This is a glimpse of some of the information that will be discussed in my next book. Please be aware that the details of this text are subject to change in the final version when the book is published. This post is for informational purposes only, and should not be considered to be medical advice. While this information is thought to be correct, some of it may be incomplete.
Are inflammatory bowel diseases contagious?
Recent research by Dheer et al. (2016) has shown that increased toll-like receptor 4 (TLR4) signaling is associated with an increase in the population and translocation of gut bacteria, and an increase in intestinal permeability.1 The effects on gut bacteria characteristics imply that increased TLR4 activation might provide the mechanism needed to substantiate the long-held theory that IBDs may be the result of a bacterial infection. And it suggests the possibility of infectious transmission.
For decades, the medical community has denied that IBDs may be transmitted from one individual to another, but experience shows that while this is not common, plenty of examples exist to show where more than one member of a household has developed an IBD. With MC, for example, not only are there multiple IBD cases in some households, but there are also examples of cases where the disease appears to have been transmitted from a human to a pet. MC is actually somewhat common in dogs. While appearances can be deceiving, and it’s certainly possible that all these cases are merely coincidental, it’s worth noting that Dheer et al. (2016) pointed out that:
Interestingly, WT mice cohoused with villin-TLR4 mice displayed greater susceptibility to acute colitis than singly housed WT mice did. The results of this study suggest that epithelial TLR4 expression shapes the microbiota and affects the functional properties of the epithelium. The changes in the microbiota induced by increased epithelial TLR4 signaling are transmissible and exacerbate dextran sodium sulfate-induced colitis. Together, our findings imply that host innate immune signaling can modulate intestinal bacteria and ultimately the host’s susceptibility to colitis. (p. 798)
WT mice are “Wild Type” mice (with no genetic modifications). Villin-TLR4 mice are genetically modified to overexpress TLR4, making them highly vulnerable to colitis and the physiological effects of colitis. While not conclusive evidence, this research certainly suggests that susceptibility to colitis, if not the disease itself, may be increased by close contact with someone who is highly susceptible to colitis. That potentially opens the door to possible contagious effects, though clearly the risk (if it exists) must be low, otherwise the transmission of IBDs between humans would be common.
1. Dheer, R., Santaolalla, R., Davies, J. M., Lang, J. K., Phillips, M. C., Pastorini, C., . . . Abreu, M. T. (2016). Intestinal epithelial toll-like receptor 4 signaling affects epithelial function and colonic microbiota and promotes a risk for transmissible colitis. Infection and Immunity, 84(3), 798-810. Retrieved from http://iai.asm.org/content/84/3/798.full