Synchronous Recurrence of Group B Streptococcal Late-Onset Sepsis in Twins

Elling, Roland; Hufnagel, Markus; Zoysa, Aruni De; Lander, Fabian; Zumstein, Katharina; Krueger, Marcus; Henneke, Philipp

doi:10.1542/peds.2013-0426

Cited by 35 publications

(26 citation statements)

References 16 publications

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“…44 Most of the studies (17/22) reported clusters occurring in neonatal intensive care units (NICUs) or special care nurseries; the remainder described clusters occurring in or originating from maternity units in regional, district or community hospitals. There were two reports of LOD in twins 35 and triplets 38 and two references describing clusters only of EOD 23 , 34 (see supplementary files). The other reported clusters involved LOD ( n = 12) or a mix of early and LOD ( n = 6) as described below.…”

Section: Neonatal Gbs Disease Clustersmentioning

confidence: 99%

Hospital clusters of invasive Group B Streptococcal disease: A systematic review

Collin

Lamb

Jauneikaite

et al. 2019

Journal of Infection

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Group B streptococcal disease Adult Neonatal Outbreak Cluster Healthcare-associated infection Systematic review s u m m a r y Objectives: To characterize outbreaks of invasive Group B Streptococcal (iGBS) disease in hospitals.Methods: Systematic review using electronic databases to identify studies describing iGBS outbreaks/clusters or cross-infection/acquisition in healthcare settings where 'cluster' was defined as ≥2 linked cases. PROSPERO CRD42018096297. Results: Twenty-five references were included describing 30 hospital clusters (26 neonatal, 4 adult) in 11 countries from 1966 to 2019. Cross-infection between unrelated neonates was reported in 19 clusters involving an early-onset ( < 7 days of life; n = 3), late-onset (7-90 days; n = 13) index case or colonized infant ( n = 3) followed by one or more late-onset cases (median serial interval 9 days (IQR 3-17, range 0-50 days, n = 45)); linkage was determined by phage typing in 3 clusters, PFGE/MLST/PCR in 8, WGS in 4, non-molecular methods in 4. Postulated routes of transmission in neonatal clusters were via clinical personnel and equipment, particularly during periods of crowding and high patient-to-nurse ratio. Of 4 adult clusters, one was attributed to droplet spread between respiratory cases, one to handling of haemodialysis catheters and two unspecified. Conclusions: Long intervals between cases were identified in most of the clusters, a characteristic which potentially hinders detection of GBS hospital outbreaks without enhanced surveillance supported by genomics.

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Section: Neonatal Gbs Disease Clustersmentioning

confidence: 99%

Hospital clusters of invasive Group B Streptococcal disease: A systematic review

Collin

Lamb

Jauneikaite

et al. 2019

Journal of Infection

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“…GBS is a well-established cause of soft tissue and bone infections, both in infants and adults (32,33). In the dermis, an important barrier against soft tissue infections caused by streptococci, resident dermal MFs constitute the main immune cell population (34).…”

Section: Dermal Mfs Require Endosomal Tlr13 For Sensing Of Gbsmentioning

confidence: 99%

“…Intradermal injection in the ear pinna of WT mice results in neutrophil recruitment and resolution of infection that are dependent on the presence of dermal MFs (3). This model is relevant for GBS, because local infections of skin and soft tissue often precede neonatal GBS sepsis (32). To verify the importance of TLR signaling, we used MyD88 2/2 mice, which are severely impaired in the sensing of surface and endosomal TLRs.…”

Section: Unc-93b (3d) Mice Incompletely Control Dissemination Of Gbs mentioning

confidence: 99%

Streptococci Engage TLR13 on Myeloid Cells in a Site-Specific Fashion

Kolter

Feuerstein

Spoeri

et al. 2016

The Journal of Immunology

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International audienceStreptococci are common human colonizers with a species-specific mucocutaneous distribution. At the same time, they are among the most important and most virulent invasive bacterial pathogens. Thus, site-specific cellular innate immunity, which is predominantly executed by resident and invading myeloid cells, has to be adapted with respect to streptococcal sensing, handling, and response. In this article, we show that TLR13 is the critical mouse macrophage (MΦ) receptor in the response to group B Streptococcus, both in bone marrow-derived MΦs and in mature tissue MΦs, such as those residing in the lamina propria of the colon and the dermis, as well as in microglia. In contrast, TLR13 and its chaperone UNC-93B are dispensable for a potent cytokine response of blood monocytes to group B Streptococcus, although monocytes serve as the key progenitors of intestinal and dermal MΦs. Furthermore, a specific role for TLR13 with respect to MΦ function is supported by the response to staphylococci, where TLR13 and UNC-93B limit the cytokine response in bone marrow-derived MΦs and microglia, but not in dermal MΦs. In summary, TLR13 is a critical and site-specific receptor in the single MΦ response to β-hemolytic streptococci

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“…Next to the lethality of GBS meningoencephalitis (5–10%), long‐term neurologic impairment of variable degrees affects up to 30 to 70% of surviving infants . GBS has been cultured from breast milk of the nursing mother and the intestinal tract of individual infants before onset of LOD and meningitis in individual cases, which suggests that GBS is acquired through the intestinal route, yet this model remains somewhat speculative. The concept that GBS dissemination happens from the intestine to the CNS is supported by the study of Poyart et al., where intestinal GBS colonization in mice in the first three weeks of life led to CNS invasion and meningoencephalitis .…”

Section: Introductionmentioning

confidence: 99%

The role of CNS macrophages in streptococcal meningoencephalitis

Gres

Kolter

Erny

et al. 2019

Journal of Leukocyte Biology

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In the healthy brain, microglia and other CNS macrophages are the most abundant immune cell type. Thus, they form the natural immune cell interface with streptococci, which are the leading cause of bacterial meningitis and encephalitis in infants and young children. In homeostasis, the blood-brain barrier allows for very limited access of immune cells circulating in the periphery. During bacterial meningoencephalitis, however, origin and fate of CNS macrophages are massively altered. This review summarizes the emerging knowledge on the sequence of reciprocal events between streptococci and CNS macrophages leading to host resistance, acute inflammation, changes in resident innate immune cells of the brain, and long-term neuronal damage. K E Y W O R D S meningitis, microglia, Streptococcus agalactiae, Streptococcus pneumoniae [The copyright line for this article was changed on 25 February 2019 after original online publication] of events can transiently severely perturb the separation of the CNS and the peripheral immune system. Thereby, long-term consequences for neurodevelopment might ensue.

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Synchronous Recurrence of Group B Streptococcal Late-Onset Sepsis in Twins

Cited by 35 publications

References 16 publications

Hospital clusters of invasive Group B Streptococcal disease: A systematic review

Hospital clusters of invasive Group B Streptococcal disease: A systematic review

Streptococci Engage TLR13 on Myeloid Cells in a Site-Specific Fashion

The role of CNS macrophages in streptococcal meningoencephalitis

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