155 Plastic bronchitis (PB) is a rare respiratory condition characterized by the formation of cohesive branching casts that result in airway obstruction (1). PB is categorized into two types based on cast histopathology. Type 1 casts are abundant in fibrin, eosinophils, and Charcot-Leyden crystals (CLCs). They have been associated with asthma and atopic diseases. Type 2 casts are composed of mucinous materials with minimal or no cellular component. They have been typically associated with congenital heart disease in patients who undergo the Fontan procedure (1). Cases of PB caused by viral respiratory tract infections in previously healthy children have recently been reported (2). The infuenza A (H1N1) pdm09 virus is the primary etiologic agent for cast formation in pediatric patients (2). Human bocavirus (HBoV) belongs to the Parvoviridae family and has been detected in nasopharyngeal specimens (3). Initially, HBoV1 was discovered in 2005, followed by HBoV2-4 in 2009 (4). HBoV1 has recently been reported as a pathogen responsible for acute respiratory tract infections, which are common in children (4,5). HBoV1 can be detected in asymptomatic children or in those infected with other respiratory viruses, but its pathologic contribution to respiratory infection remains unclear (4). This report describes a case of severe PB caused by HBoV1 in a child. A 20-month-old male patient presented with acute dyspnea. He developed cough and fever 3 days prior to admission. The patient had no history of asthma, allergies, or cardiac anomalies. He did not go abroad, and influenza A was not prevalent in the area of the patient’s residence. Upon transfer to our emergency department, he presented with tachypnea and hypoxia with a temperature of 39.1°C, heart rate of 160 beats/ min, respiratory rate of 50 breaths/min, and SpO 2 of 88–92% (with a fow rate of 8 L/min using a reservoir mask). Chest-wall retraction and decreased breath sounds over the left hemithorax were noted. Chest radiography showed atelectasis of the left lung, while computed tomography (CT) showed occlusion of the left main bronchi and no foreign bodies. Multiplex polymerase chain reaction (PCR) of a nasopharyngeal swab, using FilmArray Respiratory Panel 2.1 (FilmArray; Bio Mérieux, Marcy-l'Etoile, France) (6), revealed respiratory syncytial virus (RSV) and human parainfuenza virus (HPIV) 3. The atelectasis of the left lung worsened, and the patient was intubated for ventilatory management on day 2. Contrast- enhanced CT after tracheal intubation revealed no mass suggestive of a mediastinal tumor. On day 3, rigid Short Communication Plastic Bronchitis of Human Bocavirus 1 Detected by Comprehensive Polymerase Chain Reaction of Mucus Casts Hiroki Yabushita 1 , Shogo Otake 1 * ‡ , Shun Iida 2 , Harutaka Katano 2 , Tadaki Suzuki 2 , and Masashi Kasai 1 1 Division of Infectious Disease, Department of Pediatrics, Hyogo Prefectural Kobe Children’s Hospital, Hyogo; and 2 Department of Pathology, National Institute of Infectious Diseases, Tokyo, Japan ABSTRACT: Plastic bronchitis (PB) is a rare and severe respiratory disease characterized by the formation of branching mucus casts, resulting in airway obstruction. PB can be divided into two types. Type 1 PB is primarily caused by infammatory casts that result from allergic diseases. In type 2 PB, mucinous casts are produced in association with congenital heart disease. PB is also associated with viral respiratory infections, particularly the infuenza A (H1N1) pdm09 virus, which is the most common pathogen afecting pediatric patients. Herein, we report a case of severe type 1 PB caused by human bocavirus (HBoV)1 in a child. Multiplex polymerase chain reaction (PCR) of a nasopharyngeal swab revealed the presence of respiratory syncytial virus and human parainfuenza virus 3. However, no viruses other than HBoV1 were detected in mucus casts by real-time PCR. Consequently, we suggest that HBoV can cause PB in pediatric patients, and direct and comprehensive PCR of bronchial casts may be useful for identifying the etiologic agents. Received July 23, 2022. Accepted October 24, 2022. J-STAGE Advance Publication November 30, 2022. DOI:10.7883/yoken.JJID.2022.433 *Corresponding author: Mailing address: Division of Infectious Disease, Department of Pediatrics, Hyogo Prefectural Kobe Children’s Hospital, Hyogo, Japan. ‡ Present address: Center for Field Epidemic Intelligence, Research, and Professional Development, National Institute of Infectious Diseases, Tokyo, Japan. J1601 Iidabashi Plano stage Bld., 2-7-2 Fujimi, Chiyoda-ku, Tokyo 102-0071, Japan. Tel: +81-3-6261-5930, E-mail: shogo.ohtake@gmail. com Jpn. J. Infect. Dis., 76, 155-158, 2023