Invited Review: Maintain or Improve Piglet Gut Health around Weanling: The Fundamental Effects of Dietary Amino Acids

Gut health has significant implications for swine nutrient utilization and overall health. The basic gut morphology and its luminal microbiota play determinant roles for maintaining gut health and functions. Amino acids (AA), a group of essential nutrients for pigs, are not only obligatory for maintaining gut mucosal mass and integrity, but also for supporting the growth of luminal microbiota. This review summarized the up-to-date knowledge concerning the effects of dietary AA supplementation on the gut health of weanling piglets. For instance, threonine, arginine, glutamine, methionine and cysteine are beneficial to gut mucosal immunity and barrier function. Glutamine, arginine, threonine, methionine and cysteine can also assist with relieving the post-weaning stress of young piglets by improving gut immunological functions, antioxidant capacity, and/or anti-inflammatory ability. Glutamine, glutamate, glycine and cysteine can assist to reconstruct the gut structure after its damage and reverse its dysfunction. Furthermore, methionine, lysine, threonine, and glutamate play key roles in affecting bacteria growth in the lumen. Overall, the previous studies with different AA showed both similar and different effects on the gut health, but how to take advantages of all these effects for field application is not clear. It is uncertain whether these AA effects are synergetic or antagonistic. The interactions between the effects of non-nutrient feed additives and the fundamental effects of AA warrant further investigation. Considering the global push to minimize the antibiotics and ZnO usage in swine production, a primary effort at present may be made to explore the specific effects of individual AA, and then the concert effects of multiple AA, on the profile and functions of gut microbiota in young pigs.

Upper Esophageal Schwannoma: Rare Differential Diagnosis of Dysphagia

Esophageal schwannomas are rare primary sub mucosal tumors, 45 cases have been reported so far. We herein report the 46th case of an esophageal schwannoma from Nepal. A 60-year-old woman presented with progressivedysphagia. Oesophago-Gastro-Duodenoscopy (OGD) showed a sub mucosal mass with mucosal puckering in the upper esophagus; Computed tomography (CT) of the chest showed an upper esophageal mass of size 8x7x6cm3compressing the trachea. Bronchoscopy showed external compression of the mid trachea. The patient under went three incision VATS esophagectomy. Histopathological examination and immunohistochemical (IHC) staining confirmed the diagnosis of schwannoma.

Patent Urachus with Bladder Prolapse

We report a case of bladder prolapse through a patent urachus in a term male neonate with a large, red, tubular, mucosa lined mass inferior to the umbilical cord. A cystic mass communicating with fetal urinary bladder was detected in an antenatal ultrasound in a 26 years primigravida at 18 and 26 weeks gestation. The cyst disappeared at 35 weeks and a new solid mass was noted at the fetal abdominal wall. After birth a protruded mucosal mass inferior to the umbilical cord was noted. Urethral catherisation confirmed communication with bladder. On the second day of life excision of urachus, repair, reduction of bladder and reconstruction of abdominal wall was performed. The patient voided well and was discharged on ninth day without any complication. DOI: http://dx.doi.org/10.3126/jnps.v34i1.7877 J Nepal Paediatr Soc 2014;34(1):68-70

Early but not late administration of glucagon-like peptide-2 following ileo-cecal resection augments putative intestinal stem cell expansion

Expansion of intestinal progenitors and putative stem cells (pISC) occurs early and transiently following ileo-cecal resection (ICR). The mechanism controlling this process is not defined. We hypothesized that glucagon-like peptide-2 (GLP-2) would augment jejunal pISC expansion only when administered to mice immediately after ICR. Since recent reports demonstrated increases in intestinal insulin-like growth factor (IGF)-I following GLP-2 administration, we further hypothesized that increased intestinal IGF-I expression would correlate with pISC expansion following ICR. To assess this, GLP-2 or vehicle was administered to mice either immediately after resection (early) or before tissue harvest 6 wk following ICR (late). Histological analysis quantified proliferation and intestinal morphometrics. Serum levels of GLP-2 were measured by ELISA and jejunal IGF-I mRNA by qRT-PCR. Expansion of jejunal pISC was assessed by fluorescent-activated cell sorting of side population cells, immunohistochemistry for phosphorylated β-catenin at serine 552 (a pISC marker), percent of crypt fission, and total numbers of crypts per jejunal circumference. We found that early but not late GLP-2 treatment after ICR significantly augmented pISC expansion. Increases in jejunal IGF-I mRNA correlated temporally with early pISC expansion and effects of GLP-2. Early GLP-2 increased crypt fission and accelerated adaptive increases in crypt number and intestinal caliber. GLP-2 increased proliferation and intestinal morphometrics in all groups. This study shows that, in mice, GLP-2 promotes jejunal pISC expansion only in the period immediately following ICR. This is associated with increased IGF-I and accelerated adaptive increases in mucosal mass. These data provide clinical rationale relevant to the optimal timing of GLP-2 in patients with intestinal failure.

Enteral feeding induces diet-dependent mucosal dysfunction, bacterial proliferation, and necrotizing enterocolitis in preterm pigs on parenteral nutrition

Preterm neonates have an immature gut and metabolism and may benefit from total parenteral nutrition (TPN) before enteral food is introduced. Conversely, delayed enteral feeding may inhibit gut maturation and sensitize to necrotizing enterocolitis (NEC). Intestinal mass and NEC lesions were first recorded in preterm pigs fed enterally (porcine colostrum, bovine colostrum, or formula for 20–40 h), with or without a preceding 2- to 3-day TPN period ( n = 435). Mucosal mass increased during TPN and further after enteral feeding to reach an intestinal mass similar to that in enterally fed pigs without TPN (+60–80% relative to birth). NEC developed only after enteral feeding but more often after a preceding TPN period for both sow's colostrum (26 vs. 5%) and formula (62 vs. 39%, both P < 0.001, n = 43–170). Further studies in 3-day-old TPN pigs fed enterally showed that formula feeding decreased villus height and nutrient digestive capacity and increased luminal lactic acid and NEC lesions, compared with colostrum (bovine or porcine, P < 0.05). Mucosal microbial diversity increased with enteral feeding, and Clostridium perfringens density was related to NEC severity. Formula feeding decreased plasma arginine, citrulline, ornithine, and tissue antioxidants, whereas tissue nitric oxide synthetase and gut permeability increased, relative to colostrum (all P < 0.05). In conclusion, enteral feeding is associated with gut dysfunction, microbial imbalance, and NEC in preterm pigs, especially in pigs fed formula after TPN. Conversely, colostrum milk diets improve gut maturation and NEC resistance in preterm pigs subjected to a few days of TPN after birth.

Tropical mayhem: a chronic viral disease with superadded parasitic infection

Coexistence of two illnesses in the same patient may result in atypical manifestations of either or both diseases. A case of hepatitis B virus-related cirrhosis in a patient who presented with a pharyngeal mucosal mass lesion as a manifestation of superadded Leishmania infection is presented here. The clue to the diagnosis was the origin of the patient from an area highly endemic for leishmaniasis and the presence of unexplained polyclonal hypergammaglobulinaemia. The patient responded very well to therapy with amphotericin B with complete disappearance of the mucosal lesion.