admission. Patients with RSV infection presented with significantly higher platelet counts (P=0.003). Extreme thrombocytosis (platelet count >1000×109/L) was noticed in eight patients (8.7%), seven of them were infants with RSV bronchiolitis. All children recovered uneventfully without requiring prophylaxis with anticoagulants or platelet aggregation inhibitors. CONCLUSION: Reactive thrombocytosis is a common finding in the acute care population of children hospitalized with viral lower respiratory tract infection. It represents a reactive phenomenon and does not indicate infection of bacterial cause or severe clinical course. Routine prophylactic antiplatelet treatment or further investigations are not necessary.

[Evaluation of Ebola virus reproduction in adult ICR white mice].

The investigators studied the ability of adult ICR mice (a laboratory model that was most approximated to the wildtype populations of mice) to maintain Ebola virus (EV) reproduction in the organism. The adult ICR mice inoculated with EV during 23 passages were shown to maintain viral reproduction in the liver. The elevated levels of platelets and the early generation of fibrin and fibrinogen degradation products suggested there were hemostatic changes that did not, however, progress to severe coagulopathy. The animals were in appearance apparently, other than adynamia observed on days 5-7. Thus, the susceptibility of the adult ICR mice to EV is characterized by their ability to maintain virus reproduction in the liver without evident signs of the infection. This pattern of susceptibility in the mice shows a possible role of this rodent species in the transmissive cycle of EV.

Respiratory syncytial virus-positive bronchiolitis in hospitalized infants is associated with thrombocytosis.

BACKGROUND: Secondary thrombocytosis is associated with a variety of clinical conditions, one of which is lower respiratory tract infection. However, reports on thrombocytosis induced by viral infections are scarce. OBJECTIVES: To assess the rate of thrombocytosis (platelet count > 500 x 10(9)/L) in hospitalized infants with bronchiolitis and to investigate its potential role as an early marker of respiratory syncytial virus infection. METHODS: Clinical data on 469 infants aged < or = 4 months who were hospitalized for bronchiolitis were collected prospectively and compared between RSV-positive and RSV-negative infants. RESULTS: The rate of thrombocytosis was significantly higher in RSV-positive than RSV-negative infants (41.3% vs. 29.2%, P=0.031). The odds ratio of an infant with bronchiolitis and thrombocytosis to have a positive RSV infection compared to an infant with bronchiolitis and a normal platelet count was 1.7 (P= 0.023, 95% confidence interval 1.07-2.72). There was no significant difference in mean platelet count between the two groups. CONCLUSIONS: RSV-positive bronchiolitis in hospitalized young infants is associated with thrombocytosis.

Measurement of thrombopoietic levels: clinical and biological relationships.

Platelet production is primarily regulated by the thrombopoietic cytokine thrombopoietin (TPO). In most cases thrombopoietin serum levels are determined by the rate of c-mpl receptor-mediated degradation after TPO uptake into platelets and megakaryocytes. The contribution of increased TPO protein synthesis by a translational mechanism was recently appreciated as the cause for hereditary thrombocythemia and will have to be elucidated in other conditions of thrombocytosis in association with increased TPO levels.