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Gut bacteria are rarely shared by co-hospitalized premature infants, regardless of necrotizing enterocolitis development.

Raveh-Sadka T, Thomas BC, Singh A, Firek B, Brooks B, Castelle CJ, Sharon I, Baker R, Good M, Morowitz MJ, Banfield JF - Elife (2015)

Bottom Line: Thus, spread of potential pathogens among hospitalized infants is of great concern.We compared microbial communities in infants who did and did not develop necrotizing enterocolitis.Importantly, we demonstrate that strain-resolved comprehensive community analysis can be accomplished on potentially medically relevant time scales.

View Article: PubMed Central - PubMed

Affiliation: Department of Earth and Planetary Science, University of California, Berkeley, Berkeley, United States.

ABSTRACT
Premature infants are highly vulnerable to aberrant gastrointestinal tract colonization, a process that may lead to diseases like necrotizing enterocolitis. Thus, spread of potential pathogens among hospitalized infants is of great concern. Here, we reconstructed hundreds of high-quality genomes of microorganisms that colonized co-hospitalized premature infants, assessed their metabolic potential, and tracked them over time to evaluate bacterial strain dispersal among infants. We compared microbial communities in infants who did and did not develop necrotizing enterocolitis. Surprisingly, while potentially pathogenic bacteria of the same species colonized many infants, our genome-resolved analysis revealed that strains colonizing each baby were typically distinct. In particular, no strain was common to all infants who developed necrotizing enterocolitis. The paucity of shared gut colonizers suggests the existence of significant barriers to the spread of bacteria among infants. Importantly, we demonstrate that strain-resolved comprehensive community analysis can be accomplished on potentially medically relevant time scales.

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Comparison of CRISPR loci in Enterococcus faecalisgenomes.(A) The CRISPR-Cas loci in infants #3, #5 (earlystrain), and #8 and (B) the CRISPR locus lackingadjacent Cas proteins. The first defective repeats are shown in blue, otherrepeats are in green. The CRISPR loci are expanded below. In A,two versus three spacers have been added to the young end of the loci (leftside, adjacent to Cas) in infants #3, #5 versus #8,respectively. In B, scaffolds encoding the loci are shown ashorizontal gray bars (polymorphisms in the multi-sequence alignment aresmall vertical tic marks). The same color indicates shared sequences. Blueboxes to the left indicate that the genome encodes Cas proteins. Both loci(A and B) are identical in infants #3and #5.DOI:http://dx.doi.org/10.7554/eLife.05477.009
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fig5: Comparison of CRISPR loci in Enterococcus faecalisgenomes.(A) The CRISPR-Cas loci in infants #3, #5 (earlystrain), and #8 and (B) the CRISPR locus lackingadjacent Cas proteins. The first defective repeats are shown in blue, otherrepeats are in green. The CRISPR loci are expanded below. In A,two versus three spacers have been added to the young end of the loci (leftside, adjacent to Cas) in infants #3, #5 versus #8,respectively. In B, scaffolds encoding the loci are shown ashorizontal gray bars (polymorphisms in the multi-sequence alignment aresmall vertical tic marks). The same color indicates shared sequences. Blueboxes to the left indicate that the genome encodes Cas proteins. Both loci(A and B) are identical in infants #3and #5.DOI:http://dx.doi.org/10.7554/eLife.05477.009

Mentions: This pattern of loci with and without Cas proteins has been reported previously inE. faecalis (Palmer andGilmore, 2010). Different Cas1 sequences (types a and b) and a differentrepeat sequence were identified in E. faecalis from infants#3, #5 before antibiotic treatment, and #8, compared to thestrain in infant #5 after antibiotic treatment (Figure 4B). The repeat-spacer arrays in the loci with Cas1 typea are identical in the genotypes of E. faecalis in infant #3and in early samples from infant #5 (Figure5A), reinforcing the very high similarity of these populations deduced fromsingle copy gene sequence comparisons (Figure2). As often happens in CRISPR loci (Tyson and Banfield, 2008), a block comprising six spacers and flankingrepeats has been excised in the strain from infant #8 and three novel spacershave been added at the growing tip, versus two in infants #3 and #5(Figure 5A). Shared spacers at the olderend (distant from the Cas) imply that the strains in infants #3, #5,and #8 had a recent common ancestor.10.7554/eLife.05477.009Figure 5.Comparison of CRISPR loci in Enterococcus faecalisgenomes.


