Systemic Group B Streptococcal Disease in the Neonate: Characterization of an Oral Colonization Model Using the Suckling Rat

Weisman, Leonard E.; McKinney, Luanne; Villalobos, Raphael

doi:10.1111/j.1348-0421.1990.tb01053.x

Cited by 13 publications

(6 citation statements)

References 19 publications

(12 reference statements)

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“…Further, S. aureus and group B streptococcus, the most frequently encountered causative species of neonatal skeletal infection, may also colonize the intestine (8), particularly in hospitalized neonates, in whom the risk of osteomyelitis is increased. The ability of these bacteria to translocate from the gut into the systemic circulation has been documented in experimental animals (28,49), and may be operative when asymptomatic bacteremia develops in human neonates (44). It is interesting to note that in the present study S. aureus was not detected in the bone, despite the fact that some rat pups harbored this organism in the small intestine.…”

Section: Discussionmentioning

confidence: 34%

“…The age-dependant fall in spontaneous bacterial translocation is associated with a reduction of the intestinal permeability to small molecular weight particles (22), with the maturation of the gut-associated lymphoid tissue (23), and with the establishment of a normal gut flora (20). Whereas the spontaneous escape of bacteria from the intestine has no documented adverse effects in normal breast-fed animals, more pronounced translocation, as observed after artificial feeding (24) or induced by oral inoculation of various strains of Escherichia coli (25)(26)(27) and group B streptococcus (28), can result in septicemia (24 -28), pneumonia (28), meningitis (26,28), and death (26,28).…”

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confidence: 99%

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Gut-Derived Bone Infection in the Neonatal Rat

et al. 2001

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The risk of osteomyelitis is increased in the premature and critically ill neonate. Although potential sites of bacterial entry are present in many of these infants, the source of infection frequently cannot be established. This study was performed to assess the possible role of bacterial translocation from the intestine in the origin of bone infection using models of breast-fed and formula-fed rat pups. Newborn Sprague-Dawley rats suckled either ad libitum by the dam (n ϭ 30), or were fed a rat milk-simulated formula (n ϭ 30). After 3 d, the animals were killed, and the left femur, heart blood, mesenteric lymph nodes, liver, spleen, and terminal ileum were excised. Organs were analyzed for bacteria by standard microbiologic procedures. Bacterial translocation occurred in 23% of breast-fed rats; the bone was not infected in any of these animals. After feeding of formula diet, bacterial counts of the ileum were markedly elevated (p Ͻ 0.001), and the composition of the gut flora was disrupted. Bacterial translocation was noted in all formula-fed rats. Bone cultures were positive in 23 of 30 (77%) rats after formula-feeding (p Ͻ 0.001 versus breast-feeding). Organisms translocated to the bone included Enterococci, Proteus, Enterobacter, and Escherichia coli. Bacterial species cultured from the bone correlated with the individual colonization pattern of other extraintestinal organs and with the composition of the ileal flora. Members of the gut flora can escape the intestine and colonize the bone in formula-fed rats. The gut should be considered as a potential source for osteomyelitis in the neonate. Acute osteomyelitis in the neonate is a leading cause of destruction of the physis resulting in high rates of permanent handicaps (1-3). Because the major route of infection is via the bloodstream, opportunities for organisms to gain access to the circulation may favor the development of osteomyelitis. Premature and sick neonates represent the high-risk group, and in this population potential sites of bacterial entrance are frequently present. Many of these infants undergo vascular manipulation including insertion of central catheters for total parenteral nutrition or invasive monitoring, which have long been linked to the development of skeletal infection. In most cases, however, the origin of bacterial entry remains unknown (4). Therefore, alternative routes of infection should be considered.Among the organisms causing neonatal osteomyelitis, Staphylococcus aureus is most common, followed by group B streptococci and Gram-negative bacteria (1, 5-7). All of these organisms have the ability to colonize the neonatal gut. They may represent normal luminal residents, or members of an abnormal microflora, as frequently seen in hospitalized neonates (8). It is now widely accepted that organisms can escape from the gastrointestinal tract and invade extraintestinal organs, a process termed as bacterial translocation (9, 10). In normal adult individuals, translocation of bacteria from the gastrointestinal tract is limited by a n...

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Section: Discussionmentioning

confidence: 34%

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confidence: 99%

Gut-Derived Bone Infection in the Neonatal Rat

et al. 2001

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“…83 Often GBS contaminated breast milk leads to heavy neonatal colonization, 25 and oral administration of GBS is shown to cause systemic infection in animal studies. 22 A recent comprehensive review that summarizes data from 48 cases has shown that breast milk-associated LOGBS has a high recurrence rate and that LOGBS may occur even without RFs other than contaminated breast milk; however, 24 the mechanism underlying breast milk contamination with GBS is unclear. The “retrograde theory” assumes that neonatal colonization occurs at birth and colonization of the oral mucosa contaminates the maternal mammary ducts, owing to the negative pressure created during the sucking action of the newborn.…”

Section: Breastfeedingmentioning

confidence: 99%

“… 14 , 21 Studies in animal models have shown that oral administration of GBS leads to systemic disease. 22 The pathogenesis of LOGBS involves GBS adhesion to mucosal surfaces, followed by invasion of the epithelium and subsequently the bloodstream. Factors that mediate persistent intestinal colonization or promote the shift from intestinal colonization to invasive GBS disease remain unknown.…”

Section: Introductionmentioning

confidence: 99%

Understanding Factors in Group B Streptococcus Late-Onset Disease

Berardi¹,

Trevisani²,

Caprio³

et al. 2021

IDR

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Group B streptococcus (GBS) infection remains a leading cause of sepsis, pneumonia, and meningitis in infants. Rates of GBS early onset disease have declined following the widcespread use of intrapartum antibiotic prophylaxis; hence, late-onset infections (LOGBS) are currently a common presentation of neonatal GBS dicsease. The pathogenesis, mode of transmission, and risk factors associated with LOGBS are unclear, which interfere with effective prevention efforts. GBS may be transmitted from the mother to the infant at the time of delivery or during the postpartum period via contaminated breast milk, or as nosocomial or community-acquired infection. Maternal GBS colonization, prematurity, young maternal age, HIV exposure, and ethnicity (Black) are identified as risk factors for LOGBS disease; however, further studies are necessary to confirm additional risk factors, if any, for the implementation of effective prevention strategies. This narrative review discusses current and previous studies that have reported LOGBS. Few well-designed studies have described this condition; therefore, reliable assessment of maternal GBS colonization, breastfeeding, and twin delivery as risk factors for LOGBS remains limited.

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“…The GBS strain isolated in breast milk matches the serotype isolated from the infant’s samples may reflect that mothers and infants are colonised with the same strain, rather than implicating breast milk transmission. However, in animal studies, oral administration of GBS leads to systemic disease 38. In settings where no other source of GBS can be identified, GBS infection through breast milk seems a convincing mechanism.…”

Section: Commentarymentioning

confidence: 99%