Storage of human urine for a couple of weeks results in a great reduction of the number of enteric microbes and this renders urine a safer fertilizer compared with animal manure which requires more than 6 months for decomposition (Egigu et al. 2014).
Similar approaches might be extended to enteric microbes that contain the FHL enzyme system to improve hydrogen production from alternate carbon sources, and for the simultaneous production of value-added chemical entities derived from the anaerobic metabolism of pyruvate.
To determine if enteric microbial fermentation occurs during these prolonged extractions, potentially contributing towards the total number of identified analytes (produced ex vivo), we compared the VOCs isolated from unboiled and boiled (sterile) fecal samples and also evaluated the survival of enteric microbes at 60°C.
Additionally, as shown in Fig. 2b, when the fecal sample is heated to 60°C, the number of viable enteric microbes rapidly declines (90% of microbial viability is lost after 1 hr), with near complete absence of viability observed after 2 hours of heating.
One possibility is that the drug alters mammalian physiology by changing the composition and/or metabolism of enteric microbes.
As microbial sensors in IECs, TLR signaling constitutes the primary link between enteric microbes and epithelial cell-intrinsic NF-κB signaling.
Within the next 2 decades, global mixing, increased population density, and decreased travel times will facilitate the spread of a variety of antimicrobial-resistant pathogens such as fluoroquinolone-resistant pneumococci and enteric microbes.
For example, from the Fresh stage to the Bloat stage, enteric microbes likely contribute to putrefaction by digesting the corpse macromolecules, which in turn generates metabolic byproducts that cause the corpse to bloat (Mondor et al., 2012).
In mammals, the postnatal intestinal epithelial cells (IECs), after transitioning from a relatively germ-free fetal environment, immediately interact with enteric microbes and participate in immune surveillance against luminal pathogenic stimuli (Artis, 2008; Maynard et al, 2012).
We found little or no overlap between outbreaks of the three diseases within each region, which suggests that a combination of different factors triggered each event in each region, and that competition may have occurred between these enteric microbes for available hosts (Rabbani and Greenough 1999).
