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BackgroundPostoperative bloodstream infection (BSI) is the most important determinant of recipient morbidity and mortality after liver transplantation (LT). Children who underwent LT are at the highest risk of developing BSI because of the significant surgical intervention, use of multiple devices, and administration of immunosuppressive agents. However, information regarding the risk factors for BSI in children after LT is limited.MethodsWe retrospectively reviewed 210 children who underwent living-donor LT at the largest pediatric LT center in Japan. Patients' characteristics, blood culture results and clinical outcomes were extracted from electronic medical records. Univariate and multivariate analyses were performed to identify the risk factors for BSI.ResultsAmong the 210 LT recipients, 53 (25%) recipients experienced 86 episodes of BSI during the observational period. The source of the BSI was identified only in 38%: catheter-related BSI (27%) peritonitis (7%), urinary tract infection (2%), pneumonia (1%) and infectious endocarditis (1%). A multivariate analysis demonstrated that body weight (P = 0.03), volume of blood loss during LT (P < 0.001) and cytomegalovirus (CMV) antigenemia positivity (P = 0.04) were independently associated with the development of BSI. The risk factors for BSI differed when we analyzed the subjects according to age (≤24 months and >24 months), blood loss and pediatric end-stage liver disease/model for end-stage liver disease versus positive CMV antigenemia.ConclusionsThe volume of blood loss, postoperative CMV antigenemia positivity and body weight were associated with the development of BSI after LT in pediatric living-donor recipients. To identify the age-specific predictors of BSI in children who underwent LT, age-specific analyses are crucial.

In this article the author talks about the changes in laboratory findings in parechovirus-A infection in neonates and infants. Topics discussed include neonates and infants whose serum samples were positive for PeV-A when tested with the polymerase chain reaction (PCR) method at Nagano Red Cross Hospital, Japan, between July and October 2014, and patients received corticosteroids and intravenous immunoglobulin therapy during hospitalization.

As compared with standard intramuscular and subcutaneous vaccines, intradermal (ID) vaccines elicit a more potent immune response in both adults and children, with equivalent dosage or antigen dose sparing. Recently, various devices for ID injection have been developed; the length of needles ranges in 0.6–1.5 mm. However, skin thickness must be measured to determine optimal needle length for ID vaccines. Use of ID vaccines in infants and children is appealing because children require more vaccines than do adults; however, information on skin thickness in infants and children is limited. We used ultrasound echography to measure skin thickness in Japanese infants aged 2 months ( n = 78) and adolescents aged 13–15 years ( n = 82). Mean (range) deltoid and suprascapular skin thickness was 1.67 mm (1.16–2.39 mm) and 1.83 mm (1.24–2.60 mm), respectively, in infants and 1.81 mm (1.25–3.00 mm) and 2.43 mm (1.51–3.95 mm), respectively, in adolescents. Among infants who underwent re-measurement of skin thickness at age 6 months ( n = 11), mean deltoid skin thickness (1.84 mm) was significantly greater than at age 2 months (1.60 mm) ( P < 0.001). In contrast, no significant difference was observed in suprascapular skin thickness (1.79 mm vs. 1.67 mm, respectively; P = 0.17). Gender was not associated with skin thickness in either age group. Skin thickness was positively correlated with body weight in adolescents ( r = 0.43, P < 0.001 in deltoid region; r = 0.30, P = 0.01 in suprascapular region). In conclusion, this is the first study to evaluate skin thickness in different age groups of children, including at age 2 months. Skin thickness gradually increased from age 2 months to age 13–15 years, but no consistent trend was noted in analysis stratified by measurement site, gender, or age. These findings suggest that an appropriate length of ID device needle for infants and children is likely to be less than 1.2 mm and a special device with shorter length of needle is warranted for infants and children. [ABSTRACT FROM AUTHOR]

Four infants born prematurely presented with multiple apnea episodes caused by human parechovirus type 3 (HPeV3) infection. All patients required oxygen supplementation, and one patient required mechanical ventilation. HPeV3 infection might be included in the differential diagnosis of apnea in neonates and young infants, especially those born prematurely. [ABSTRACT FROM AUTHOR]

Background Parechovirus-A3 (PeV-A3) causes severe disease, including sepsis and meningoencephalitis in young infants. The first case of PeV-A3 was reported in Japan in 1999 and, although epidemics have been reported every 2 to 3 years in more than 20 countries, no major epidemic has occurred in Japan since 2014. Methods This prospective study included febrile infants (<4 months of age) admitted at Niigata University and its affiliated hospitals, which serve about 2.5 million people, during the period from 2014 to 2018. Neonates and infants younger than 4 months presenting with fever and suspected of having viral sepsis underwent serum and/or cerebrospinal fluid (CSF) testing by real-time PCR for parechovirus-A (PeV-A) and enteroviruses (EVs), and for herpes simplex viruses, if suspected. Bacterial infection was excluded on the basis of the results of bacterial culture of blood, urine, and/or CSF. PeV-A genotype was identified by examining the viral protein 1 (VP1) sequence, and the phylogenetic tree of the VP1 sequence was constructed. Results Of the 277 patients evaluated, 135 (49%) were positive for PeV-A (n = 74, 27%) or EVs (n = 61, 22%). Among PeV-A patients, most had PeV-A3 (n = 69; 93%), followed by PeV-A4 (n = 4; 5%). There was a PeV-A3 epidemic in 2014 (n = 43); however, no cases were reported in 2015. In 2016–2018, small numbers of PeV-A3 cases were reported: 10 in 2016, 7 in 2017, and 9 in 2018. In contrast, EV cases were reported throughout this period: 8 in 2014, 22 in 2015, 10 in 2016, 5 in 2017, and 16 in 2018. When data were analyzed by season, the PeV-A3 detection rate in summer (June-August) was 93% (40/43) in 2014 and 65% (17/26) during 2016–2018, indicating an increase in the number of PeV-A3 cases in seasons other than summer. Phylogenetic analysis showed that PeV-A3 strains during 2016–2018 were part of a cluster of epidemics in 2011 and differed from those in 2014. Conclusion After the major PeV-A3 epidemics in 2014, we observed changes in the PeV-A3 epidemic profile, namely, a small, but constant, number of cases every year in Niigata, Japan. A future study should investigate if this trend has continued in Japan and other countries and identify the causes of this change in epidemic profile. Disclosures All authors: No reported disclosures. [ABSTRACT FROM AUTHOR]

