Viral diarrheas

Etiology: Caliciviridae family

Caliciviruses got their name from the Latin word calyx, which translates to "cup". This is due to their characteristic morphology. All human enteric caliciviruses, based on genome organization, antigenic, and genetic properties, are divided into two main genera:

1. Noroviruses (prototype: Norwalk-like viruses, NLV).
2. Sapoviruses (prototype: Sapporo-like viruses, SLV).

Genetics and classification of noroviruses: The pathogens are divided into three genogroups. Only the first (GI) and second (GII) genogroups are pathogenic to humans. The first includes seven clusters (GI/1 – GI/7), and the second includes eight clusters (GII/1 – GII/8). The third genogroup consists of two clusters that are completely non-pathogenic to humans but cause disease in animals (e.g., cattle and pigs). The division into clusters is based on differences in the RNA-dependent RNA polymerase region of the genome, as well as the region encoding capsid proteins. The amino acid sequences of noroviruses match by approximately 80% within a single cluster, but across the entire genome, identity is only 44–55%.

Sapovirus characteristics: Unlike noroviruses, the genetic apparatus of sapoviruses is significantly more conserved. They are also divided into at least three genogroups, of which only the first and second are recognized as pathogenic to humans. A common property of both genera is their high environmental stability.

Clinical presentation of severe gastroenteritis

The disease often manifests after consuming food of questionable quality (e.g., purchased "street-side" while traveling). Symptom development is rapid:

• Onset: sudden recurrent vomiting accompanied by signs of intoxication (chills, weakness, initial subfebrile temperature up to 37.5°C).
• Peak: within 1.5–2 hours, profuse watery diarrhea joins. Amidst unrelenting vomiting and diarrhea, headache and pronounced weakness rapidly increase.

Objective status in developing complications: A clinical picture of shock develops. Body temperature drops to subnormal values (hypothermia, e.g., 35.6°C). The skin becomes pale, hands and feet cold to the touch, and acrocyanosis appears. Mucous membranes and skin are dry, tissue turgor is sharply reduced. Tachycardia is registered in the cardiovascular system (weak pulse, up to 120 bpm), muffled heart sounds, and pronounced hypotension (blood pressure drops to 60/30 mmHg). Anuria develops due to impaired renal perfusion (the bladder is empty upon catheterization). Due to electrolyte loss, lower extremity muscle cramps occur. Meanwhile, the abdomen participates in breathing, peristalsis is preserved, rumbling is auscultated, and there are no peritoneal irritation signs.

Laboratory monitoring in emergency conditions

To accurately determine the degree of dehydration and calculate an adequate volume of anti-shock therapy, it is necessary to assess the patient's body weight before the onset of the disease. Extended laboratory monitoring includes determining the following parameters:

• Hemodynamics and volemic status: Central venous pressure (CVP), hematocrit (Ht).
• Acid-base balance (ABB): Blood pH level, gas composition, buffer base deficit.
• Electrolyte balance: Concentration of sodium (Na+), potassium (K+), and chloride (Cl-) ions.
• Renal function: Urea and residual nitrogen levels (markers of acute renal failure against the background of anuria).

Principles of combination therapy

Treatment tactics are based on strict dietary therapy and staged pharmacological intervention. The diet is based on the exclusion of whole milk, as well as strict restriction of carbohydrates, fresh vegetables, and fruits.

Infusion tactics:

1. First stage (Rehydration): Intravenous administration exclusively of polyionic solutions. The goal is complete compensation of water and electrolyte losses.
2. Second stage (Anti-shock therapy): If shock phenomena persist or worsen (indicating the dominance of the infectious-toxic component over hypovolemia), colloidal solutions (dextran, Polyglukin), fresh frozen plasma (FFP), and corticosteroid drugs are added to the regimen.

Medical support:

• Multienzyme preparations: to restore normal enzymatic status of the gastrointestinal tract (Creon, Festal, Pancreatin, Mezim-forte, Panzynorm-forte).
• Symptomatic agents: drugs with proven clinical efficacy — antispasmodics (No-shpa, Papaverine) and adsorbents/astringents (Smecta, Polyphepan, Carbolen).
• Probiotics: preference is given to agents based on lactobacilli (Acilakt, Bactisubtil, Lactobacterin).

The issue of prescribing broad-spectrum antibacterial drugs (etiotropic therapy) is decided individually. They are indicated only in severe cases, the presence of serious complications, or a real threat of generalization of the intestinal infection. Specific prophylaxis (vaccination) is currently only at the stage of active development.

Class and exam questions

What else to study on this topic

• Method for calculating infusion therapy volume using nomograms and degrees of dehydration
• Interpretation of acid-base balance (ABB) parameters in shock
• Mechanism of action of lactobacillus-based probiotics in viral intestinal infections
• Differential diagnosis of hyperosmolar and secretory diarrhea
• Indications and contraindications for prescribing colloidal solutions in toxic shock

Other topics in the "Acute Intestinal Infections" section

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