Our patients with NEC are similar to patients described in the literature1,3,10-12, except for a significant difference in sex distribution betwen the two groups. All infants with NEC were males. This observation could possibly be biased because of the small number of patients in this study. Although aetiology and pathophysiology of NEC remains unclear, many perinatal events have been implicated in its pathogenesis5-10,14,15. These factors are thought to be the cause of systemic hypoxia and local tissue hypoxemia4,16. However, many controlled studies have contradicted this hypothesis as these factors are not lust confined to NEC infants but are also common in other high risk infants who do not develop NEC11,17-20. Similarly we also did not find these factors to be predictive of NEC. Other factors e.g., enteral feeds, increments in volume/day and type of feedings were also examined. No differences were found between the groups. Two infants who developed NEC in our series were never fed. These observations do not support previous reports which suggest that aggressive feeding practices have an adverse effect14,15,21. All our infants received mixed feedings e.g., breast milk, regular infant formula and enfalac premature formula. Therefore protective effect of breast milk22 could not be determined. Nonetheless NEC has been reported in infants who were never fed23 or exclusively breast fed19. The role of bacteria in the pathogenesis of NEC remains controversial. There is sufficient evidence to support the hypothesis that an infectious agent contributes to the etiology of NEC e.g., clinical features resembling sepsis, epidemic clustering of cases and interruption of epidemics by infection control measures. Although no common bacterium or virus has been isolated as the cause of NEC, nonetheless, clustering of instances have occurred in the nurseries associated with agents such as escherichia coli, klebsiella, pseudomonas, enterobacter cloacae, salmonella and clostridial species24-29. Of these the bacteria most commonly linked with NEC are klebsiella30, escherichia coli24 and clostridia31. The mechanism by which these bacteria cause the disease is not clear. Lawrence et al32 postulated that the immature intestine of human neonates may be vulnerable to damage by bacterial toxins following initial colonisation with bacteria. Others have postulated changes in the gut milieu causing suppression of competitive strains of bacteria and overgrowth of virulent bacteria30. Other studies have also suggested that clostridial exotoxm is capable of causing direct mucosal injury31. In this study infants with NEC had a significantly higher frequency of septicemia i.e., 6/9 (66%) vs 5/31 (16%) in control group (P< 0.01). The organisms isolated were pseudomonas (peritoneal fluid and blood in two different patients respectively), kiebsiella (from blood and peritoneal fluid in the same patient), enterobacter cloacae (blood), enterococcus (blood) and staph aureus (blood) in each of the last 3 patients respectively. The frequency of positive blood culture was higher than the 30-35% reported in the literature33,34. It is possible that bacterial proliferation may have been responsible for initial injury to the immature intestinal mucosa and predisposed to NEC in our patient population. Although NEC is amultifactorial disease, sepsis may bean important predisposing factor in premature infants in developing countries. With the advent of neonatal intensive care units, this disease will also become more prevalent in this part of the world. Newborn infants especially preterm infants, who present with signs of sepsis and gastrointestinal disturbances, should be thoroughly investigated for this problem.
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