Identification of major clonal complexes and toxin producing strains among Staphylococcus aureus associated with atopic dermatitis.

Staphylococcus aureus promotes the onset and severity of atopic dermatitis (AD), which is exacerbated by superantigen toxins SEB and SEC. The genetic identity of these isolates, and their relationship to common hospital- or community-associated methicillin resistant S. aureus (HA-MRSA and CA-MRSA) has not been defined. We conducted spa typing, partial multi-locus sequence typing (MLST), and toxin profiling (seb, sec, lukS-PV) of S. aureus from 119 pediatric and 40 adult AD patients. MLST clonal complexes CC45, CC5, CC15, CC1, CC8 and CC30 accounted for 79% of isolates, representing the same major groups reported for nosocomial S. aureus in hospital intensive care units. The highest disease severity was associated with CC1, which was significantly greater relative to CC15 (p = 0.017) or CC30 (p = 0.040), but with no significant difference relative to CC45, CC5 or CC8. Although there were two few lukS-PV, seb or sec isolates to infer a role in disease severity, CC45 was identified as a source of SEC producing strains, and lukS-PVL was associated with a small number of CC5 pediatric isolates. CC1 harbored the only CA-MRSA that was identified, and was a source of isolates that expressed both seb and sec, and closely resembled the USA400 strain of CA-MRSA.

Glucose intolerance and insulin resistance in extremely premature newborns, and implications for nutritional management.

UNLABELLED: Glucose intolerance and postnatal growth retardation are commonly seen in low-gestation newborns. In contrast to the nutrient compositions of parenteral and enteral nutrition, fetuses at equivalent gestational ages receive much more amino acids (protein) but less glucose and lipids through placental transfer. CONCLUSION: A nutrition regime that simulates placental nutrient delivery would potentially minimize glucose intolerance and facilitate early attainment of normal growth velocity with normal body composition after preterm birth.

Somatotropic axis derangement as an underlying factor in the genesis of retinopathy of prematurity.

UNLABELLED: Recent research data suggest a significant role of prolonged low serum insulin-like growth factor (IGF)-I concentration in the genesis of retinopathy of prematurity (ROP). Evidence also reveals significant early postnatal nutritional deficits and growth deceleration among premature newborns. CONCLUSION: Since serum IGF-I concentration is positively related to nutritional status, particularly protein nutrition, it would suggest that protein under-nutrition may be a major determinant of low serum IGF-I concentration and in the high risk of ROP.

Postnatal growth, neurodevelopment and altered adiposity after preterm birth--from a clinical nutrition perspective.

UNLABELLED: Evidence reveals a dilemma that under-nutrition and growth retardation during brain growth are associated with neurodevelopmental deficits, and nutritional supplement resulting in catch-up growth and relative visceral adiposity leads to metabolic/cardiovascular morbidities. Hyperinsulinaemia secondary to insulin resistance appears to play a central role in the development of visceral adiposity through its action on adipocyte beta3-adrenoceptor. CONCLUSION: Optimal nutritional management to minimize hyperinsulinaemia and insulin resistance may potentially improve neurodevelopment and facilitate catch-up growth with normal body composition.

Oligonephropathy, developmental programming and nutritional management of low-gestation newborns.

UNLABELLED: Intrauterine growth retardation is associated with oligonephropathy and the risk of hypertension and renal disease in adulthood. Animal study data show that nephron density is directly related to protein nutrition status during nephrogenesis. Among infants born at low gestation, postnatal growth retardation and major deficits in energy and protein intake have been reported. CONCLUSION: Since nephrogenesis occurs mainly in late gestation, increasing protein intake during nephrogenesis could minimize the risk of long-term morbidities associated with oligonephropathy.

Influence of early postnatal nutritional management on oxidative stress and antioxidant defence in extreme prematurity.

UNLABELLED: The increased survival of infants born at mid-gestation in the last decade is associated with significant oxygen free radical-mediated morbidities. Resuscitation with 100% oxygen, oxidant load from parenteral nutrition fluids, and oxidant stress inherent to the systemic inflammatory state subsequent to infection and tissue injury are all contributory. CONCLUSION: Improving early postnatal protein nutrition and the formulation of parenteral nutrition fluids would potentially reduce the oxidative stress and enhance the antioxidant defence of extremely premature newborns.

