Staphylococcus aureus Enterocolitis: An Underrecognized Mimic of Clostridium difficile

The article by Dalal et al 1 published in this issue of Infectious Diseases in Clinical Practice raises awareness of an oftentimes-forgotten gastrointestinal pathogen: Staphylococcus aureus. Although stories of Clostridium difficile diarrhea and infection have become ubiquitous in the media because of its rampant spread and attributable deaths in 2004 and 2005, S. aureus, particularly methicillin-resistant S. aureus, assumed a similar role with respect to recurrent skin and soft tissue infections and necrotizing pneumonias. For these reasons, and the fact that S. aureus enteritis is usually associated with food poisoning, many clinicians have neglected the potential role of S. aureus as a gastrointestinal pathogen that causes a clinical presentation very similar to infection by C. difficile. Whether there is a correlation between skin colonization of S. aureus and gastrointestinal colonization or diarrheal illness is not known. As reported by Dalal et al, diarrhea due to S. aureus is not uncommon. Multiple citations have demonstrated its role as a pathogen, either methicillin-resistant or methicillinsensitive and antibiotic-associated or sporadic. Presentation can be very similar, if not identical, to a typical patient with C. difficile infection with multiple liquid stools, leukocytosis, fever, and abdominal pain. The difficulty lies in that C. difficile is much more common as an antibiotic-associated infectious diarrhea pathogen than S. aureus. It is also problematic that S. aureus is often a member of the normal microbiologic flora of the gastrointestinal tract. In addition, clinicians who use oral vancomycin as their primary treatment of choice for C. difficile infection may be concurrently and inadvertently treating S. aureus and C. difficile. Dalal et al report their use of Gram stains of fecal smears in conjunction with fecal cultures. Because of the presence of S. aureus as normal enteric flora, the stain must be interpreted with caution. Most microbiology laboratories will not report growth of S. aureus in the stool or the presence of organisms resembling S. aureus on fecal stains unless specifically requested, and it cannot be assumed that they will. In addition, because there are no specific guidelines to help determine the amount of growth that should be considered sufficient or likely to be causative for diarrheal disease, these cultures must also be interpreted with caution. Again, the same must be said of fecal stains. Few studies, if any, have made direct correlations of the colony counts with the incidence of diarrhea. However, abstracts and case series that have been published suggest that growth of moderate to predominant S. aureus should be considered a pathogen in the appropriate clinical setting especially in those cases where patients have had presumptive C. difficile infection with nonresponse to metronidazole and persistently negative C. difficile toxin assays. These same studies did report the presence of enterotoxin; however, testing for the entire panel of S. aureus enterotoxins is not routinely available in most hospital laboratories. With the difficulties mentioned and the relative uncertainty as to the prevalence of the pathogen as a cause of antibiotic-associated diarrhea, S. aureus should be considered a pathogen if there are supporting clinical factors. These should include patients who (1) have a diarrheal disease, (2) have at least moderate S. aureus reported on their fecal cultures, (3) have a diarrheal disease that is unresponsive to metronidazole, and (4) may have persistently negative C. difficile toxin assays. Guidelines in development on the treatment of C. difficile Editorial Comment