Influenza B Virus Infection in Pediatric Solid Organ Transplant Recipients

PEDIATRICS ◽  
1994 ◽  
Vol 94 (2) ◽  
pp. 225-229
Author(s):  
Teri Jo Mauch ◽  
Tim Myers ◽  
Clifford E. Kashtan ◽  
Susan Bratton ◽  
Elliot Krane ◽  
...  

Objective. Influenza B virus causes epidemic infection in normal children, but only one case of infection in an immunocompromised solid organ transplant (SOT) recipient has been reported. Characterization of the clinical course of influenza B virus infection in pediatric SOT recipients may increase the utilization of preventive and therapeutic interventions by pediatricians caring for these immunocompromised children. Design. Retrospective chart review of patients whose respiratory viral cultures yielded influenza B from January 1989 through March 1992. Patients. Twelve pediatric SOT recipients with influenza B virus infection were identified. These included five renal, four hepatic, and three cardiac allograft recipients, ranging from 19 months to 17 years 9 months of age (median 6 years 2 months). The post-transplant interval ranged from 6 weeks to 4 years 6 months (average 26.7 months). No patient had been immunized against influenza. Exposure histories were documented for eight children; five of these occurred in the hospital. Results. Clinical symptoms included fever (12/12), respiratory (11/12), or gastrointestinal complaints (8/12). Five patients had neurologic involvement; one died of uncal herniation. Ten children were hospitalized (median duration, 3 days; range, 2 to 79 days). Two patients (post-transplant interval, 3 to 8 months) required mechanical ventilation, and one of these received aerosolized ribavirin. Three children had concurrent allograft rejection. Conclusions. Influenza B infection is potentially life-threatening in pediatric SOT recipients. We recommend annual immunization of pediatric SOT recipients, their household contacts, and health care workers. Prospective studies are needed to evaluate the efficacy of influenza vaccination in pediatric SOT recipients.

2021 ◽  
Vol 10 (Supplement_1) ◽  
pp. S1-S1
Author(s):  
T Kitano ◽  
M Science ◽  
N Nalli ◽  
K Timberlake ◽  
U Allen ◽  
...  

Abstract Background Solid-organ transplant (SOT) patients are more vulnerable to infections by antimicrobial-resistant organisms (AROs) because of their hospital exposure, compromised immune systems, and antimicrobial exposure. Therefore, it may be useful for transplant facilities to create transplant-specific antibiograms to direct empirical antimicrobial regimens and monitor trends in antimicrobial resistance. Methods SOT (i.e., lung, liver, renal, and heart) antibiograms were created using antimicrobial susceptibility data on isolates from 2012 to 2018 at The Hospital for Sick Children, a tertiary pediatric hospital and transplant center in Toronto, Ontario. The Clinical Laboratory Standards Institute (CLSI) guidelines were followed to generate the antibiograms. The first clinical isolate of a species from a patient in each year was included irrespective of body site; duplicates were eliminated and surveillance cultures were excluded. Results from 2 years of data were pooled on a rolling basis to achieve an adequate sample size in both SOT and hospital-wide antibiogram. The SOT antibiogram was then compared with the hospital-wide antibiogram of the compatible 2 pooled years from 2012 to 2018. For subgroup analyses in the SOT population, organ-specific antibiograms and transplant timing-specific antibiograms (pretransplant, post-transplant <1 year, and post-transplant ≥1 year) between transplant and sample collection dates were analyzed. All proportions were compared using the χ 2 test. Results The top 5 organisms in one (2 year) analysis period of the SOT antibiogram were Escherichia coli (n = 29), Staphylococcus aureus (n = 28), Pseudomonas aeruginosa (n = 20), Enterobacter cloacae complex (n = 18), and Klebsiella pneumoniae (n = 17). For E.coli, susceptibility in the SOT antibiogram was significantly lower than those in the hospital-wide antibiogram in 2017/2018 for ampicillin (27% vs. 48%; P = 0.015), piperacillin/tazobactam (55% vs. 87%; P < 0.001), cefotaxime (59% vs. 88%; P < 0.001), ciprofloxacin (71% vs. 87%; P = 0.007) and cotrimoxazole (41% vs. 69%; P < 0.001), but not significantly different for gentamicin (94% vs. 91%; P = 0.490), tobramycin (88% vs. 90%; P = 0.701) and amikacin (100% vs. 99%; P = 0.558). These findings were consistent throughout the study period in E.coli. There was no statistically significant difference between the SOT and hospital-wide antibiograms for other organisms. There were no significant differences in susceptibility between organ-specific antibiograms or transplant timing-specific antibiograms in 2012–2018. Conclusions We found that E.coli from the SOT population had a significantly lower sensitivity to all antimicrobials, except aminoglycosides, compared with those from the hospital-wide population. Other organisms had similar susceptibility to the hospital-wide population. Developing a SOT antibiogram will assist in revising and improving empiric treatment guidelines for this population.


2012 ◽  
Vol 205 (6) ◽  
pp. 895-905 ◽  
Author(s):  
Christopher D. Paddock ◽  
Lindy Liu ◽  
Amy M. Denison ◽  
Jeanine H. Bartlett ◽  
Robert C. Holman ◽  
...  

2021 ◽  
Vol 7 (5) ◽  
pp. 327
Author(s):  
Nipat Chuleerarux ◽  
Achitpol Thongkam ◽  
Kasama Manothummetha ◽  
Saman Nematollahi ◽  
Veronica Dioverti-Prono ◽  
...  

