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Necrotizing enterocolitis (NEC) is a serious disease that affects the bowel of premature infants in the first few weeks of life. This review is available through the The Cochrane Library, which contains more than 5,300 research reviews produced by an international network of over 28,000 research experts and consumer representatives from 120 countries. Researchers in the United Kingdom have found evidence suggesting that some probiotics are unable to protect preemies from potentially fatal health conditions.
A study of 1,300 preemies found that probiotics could not prevent potentially fatal conditions such as sepsis and necrotizing enterocolitis. Researchers split the 1,300 preemies into two groups, one with probiotics and the other with placebos. Although some probiotics may have little ability to save the lives of preemies, other sources of nutrition can.
One study found preemies given breast milk from their mothers were 46 to 90 percent less likely to develop retinopathy of prematurity, a condition that can cause permanent blindness.
Science, Technology and Medicine open access publisher.Publish, read and share novel research. Although the cause of NEC is not entirely known, milk feeding and bacterial growth play a positive role.
CIHR funds the Canadian Cochrane Centre as part of its mission to facilitate evidence-based health decisions. Probiotics are found in many foods and can have a role in protecting against some bacterial infections. The group with probiotics still suffered life-threatening health conditions, compared to 12 percent in the placebo group. Future studies will look into alternative probiotics for protecting preemies from potentially fatal infections. In previous blogs, we have discussed how breast milk can prevent conditions such as necrotizing enterocolitis or retinopathy of prematurity.
Despite the bad news that probiotics may not be helpful, preemies and their families are not without options.
Risk factorsSo far, four major risk factors for NEC have been defined with prematurity being the most consistent. Probiotics (dietary supplements containing potentially beneficial bacteria or yeast) have been used to prevent NEC. Foods such as yogurt, sauerkraut, dark chocolate and miso soup contain high levels of probiotics. In addition, 9 percent in the probiotic group suffered necrotizing enterocolitis, compared to 10 percent in the placebo group. Toll-like receptors (TLR) and nucleotide-binding oligomerisation domain-like (NOD) receptors recognise patterns of bacterial signals.
At 36 weeks gestation there is a sharp decrease in the incidence of NEC, supporting the concept that gut maturation provides significant protection against development of the disease [4]. A Cochrane updated Review of studies found that the use of probiotics reduces the occurrence of NEC and death in premature infants born less than 1500 grams. Scanty mucus and reduced antimicrobial factors allow bacteria to adhere to enterocytes, activating NFKB via TRL leading to enterocyte apoptosis, necrosis and loosening of tight junctions. Broadbent2[1] Department of Microbiology and Immunology, Otago School of Medical Sciences, University of Otago, New Zealand[2] Department of Women and Children’s Health, Dunedin School of Medicine, University of Otago, New Zealand1. Nevertheless, NEC in term and high birth-weight infants is not unknown, although the risk factors appear to be somewhat different [4,6,13]. There is insufficient data with regard to the benefits and potential adverse effects in the most at risk infants less than 1000 grams at birth. Bacterial translocation may be increased by presence of enteric viruses or microbial and other toxins. IntroductionNecrotising enterocolitis (NEC) is a progressive disease of the neonatal intestine beginning in the distal ileum and proximal colon and characterised by inflammatory necrosis [1,2].
The introduction of enteral feeds, particularly formula milk, and subsequent colonisation of the neonatal intestinal tract with bacteria are believed to be significant risk factors in the development of NEC [4,6,19]. It typically affects low birth-weight, preterm infants who account for the majority (70–90%) of cases [3–5].
Not only does formula milk lack the gastrointestinal protective, anti-inflammatory and maturation factors present in breast milk, it can be a source of Cronobacter sakazakii, a neonatal pathogen implicated in some cases of NEC [19]. Diversity of enteric microbiota and normal gut motility prevent a bloom of one type of bacteria. Since the 1960s, advances in medical care have raised the survival rate for preterm infants with increasingly shortened gestation periods, resulting in a concomitant surge in NEC cases. Early research concentrated on the role of hypoxia and ischaemia, with the idea that the subsequent mucosal injury due to lack of oxygenation initiates NEC through promotion of bacterial translocation and the inflammatory cascade [1]. The overall incidence of NEC is generally accepted as ranging from <1% to 5% of neonatal intensive care unit (NICU) admissions, or up to 5 cases per 1,000 live births [4–6].


Many animal models of NEC have subsequently relied on reproducing this type of damage [5,20,21]. Kosloske et al suggested the ‘dive reflex’, whereby blood flow is diverted away from the GI tract to vital organs, as one mechanism of intestinal injury but current opinion, based on analyses of risk factors over several decades, favours a secondary role for hypoxia-ischaemia [5].
Caplan reported NEC rates for VLBW infants vary greatly across countries, ranging from 1.5% in Japan to 28% in Hong Kong, with racial disparity apparent in VLBW black infants who have an increased risk and greater associated mortality [5,8]. Nevertheless, the fact that NEC most commonly occurs in the distal ileum and proximal colon, the watershed areas of the mesenteric arteries, suggests inadequate or disordered blood circulation constitutes a risk factor in some circumstances [1,22]. Despite advances in neonatal care, the overall mortality remains high at around 20–30% [3,8-10]. Prenatal circulatory events, umbilical and aortic catheterisation with dispersion of small emboli and congenital heart disease have been linked to NEC, but occur in a minority of cases [2,4].