Gut bacteria are rarely shared by co-hospitalized premature infants, regardless of necrotizing enterocolitis development.

Raveh-Sadka T, Thomas BC, Singh A, Firek B, Brooks B, Castelle CJ, Sharon I, Baker R, Good M, Morowitz MJ, Banfield JF - Elife (2015)

Comparison of CRISPR loci in Enterococcus faecalisgenomes.(A) The CRISPR-Cas loci in infants #3, #5 (earlystrain), and #8 and (B) the CRISPR locus lackingadjacent Cas proteins. The first defective repeats are shown in blue, otherrepeats are in green. The CRISPR loci are expanded below. In A,two versus three spacers have been added to the young end of the loci (leftside, adjacent to Cas) in infants #3, #5 versus #8,respectively. In B, scaffolds encoding the loci are shown ashorizontal gray bars (polymorphisms in the multi-sequence alignment aresmall vertical tic marks). The same color indicates shared sequences. Blueboxes to the left indicate that the genome encodes Cas proteins. Both loci(A and B) are identical in infants #3and #5.DOI:http://dx.doi.org/10.7554/eLife.05477.009
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4384745&req=5

fig5: Comparison of CRISPR loci in Enterococcus faecalisgenomes.(A) The CRISPR-Cas loci in infants #3, #5 (earlystrain), and #8 and (B) the CRISPR locus lackingadjacent Cas proteins. The first defective repeats are shown in blue, otherrepeats are in green. The CRISPR loci are expanded below. In A,two versus three spacers have been added to the young end of the loci (leftside, adjacent to Cas) in infants #3, #5 versus #8,respectively. In B, scaffolds encoding the loci are shown ashorizontal gray bars (polymorphisms in the multi-sequence alignment aresmall vertical tic marks). The same color indicates shared sequences. Blueboxes to the left indicate that the genome encodes Cas proteins. Both loci(A and B) are identical in infants #3and #5.DOI:http://dx.doi.org/10.7554/eLife.05477.009
Mentions: This pattern of loci with and without Cas proteins has been reported previously inE. faecalis (Palmer andGilmore, 2010). Different Cas1 sequences (types a and b) and a differentrepeat sequence were identified in E. faecalis from infants#3, #5 before antibiotic treatment, and #8, compared to thestrain in infant #5 after antibiotic treatment (Figure 4B). The repeat-spacer arrays in the loci with Cas1 typea are identical in the genotypes of E. faecalis in infant #3and in early samples from infant #5 (Figure5A), reinforcing the very high similarity of these populations deduced fromsingle copy gene sequence comparisons (Figure2). As often happens in CRISPR loci (Tyson and Banfield, 2008), a block comprising six spacers and flankingrepeats has been excised in the strain from infant #8 and three novel spacershave been added at the growing tip, versus two in infants #3 and #5(Figure 5A). Shared spacers at the olderend (distant from the Cas) imply that the strains in infants #3, #5,and #8 had a recent common ancestor.10.7554/eLife.05477.009Figure 5.Comparison of CRISPR loci in Enterococcus faecalisgenomes.

Bottom Line: Thus, spread of potential pathogens among hospitalized infants is of great concern.We compared microbial communities in infants who did and did not develop necrotizing enterocolitis.Importantly, we demonstrate that strain-resolved comprehensive community analysis can be accomplished on potentially medically relevant time scales.

View Article: PubMed Central - PubMed

Affiliation: Department of Earth and Planetary Science, University of California, Berkeley, Berkeley, United States.

ABSTRACT
Premature infants are highly vulnerable to aberrant gastrointestinal tract colonization, a process that may lead to diseases like necrotizing enterocolitis. Thus, spread of potential pathogens among hospitalized infants is of great concern. Here, we reconstructed hundreds of high-quality genomes of microorganisms that colonized co-hospitalized premature infants, assessed their metabolic potential, and tracked them over time to evaluate bacterial strain dispersal among infants. We compared microbial communities in infants who did and did not develop necrotizing enterocolitis. Surprisingly, while potentially pathogenic bacteria of the same species colonized many infants, our genome-resolved analysis revealed that strains colonizing each baby were typically distinct. In particular, no strain was common to all infants who developed necrotizing enterocolitis. The paucity of shared gut colonizers suggests the existence of significant barriers to the spread of bacteria among infants. Importantly, we demonstrate that strain-resolved comprehensive community analysis can be accomplished on potentially medically relevant time scales.

Show MeSH
Related in: MedlinePlus