Background: Cytomegalovirus (CMV) and invasive aspergillosis (IA) cause high morbidity and mortality in solid organ transplant (SOT) recipients. There are conflicting data with respect to the impact of CMV on IA development in SOT recipients. Methods: A literature search was conducted from existence through to 2 April 2021 using MEDLINE, Embase, and ISI Web of Science databases. This review contained observational studies including cross-sectional, prospective cohort, retrospective cohort, and case-control studies that reported SOT recipients with post-transplant CMV (exposure) and without post-transplant CMV (non-exposure) who developed or did not develop subsequent IA. A random-effects model was used to calculate the pooled effect estimate. Results: A total of 16 studies were included for systematic review and meta-analysis. There were 5437 SOT patients included in the study, with 449 SOT recipients developing post-transplant IA. Post-transplant CMV significantly increased the risk of subsequent IA with pORs of 3.31 (2.34, 4.69), I2 = 30%. Subgroup analyses showed that CMV increased the risk of IA development regardless of the study period (before and after 2003), types of organ transplantation (intra-thoracic and intra-abdominal transplantation), and timing after transplant (early vs. late IA development). Further analyses by CMV definitions showed CMV disease/syndrome increased the risk of IA development, but asymptomatic CMV viremia/infection did not increase the risk of IA. Conclusions: Post-transplant CMV, particularly CMV disease/syndrome, significantly increased the risks of IA, which highlights the importance of CMV prevention strategies in SOT recipients. Further studies are needed to understand the impact of programmatic fungal surveillance or antifungal prophylaxis to prevent this fungal-after-viral phenomenon.


Author(s):  
Pınar YAZICI ÖZKAYA ◽  
Eşe Eda TURANLI ◽  
Hamdi METİN ◽  
Ayça Aydın UYSAL ◽  
Candan ÇİÇEK ◽  
...  

2019 ◽  
Vol 58 (3) ◽  
pp. 441-445 ◽  
Author(s):  
Toshimasa Shimizu ◽  
Naoki Iwamoto ◽  
Momoko Okamoto ◽  
Yushiro Endo ◽  
Sosuke Tsuji ◽  
...  

2012 ◽  
Vol 18 (5) ◽  
pp. 869-872 ◽  
Author(s):  
Suzan D. Pas ◽  
Rob A. de Man ◽  
Claudia Mulders ◽  
Aggie H.M.M. Balk ◽  
Peter T.W. van Hal ◽  
...  

Vaccine ◽  
2001 ◽  
Vol 19 (11-12) ◽  
pp. 1446-1455 ◽  
Author(s):  
Ze Chen ◽  
Shin-etsu Kadowaki ◽  
Yukari Hagiwara ◽  
Tomoki Yoshikawa ◽  
Tetsutaro Sata ◽  
...  

mBio ◽  
2018 ◽  
Vol 9 (2) ◽  
Author(s):  
Mira C. Patel ◽  
Kari Ann Shirey ◽  
Marina S. Boukhvalova ◽  
Stefanie N. Vogel ◽  
Jorge C. G. Blanco

ABSTRACT Host-derived “danger-associated molecular patterns” (DAMPs) contribute to innate immune responses and serve as markers of disease progression and severity for inflammatory and infectious diseases. There is accumulating evidence that generation of DAMPs such as oxidized phospholipids and high-mobility-group box 1 (HMGB1) during influenza virus infection leads to acute lung injury (ALI). Treatment of influenza virus-infected mice and cotton rats with the Toll-like receptor 4 (TLR4) antagonist Eritoran blocked DAMP accumulation and ameliorated influenza virus-induced ALI. However, changes in systemic HMGB1 kinetics during the course of influenza virus infection in animal models and humans have yet to establish an association of HMGB1 release with influenza virus infection. To this end, we used the cotton rat model that is permissive to nonadapted strains of influenza A and B viruses, respiratory syncytial virus (RSV), and human rhinoviruses (HRVs). Serum HMGB1 levels were measured by an enzyme-linked immunosorbent assay (ELISA) prior to infection until day 14 or 18 post-infection. Infection with either influenza A or B virus resulted in a robust increase in serum HMGB1 levels that decreased by days 14 to 18. Inoculation with the live attenuated vaccine FluMist resulted in HMGB1 levels that were significantly lower than those with infection with live influenza viruses. RSV and HRVs showed profiles of serum HMGB1 induction that were consistent with their replication and degree of lung pathology in cotton rats. We further showed that therapeutic treatment with Eritoran of cotton rats infected with influenza B virus significantly blunted serum HMGB1 levels and improved lung pathology, without inhibiting virus replication. These findings support the use of drugs that block HMGB1 to combat influenza virus-induced ALI. IMPORTANCE Influenza virus is a common infectious agent causing serious seasonal epidemics, and there is urgent need to develop an alternative treatment modality for influenza virus infection. Recently, host-derived DAMPs, such as oxidized phospholipids and HMGB1, were shown to be generated during influenza virus infection and cause ALI. To establish a clear link between influenza virus infection and HMGB1 as a biomarker, we have systematically analyzed temporal patterns of serum HMGB1 release in cotton rats infected with nonadapted strains of influenza A and B viruses and compared these patterns with a live attenuated influenza vaccine and infection by other respiratory viruses. Towards development of a new therapeutic modality, we show herein that blocking serum HMGB1 levels by Eritoran improves lung pathology in influenza B virus-infected cotton rats. Our study is the first report of systemic HMGB1 as a potential biomarker of severity in respiratory virus infections and confirms that drugs that block virus-induced HMGB1 ameliorate ALI.


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