Project description:We evaluated enterovirus D68 seroprevalence in Kansas City, Missouri, USA, from samples obtained during 2012-2013. Neutralizing antibodies against Fermon and the dominant 2014 Missouri isolate were universally detected. Titers increased with age. Widespread circulation of enterovirus D68 occurred before the 2014 outbreak. Research is needed to determine a surrogate of protection.
Project description:Here, we report 17 nearly complete genome sequences of enterovirus D68 (EV-D68) isolated from Kansas City, MO, in 2018. Phylogenetic analysis suggests that these strains belong to subclade B3, similar to the ones that caused the 2016 epidemics in the United States but different from the 2014 outbreak B1 strains.
Project description:A fall 2016 outbreak of enterovirus D68 infection in St. Louis, Missouri, USA, had less effect than a fall 2014 outbreak on hospital census, intensive care unit census, and hospitalization for a diagnosis of respiratory illness. Without ongoing surveillance and specific testing, these cases might have been missed.
Project description:Enterovirus D68 (EV-D68) was rarely observed prior to a widespread outbreak in 2014. We observed its reemergence in St. Louis in 2016 and sequenced the EV-D68 genomes from two patient samples. The 2016 viruses in St. Louis differed from those we had sequenced from the 2014 outbreak but were similar to other viruses circulating nationally in 2016.
Project description:Among known parechovirus (PeV) types infecting humans, PeV-A3 (formerly HPeV3) and PeV-A1 (formerly HPeV1) are associated with pediatric central nervous system (CNS) infections. The prevalence of PeV-A3 among hospitalized infants with sepsis-like illness and viral CNS infection is well described; however, the contribution of PeV-A4 to infant CNS infection is relatively unexplored. We report the first 11 U.S. cases of PeV-A4 CNS infections occurring in Kansas City infants during 2010 to 2016 and compare the clinical presentation with that of PeV-A3. PeV-positive cerebrospinal fluid (CSF) specimens from 2010 to 2016 underwent sequencing for genotyping. Among all PeV-CSF positives, PeV-A4 was detected in 11 CSF samples from 2010 to 2016. PeV-A4 was first detected in 2010 (n = 1/4), followed by detections in 2014 (n = 1/39), 2015 (n = 6/9), and 2016 (n = 3/33). The median age of PeV-A4-infected infants in weeks (median, 4; range, 1 to 8) was similar to that of infants infected with PeV-A3 (median, 4; range, 0.25 to 8). Clinical characteristics of PeV-A4 (n = 11) were compared with those of select PeV-A3-infected children (n = 34) with CNS infections and found to be mostly similar, although maximum temperature was higher (P = 0.017) and fever duration was shorter (P = 0.03) for PeV-A4 than for PeV-A3. Laboratory test results were also similar between genotypes, although they showed significantly lower peripheral white blood cell (P = 0.014) and absolute lymphocyte (P = 0.04) counts for PeV-A4 infants. Like PeV-A3, PeV-A4 caused summer-fall seasonal clusters of CNS infections in infants, with mostly similar presentations. Further surveillance is necessary to confirm potential differences in laboratory findings and in fever intensity/duration.
Project description:BackgroundEnterovirus D68 (EV-D68) has been infrequently reported historically, and is typically associated with isolated cases or small clusters of respiratory illness. Beginning in August, 2014, increases in severe respiratory illness associated with EV-D68 were reported across the USA. We aimed to describe the clinical, epidemiological, and laboratory features of this outbreak, and to better understand the role of EV-D68 in severe respiratory illness.MethodsWe collected regional syndromic surveillance data for epidemiological weeks 23 to 44, 2014, (June 1 to Nov 1, 2014) and hospital admissions data for epidemiological weeks 27 to 44, 2014, (June 29 to Nov 1, 2014) from three states: Missouri, Illinois and Colorado. Data were also collected for the same time period of 2013 and 2012. Respiratory specimens from severely ill patients nationwide, who were rhinovirus-positive or enterovirus-positive in hospital testing, were submitted between Aug 1, and Oct 31, 2014, and typed by molecular sequencing. We collected basic clinical and epidemiological characteristics of EV-D68 cases with a standard data collection form submitted with each specimen. We compared patients requiring intensive care with those who did not, and patients requiring ventilator support with those who did not. Mantel-Haenszel χ(2) tests were used to test for statistical significance.FindingsRegional and hospital-level data from Missouri, Illinois, and Colorado showed increases in respiratory illness between August and September, 2014, compared with in 2013 and 2012. Nationwide, 699 (46%) of 1529 patients tested were confirmed as EV-D68. Among the 614 EV-D68-positive patients admitted to hospital, age ranged from 3 days to 92 years (median 5 years). Common symptoms included dyspnoea (n=513 [84%]), cough (n=500 [81%]), and wheezing (n=427 [70%]); 294 (48%) patients had fever. 338 [59%] of 574 were admitted to intensive care units, and 145 (28%) of 511 received ventilator support; 322 (52%) of 614 had a history of asthma or reactive airway disease; 200 (66%) of 304 patients with a history of asthma or reactive airway disease required intensive care compared with 138 (51%) of 270 with no history of asthma or reactive airway disease (p=0·0004). Similarly, 89 (32%) of 276 patients with a history of asthma or reactive airway disease required ventilator support compared with 56 (24%) of 235 patients with no history of asthma or reactive airway disease (p=0·039).InterpretationIn 2014, EV-D68 caused widespread severe respiratory illness across the USA, disproportionately affecting those with asthma. This unexpected event underscores the need for robust surveillance of enterovirus types, enabling improved understanding of virus circulation and disease burden.FundingNone.
Project description:Background:Infection with parechovirus type 3 (PeV3) can cause severe neurologic and sepsis-like illness in young infants; clinical and epidemiologic descriptions have been limited. We aimed to characterize PeV3 illness and explore risk factors for acquisition in a cluster of neonatal cases at Children's Mercy Hospital in Kansas City, Missouri. Methods:Cerebrospinal fluid specimens were obtained from infants aged <180 days who were hospitalized with sepsis-like illness or meningitis between June 1 and November 1, 2014. PeV-positive specimens were sequenced at the Centers for Disease Control and Prevention. We reviewed the medical and birth charts of the infants and performed face-to-face parent interviews. We analyzed characteristics according to infant age and intensive care admission status. Results:We identified 35 cases of PeV infection in infants aged 5 to 56 days. Seven infants required intensive care (median age, 11 days vs 27 days among those who did not require intensive care; P = .0044). Six of these 7 infants had neurologic manifestations consistent with seizures, and all 6 of them were treated with acyclovir but subsequently tested negative for herpes simplex virus. Virus sequences formed 2 lineages, both of which were associated with severe illness. Half of the infants were reported to have household contacts who were ill during the week before onset. Infants aged ?7 days at onset were more likely to have been delivered at the same hospital. Conclusions:PeV3 can cause severe neurologic illness in neonates, and younger infants are more likely to require intensive care. PeV3 should be considered along with herpes simplex virus and other pathogens when evaluating young infants with sepsis-like illness or meningitis. More widespread testing for PeV3 would enable us to gain a better understanding of the clinical scope and circulation of this virus.