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Background This open-label, single-arm, phase 3 study evaluated safety and immunogenicity of the 13-valent pneumococcal conjugate vaccine (PCV13) in pneumococcal vaccine-naive Japanese individuals aged 6–64 years at increased risk of pneumococcal disease (PD). Methods Participants received 1 PCV13 dose. Reactogenicity events were recorded for 7 days (individuals aged 6- to 17-year-old) or 14 days (individuals aged 18 to 64 years old) postvaccination. Adverse events (AEs) were collected for 1 month postvaccination. Opsonophagocytic activity (OPA) and anticapsular immunoglobulin G (IgG) geometric mean concentrations (GMCs) were measured for vaccine serotypes before and 1 month postvaccination. Post hoc analyses compared immunogenicity in participants categorized as at-risk (immunocompetent but having chronic medical conditions associated with increased PD risk) or high-risk (immunocompromised due to diseases/conditions and/or medications). Results 206 participants aged 6- to 17-year-old (n = 53) and 18 to 64 years old (n = 153) completed the study. Reactogenicity events were generally mild to moderate in severity. AEs were reported in 16% (33/206) of participants; 1.0% (2/206) were severe. Six AEs were vaccine-related; most were associated with local reactions. No serious AEs occurred. Circulating antibody levels for all 13 serotypes increased postvaccination. OPA geometric mean fold rises (GMFRs) from prevaccination to 1 month postvaccination were 5.5–61.7; lower limits of the 2-sided, 95% CI were > 1 for all serotypes. IgG GMFRs were consistent with OPA analyses. In post hoc analyses, 55.8% (115/206) and 44.2% (91/206) of participants were categorized as at risk and at high risk of PD, respectively; OPA GMFRs from prevaccination to 1 month postvaccination were 3.9–635.1, with lower limits of the 2-sided 95% CIs > 1 for all 13 serotypes across these risk groups; IgG GMFRs were consistent with OPA analyses. Conclusions PCV13 was well tolerated and immunogenic in Japanese individuals aged 6–64 years considered at increased risk of PD. Results were broadly comparable with past PCV13 studies in other Japanese and non-Japanese populations. Registration number: NCT03571607; JapicCTI-184024.

We herein report a case of pulmonary tumor embolism caused by hematogenous metastasis that mimicked pulmonary thromboembolism in a 62-year-old Japanese woman with a history of uterine corpus carcinosarcoma. The case suggests that tumor embolism must be included in the differential diagnoses of respiratory symptoms in patients with a history of malignancy. It also illustrates the usefulness of such findings as beaded, dilated pulmonary arteries by computed tomography (CT) and high (18)F-fluorodeoxyglucose (FDG) uptake by fusion FDG positron emission tomography/CT imaging for differentiating a pulmonary tumor embolism from pulmonary thromboembolism.

A 72-year-old man was admitted to the intensive care unit of our hospital with acute respiratory distress syndrome (ARDS). A chest CT scan showed diffuse consolidations and ground-glass opacities in both lungs. We diagnosed ARDS secondary to community-acquired pneumonia. We then started mechanical ventilation with airway pressure release ventilation and treated him with antibiotics, peramivir, and corticosteroids, despite negative results for a rapid antigen test for influenza. Bronchial lavage on day 10 showed blood-tinged fluid and hemosiderin-laden macrophages, but no bacteria or fungi. Real-time reverse-transcriptase polymerase chain reaction testing yielded a positive result for pandemic influenza A (H1N1). The mechanical ventilator was removed on day 15, corticosteroid administration was discontinued on day 22 and antibiotics were discontinued on day 23. However, he had a fever on day 28, pleural pain and dyspnea on day 29, and exacerbation of the infiltration as demonstrated on chest CT on day 30. On day 31, repeat bronchoalveolar lavage showed an increase in the number of total cells which were lymphocyte-predominant, but there were no pathogens. We believed that this clinical exacerbation might have occurred due to the re-exacerbation of pandemic influenza A (H1N1) pneumonia due to the cessation of corticosteroids. The re-administration of corticosteroids was effective, and were eventually tapered. Currently, the use of corticosteroid therapy for severe pandemic influenza A (H1N1) pneumonia is controversial, but even the late administration of corticosteroid therapy may be effective. However, this case also suggests that the early administration of corticosteroid therapy as immunomodulation might be effective in selected cases, and that cessation of such therapy during the early phase of ARDS may cause exacerbation of clinical symptoms.

A 60-year-old man was admitted because of fever, headache, and difficulty in walking. Respiratory symptoms included only mild cough, but crackles were present on auscultation at the right lung base, the chest roentgenogram and computed tomography scans showed consolidation in the right lower lobe. Laboratory findings revealed hyponatremia, elevated liver function test values and creatine phosphokinase, and Legionella pneumophila antigen in urine. Neurological examination revealed mild mental status change, dysmetria, dysarthria, and ataxic gait. Diffusion-weighted magnetic resonance imaging (MRI) of the brain, performed at the time of admission, revealed regions of high intensity in the splenium corpus callosum. We diagnosed Legionnaires' pneumonia accompanied by clinically mild encephalitis/encephalopathy with a reversible splenial lesion (MERS), and started treatment with ciprofloxacin and methylprednisolone at 1 mg/kg/day. Neurological symptoms gradually improved. On day 6 after admission, mild dysarthria and ataxic gait remained, a 123-IMP single photon emission computed tomography revealed no abnormality. On day 15 after admission, the only neurological symptom was mild ataxic gait; the MRI scans showed no abnormalities. On day 29 after admission, neurological symptoms were completely resolved. This is the first reported case of Legionnaires' pneumonia accompanied by clinically mild encephalitis/encephalopathy with a reversible splenial lesion (MERS) was treated with not only antibiotics but also corticosteroid.