Background Parechovirus-A3 (PeV-A3) and enteroviruses (EVs) are the most common viral causes of neonatal and infantile sepsis. We previously reported that the clinical manifestations of PeV-A3 infection—e.g. high body temperature, tachycardia, and poor peripheral circulation, but not cerebrospinal fluid (CSF) pleocytosis—tend be more severe than those of EV infection. We tested the hypothesis that innate immune responses to PeV-A3 and EVs are distinct. Methods Using serum and CSF samples, we investigated immune responses of febrile neonates and infants <4 months in Niigata, Japan, from 2015 through 2018. PeV-A and EV infections were diagnosed with real-time PCR. PeV-A3 infection was diagnosed by sequence analysis of the VP1 region. The control was clinically well patients without serum and CSF findings suggestive of bacterial or viral etiology. The Milliplex MAP human cytokine/chemokine magnetic bead panel (Merck Millipore, Germany) was used to analyze 22 cytokines/chemokines related to innate immunity in serum and CSF. Results We evaluated 14 PeV-A3-infected and 15 EV-infected patients and 8 controls. Serum levels of proinflammatory cytokines/chemokines (fractalkine, interferon-α2, interleukin [IL]-1 receptor α, IL-6, IL-8, and IL-15) were significantly higher in PeV-A3-infected patients than in EV-infected patients (P < 0.005). Serum cytokine/chemokine profiles of EV-infected patients did not differ from those of controls. However, while most pro- and anti-inflammatory cytokines/chemokines in CSF were elevated in EV-infected patients, levels were low or undetectable in PeV-A3-infected patients and controls (P < 0.005). Conclusion PeV-A3-infected patients had high serum levels of proinflammatory cytokines/chemokines, which may explain why clinical manifestations were more severe in this patient group than in EV-infected patients. Conversely, the limited or nonexistent innate immune response in CSF from PeV-A3-infected patients might explain the absence of CSF pleocytosis. These findings improve our understanding of the differing pathophysiological characteristics of PeV-A3 and EV infection in neonates and young infants. Disclosures All Authors: No reported Disclosures. [ABSTRACT FROM AUTHOR]

Background Parechovirus-A3 (PeV-A3) is an emerging pathogen causing sepsis and meningoencephalitis in neonates and young infants. We previously reported that maternal antibodies against PeV-A3 are important to protect neonates and young infants from the infection. Recent studies showed that (1) breastfeeding had a protective effect against enterovirus, which is closely-related virus to PeV-A, and (2) human breast milk (HBM) neutralized enterovirus in vitro. Currently, no report is available related to the antiviral effect of HBM against PeV-A3. Methods HBM (colostrum, 3–5 days after childbirth; mature milk, 1 month after childbirth) and serum (within ± 1 week of child's birthday) samples were obtained from mothers at obstetrics clinic in Niigata, Japan. Neutralizing antibody titers (NATs) against PeV-A3 were measured using the Vero cells. Results The anti-PeV-A3 NATs of colostrum (n = 32) ranged from 1:8 to 1:2048, those ≥1:32 was 59% (19/32). Whereas, the anti-PeV-A3 NATs of mature milk ranged from 1:8 to 1:96. and those ≥1:32 was 20% (2/20) (P < 0.001). The median NATs anti-PeV-A3 was higher in colostrum (1:32) compared with mature milk (1:8) (P < 0.001). There was a strong positive correlation between the NATs of colostrum and serum (r = 0.604, P < 0.001, Figure). Conclusion This study showed that HBM had high NATs against PeV-A3, which was correlated with serum NATs. Further studies are necessary to investigate which components of HBM has antiviral effects against PeV-A3. Disclosures All authors: No reported disclosures. [ABSTRACT FROM AUTHOR]

• An infant with acute heart failure due to dilated cardiomyopathy was hospitalized. • Parechovirus A1 (PeV-A1) was detected in blood, stool, and throat swab samples from the patient. • PeV-A1 infection could trigger exacerbation of myocardial diseases in children. • PeV-A1 infection needs to be included as a cause of worsening myocardial diseases in children. Parechovirus A1 (PeV-A1) often causes mild respiratory or gastrointestinal disease. Herein we report a case of acute heart failure due to dilated cardiomyopathy exacerbated by acute PeV-A1 infection in a 10-month-old infant. He was brought to our hospital with acute respiratory distress and compensated shock. Echocardiogram showed a dilated left ventricle and severe mitral regurgitation, consistent with dilated cardiomyopathy. PeV-A1 infection was confirmed by (1) positive PCR test results for PeV-A in multiple anatomical sites, including blood, stool, and throat, (2) the genetic sequence of viral protein, and (3) an increase in paired serum PeV-A1-specific neutralizing antibody titers. A few, scattered case reports in infants and young children also indicate the association between myocarditis and/or dilated cardiomyopathy and PeV-A1 infection. In conclusion, PeV-A1 infection could be associated with exacerbation of myocardial diseases in infants and young children; thus PeV-A1 needs to be evaluated as a viral cause of such a condition. [ABSTRACT FROM AUTHOR]