Objective To investigate the relationship between viral load and secondary transmission in novel coronavirus disease 2019 (COVID-19). Methods Epidemiological and clinical data were obtained from immunocompetent laboratory-confirmed patients with COVID-19 who were admitted to and/or from whom viral loads were measured at Toyama University Hospital. Using a case-control approach, index patients who transmitted the disease to at least one other patient were analysed as “cases” (index patients) compared with patients who were not the cause of secondary transmission (non-index patients, analysed as “controls”). The viral load time courses were assessed between the index and non-index symptomatic patients using non-linear regression employing a standard one-phase decay model. Results In total, 28 patients were included in the analysis. Median viral load at the initial sample collection was significantly higher in symptomatic than in asymptomatic patients and in adults than in children. Among symptomatic patients (n = 18), non-linear regression models showed that the estimated viral load at onset was higher in the index than in the non-index patients (median [95% confidence interval]: 6.6 [5.2–8.2] vs. 3.1 [1.5–4.8] log copies/μL, respectively). In adult (symptomatic and asymptomatic) patients (n = 21), median viral load at the initial sample collection was significantly higher in the index than in the non-index patients (p = 0.015, 3.3 vs. 1.8 log copies/μL, respectively). Conclusions High nasopharyngeal viral loads around onset may contribute to secondary transmission of COVID-19. Viral load may help provide a better understanding of why transmission is observed in some instances, but not in others, especially among household contacts.

To investigate the relationship between viral load and secondary transmission in novel coronavirus disease 2019 (COVID−19), we reviewed epidemiological and clinical data obtained from immunocompetent laboratory-confirmed patients with COVID−19 at Toyama University Hospital. In total, 28 patients were included in the analysis. Median viral load at the initial sample collection was significantly higher in adults than in children and in symptomatic than in asymptomatic patients. Among symptomatic patients, non−linear regression models showed that the estimated viral load at onset was higher in the index (patients who transmitted the disease to at least one other patient) than in the non−index patients (patients who were not the cause of secondary transmission; median [95% confidence interval]: 6.6 [5.2−8.2] vs. 3.1 [1.5−4.8] log copies/µL, respectively). High nasopharyngeal viral loads around onset may contribute to secondary transmission of COVID−19.

Mycobacterium bovis infection after intravesical Bacillus Calmette-Guérin (BCG) therapy is rare. A 65-year-old Japanese man with history of bladder cancer and intravesical BCG therapy, presented with low-grade fever. An aneurysm with perianeurysmal fluid was suspected and endovascular aortic repair was performed. After 160 days, he developed blood-streaked sputum and computed tomography images revealed that the perianeurysmal fluid area was increasing in size. A multiplex polymerase chain reaction using sputum identified M. bovis. Treatment with anti-tuberculosis drugs reduced the size of the perianeurysmal fluid area. After intravesical BCG therapy, the possibility of M. bovis infection should be considered, thus further investigations are required.

A 53-year-old man was admitted to the hospital with a diagnosis of cellulitis and osteomyelitis. Twenty-four days after the initiation of daptomycin and sulbactam/ampicillin, he developed a fever and pulmonary infiltration. Bronchoalveolar lavage revealed a high number of eosinophils, while an intracutaneous test revealed positivity for daptomycin. The patient improved after discontinuing antimicrobial therapy. The plasma daptomycin minimum concentration (Cmin) was elevated (27.4 μg/mL), but plasma protein binding of daptomycin was low (87.8%). Although the pathophysiology of eosinophilic pneumonia remains unclear, antigenic stimulation due to daptomycin accumulation in the alveoli may have caused continuous immune activation.

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