KI and WU Polyomaviruses in Children, France

KI and WU Polyomaviruses in Children, France

In France, from November 2006 through June 2007, nasopharyngeal aspirates were obtained from 537 children who were <5 years of age and who had acute respiratory tract disease. The aspirates were tested for respiratory syncytial virus (RSV); infl uenza virus types A and B; parainfl uenza virus types 1, 2, and 3; and adenoviruses (AdVs) by direct immunofl uorescence assay. The aspirates were also tested for human metapneumovirus (HMPV) by an enzyme immunoassay (HMPV EIA, Biotrin, Lyon, France) and for the human bocavirus (HBoV) by PCR (3). Samples were placed on MRC5 cell monolayers for virus isolation.
Nucleic acid extracts were tested for KIPyV and WUPyV DNA by PCR. KIPyV detection was performed by using a nested PCR approach that targeted the VP1 capsid gene as described by Allander et al. (1). For WUPyV detection, primers targeted the predicted 3′ end of the large T antigen coding region as described by Gaynor et al. (2). The amplifi cation specifi city was assessed by sequencing the PCR product; sequences were deposited in GenBank (WUPyV isolates, accession no. AM778536-48; KIPyV isolates, accession no. AM849808-10).
A total of 13 (2.4%) samples were positive for WUPyV; of these 4 (30.8%) were co-infected with another virus. The 13 children with samples positive for WUPyV had a median age of 11.2 (2-48) months and the male/ female sex ratio was 2.2. KIPyV DNA was detected in samples from 3 (0.6%) boys (ages 10, 18 and 30 months); 1 of those samples was co-infected with RSV and HMPV.
Sequences of WUPyV and KIPyV isolates varied little from each other and from other GenBank sequences, which suggests that these polyomaviruses are genetically conserved viruses. Clinical characteristics of children infected with WUPyV and KIPyV are retrospectively recorded (Table). All children recovered and were able to return home within 1 to 10 days, with the exception of 1 child. This child had been hospitalized since birth for congenital myopathy; nosocomial acquisition or vertical transmission of the WUPyV is suspected.
Our data are in agreement with the 2 original reports that show that the new KI and WU polyomaviruses may be detected in respiratory secretions from patients with respiratory diseases (1,2). WUPyV was detected in 2.4% of children <5 years of age who were hospitalized with respiratory tract disease, which is in accordance with the 2% incidence reported by Gaynor et al. (2). The 0.6% prevalence observed for KIPyV PCR is also in agreement with data reported from Sweden (1) and Australia (4). A seasonal change in the presence of WUPyV was not observed; however, all KIPyV isolates were found only during January.
KIPyV and WUPyV were mainly detected in samples from children with lower respiratory tract disease, such as bronchiolitis or atypical pneumonia, and in samples from children with exacerbated asthma. These preliminary data on the likely role of these viruses as respiratory pathogens need to be interpreted with caution. Aspirates were obtained only from those with observed symptoms; no asymptomatic controls were tested. Detection of WUPyV and KIPyV in respiratory samples may simply refl ect a respiratory transmission route as previously suggested for BK virus and JC virus (5). Another virus was in aspirates from 31% of the children with KI and WU polyomaviruses. Substantial rates of codetection were also reported in the initial descriptions of both WUPyV and KIPyV (1,2). More recently, Bialasiewicz et al. reported a 25% rate of codetection of KIPyV with another pathogen (4). These high rates of co-  infection raise questions about the real pathogenic role of these viruses. As with other polyomaviruses, WUPyV and KIPyV could establish persistent and latent infections with likely asymptomatic reactivations (5), and detection of these viruses could also refl ect a long-term shedding from previous acute episode. Recently

Milk Replacers and Bovine Spongiform Encephalopathy in
Calves, Japan To the Editor: Milk replacers produced from a specifi c feed factory in Japan were suspected of being associated with a cluster of bovine spongiform encephalopathy (BSE) infection in calves. We conducted a case-control study to test this association.
In Japan, BSE infection has been confi rmed in 32 calves as of the end of May 2007; 13 of these calves were born between December 1995 and August 1996. One BSE-infected calf was born in 1992 and had an atypical BSE phenotype (1). Because no BSEinfected calves were born in 1997 and 1998, we considered that those born in 1995 and 1996 formed an independent temporal cluster (Figure). Epidemiologic investigation showed that all 13 calves were fed milk replacers produced by a specifi c factory. Ten calves were born in Hokkaido, and 3 were born in the Kanto region, which is ≈800 km away from Hokkaido.
In the case-control study, all farms where the 13 BSE-infected calves were born and raised for at least 1 year were defi ned as case farms. Control farms were defi ned as dairy farms where no BSE calves had been reported. Candidates for control farms comprised 200 randomly selected farms, which were located in 23 prefectures where the milk replacers were distributed. We used a national cattle identifi cation database for random selection. Veterinary offi cers from the local government interviewed farmers in November and December 2006 and requested that they complete a questionnaire on farming practices in 1996, including herd size and use of milk replacers and calf concentrates. For the case farms, information previously obtained from outbreaks was used. Of the 200 potential control farms, 154 farms were used as controls. Forty-six farms were excluded; 24 farmers did not respond or could not specify the use of milk replacers; and 22 farms had either closed or farmers did not respond for miscellaneous reasons.
Among the 154 control farms, 36 farms (23%) used the milk replacers from the specifi c factory, 89 farms (58%) used other milk replacers, and 29 farms (19%) did not use milk replacers. Since 1 case farm lacked