Streptococcal Neonatal Osteomyelitis

Lai, Tony Kwan; Hingston, James; Scheifele, David W.

doi:10.1001/archpedi.1980.02130190077025

Cited by 5 publications

(4 citation statements)

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“…The source of the organism is the genital tract of the infected infant's mother (3). Common manifestations of GBS disease in neonates include pneumonia, septicemia, meningitis, bacteremia, and bone or joint infections (3,6,19,24). Invasive disease caused by GBS has also been recognized in adults (8,32).…”

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confidence: 99%

Role of Tumor Necrosis Factor Alpha, Interleukin-1β, and Interleukin-6 in a Mouse Model of Group B Streptococcal Arthritis

et al. 1999

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Intravenous inoculation of CD1 mice with 107 CFU of type IV group B Streptococcus (GBS IV) results in a high incidence of diffuse septic arthritis. In this study the roles of tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), and IL-6 in articular pathology were evaluated. Cytokine levels were quantified in the serum and joints by enzyme-linked immunosorbent assay in mice injected with GBS IV and tested or not tested with pentoxifylline (PTF), a methylxanthine that affects cytokine production. PTF was administered intraperitoneally at a dose of 1 mg/mouse (50 mg/kg of body weight) 1 h after GBS infection and then at 24-h intervals for 4 days. High levels of IL-1β and IL-6, but not TNF-α, were detected in the joints of mice injected with GBS IV from 5 to 15 days after infection, when articular lesions were most frequent and severe. IL-1β and IL-6 concentrations in the joints significantly (P < 0.001) exceeded those detected in the serum, confirming a strong local production. PTF treatment resulted in a strong reduction of cytokine production and in a marked decrease in both the incidence and severity of arthritis. Inoculation of exogenous murine recombinant IL-1β or IL-6 in mice treated with GBS IV plus PTF resulted in an incidence and severity of articular lesions similar to those obtained with inoculation of GBS IV alone. No significant effect was obtained with TNF-α administration. These data show a strong involvement of IL-1β and IL-6, but not TNF-α, in the pathogenesis of GBS arthritis.

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confidence: 99%

Role of Tumor Necrosis Factor Alpha, Interleukin-1β, and Interleukin-6 in a Mouse Model of Group B Streptococcal Arthritis

et al. 1999

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“…Pregnant women who are carriers of GBS have the potential to transmit GBS to their newborn infants, and GBS are one of the first pathogenic organisms that newborns may encounter at birth. Common manifestations of GBS diseases include pneumonia, septicemia, meningitis, bacteremia, and bone or joint infections, such as septic arthritis and osteomyelitis (8, 9). With the advent of intrapartum prophylaxis in 1999, the rate of early onset GBS infection has decreased, but it is still quite high in premature infants (10).…”

Section: Introductionmentioning

confidence: 99%

Group B Streptococci Induce Proinflammatory Responses via a Protein Kinase D1–Dependent Pathway

Upadhyay

Park

Yoon

et al. 2017

The Journal of Immunology

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Group B streptococci (GBS) are one of the leading causes of life-threatening illness in neonates. Proinflammatory responses to GBS mediated through host innate immune receptors play a critical role in the disease manifestation. However, the mechanisms involved in proinflammatory responses against GBS, and the contribution of signaling modulators involved in host immune defense, have not been fully elucidated. In the present study, we investigated the role of protein kinase D1 (PKD1) in the proinflammatory responses to GBS. We found that both live and antibiotic-killed GBS induce activation of PKD1 through a pathway that is dependent on the Toll-like receptor signaling adaptor MyD88 and its downstream kinase IRAK1, but independent of TRAF6. Our studies using pharmacological PKD inhibitors and PKD1-knockdown macrophages revealed that PKD1 is indispensable for GBS-mediated activation of MAPKs and NF-κB and subsequent expression of proinflammatory mediators. Furthermore, systemic administration of a PKD inhibitor protects D-galactosamine-sensitized mice from shock-mediated death caused by antibiotic-killed GBS. These findings imply that PKD1 plays a critical regulatory role in GBS-induced proinflammatory reactions and sepsis, and inhibition of PKD1 activation together with antibiotic treatment in GBS-infected neonates could be an effective way to control GBS diseases.

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“…In the newborn, staphylococcus aureus, hemolytic streptococci and aerobic Gram-negative rods are most commonly found. The increasing prevalence of methicillin-resistant staphylococcus aureus is an emerging problem in pediatrics [65][66][67][68][69][70][71][72][73][74][75].…”

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confidence: 99%

Neonatal Osteomyelitis and Septic Arthritis

2021

IJOR

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The purpose of this editorial is to perform an extensive review of the relevant international literature about neonatal osteomyelitis and septic arthritis, to indicate the value of clinical suspicion and of regular osteoarticular examination for the early diagnosis and treatment of the disease in the septicemic neonate or in the preterm infant, even when initial empiric antibiotic therapy is used, and to present illustrative cases.

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Streptococcal Neonatal Osteomyelitis

Cited by 5 publications

References 1 publication

Role of Tumor Necrosis Factor Alpha, Interleukin-1β, and Interleukin-6 in a Mouse Model of Group B Streptococcal Arthritis

Role of Tumor Necrosis Factor Alpha, Interleukin-1β, and Interleukin-6 in a Mouse Model of Group B Streptococcal Arthritis

Group B Streptococci Induce Proinflammatory Responses via a Protein Kinase D1–Dependent Pathway

Neonatal Osteomyelitis and Septic Arthritis

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