Etiology and age-related features
The etiological structure of acute intestinal infections is constantly expanding. All pathogens can be divided into three main groups:
- Bacterial: pathogenic enterobacteria (Salmonella, Shigella, Campylobacter, Yersinia, various classes of Escherichia), as well as opportunistic flora (Klebsiella, Proteus, Pseudomonas aeruginosa).
- Viral: rotaviruses, enteroviruses, adenoviruses, and caliciviruses.
- Protozoa and fungi: Giardia (Giardia), Cryptosporidium, Entamoeba histolytica.
Viral diarrhea and infections caused by opportunistic flora, Campylobacter, and Escherichia predominate in young children. In older children, classic bacterial infections come to the forefront: salmonellosis, shigellosis, and yersiniosis.
High susceptibility in infants is due to the anatomical and physiological immaturity of the gastrointestinal tract: low gastric juice acidity and insufficient concentration of secretory immunoglobulin A (IgA).
Mechanisms of diarrhea development
The pathogenesis of acute intestinal infections depends on the nature of the pathogen. There are two main mechanisms of diarrheal syndrome: invasive and secretory. Frequently, they operate simultaneously.
In viral infections (e.g., rotavirus), the mechanism is mixed:
- Osmotic component: viruses destroy mature enterocytes on the villi of the small intestine. Because of this, the synthesis of disaccharidases decreases. Unhydrolyzed carbohydrates accumulate in the intestinal lumen, which increase osmotic pressure and draw in water.
- Secretory component: rotaviruses produce non-structural proteins. In particular, the NSP4 protein acts as a true viral enterotoxin—it activates the enteric nervous system and stimulates the direct release of water and electrolytes into the intestinal lumen.
In bacterial lesions, endotoxins (lipopolysaccharides) released upon bacterial death play a key role. They stimulate fluid secretion and, upon entering the systemic circulation, cause severe intoxication up to endotoxic shock.
Clinical picture and topical diagnosis
The incubation period averages 2–3 days, but can be reduced to a few hours in foodborne transmission. The disease begins acutely with fever, vomiting, abdominal pain, and changes in stool consistency.
Stool evaluation is a crucial criterion indicating the level of gastrointestinal tract involvement:
| Infection | Macroscopic stool characteristics |
|---|---|
| Dysentery | Scanty ("rectal spit"), contains mucus, blood, and pus |
| Salmonellosis | "Bog slime" appearance ( greenish), often with blood |
| Yersiniosis | Abundant, foul-smelling, with greens and mucus |
| Escherichiosis | Abundant, watery, bright yellow |
| Rotavirus | Watery, abundant, without visible pathological impurities |
In addition to stool, additional signs are important. For example, pronounced meteorism is typical for escherichiosis and salmonellosis in infants. Hepatosplenomegaly indicates generalization of the process and is often found in salmonellosis. The presence of polymorphic exanthema is specific to yersiniosis.
Principles of laboratory diagnostics
A number of laboratory methods are used to confirm the clinical diagnosis. The main rule is that material for pathogen isolation must be collected strictly before the start of antibacterial therapy.
- Bacteriological/virological stool examination: the primary method for etiological identification.
- Rapid tests: PCR, ELISA, latex agglutination. They allow for the rapid detection of pathogen antigens or DNA/RNA.
- Serological methods: searching for specific antibodies in the blood (passive hemagglutination assay, complement fixation test). Informative no earlier than the 5th day from the onset of the disease.
- Microscopy (coprogram): shows the severity of inflammation. In dysentery, an abundance of leukocytes and erythrocytes is detected in the stool, whereas in viral diarrhea, inflammatory changes are completely absent.
To easily remember stool characteristics in bacterial infections, associate: dysentery — "scanty blood" (distal colitis), salmonellosis — "green slime" (higher involvement), escherichiosis — "yellow water" (small intestine).
Class and exam questions
What causes the seasonality of different intestinal infections?
Bacterial pathogens (e.g., Shigella) multiply more intensively in warmth, resulting in a summer-autumn peak. Viral diarrhea, conversely, is more stable and spreads more actively during the winter period.
Why does osmotic diarrhea develop in rotavirus infection?
The virus destroys the villi of the small intestine, resulting in the loss of disaccharidase enzymes. Unhydrolyzed sugars remain in the intestinal lumen and draw in water according to the law of osmosis.
How does the transmission route affect the scale of morbidity?
The contact-household route (via toys, dirty hands) usually causes single (sporadic) cases. Food and water routes cause major group outbreaks.
What else to study on this topic
- Criteria for assessing the severity of dehydration (exicosis) and types of electrolyte loss.
- Extraintestinal pathology mimicking acute intestinal infections (appendicitis, meningitis, diabetic ketoacidosis).
- Life-threatening complications: hypovolemic shock, acute kidney injury, hemolytic uremic syndrome.
- Long-term consequences of acute intestinal infections: secondary lactase deficiency and irritable bowel syndrome.
- Features of parasitic infections using the pathogenesis of cryptosporidiosis as an example.
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Other topics from the section «Chapter 12. Infectious and parasitic diseases»
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