Impact of Rotavirus Vaccination on Hospital-Acquired Rotavirus Gastroenteritis in Children

DISCUSSION

In the 2007–2008 rotavirus season, we noted a 82% decline in CA rotavirus admissions from the previous median of the 2003–2007 season. These data mirror other published studies from the 2007–2008 season that noted a significant decrease (67%–87%) in CA rotavirus^10,11,13,18 and in all-cause acute gastroenteritis hospitalization rates.¹⁴ Because only 31% of US children younger than 2 years old had completed 3 doses of vaccine, with single-dose administration rates of 56% by the 2007–2008 season, this strongly suggests herd immunity.^10,13,19 In contrast, CA RSV and CA influenza hospital admission rates remained stable. The slight increase in CA rotavirus infections in the 2008–2009 season compared with the 2007–2008 season was similar to national data.¹⁵

Hospital acquisition of rotavirus infections occurs frequently. A recent review determined that roughly 27% of children hospitalized with rotavirus (16 000–19 000 hospitalizations per year) have acquired rotavirus infection while hospitalized for another condition.^9,20,–,22 This equates to transmission of rotavirus from 1 in every 3 children admitted with CA rotavirus to another hospitalized child. Similarly, we found that HA rotavirus accounted for ∼19% of the total inpatient rotavirus burden at CMH before 2007–2008. Potential reasons for the frequent transmission of rotavirus in the hospital include the large number of rotavirus virions shed in stool, the low rotavirus infectious dose, and prolonged shedding, which has been observed in hospitalized children.^2,23,–,25 One group concluded that because the percentage of rotavirus in the hospital that is HA has remained stable for 20 years, more stringent infection-control practices would not likely impact the burden of HA rotavirus.²² Many groups have speculated that interventions that impact CA rotavirus hospital admissions (eg, vaccination) might also impact HA rotavirus rates.^{3,6,7,9,21,22}

The substantial decline in CA rotavirus rates prompted us to evaluate whether HA rotavirus rates might be impacted as well. Coincident with the decrease in CA rotavirus rates, we documented a significant decrease in HA rotavirus rates in 2007–2008, in contrast with the stability of HA RSV and HA influenza rates. Potential reasons for this include fewer hospitalizations of children with CA rotavirus, resulting in less risk of transmission, and fewer hospitalized children may be at risk of rotavirus infection because of previous rotavirus vaccination. This study was unable to differentiate between these possibilities. Our data differ from those of children admitted to a pediatric hospital in Philadelphia, in which the absolute number of HA cases in 2007–2008 remained unchanged from 2005 to 2006.¹¹ The methods for identifying HA cases in that study were not detailed, and the reasons for differences in our results are not readily apparent.¹¹ The decrease in HA rotavirus rates we observed in 2007–2008 was sustained in 2008–2009.

To control for changes in infection control within the hospital and to control for changes in the year-to-year number of CA admissions, we also evaluated the rates of transmission (HA infections and CA infections) of rotavirus, RSV, and influenza. Thus, changes in infection control that lower the number of HA infections will result in a fall in the rate of transmission. The rate of transmission for rotavirus (median: 0.27 for the 2003–2008 seasons) remained unchanged and much higher than for influenza or RSV (Fig 3). Thus, for every 4 CA rotavirus hospital admissions, at least 1 child will acquire rotavirus while hospitalized for other reasons. Although we noted continued improvement in our independently observed hand-hygiene compliance, a corresponding decrease in the HA and CA rotavirus transmission rate did not occur. A potential explanation is that the 10% absolute increase in hand-hygiene compliance at CMH was insufficient to substantially impact HA rates. Our data confirm the opinion of others, which is that more stringent infection-control practices would be unlikely to impact the burden of HA rotavirus disease²² and also confirm the hypothesis that vaccination, by impacting CA rotavirus hospital admissions, might decrease HA rotavirus rates.^{3,6,7,9,21,22} Thus, community-based rotavirus vaccination efforts should be encouraged as a strategy for impacting the substantial burden of HA rotavirus.

One potential explanation for the decline in HA rotavirus rates would be a subtle unrecognized change in CMH's infection prevention and control efforts. Thus, we used other common pediatric viral pathogens (RSV and influenza) as comparators. Transmission of RSV occurs primarily by contact with contaminated secretions and via fomites with some transmission by large particle droplets at short distances (<3 ft).¹⁶ Thus, for both rotavirus and RSV, hand-hygiene and barrier precautions are considered crucial to prevention and containment.^17,26 Other groups^26,–,28 also have compared HA rotavirus and RSV and observed a similar burden of disease. Limited evidence exists that rotavirus also may undergo airborne transmission^9,20; thus, influenza also was used as a comparator.¹⁶ Rates of RSV and influenza transmission in our study were similar to rates observed in other studies.^29,30 The failure to observe any change in HA RSV and HA influenza rates in 2007–2008 strongly argues against a subtle unrecognized change in the methods of infection prevention and control as responsible for the decline in HA rotavirus rates.

Limitations of this study include the fact that these data are retrospective and from a single, large, tertiary care center. We may have missed hospitalized patients with mild gastroenteritis symptoms, but these patients likely would have been missed consistently each year.²¹ It could be argued that the use of rapid antigen testing, particularly for influenza, resulted in the underdiagnosis of viral pathogens, because of the low sensitivity in clinical practice of the rapid antigen test.³¹ This limitation, however, is unlikely to have impacted our conclusions because the same rapid antigen kits were used throughout the study and a symmetric underdetection of both CA and HA infections likely occurred. We also could not include data for RSV and influenza in 2008–2009 because of the onset of the pandemic 2009 H1N1 influenza that resulted in the implementation of many new infection-control strategies. The first of these measures occurred coincident with our last case of HA rotavirus in May 2009 and occurred after 75% of the CA rotavirus had occurred. Thus, it is unlikely that these efforts significantly impacted the risk of HA rotavirus. Because of our study design, we lack genotype data for the identified HA isolates, which would allow us to determine genetic relatedness of the HA isolates. We also were unable to assess the impact on hospital cost and severity of illness.

Important strengths of this study include the multiple years of baseline data from 2003 to 2007 and inclusion of comparison data from other common pediatric HA viral pathogens (RSV and influenza). These data provide the context in which to the substantial decline in both CA and HA rotavirus disease that began in 2007–2008.