An estimated 20-40% of infants with NEC require surgery, which has a case fatality rate of up to 50%, the smallest, least mature infants having the worst prognosis [5]. Preterm neonates are more susceptible to hypoxia and intestinal ischaemia than term neonates because of poor vascular resistance [1,4,22].
Most cases of NEC are sporadic with no clear seasonal distribution, but outbreaks have been documented [5]. However, there is a stronger association between NEC, prematurity, enteral feeding and the presence of bacteria in the GI tract than hypoxia-ischaemia [1,5,22]. Treatment of NEC is mainly supportive with the administration of broad-spectrum antibiotics while surgery is indicated for intestinal perforation or removal of necrotic bowel segments. NEC complications and sequelae include serious neurodevelopmental delay, poor growth, intestinal obstruction due to scarring, short bowel syndrome, and liver failure due to prolonged hyperalimentation [6,9]. The terms TANEC (Transfusion Associated NEC) and TRAGI (Transfusion-Related Acute Gut Injury) have been coined, referring to this association [25,31]. Clinical classificationThe classification system of Bell has historically proved important in defining three main stages: suspected, definite and advanced NEC [11]. A recent meta-analysis examining evidence for the association concludes that recent transfusion is associated with NEC, and that transfusion-associated NEC has a higher risk of mortality than NEC which was not preceded by transfusion [25]. Modifications to Bell’s criteria have provided a more detailed system of clinical staging as shown in Table 1 [12,13].
However, Gordon et al and others have challenged the belief that NEC is a single entity, preferring to view it as an umbrella term for a number of separate diseases with some common features [13,14].
Prior to concern about TRAGI, Doppler studies have shown a decrease in neonatal superior mesenteric blood flow during and after blood transfusion [32].
Although relatively uncommon, conditions, which mimic neonatal NEC, such as focal bowel perforation, intussusception, ecchymotic colitis, appendicitis and shigellosis, have been reported and may complicate the clinical diagnosis [14-18].
The reason for this is not clear, but blood transfusion appears to have wide-ranging effects on haemodynamics, possibly as a result of changes in the microcirculation. Digestion of food requires a major increase in gut blood supply and it has been suggested that limiting or ceasing milk feeds before, during and after a blood transfusion in susceptible babies may decrease the risk of TRAGI.
Any trial of an intervention for TRAGI prophylaxis would need large numbers, requiring a multicentre approach.There are other characteristics of the preterm infant favouring the development of NEC. The combination of poor gut motility and under-production of mucous decreases clearance and increases exposure of the epithelium to potentially harmful components of the luminal contents [1,5,19]. Moreover, induction of foetal hypoxia can further reduce postnatal intestinal motility [1]. Bacterial overgrowth, as indicated by a positive hydrogen breath test, is considered to be a further consequence of delayed transit time and may promote NEC through increasing bacterial translocation from the intestinal lumen into the tissues or through exposure to high concentrations of bacterial antigens [33,34]. More recently, it has been proposed that genetic polymorphisms in the genes encoding the interleukin (IL) 4 binding receptor alpha chain and the chemokine IL-8 may also be a risk factor for NEC [35]. Breastfeeding, handling by the mother and exposure to environmental bacteria create further opportunities for gaining new species [6].
Colonisation takes place in the first few days of life and is influenced by a multitude of factors such as mode of delivery, type of feeding (breast milk or formula), gestation age, hospitalisation, the surrounding environs, maternal infection and antibiotic therapy, with mode of delivery and type of feeding considered the most significant [36].
Whereas breast fed infants are regarded as having an enteric microbiota rich in bifidobacteria, a more diverse microbiota, including potentially pathogenic groups such as Clostridium and Enterobacteriaceae, has been traditionally associated with formula fed infants.
However, modern infant formulas more closely represent breast milk, shifting the gut microbiota towards beneficial species such as lactobacilli [19,36]. Breast-fed infants are less likely to develop NEC as breast milk contains many protective bioactives [1]. The initial neonatal microbiota consists of facultative anaerobic bacteria such as Enterobacteriaceae, enterococci, streptococci and staphylococci, which are present within days of birth [33].
These bacteria consume oxygen providing the reducing conditions required for the growth of obligate anaerobes, typically bifidobacteria, clostridia and Bacteroides, appearing one to two weeks later [33,36]. It is well established that the intestinal microbiota has a profound effect on gut health, influencing physiology and metabolism, as well as maturing the infant immune system and protecting against pathogens [19,33].
However, in the preterm infant, the normal succession of bacterial colonisers may be interrupted by the administration of broad-spectrum antibiotics, gut immaturity, acquisition of nosocomial bacteria in the NICU and placement of orogastric or nasogastric feeding tubes, resulting in a more restricted enteric microbiota with delayed colonisation with bifidobacteria and without the individual differences seen in the healthy, term neonate [6,33,37].


