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Fecal Bacteria Overpower Highly Contagious C. diff Strain

A mix of six different bacteria found naturally in the healthy gut system of mice and isolated from feces can succeed where antibiotics fail, and eradicate murine infection by highly contagious strains of the Gram-positive anaerobe Clostridium difficile, including the human epidemic 027/BI strain, report scientists at the Wellcome Trust Sanger Institute. The findings point to a promising approach for treating antibiotic-resistant C. difficile infection and controlling its spread by harnessing naturally occurring microbial communities.

Studies by Gordon Dougan, Ph.D., and colleagues demonstrated that the 027/BI strain of C. difficile establishes a persistent and highly contagious infection in mice that is associated with high levels of spore shedding (supershedding), chronic intestinal pathology, and persistent dysbiosis; essentially an imbalance in intestinal microbiota. While treating these infected animals using the antibiotic vancomycin rapidly suppressed C. difficile excretion to below the culture detection limit, as soon as the drug was withdrawn, the bacterium invariably took hold again and high-level shedding was evident within a week.

Human studies have suggested that as an alternative to antibiotic therapy, administration of homogenized feces from a healthy donor can treat recurrent C. difficile infection by reintroducing the right mix of healthy gut bacteria that can overpower the pathogen. When the Sanger team tested this form of treatment in their supershedding 027/BI C. difficile mouse model, they found that just a single oral treatment of homogenized feces from a healthy mouse donor suppressed shedding levels in the infected animals to below detection limits within just days. The treatment worked every time, and suppression of shedding was associated with a marked loss in contagiousness. Encouragingly, and in contrast with vancomycin therapy, bacterial suppression lasted for months after just a single treatment. The recipient animals in addition demonstrated restored intestinal pathology and a reduction in the expression of proinflammatory genes associated with supershedding C. difficile.
 
 

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