Treatment of acute intestinal infections

Approaches to the treatment of severe toxic infections

Upon the development of acute respiratory failure (e.g., associated with botulism), patients immediately undergo mechanical ventilation (artificial lung ventilation). The main indications for intubation include apnea, tachypnea exceeding 40 respiratory movements per minute, and severe hypoxemia where the oxygen level drops below 50 mm Hg and carbon dioxide exceeds 60 mm Hg. A decrease in vital capacity and any mechanical airway obstruction are also alarming signals. The apparatus is disconnected only after the patient fully recovers the ability to breathe independently.

Nutrition for patients with swallowing disorders is administered via a probe, and in severe situations, parenteral nutrition is initiated. Quality nursing care is extremely vital: it prevents such formidable consequences as bedsores, positional injuries, muscular atrophy, and the development of hypostatic pneumonia.

The physician is obligated to prescribe antibacterial drugs. For this purpose, metronidazole, tetracycline, ampicillin, chloramphenicol, or third-generation cephalosporins are used in average therapeutic doses. The primary task of antibiotics is to halt the reproduction of the microorganism, stop its toxin production in the intestinal lumen, and prevent secondary bacterial flora colonization. Additionally, vitamin therapy, ATP preparations, cocarboxylase, and cardiovascular agents are prescribed. A patient is discharged exclusively after the full recovery of voice, articulation, and swallowing (complete regression of bulbar syndrome).

Preventive measures and focus containment

To prevent outbreaks of infections, strict sanitary supervision is required over how semi-finished meat, fish, and vegetable products are harvested, transported, and stored. Under domestic and industrial conditions, it is extremely important to adhere to a strict canning regimen. If a product raises the slightest doubt, it should undergo full thermal processing prior to consumption to guarantee the destruction of the deadly botulinum toxin.

Risk groups, such as laboratory staff constantly working with toxins, are subject to specific prophylaxis via the administration of polyanatoxin. If a case of infection has already been recorded, all individuals who consumed suspicious food along with the patient are urgently administered botulinum antitoxins. Intramuscularly, types A, B, and E antitoxins are used (strictly 2,000 international units of each type). Daily medical observation is mandatory for these contacts for a period of 10 to 12 days.

Diagnostics and differential search

The search for the cause of the disease always begins with a thorough collection of the epidemiological history. The physician pays attention to the consumption of suspicious canned goods, dried fish, or vacuum-packed products over the past 24 hours (the period can extend up to six days). It is alarming if the patient complains of marked general weakness, a short-term blood pressure spike, and severe dryness of the oral mucous membranes that does not correspond at all to actual fluid losses from diarrhea.

For accurate identification of the pathogen in coprofiltrates, saliva, urine, or operative material, enzyme-linked immunosorbent assay (ELISA) is used. This method has a sensitivity of about eighty percent. When establishing a definitive diagnosis, it is often necessary to rule out other diseases:

• Yersiniosis: differs from salmonellosis by the presence of numerous extraintestinal manifestations (arthropathies, rash, "strawberry tongue" sign, jaundice).
• Acute appendicitis: in this condition, pain always precedes fever and dyspepsia, whereas in the abdominal form of yersiniosis, intoxication and diarrhea appear first.
• Acute viral hepatitis: differs in that with the appearance of skin jaundice, preicteric symptoms (flu-like or arthralgic) abruptly disappear, and a tenfold or greater increase in transaminases is observed in the biochemical blood analysis.

Pathogenesis cascade of gram-negative infections

The mechanism of development of a systemic intestinal infection (using salmonellosis as an example) includes several sequential and interrelated stages. First, the gram-negative microorganism invades the host tissues. Then, it begins to actively secrete pathogenicity factors, specifically lipopolysaccharides (endotoxins) and exotoxins. At the site of bacterial reproduction, a local primary tissue reaction occurs, the intensity of which largely depends on the functioning of the body's endogenous antimicrobial systems.

Next, systemic cell activation takes place with the release of a massive amount of protein and lipid mediators: interleukins, prostaglandins, tumor necrosis factor, leukotrienes, and interferons. This mediator storm triggers a large-scale systemic reaction. The vascular endothelium is damaged, microcirculation is severely disrupted, and disseminated intravascular coagulation syndrome develops. Concurrently, the functions of the central nervous, cardiovascular, and respiratory systems, as well as the liver, are impaired. The final and most severe stage of this pathogenetic cascade is the development of fatal multiple organ dysfunction syndrome (MODS).

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Clinical presentation and laboratory diagnostics of cholera
• Features of the course of bacterial food poisoning
• Typhoid fever: symptomatology and hemogram at the peak of the disease
• Clinical features and mechanisms of development of shigellosis
• Symptom complex of viral gastroenteritis

Other topics in the "Acute Intestinal Infections" section

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