Nutritionally regulated hormonal factors in prolonged postnatal growth retardation and its associated adverse neurodevelopmental outcome in extreme prematurity.

Recent published data show that at hospital discharge, most infants born at <30 weeks of gestation would not achieve the median birth weight of the reference fetus at the same postconceptional age, and many would be less than the 10th centile. Estimating from the current recommendations of calorie and protein intakes, these infants accrue large deficits in intakes of protein and calorie during the first weeks of life. Postnatal growth retardation over a prolonged period of time is related to neurodevelopmental delays. While a total energy intake of 120 kcal/kg/day has generally been considered adequate, protein requirement in low gestation infants remains a matter for debate. Increasing the dietary protein:calorie ratio has previously been proposed as a strategy to enhance growth and to achieve a body composition similar to that of the reference fetus. Previous study data reveal that serum insulin-like growth factor I (IGF-I) concentration is positively correlated with protein intake, and nitrogen retention, in turn, is positively correlated with serum IGF-I concentration. Remarkably, elevated serum growth hormone but low serum IGF-I concentrations have been reported in low gestation infants and in infants with intrauterine growth retardation, suggesting IGF-I being a nutritionally regulated hormonal factor in the postnatal growth retardation. As neurodevelopment in extreme prematurity is likely affected by multiple factors, we hypothesize that a combined strategy of the previously proposed hormonal supplement with hydrocortisone and tri-iodothyronine together with increased dietary protein intake (progressively increasing from 1.5 g/kg/day intravenously administered amino acids immediately after birth, then 3.6 g/100 kcal at approximately 125 kcal/kg/day when enterally fed till the infant reaches a body weight of >or=1.8 kg and at >or=50th centile weight of the reference fetus at the same postconceptional age) would likely be synergistic and more effective in improving neurodevelopmental outcome.

Hormonal factors in the morbidities associated with extreme prematurity and the potential benefits of hormonal supplement.

Cortisol and thyroid hormones are known to modulate the maturation of various fetal organ systems, enzymes, and biochemical pathways. The cortisol furnished by the structural and biochemical immature fetal adrenal gland renders the extremely premature infants relatively cortisol deficient in comparison with the term newborns. The premature infants also have elevated fetal androgens, the production of which persists until approximately 42 weeks of postconceptional age. The androgens produced by the fetal adrenal cortex and the müllerian inhibiting substance produced by the fetal testis have antiglucocorticoid and inhibitory effects on human fetal lung growth and maturation in vitro. Hypothalamic-pituitary-thyroid axis and thyroid function are also immature in extreme prematurity. In addition, there is reduced tissue thyroid hormone responsiveness. Superimposed on this is the reduced thyroid function seen in non-thyroidal illness in which elevated cytokine levels have been implicated. Repeated courses of antenatal steroids and high-dose postnatal dexamethasone appear to be deleterious to lung and brain development. This may be through inhibition of cell replication and catabolism as well as decreased thyroid-stimulating hormone secretion and reduced peripheral conversion of T(4) to T(3). Furthermore, dexamethasone has been found to enhance neurosteroid production in the immature brain, potentially altering brain development. Considered together, the relative cortisol deficiency/androgen excess and reduced thyroid function as well as prolonged high-dose postnatal dexamethasone therapy in these infants may be important factors in their high degree of morbidity. We propose to restrict antenatal steroids to a single course and hypothesize that the overall outcome of low-gestation infants would be improved with (1) hydrocortisone (i.v./p.o.) supplement at a fixed dose of 0.5 mg/kg birth weight every 12 h in infants <30 weeks of gestation from birth till 32 weeks of postconceptional age and (2) T(3) (i.v./p.o.) supplement at a fixed dose of 0.4 microg/kg birth weight every 12 h in those <27 weeks of gestation from birth till 32 weeks of postconceptional age.