High turnover rate of <i>Escherichia coli</i> strains in the intestinal
 
flora of infants in Pakistan

Adlerberth, Ingegerd; Jalil, F; Carlsson, B.; Mellander, Lotta; Hanson, Lars Å.; Larsson, Peter; Khalil, K; Wold, Agnes E.

doi:10.1017/s0950268898001484

Cited by 89 publications

(91 citation statements)

References 45 publications

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“…During the first 6 mo of life, a mean number of 1.5 strains per infant were identified, which contrasts sharply to the 8.5 strains found on average in Pakistani infants (35). One may also compare the 2.1 different E. coli strains found during the first 12 mo in our study with the average 4.2 strains found in Swedish infants followed until 11 or 18 mo of age during the 1980s (36).…”

Section: Discussioncontrasting

confidence: 72%

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Escherichia coli in Infants' Intestinal Microflora: Colonization Rate, Strain Turnover, and Virulence Gene Carriage

et al. 2003

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Colonization by Escherichia. coli in infants might have decreased in the last decades, owing to changes in hospital routines and family lifestyle. In this study, the E. coli flora was characterized in 70 healthy Swedish infants followed for the first year of life. E. coli was isolated from rectal swabs obtained at 3 d of age and quantified in fecal samples collected at 1, 2, 4, and 8 wk of age and at 6 and 12 mo of age. Strains were typed using random amplified polymorphic DNA, and their virulence factor genes were identified by multiplex PCR. Colonization by E. coli occurred late; only 61% of the infants were positive by 2 mo of age. The turnover of individual strains in the microflora was slow (1.5 strains per infant during 6 mo, 2.1 during 1 y). Environmental factors, such as siblings, pets, or feeding mode, did not influence colonization kinetics or strain turnover rate. Genes encoding type 1 fimbriae, P fimbriae, and hemolysin were significantly more common in E. coli strains persisting for at least 3 wk in the microflora than in transient strains. The P-fimbrial class III adhesin gene was more common in E. coli from children who had a cat in their homes than in E. coli from children without pets (p ϭ 0.01); this adhesin type is common in E. coli from cats. The late colonization and low E. coli strain turnover rate suggest limited exposure of Swedish infants to E. coli. Our results confirm that P fimbriae and other virulence factors facilitate persistence of E. coli in the human colonic microflora. Escherichia coli is one of the first bacterial species to colonize the infant's intestines. In the 1970s, E. coli usually appeared in the baby's feces a few days after birth (1, 2), as a sign of its establishment in the intestinal microflora (3, 4). E. coli colonizing the newborn infant may originate in the maternal fecal flora (5), but E. coli strains are also commonly spread at maternity wards via the nursing staff, especially during periods of high bed-occupancy and staff workload (6). We have recently reported that Staphylococcus aureus has become a major colonizer of the infant gut (7), which may be a sign of reduced competition from other microbes. E. coli and other fecal bacteria might be less easily spread today, because of increased hygiene in hospitals and families.Some E. coli strains persist in the intestinal microflora of an individual for months or years (resident strains), whereas others (transient strains) disappear within a few weeks (8). Resident E. coli strains display certain characteristics that enable them to persist in the intestinal microflora, e.g. the expression of P fimbriae and capacity to adhere to colonic epithelial cells (9 -12). P fimbriae are composed of a fimbrial rod with a tip adhesin that exists in three varieties, termed papG classes I, II, and III. These recognize the Gal␣134Gal␤ disaccharide, with slight differences in binding specificity (13). The class II variety of the papG adhesin is common among E. coli causing pyelonephritis (14), whereas the class III variety is comm...

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Section: Discussioncontrasting

confidence: 72%

“…The carriage rates of these genes were similar to those observed in E. coli isolated from the intestinal flora of Swedish schoolgirls in the 1970s (10), but higher than among E. coli isolated from Pakistani infants (9), which confirms that commensal E. coli populations may differ in different geographic areas (35,44).…”

