Intestinal Dysbiosis

Normal microflora and its functions

Microorganisms of the digestive tract perform a number of critical tasks to maintain the body's homeostasis:

• Digestive and synthetic role: Bacterial enzymes break down substances that could not be digested in the small intestine (pectins, cellulose, and hemicellulose). They also synthesize vitamin K and B vitamins. Microbial synthesis partially covers human natural requirements for these nutrients.
• Metabolism: Normal flora processes undigested food residues, forming metabolites that are absorbed and incorporated into general metabolism. With the participation of microflora, the metabolism of cholesterol, bilirubin, proteins, phospholipids, bile, and fatty acids takes place. An important point is that bacteria regulate the enterohepatic circulation of bile components, directly affecting liver function.
• Inactivation and decomposition: Bacteria, often together with the GI tract's own proteolytic enzymes, destroy enterokinase, alkaline phosphatase, amylase, and trypsin. They also break down organic compounds and bile acids with the release of ammonium salts, amines, and various organic acids.

How microbiocenosis is formed

In utero, the gastrointestinal tract is completely sterile. Initial colonization by microflora occurs during the intranatal period: passing through the mother's birth canal, the fetus receives the first portions of bacteria. Due to the physiological immaturity of the local immune system (MALT system), completely different pools of microbes can multiply at this time.

In the early neonatal period (the first 6–8 days), a stage of transient dysbiosis with a variegated flora composition develops. Then, as immunity matures, the stabilization stage sets in. A healthy microbiocenosis looks like this:

1. Obligate flora (up to 95%): strict anaerobes — bifidobacteria and bacteroides.
2. Associated flora: non-pathogenic E. coli, lactobacilli.
3. Facultative flora (no more than 1%): aerobic opportunistic bacteria.

Early breastfeeding is critical for the proper formation of a balance. Natural feeding promotes the colonization of the GI tract with protective flora. Artificial formulas, conversely, often lead to imbalance: a decrease in the number of bifidobacteria and the proliferation of proteus, staphylococci, and enterococci. If early feeding is contraindicated for a premature infant due to a severe condition, a few drops of mother's milk are administered directly into the mouth using a pipette as a prophylaxis.

Development of dysbiosis and clinical picture

Various risk factors provoke a shift in microbiocenosis. These include maternal causes (vaginal dysbiocenosis), organizational and regimen defects (late breastfeeding, poor hygienic care, circulation of hospital strains), as well as iatrogenesis (prolonged antibiotic therapy, use of parenteral nutrition). Because of this, rapid growth of opportunistic strains (yeasts, staphylococci, proteus) begins.

The severity of the process is divided into four degrees. A common sign for all stages is a progressive decrease in the titer of protective bifidobacteria and lactobacilli.

• Stages I and II: anaerobes quantitatively predominate over aerobes. Clinically, these stages proceed predominantly latently.
• Stages III and IV: aerobic flora catches up in quantity with anaerobic flora or begins to exceed it. A manifest clinical picture develops.

Clinical manifestations:

• Dyspeptic syndrome: accompanied by flatulence, regurgitation, and a noticeable decrease in appetite.
• Motor disorders: manifested by increased intestinal peristalsis.
• Stool changes: it becomes loose, with an admixture of green. The appearance of undigested food lumps indicates the development of steatorrhea and creatorrhea.

Secondary malabsorption

Nutrient malabsorption is closely associated with gastrointestinal diseases, which are often accompanied by dysbiosis. The secondary form of malabsorption arises against the background of anatomical defects (for example, after gastric resection or bowel resection), inflammatory diseases, as well as pathologies of the pancreas and hepatobiliary system. The main principle of therapy is etiopathogenetic treatment of the underlying disease, which is supplemented by enzyme replacement therapy.

Class and exam questions

What else to study on this topic

• Pathogenesis of secondary malabsorption in anatomical intestinal defects
• Mechanisms of digestive enzyme inactivation by microflora
• The role of enterohepatic circulation of bile acids in metabolism
• Features of the formation of local GI immunity (MALT system) in the intranatal period
• Characteristics of hospital microorganism strains and their impact on newborns

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.