Etiology

SBBO is a syndrome that can cause functional and morphological abnormalities of the digestive tract, resulting in a disturbance in the homeostasis of the bacterial flora in the small intestine and a consequent imbalance of the mechanisms that control the flora.5,6 Therefore, for better understanding of the development of SBBO, the microflora that is normally found in the digestive tract and its regulatory mechanisms are briefly described.

It is generally accepted that the upper digestive tract (stomach, duodenum, jejunum) is sterile, as found in 70% of the population, or may present a scarce microflora made up of facultative microorganisms, predominantly Gram-positive bacteria. The concentration of bacteria (Streptococcus, Lactobacillus, aerobes and diphtheroids) and yeast is normally no greater than 104 colonies/ml in the fluid of the small bowel. These micro-organisms come from the oral cavity, colonizing the upper small intestine after surviving the gastric juice. The terminal portion of the ileum comprises a transition zone and the microbiota begins to change with the appearance of Gram-negative bacteria, such as coliforms and bacteroids. The ileocecal valve acts as a true barrier, separating the Gram-positive species, which predominate in the upper small intestine, from the Gram-negative species, which inhabit the colon, where the anaerobic bacterial population represents the main portion of colonic microflora. Bacteroids, anaerobic Lactobacilli and Clostridium spp are the main components of the colonic flora and exist in concentrations ranging between 108 and 1011 colonies/ml, surpassing the facultative or aerobic microflora in a proportion of 1000-10 000: 1. Table 13.1 shows the microflora of various segments of the digestive tract.5-7

The maintenance of the intestinal microbiota with the characteristics mentioned above depends upon the action of various regulatory mechanisms, such as diet, digestive tube motility, gastric acidity, the intestinal immunological system and the integrity of the ileocecal valve.5,6

Diet type

Animals raised in sterile environmental conditions, including feed, are different from animals raised under normal conditions that present digestive tract colonization. Animals free of bacteria

Table 13.1 Microflora of the digestive tract

Concentration of

Site micro-organisms/ml

Description

Stomach, duodenum, <104

mostly Gram-positive,

jejunum, proximal ileum

Streptococcus, Lactobacillus,

diphtheroids and yeast

Distal ileum 105- 108

besides organisms of the proximal

digestive tract, Gram-negative,

Bacteroides and coliforms

Colon 109- 1011

mostly anaerobic bacteria, 95%

Bacteroides, Clostridium and

bifidobacteria

Stool 1012

same as the colon

present a dilated cecum, underdeveloped lymphatic tissue and reduced levels of immunoglobulins in the serum. The intestinal wall of these animals is thinner, and lymphoplas-mocytic infiltration is not observed in the lamina propria as in animals raised in normal environments, which present digestive tube colonization.1,5 In the human being, during gestation, the intestine of the fetus is sterile. Shortly after birth, the intestine of the newborn is rapidly colonized by bacteria from the vaginal canal of the mother and from the environment. However, the bacterial flora also depends on the type of milk used in the diet. In infants who receive breast milk, Lactobacillus bifidus predominates and represents from 95% to 99% of the bacteria in the intestinal lumen. When an unweaned infant is fed with milk-based formulas, in addition to the bifidobacteria, bacteroids and anaerobes also appear.5,7

It is noteworthy that coprophagous animals present a greater number of bacteria in the proximal small intestine than do humans, but in the colon the number of bacteria is similar.6 Under suitable environmental conditions, especially when climatic conditions are favorable, humans may ingest food with higher quantities of bacteria that are able to defeat the antibacterial barriers of the digestive tube.6 Bacterial contamination of the lacteal contents of feeding bottles prepared in households for infants is observed frequently in developing countries, and is more frequent in families of low socioeconomic status.8

Gastric acid secretion

Gastric acid secretion is considered one of the most important factors for the regulation of small-intestine microflora, because it destroys a large amount of the bacteria that come from the oral cavity or from ingested food. In patients with hypochlorhydria or achlorhydria, secondary to gastrectomy or the use of antacids, an increase in the number of proximal small-intestine bacteria can be observed. In the small intestine, the digestive pancreatic and biliary secretions work together to control the intestinal microbiota.5,6

Digestive tract motility

Propelling peristaltic movements in the cranio-caudal direction plays an important role in the maintenance of intestinal microbiota. Dixon's classic study9 demonstrated, by inoculating the intestinal lumen with a mixture of erythrocytes marked with radioactive chromium and bacteria, that peristaltic movements are fundamental in the elimination of these elements. The integrity of the autonomic nervous system and the intestinal musculature are fundamental for the maintenance of intestinal motility. For example, in intestinal pseudo-obstruction syndrome, which is associated with profound abnormalities of intestinal motility, SBBO is frequent.10

Intestinal mucosal immunity

Intestinal mucosal immune responses are different from those that occur systemically. One of the fundamental differences is the production of immunoglobulin A (IgA), which is secreted in the intestine. IgA is the main class of antibodies produced in the intestine, as illustrated by the larger number of IgA-producing cells: a proportion of 20 for each IgG-producing cell and three for each producing IgM. Secretory IgA differs from serum IgA, as it is in dimeric form, created by the secretory piece, which confers resistance against proteolysis in the intestinal lumen. Secretory IgA can impede the adherence of micro-organisms to the surface of enterocytes, an important control mechanism to prevent SBBO. It is important to emphasize that newborns have a smaller population of plasma cells in the lamina propria, which explains their reduced ability to respond to local antigenic stimuli. At this stage of life, the colostrum and mother's milk are rich in secretory IgA and play an important role in the newborn's defense mecha-nism.5,7,11

Ileocecal valve

This valve acts as a barrier separating Grampositive bacteria that inhabit the proximal small intestine from the Gram-negative bacteria and anaerobes that comprise the colonic bacterial flora. In the absence of the ileocecal valve due to intestinal resection, a retrograde colonization of the small intestine with bacteria that are normally found only in the colon is observed.6

SBBO develops when an alteration of one or more of the intestinal mucosa regulatory mechanisms occurs. Theoretically, bacteria responsible for SBBO may come either from the environment, by the ingestion of contaminated food or water, or from the colonic microflora itself, as a result of proximal colonization due to intestinal motility disturbances or ileocecal valve functional insufficiency.

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