Section: Discussionsupporting

confidence: 71%

Escherichia coli in Infants' Intestinal Microflora: Colonization Rate, Strain Turnover, and Virulence Gene Carriage

et al. 2003

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“…aureus is foremost a skin bacterium and has previously been incriminated in the pathogenesis of eczema, because S. aureus are often found colonising eczematous skin lesions, aggravating the lesion and because IgE antibodies to S. aureus superantigen may be found in such cases [15]. However, we have recently observed that S. aureus has become a quite common inhabitant of the gut microbiota in Swedish infants [16,17], probably as a result of decreased competition from ''classical'' faecal bacteria, whose circulation has decreased strongly in today's highly hygienic hospitals and homes [18,19]. Of S. aureus strains colonising the neonatal gut, approximately 45% have the capacity to produce a toxin with superantigenic function [16,17].…”

mentioning

confidence: 97%

Neonatal exposure to staphylococcal superantigen improves induction of oral tolerance in a mouse model of airway allergy

et al. 2009

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The hygiene hypothesis suggests that lack of microbial stimulation in early infancy may lead to allergy, but it has been difficult to identify particular protective microbial exposures. We have observed that infants colonised in the first week(s) of life with Staphylococcus aureus have lower risk of developing food allergy. As many S. aureus strains produce superantigens with T-cell stimulating properties, we here investigate whether neonatal mucosal exposure to superantigen could influence the capacity to develop oral tolerance and reduce sensitisation and allergy. BALB/c mice were exposed to staphylococcal enterotoxin A (SEA) as neonates and fed with OVA as adults, prior to sensitisation and i.n. OVA challenge. Our results show that SEA pre-treated mice are more efficiently tolerised by OVA feeding, as shown by lower lung-cell infiltration and antigen-specific IgE response in the SEA pre-treated mice, compared with sham-treated mice. This was not due to deletion or anergy of lymphocytes by SEA treatment, because the SEA pre-treated mice that were fed with PBS showed similar inflammatory response as the sham-treated PBS-fed mice. Our results suggest that strong T-cell activation in infancy conditions the mucosal immune system and promotes development of oral tolerance.Key words: Allergic sensitisation . Mucosal immunity . Staphylococcal enterotoxin A . Tolerance Supporting Information available online IntroductionAllergies have increased markedly in Western industrialised countries, where they now afflict every third child. Allergies are linked to wealth, good education and small families, observations that have given rise to the hygiene hypothesis, according to which the developing immune system should be exposed to appropriate microbial stimulation in early childhood in order to mature correctly and for allergies to be avoided [1,2]. The hygiene hypothesis is also supported by experimental data. Germ-free animals are less prone to develop oral Ã These author contributed equally to this work. Eur. J. Immunol. 2009. 39: 447-456 DOI 10.1002 Immunomodulation 447 tolerance than animals reared conventionally [3,4]. Oral tolerance is induced by passage of antigens over the gut mucosa, prevents against both Th1-and Th2-dominated immune responses [5] and includes development of Treg [6,7]. Natural thymic-dependent Treg (CD4 1 CD25 hi FoxP3 1 ) are fundamental in protection against autoimmunity, gut inflammation and IgE responses. This cell subset has reduced functional capacity in germ-free animals [8].The strongest T-cell activators known are the ''superantigens'', exotoxins produced by certain pathogenic bacteria such as Staphylococcus aureus. These include staphylococcal enterotoxin A, B, C, D and E, as well as toxic shock syndrome toxin-1. The superantigen binds to the variable part of the TCR and to the MHC class II molecule, thereby ''mimicking'' antigen recognition, which leads to T-cell activation [9][10][11][12]. As many as 10-30% of all T cells can become activated by a certain superantigen compared with o0...

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“…7,8 Along with an increased hygienic lifestyle, it has been shown that E. coli colonization is delayed in Swedish infants. Instead, coagulase-negative staphylococci and/or Staphylococcus aureus are the first colonizers, possibly due to reduced competition from traditional fecal bacteria, such as E. coli.…”

Section: The Gut Microbiota In Western Infants and Potential Consequementioning

confidence: 99%

“…9 Moreover, the early gut flora of Swedish infants have a lower diversity and strain turn-over rate than the flora of infants in developing countries. 8,10 Whether the changes in the bacterial colonization pattern that appear to have taken place during the last decades will influence child health is not clear, but diseases caused by deficiencies in immune regulation, including allergies, Crohn disease and type-1 diabetes, have increased in Western countries. Today, B cell-mediated allergic disorders are a major public health issue.…”

Section: The Gut Microbiota In Western Infants and Potential Consequementioning

confidence: 99%

Infant B cell memory and gut bacterial colonization

Rudin

Lundell

2012

Gut Microbes

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High turnover rate of Escherichia coli strains in the intestinal flora of infants in Pakistan

Cited by 89 publications

References 45 publications

Escherichia coli in Infants' Intestinal Microflora: Colonization Rate, Strain Turnover, and Virulence Gene Carriage

Escherichia coli in Infants' Intestinal Microflora: Colonization Rate, Strain Turnover, and Virulence Gene Carriage

Neonatal exposure to staphylococcal superantigen improves induction of oral tolerance in a mouse model of airway allergy

Infant B cell memory and gut bacterial colonization

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