The relationship between delayed succession, bacterial overgrowth and NEC is discussed in more detail elsewhere in this chapter.2. The role of microbes in NECThe belief bacteria are crucial for the development of NEC stems from a number of clinical and experimental findings.
In two studies totalling over 100 infants, Santulli et al and Schullinger et al were the first to credibly establish bacterial colonisation of the neonatal intestine was a requirement for this disease [38,39]. NEC does not usually occur immediately post-partum but some days later, when feeding has usually commenced and there is ample opportunity for substantial intestinal colonisation.
The reason for this difference is not entirely clear, but it may relate to a difference in pathophysiology, with bowel ischaemia being the predominant factor in early-onset NEC and cytokine priming being the predominant factor in late-onset NEC. The case for bacterial colonisation is further strengthened by the absence of NEC in ischaemic, ileal segments of germ-free rats and in infants who are stillborn [42,43]. Regardless of the initiating factors, pathological changes certainly involve bacteria as the intramural gas produced in pneumatosis intestinalis contains hydrogen of bacterial origin [44]. Demonstration of bacteria and bacterial DNA in the intestinal wall of resected segments from NEC infants supports this finding [45,46]. Epidemiological studies also indicate NEC has an infectious origin as it may occur in clusters of related cases which are amenable to infection control measures [47]. Moreover, prevention of NEC has been achieved through the administration of enteral antibiotics [48]. Bacteraemia and endotoxinaemia are frequent complications of NEC but are more likely to be sequelae rather than the actual cause [49,50]. Microbes implicated in the aetiology of NECEnteric anaerobesAmong the enteric anaerobes, Clostridium species are notorious for their proteolytic, saccharolytic, toxin and gas producing activities, making them ideal candidate microorganisms for the specific pathogen theory.
Pederson et al emphasised the similarities between neonatal NEC and gas gangrene of the bowel, suggesting that ischaemic lesions were ideal sites for clostridial invasion, the anaerobic conditions of the bowel favouring conversion of the spores to toxin-producing bacteria [51]. Studying the histology of resected intestinal segments from NEC infants led these researchers to conclude Clostridium perfringens (C. Parallels were drawn with pigbel, an acute necrotising enterocolitis common in older children and adults in Papua New Guinea, caused by type C porcine Clostridium perfringens [52,53].
As the oxygen tension of healthy tissue is likely to inhibit growth of clostridia, pre-existing tissue necrosis may be exigent. The hypothesis that clostridial alpha-toxin plays a major role in NEC has never been proven [57].C. Somewhat surprisingly, colonisation with this microbe seems not to be a risk factor for NEC, probably because the neonatal bowel is tolerant to C. Other intestinal anaerobic genera have not been fully investigated, probably due to the difficulty of culturing under strict anaerobic conditions. Despite the prevailing view that non-sporing anaerobes are frequently absent in the intestinal tract of preterm infants, a DNA-based study indicated Bacteroides were abundant, and a review of anaerobic bacteraemia in a NICU carried out by Noel et al indicated anaerobic bacteraemia was frequently linked to NEC [63,64]. It is likely that further culture-independent studies will be able to better define the contribution these bacteria make to the pathogenesis of NEC.StaphylococciCoagulase negative staphylococci (CoNS) are commonly found in the stools of NEC infants and have been associated with significant disease [65,66]. The role of staphylococcal delta(?)-toxin was examined by Scheifele et al and Scheifele and Bjornson, who believed that toxin positive CoNS were enteropathic [67,68]. Moreover, it could be detected in the stools of infants colonised with ?-toxin producing CoNS [67,68].We investigated 25 CoNS isolates from the stools of six NEC and six control infants in Dunedin Hospital NICU.
A diagnosis of NEC was made on the basis of clinical indications and pneumatosis intestinalis or peritonitis on X-ray as described previously [69].
PCR primers for the ?-toxin gene were based on sequence data published by Tegmark et al and PCR conditions were as described by McIntosh [70,71].
The results, summarised in Table 2, suggest that the ?-toxin gene was frequently present in CoNS isolated from the infants (23 of 25 isolates) but that insufficient toxin was produced to cause a CPE in either of the cell lines tested compared to the Staphylococcus aureus control, which induced cell death.
The toxic strain was positive for the ?-toxin gene by PCR and Southern hybridisation, although we lacked the specific antibody required to ultimately prove the cytopathic activity was ?-toxin mediated.
The ?-toxin theory has been largely dismissed, but our research suggests there may be occasional strains of S.
The findings of Scheifele et al may reflect the dominance of such strains at a particular time in their NICU. There is one instance of a small outbreak of NEC and bacteraemia associated with a ?-toxin-producing methicillin resistant S.
In addition, preterm infants exhibit deficiencies in immune responses to CoNS, suggesting they may cause more aggressive infections in this group compared to term neonates [75].
Large, relatively stable reservoirs of CoNS have been identified in the faces, ear region, axillae and nares of preterm infants, with smaller, less stable populations elsewhere on the skin, indicating the widespread presence of this group of bacteria and their easy access to the GI tract [76].



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