Rectal cultures from Swedish and Pakistani hospital-delivered newborn infants were analysed regarding the early acquisition of enterobacteria. Swedish infants were delivered vaginally, Pakistani infants were delivered either vaginally or by caesarean section. The Swedish infants were all breast-fed, whereas breastfeeding was incomplete and often started late among the Pakistani infants. Both groups of Pakistani infants were more rapidly colonized with enterobacteria than were the Swedish infants. Cultures from Swedish infants seldom yielded more than one kind of enterobacteria; E. coli and Klebsiella were most frequently isolated. E. coli dominated in both Pakistani groups, but especially caesarean section delivered infants were in addition often colonized with Proteus, Klebsiella, Enterobacter or Citrobacter species. Breastfeeding from the first day of life reduced colonization with Klebsiella/Enterobacter/Citrobacter. The results suggest that environmental exposure, delivery mode and early feeding habits all influence the early intestinal colonization with enterobacteria.

The Escherichia coli flora of infants in developed countries is dominated by one or a few strains which persist for prolonged periods of time, but no longitudinal studies have been performed in developing countries. To this end, we studied the rectal enterobacterial flora in 22 home-delivered Pakistani infants during their first 6 months of life. Three colonies were isolated and species typed on each of 11 sampling occasions. E. coli isolates were strain typed using electromorphic typing of cytoplasmic enzymes, and their O serogroups were determined. There was a very rapid turnover of enterobacterial strains in the rectal flora of individual infants. On average, 8.5 different E. coli strains were found per infant, and several biotypes of other enterobacteria. Less than 50% of the infants were colonized with E. coli from their mothers, but strains of maternal origin were four times more likely to persists in the infants' flora than other E. coli strains. Enterobacteria other than E. coli were always of non-maternal origin, and Enterobacter cloacae and Klebsiella pneumoniae biotypes recovered from contaminated feeds were later identified in the infants' rectal flora. An early colonization with klebsiella or enterobacter was significantly associated with diarrhoea during the neonatal period, although these bacteria were not likely to be the cause of the disease. The results suggest that poor hygienic conditions result in an unstable and diverse enterobacterial flora, which may influence infant health.

Background: Substantial evidence exists linking small size at birth to later-life susceptibility to chronic disease. Evidence is also emerging that some components of immune function may be programmed in early life. However, this evidence is limited and requires confirmation. Objective: We investigated the association between size at birth and response to vaccination in a cohort of 257 adults (mean age: 29.4 y; 146 men) born in an urban slum in Lahore, Pakistan, during 1964Pakistan, during -1978. Design: A single dose of Vi polysaccharide vaccine for Salmonella typhi and 2 doses of rabies vaccine were given to each subject. Antibody titers were measured in prevaccination serum samples (Vi) and in postvaccination samples (Vi and rabies). Results:The mean birth weight of the subjects was 3.24 kg; 14% of the subjects had low birth weights (2.5 kg). Vaccine responses were not consistently associated with contemporary variables (month of study, sex, current age, or indicators of wealth). Response to typhoid vaccination was positively related to birth weight (anti-Vi immunoglobulin G: r ҃ 0.138, P ҃ 0.031; anti-Vi immunoglobulin M: r ҃ 0.197, P ҃ 0.034). Response to the rabies vaccine was not significantly associated with birth weight. Conclusions: These findings add to a growing body of evidence suggesting that components of the immune system may be permanently programmed by events in early life. The contrasting effects on typhoid and rabies responses suggest that antibody generation to polysaccharide antigens, which have greater B cell involvement, is compromised by fetal growth retardation.Am J Clin Nutr 2004; 80:453-9.