Parotitis is usually associated with mumps viral infections, but since trivalent measles–mumps–rubella vaccine started to be administrated in different countries, the burden of the disease has been steadily reduced. Nowadays the parotitis cases are usually related to other viral infections in countries with high vaccination coverage.1,2 Although Epstein Barr virus (EBV) has been recognized as the most frequently detected microorganism, other respiratory viruses such as parainfluenza virus (PIV) or adenovirus1 have been described associated with parotitis.
The human bocavirus (HBoV) has been identified in respiratory infections in children in a large number of studies, mainly in infants less than 2 years of age during late autumn3 being recurrent wheezing episodes and fever the most frequent symptomatology. To date, only two cases of parotitis have been reported associated with bocavirus infection, one of which being a coinfection with PIV 3.1,2 These two cases were detected in two prospective studies that surveyed the frequency of several viruses in sporadic parotitis in Korea and U.S.A. The authors observed an incidence of HBoV infection of 0.4–1% in their studied cases.
We report a child with parotitis and an acute respiratory tract infection in whom HBoV was the only virus identified.
A 17-month-old male, with a history of recurrent wheezing presented at the emergency room in November with 48h of left parotid swelling. He had had fever for a few hours (maximum 39.2°C), and respiratory distress that had not improved despite receiving bronchodilators and amoxicillin-clavulanate for two days. Physical examination revealed high fever, left parotid inflammation without erythema, expiratory wheezing and hypoxaemia, requiring admission and treatment with bronchodilators and oxygen therapy. The chest X-ray demonstrated an infiltrate in the right middle lobe. Cervical ultrasound revealed an enlarged left parotid gland, with multiple internal lesions of low echogenicity in relation to intraglandular inflammatory changes. Intraglandular adenopathy and bilateral laterocervical chains were also observed. The blood test showed normal haemoglobin and platelets; 13,000 leukocytes (44% neutrophils); C-reactive protein 41mg/L and amylase 381U/L. Blood culture was negative, and a multiplex polymerase chain reaction in nasopharyngeal aspirate taken at admission (CLART® Pneumovir array assay that identifies adenovirus, metapneumovirus A,B, parinfluenza 1,2,3,4, rhinovirus, respiratory syncytial virus A,B, bocavirus, influenza A,B,C, enterovirus and coronavirus 229E, OC43 & NL63) was positive for HBoV. Mumps serology detected negative IgM and positive IgG titres. He remained afebrile during admission, with improvement in his respiratory distress and disappearance of parotid swelling, then being discharged within 3 days.
Two weeks after admission the patient was asymptomatic, cervical ultrasound was normal except for some intraparotid adenopathy, and amylase titre was 77U/L. Control nasopharyngeal aspirate in this moment was negative.
Human bocavirus has been associated with lower respiratory tract infections, mainly wheezing and pneumonia, in young children.3–5 It has also been described as a causative agent of upper respiratory tract infections, mainly adenoiditis and otitis, demonstrating its affinity with this type of tissues.6,7 To date, only in two cases has HBoV been associated with mumps but its pathogenic role as a causative agent of parotitis is discussed, since in one case it has been detected in coinfection with PIV 3.1,2 However, the parotid gland could be a target of infection for this virus, as occurs in adenoids, where some authors have identified HBoV in up to 43% of the specimens obtained from children with adenoidal disease.7
Our patient had the typical symptomatology associated with HBoV infections with a wheezing episode, and with infiltrate in the chest X-ray. In addition, he was in the most frequent age-range for this virus infection, developing the disease during late autumn when most HBoV infections occur.3 The analytical data were also consistent with those described in HBoV infections.3 Bacterial agents were not detected. He was correctly vaccinated and mumps serology showed the presence of IgG titres. Acute EBV infection was also ruled out. The clinical picture evolved favourably and the nasopharyngeal aspirate control was negative two weeks after the acute episode. Although causality of HBoV is difficult to establish, serology has demonstrated that HBoV has a pathogenic role in respiratory infections.8–10 Unfortunately in our centre we do not have HBoV serology available, but we think that our case adds to those already described to make it consider that it may have an etiological role.
We consider that HBoV should be taken into consideration as an infrequent but possible causative agent of acute parotitis in young children. Prospective studies should be designed to verify the truly pathogenic role in parotitis cases.
