L. monocytogenes is widely distributed throughout the environment including soil, water, and decaying
vegetation. L. monocytogenes exists in the feces of animals and putrescent tissues, showing a high osmotic pressure
tolerance and the ability to proliferate in temperatures ranging from 1 to 45°C 2]. The gastrointestinal mucous membrane is considered to be the most common source
of infection 1].
L. monocytogenes has the ability to pass the intestinal barrier. The primary method of entry into
endothelial cells is believed to be via a zipper-like mechanism 7]. Invasion proteins on the surface of the bacteria, like Internalin A, Internalin
B, and P60, help the bacterium bind to host surface receptors 8]. This ability is thought to trigger bacterial translocation (BT).
BT is considered to be the mechanism underlying sepsis due to L. monocytogenes. The phenomenon of enteral bacteria moving outside of the intestinal tract was described
a century ago in animal experiments 9]. BT was defined as “the passage of viable bacteria from the gastrointestinal tract
through the epithelial mucosa into the lamina propria and then to the mesenteric lymph
nodes and possibly other organs†10]. The intestinal tract then came to be thought of as a new source of infection. At
present, microbial translocation, i.e., the concept of BT, is recognized as involving
not only live bacteria but also components of dead bacteria and bacterial factors
such as endotoxin 11]. L. monocytogenes is thought to invade intestinal epithelial cells and the mucous membrane lamina propria
via various routes and to become an internalization of macrophages and lymphocytes,
subsequently migrating to remote organs through lymphatic vessels 7].
The mechanisms of BT are considered to be (1) a change in enterobacterial flora, (2)
failure of the intestinal tract barrier, and (3) diminished host immunity. The enterobacterial
flora maintains an equilibrium allowing fungi and bacteria to coexist. When this enterobacterial
flora balance is compromised by antimicrobials, antacids, ileus, or fecal impaction,
pathogenic microbes and toxins proliferate abnormally in the intestinal tract, and
this leads to contact with intestinal epithelia. The intestinal tract barrier is an
epithelial structure that functions as a mechanical barrier and also provides a mucous
membrane layer to protect the organism from excessive intestinal tract peristalsis
and digestive juices such as gastric acid and bile acid. With the atrophy of intestinal
tract disuse, ischemia may occur due to shock, malnutrition, hepatic cirrhosis, arterial
clotting, inflammatory bowel disease, or radiation exposure, leading to barrier function
failure, and pathogenic microbes can then come into contact with the intestinal mucosa.
The intestinal mucosa then becomes hyper-permeable, facilitating invasion by pathogenic
microbes. The intestinal tract has an immunologic barrier function and harbors local
immune factors including neutrophils, macrophages, and gut-associated lymphoid tissue
(GALT) of the terminal ileum. GALT is the most immunologically active tissue in the
human body. Decreasing immune cells in GALT, due to nutritional management designed
to avoid the gastrointestinal tract, reduces local immunity by causing IgA secretion
disorders in the intestinal epithelia, compromised host immunity, and diminished host
immuno-responsiveness to invasive pathogens from the intestinal tract. These alterations
can all promote invasion by pathogens. It is thought that myeloablation with chemotherapy
and the associated reduction in host immunity, direct damage to the intestinal mucosa
by chemotherapy, intestinal tract obstruction by tumors with peritoneal dissemination,
and constipation due to impaired bowel movements associated with disease states or
treatment can lead to BT.
Normalization of the aforementioned processes is necessary for the prevention and
treatment of BT. In other words, for prevention of BT it is necessary to (1) control
the enterobacterial flora, (2) maintain the intestinal tract barrier, (3) control
immuno-responsiveness, and (4) maintain the intestinal tract blood supply. To achieve
the prevention and treatment of BT, attention is being paid to the administration
of probiotics and prebiotics 12], 13], glutamine 14], polyethylene glycol 15], and dobutamine 16]. In addition, to control immuno-responsiveness, endotoxin adsorption with blood adsorption
therapy using a polymyxin B column was reported to be useful 17], 18].
As in our case, with the source of infection being unclear, the sepsis often progresses.
BT is potentially involved in the infectious process by various mechanisms and must,
in the intestinal tract, be regarded as an important source of infection. Thus, it
is necessary to prevent BT as well as to implement infection control procedures.