Diminshed Igg, but Not Complement C3 or C4 or Factor B, Precedes Nosocomial Becterial Sepsis in Very Low Birth Weight Neonates

Lassiter, Herbert A.; Tanner, Jerome E.; Cost, Karen M.; Steger, Sebastian; Vogel, Rainer

doi:10.1097/00006454-199109000-00008

Cited by 13 publications

(6 citation statements)

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“…It is well-recognized that in newborn infants the immune system is impaired (1, 2, 5-7) and severe pyogenic infections are encountered frequently (1-4). The complement system, which provides essential host defenses against bacterial infections (8)(9)(10)(11)(12), has been found to be reduced and dysfunctional in newborns (7,(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23), and this probably plays a significant role in the immune incompetence of these patients. Other factors are certainly involved, since the rate of severe infections falls considerably after the first 3 months of life, while hypocomplementemia is still present in infants at this age.…”

Section: Discussionmentioning

confidence: 99%

“…Complement activity, which is essential for the opsonization and destruction of invading microorganisms (8)(9)(10)(11)(12), has been reported to be abnormal in neonates. The level of serum haemolytic activity and the complement components of the classical and alternative pathways of full-term newborn infants has been reported to be significantly reduced as compared to adult levels (7,(13)(14)(15)(16)(17)(18)(19)(20)(21).…”

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confidence: 99%

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The development of the complement system after 28 weeks' gestation

et al. 1997

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The results of these studies are: (i) complement levels and activity were significantly reduced in preterm and full-term neonates when compared with adult levels, with the exception of C7 which was within the normal range in most infants. C8 and C9 were the most markedly reduced at all gestational ages. (ii) Complement levels correlated significantly with gestational age, but not with birth-weight, type of delivery, or gender. (iii) Between 28 and 33 weeks' gestation, there appeared to be almost no development of the complement system.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

The development of the complement system after 28 weeks' gestation

et al. 1997

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“…Deficiencies in complement factor C3 and IgG are associated with a higher risk of neonatal CoNS-associated sepsis (Lassiter et al, 1991). Furthermore, in a study using an ex-vivo whole-blood sepsis model, S. epidermidis induced significantly lower complement activation in neonatal compared to adult blood (Granslo et al, 2013).…”

Section: Immunity Against S Epidermidis During Sepsismentioning

confidence: 99%

Host Response to Staphylococcus epidermidis Colonization and Infections

Nguyen

Park

Otto

2017

Front. Cell. Infect. Microbiol.

110

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The majority of research in the Staphylococcus field has been dedicated to the understanding of Staphylococcus aureus infections. In contrast, there is limited information on infections by coagulase-negative Staphylococci (CoNS) and how the host responds to them. S. epidermidis, a member of the coagulase-negative Staphylococci, is an important commensal organism of the human skin and mucous membranes; and there is emerging evidence of its benefit for human health in fighting off harmful microorganisms. However, S. epidermidis can cause opportunistic infections, which include particularly biofilm-associated infections on indwelling medical devices. These often can disseminate into the bloodstream; and in fact, S. epidermidis is the most frequent cause of nosocomial sepsis. The increasing use of medical implants and the dramatic shift in the patient demographic population in recent years have contributed significantly to the rise of S. epidermidis infections. Furthermore, treatment has been complicated by the emergence of antibiotic-resistant strains. Today, S. epidermidis is a major nosocomial pathogen posing significant medical and economic burdens. In this review, we present the current understanding of mechanisms of host defense against the prototypical CoNS species S. epidermidis as a commensal of the skin and mucous membranes, and during biofilm-associated infection and sepsis.

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“…Although MBL affinity to S. epidermidis is significantly reduced compared to that of S. aureus [68], the MBL and classical complement pathways are indispensable for mediating rapid PMN-phagocytic killing of S. epidermidis in suspension [70, 71•]. Furthermore, deficiencies in complement factor C3 and IgG, essential factors for activation of the complement cascade, have been related to greater risk for CoNS-associated sepsis in neonates [72]. Whether there is an association between low circulating MBL levels and increased risk of infection in neonates [73, 74] remains to be addressed.…”

Section: Interaction Of S Epidermidis With Innate Host Defensementioning

confidence: 99%

Understanding the significance of Staphylococcus epidermidis bacteremia in babies and children

Cheung

Otto

2010

Current Opinion in Infectious Diseases

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Purpose of review This review provides an overview of Staphylococcus epidermidis bacteremia/sepsis and Coagulase-negative staphylococci (CoNS) infections in neonates and children. Recent findings The incidence of S. epidermidis and CoNS sepsis in neonates is still very high and preventing and treating disease remains difficult. There has been recent progress in understanding pathogenesis of S. epidermidis infection, interaction of S. epidermidis with host defenses, and risk factors for the development of S. epidermidis disease. For example, we have gained more insight into the development of biofilm-associated catheter infections, which are responsible for recurrent CoNS infections in hospitalized premature neonates and are especially difficult to treat owing to intrinsic resistance of biofilms to antibiotics. Summary Biofilm-associated catheter infections by S. epidermidis occur frequently in neonates and adults. S. epidermidis bloodstream infections are particularly problematic in neonates. Prophylaxis in the form of eradicating colonizing S. epidermidis may be a double-edged sword, as S. epidermidis colonization may be beneficial to the host. New drugs may arise from a better understanding of S. epidermidis virulence and analysis of risk factors may help identify neonates susceptible to bacterial sepsis. However, reducing morbidity should always begin by increasing hygiene in hospital settings to reduce the introduction of potentially harmful opportunistic pathogens such as S. epidermidis on indwelling medical devices or during surgery.

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Diminshed Igg, but Not Complement C3 or C4 or Factor B, Precedes Nosocomial Becterial Sepsis in Very Low Birth Weight Neonates

Cited by 13 publications

References 0 publications

The development of the complement system after 28 weeks' gestation

The development of the complement system after 28 weeks' gestation

Host Response to Staphylococcus epidermidis Colonization and Infections

Understanding the significance of Staphylococcus epidermidis bacteremia in babies and children

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