BackgroundSince 1985, two antigenically distinct lineages of influenza B viruses (Victoria-like and Yamagata-like) have circulated globally. Trivalent seasonal influenza vaccines contain two circulating influenza A strains but a single B strain and thus provide limited immunity against circulating B strains of the lineage not included in the vaccine. In this study, we describe the characteristics of influenza B viruses that caused respiratory illness in the population in Italy over 13 consecutive seasons of virological surveillance, and the match between the predominant influenza B lineage and the vaccine B lineage, in each season.MethodsFrom 2004 to 2017, 26,886 laboratory-confirmed influenza cases were registered in Italy, of which 18.7% were type B. Among them, the lineage of 2465 strains (49%) was retrieved or characterized in this study by a real-time RT-PCR assay and/or sequencing of the hemagglutinin (HA) gene.ResultsCo-circulation of both B lineages was observed each season, although in different proportions every year. Overall, viruses of B/Victoria and B/Yamagata lineages caused 53.3 and 46.7% of influenza B infections, respectively. A higher proportion of infections with both lineages was detected in children, and there was a declining frequency of B/Victoria detections with age. A mismatch between the vaccine and the predominant influenza B lineage occurred in eight out of thirteen influenza seasons under study. Considering the seasons when B accounted for > 20% of all laboratory-confirmed influenza cases, a mismatch was observed in four out of six seasons. Phylogenetic analysis of the HA1 domain confirmed the co-circulation of both lineages and revealed a mixed circulation of distinct evolutionary viral variants, with different levels of match to the vaccine strains.ConclusionsThis study contributes to the understanding of the circulation of influenza B viruses in Italy. We found a continuous co-circulation of both B lineages in the period 2004–2017, and determined that children were particularly vulnerable to Victoria-lineage influenza B virus infections. An influenza B lineage mismatch with the trivalent vaccine occurred in about two-thirds of cases.
We observed five IMD cases due to the same switched MenB strain. The hypervirulent B:P1.5-1,10-8:F3-6:ST-11(cc11) strain, probably switched from C-cc11, is of concern due to the observed high virulence and case fatality rates. All the patients shared the same place of probable exposure. The molecular characterization of the invasive strain allowed the outbreak to be confirmed, which was then controlled through timely public health action.
The aim of this study was to evaluate the antimicrobial susceptibilities of 866 Neisseria meningitidis invasive strains during 11 years of surveillance in Italy. Two and six strains were resistant to ciprofloxacin and rifampin, respectively.
We describe a fatal case of myopericarditis presenting with cardiac tamponade in a previously healthy 11-year-old child. Pandemic H1N1 2009 influenza A virus sequences were identified in throat and myocardial tissues and pericardial fluid, suggesting damage of myocardial cells directly caused by the virus. CASE REPORTHere, we report a fatal case of myopericarditis presenting with cardiac tamponade associated with infection with the pandemic A/H1N1 2009 influenza virus in a previously healthy 11-year-old girl with no known risk factors, including obesity, for severe, complicated pandemic influenza.The patient developed a high fever (39.2°C) with coughing and vomiting on the evening of 28 October. The next morning, she was visited by a general practitioner, who prescribed antipyretic, antibiotic, and cortisone treatments. About 36 h after the onset of symptoms, the girl presented to the emergency unit of the district hospital with asthenia and dizziness. She was pale and afebrile at 35°C, with tachycardia of 140 beats/min and tachypnea of 32 breaths/min. Routine blood samples were analyzed. The white blood cell count was elevated at 23.8 ϫ 10 9 cells/liter, and C-reactive protein was elevated at 21.6 mg/liter. Her creatine kinase (CK) level was elevated at 5,814 IU/liter (normal range, 26 to 140 IU/liter), the troponin level was 4.24 ng/ml (normal range, 0 to 0.060 ng/ml), the myoglobin level was 1,849.4 ng/ml (normal range, 12 to 76 ng/ml), and the lactate dehydrogenase level was 1,408 IU/liter (normal range, 266 to 500 IU/liter). Her chest X-ray was reported to be clear. An electrocardiogram (ECG) showed sinus tachycardia with diffuse ST segment elevation. An urgent echocardiogram was performed, which demonstrated normal ventricle size, severely compromised pump function (ejection fraction, 20 to 30%), diffuse ipokinesia, and a small pericardial effusion, consistent with myopericarditis with a predominant myocarditic component. Metabolic lactic acidosis was also detected and treated with intravenous administration of Na ϩ -HCO 3 . Because of the need for specialized care and treatment, the patient was transferred to a regional pediatric hospital, but during ambulance transport she had loss of consciousness and needed respiratory assistance. Clinical conditions worsened during transfer to the pediatric intensive care unit (ICU): a peripheral pulse was absent, the central pulse was weak, and the capillary refill time was Ͼ5 s. Cardiac frequency (CF) detected by the monitor was 110 beats/min with a wide QRS interval. CF rapidly decreased. Atropine was administered, and cardiopulmonary resuscitation (CPR) maneuvers were performed. The central pulse became absent, and the echocardiogram showed no contractile activity.The pathological exam showed macroscopic changes such as increased ventricular size (left ventricle thickness, 2.2 cm; right ventricle thickness, 0.35 cm); the left/right ventricle size ratio was 6.28, versus a normal value of 3.1. Pericardial effusion (150 ml) was detected. Pulmonary congestion leading ...
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