Weight loss during ambulatory tube weaning: don't put the feeds back up.

OBJECTIVE: To describe the prevalence of weight loss during tube weaning and its impact on wean duration and growth. SETTING: Tertiary feeding clinic, UK. PATIENTS: All children seen for weaning from long-term enteral feeding between 2008 and 2016. INTERVENTIONS: Outpatient withdrawal of enteral feeding. DESIGN: Case series of children being weaned from tube feeding, documenting clinical details, periods of weight loss and timing of feed changes, as well as height and weight at baseline and within 1 year after feed cessation. MAIN OUTCOME MEASURES: Amount and frequency of weight loss, wean duration, change in body mass index (BMI) and height SD z score. RESULTS: Weaning was attempted in 58 children, median age 2.7 years, and 90% had stopped feeds after median (range) 5.9 (1-40) months. Weight loss was seen in 51 (88%) children and was more common and severe in children with initially higher BMI. Time to feed cessation reduced by median 4.9 months between 2008-2011 and 2012-2016, while having feeds increased prolonged the wean duration, by median 13 months. After feed cessation, mean (95% CI) BMI had dropped by 0.84 (0.5 to 1.2) z scores, but neither change in BMI, nor the amount and frequency of weight loss, related to growth. CONCLUSIONS: Short-term weight loss is to be expected during tube weaning and is not associated with compromised growth. It is important to avoid overfeeding enterally fed children and not to increase feeds again in response to weight loss.

Improved growth, tolerance and intake with an extensively hydrolysed peptide feed in infants with complex disease.

BACKGROUND & AIMS: Infants with complex medical conditions often display faltering growth due to elevated nutritional requirements, poor intake and intolerance of feeding with malabsorption and maldigestion. As a result their nutritional management can be extremely challenging and enteral nutritional support is required. This study aimed to investigate the effectiveness, tolerance and acceptability of nutritional support with a specially formulated, paediatric peptide feed in infants with complex disease and signs of growth faltering with their current nutritional management. METHODS: This prospective intervention study investigated gastrointestinal (GI) tolerance, nutritional intake and compliance with feeding, anthropometry and growth in 18 infants (mean age 6.11 months ± 4.69, mean weight 4.97 kg ± 1.71) during 28 days of enteral nutritional support with a paediatric (1 kcal/ml) readymade peptide feed. RESULTS: GI tolerance to nutritional support with a peptide enteral feed was good and either improved or remained stable over the study. Compliance was excellent (94.0% ± 12.6), total energy intake improved (+23 ± 42 kcal/kg, p = 0.037) and mean weight (0.61 kg ± 0.31, p = 0.0001), length (1.89 ± 1.77 cm, p = 0.0001), head circumference (1.33 ± 1.29 cm, p = 0.001), weight for length Z score (p < 0.05), and weight for age Z score (p < 0.05) significantly improved. Sixty one percent (n = 11) of the infants showed signs of increased growth velocity, moving upwards in terms of their centiles. All 18 infants continued with the paediatric, peptide enteral feed once the study was complete. CONCLUSIONS: This prospective study showed that nutrition support with a specially formulated, paediatric peptide readymade feed was well tolerated, helped to promote growth, and can be considered suitable for use in infants with complex disease and faltering growth who are unable to tolerate a whole protein feed.

Genetic recombination between human and animal parasites creates novel strains of human pathogen.

Genetic recombination between pathogens derived from humans and livestock has the potential to create novel pathogen strains, highlighted by the influenza pandemic H1N1/09, which was derived from a re-assortment of swine, avian and human influenza A viruses. Here we investigated whether genetic recombination between subspecies of the protozoan parasite, Trypanosoma brucei, from humans and animals can generate new strains of human pathogen, T. b. rhodesiense (Tbr) responsible for sleeping sickness (Human African Trypanosomiasis, HAT) in East Africa. The trait of human infectivity in Tbr is conferred by a single gene, SRA, which is potentially transferable to the animal pathogen Tbb by sexual reproduction. We tracked the inheritance of SRA in crosses of Tbr and Tbb set up by co-transmitting genetically-engineered fluorescent parental trypanosome lines through tsetse flies. SRA was readily transferred into new genetic backgrounds by sexual reproduction between Tbr and Tbb, thus creating new strains of the human pathogen, Tbr. There was no evidence of diminished growth or transmissibility of hybrid trypanosomes carrying SRA. Although expression of SRA is critical to survival of Tbr in the human host, we show that the gene exists as a single copy in a representative collection of Tbr strains. SRA was found on one homologue of chromosome IV in the majority of Tbr isolates examined, but some Ugandan Tbr had SRA on both homologues. The mobility of SRA by genetic recombination readily explains the observed genetic variability of Tbr in East Africa. We conclude that new strains of the human pathogen Tbr are being generated continuously by recombination with the much larger pool of animal-infective trypanosomes. Such novel recombinants present a risk for future outbreaks of HAT.