With regard to patients suffering form spontaneous bacterial peritonitis, it seems counterintuitive that those patients tend to NEVER have anerobes as the causative agents despite the common leakage theory that should allow anerobes (that fill the gut) to leak whenever the opportunity is present? Is the leakage theory a sloppy theory? Do we need to tinker it a little bit? Should we adapt a new theory?! Or, should we go playing more in our labs hoping to uncover the real etiology and decipher this anerobes enigma?