Publications by authors named "Mike A Carl"

Surgical removal of the intestine, lifesaving in catastrophic gastrointestinal disorders of infancy, can result in a form of intestinal failure known as short bowel syndrome (SBS). Bloodstream infections (BSIs) are a major challenge in pediatric SBS management. BSIs require frequent antibiotic therapy, with ill-defined consequences for the gut microbiome and childhood health.

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Introduction: Very low birth weight (VLBW) neonates (< 1500 g) are commonly exposed to prolonged antibiotic courses related to concerns for presumed early onset sepsis often with unclear indications. While antibiotics can be life-saving medications, prolonged antibiotic exposure (> 5 days) increases an infant's risk for necrotizing enterocolitis, late onset sepsis, colonization or infection with resistant organisms, and death. The aim of this study is to describe clinical and laboratory factors that influence the length of initial antibiotic courses in VLBW neonates.

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Background: Late-onset sepsis is a major problem in neonatology, but the habitat of the pathogens before bloodstream invasion occurs is not well established.

Methods: We examined prospectively collected stools from premature infants with sepsis to find pathogens that subsequently invaded their bloodstreams, and sought the same organisms in stools of infants without sepsis. Culture-based techniques were used to isolate stool bacteria that provisionally matched the bloodstream organisms, which were then genome sequenced to confirm or refute commonality.

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Article Synopsis
  • Sophisticated T6SS in Pseudomonas aeruginosa helps bacteria exchange information by delivering antibiotic effectors that target cell walls of neighboring bacteria.
  • A wide variety of peptidoglycan-degrading enzymes have been identified as T6SS effectors, which are crucial for bacterial competition.
  • These effectors are linked with immunity proteins to prevent self-harm, highlighting the evolutionary pressure for such systems in different environments, including those relevant to human health.
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Article Synopsis
  • - The type VI secretion system (T6SS) in Pseudomonas aeruginosa allows the bacteria to inject effector proteins, including Tse2, into other Gram-negative cells to inhibit their growth, thus enhancing P. aeruginosa's own survival and competitiveness.
  • - Tse2 induces a state of quiescence, meaning it stops recipient cells from growing without killing them, and is countered by an immunity protein called Tsi2, which prevents damage to the donor bacteria.
  • - Researchers determined the structure of Tsi2, revealing it works differently from other known immunity proteins, and found specific regions essential for its interaction with Tse2, highlighting unique aspects of this toxin-immunity system in bacteria.
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Bacteria that live in the environment have evolved pathways specialized to defend against eukaryotic organisms or other bacteria. In this manuscript, we systematically examined the role of the five type VI secretion systems (T6SSs) of Burkholderia thailandensis (B. thai) in eukaryotic and bacterial cell interactions.

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The functional spectrum of a secretion system is defined by its substrates. Here we analyzed the secretomes of Pseudomonas aeruginosa mutants altered in regulation of the Hcp Secretion Island-I-encoded type VI secretion system (H1-T6SS). We identified three substrates of this system, proteins Tse1-3 (type six exported 1-3), which are coregulated with the secretory apparatus and secreted under tight posttranslational control.

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The Dr family of Escherichia coli adhesins are virulence factors associated with diarrhea and urinary tract infections. Dr fimbriae are comprised of two subunits. DraE/AfaE represents the major structural, antigenic, and adhesive subunit, which recognizes decay-accelerating factor (DAF) and carcinoembryonic antigen (CEA)-related cell adhesion molecules (CEACAMs) CEA, CEACAM1, CEACAM3, and CEACAM6 as binding receptors.

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