Typhoid fever

Foodborne toxicoinfections and viral gastroenteritis

Differential diagnosis of intestinal infections requires the exclusion of a wide range of bacterial and viral agents. Main bacterial causes include salmonellosis, enterotoxigenic Escherichia coli infections, staphylococcal infection, and proteus infection.

Clinical presentation of bacterial foodborne toxicoinfections:

• Pain is localized in the upper abdomen and around the umbilicus.
• Profuse diarrhea develops. Stools may be foul-smelling, greenish, but pathological admixtures are absent throughout the course of the disease.
• Signs of dehydration are present (from grade I to III).
• In severe cases, convulsions, hypotension, collapse, and infectious-toxic shock develop.
• The course is characterized by rapid recovery with the synchronous resolution of toxoxicosis and gastroenteritis.

Materials for bacteriological examination include stool, vomitus, gastric lavage fluid, and suspected food products. For salmonellosis, serological testing (antibody detection via indirect hemagglutination assay) is also used.

Viral gastroenteritis: Caused by rotaviruses, caliciviruses, enteric adenoviruses, as well as Norwalk and Norwalk-like viruses. Most commonly registered as outbreaks in organized childcare settings. They are characterized by moderate short-term intoxication, vomiting dominating over diarrhea, absence of marked dehydration, and atypical abdominal pain.

Poisonous mushroom poisonings

Mushroom poisonings are most frequently observed from mid-summer to early autumn. Symptoms depend on the specific toxin involved.

Effects of amanitohaemolysin and amanitotoxin: The latent period ranges from 6 to 24 hours. Severe abdominal pain, profuse vomiting, and violent diarrhea (sometimes bloody) develop. Patients complain of intense thirst, weakness, headache, and dizziness. Neurological disorders (hallucinations, delirium) are possible. Dehydration develops, and by days 2–3, signs of hepatorenal syndrome appear (jaundice, anuria).

Effects of muscarine and muscaridine: The latent period is shorter—from 1 to 6 hours. Symptoms include profuse sweating, salivation, bronchorrhea, nausea, vomiting, and diarrhea with colicky pain. Nervous system manifestations include dizziness, pinpoint pupils (miosis), altered mental status, agitation, delirium, hallucinations, up to coma.

Cholera: clinical presentation and management

Cholera requires mandatory hospitalization based on epidemiological indications. The disease proceeds with normal or subnormal temperature, a painless abdomen, and no preceding nausea before vomiting.

Symptoms of dehydration in cholera:

• Sharpened facial features, sunken eyes.
• Decreased skin turgor ("cholera fold").
• Maceration of the skin of the hands ("washerwoman's hands").
• Dry mucous membranes, raspy voice, oliguria.
• Drop in blood pressure, rapid and weak pulse.
• Tonic convulsions ("stork leg", "obstetrician's hand", gladiator or wrestler posture).

Definitive diagnosis is confirmed bacteriologically (stool and vomitus culture).

Rehydration therapy: The goal is restoration of water and electrolyte balance. Includes 2 phases:

1. Initial phase: correction of pre-hospital losses (lasts no more than 2 hours).
2. Maintenance phase: correction of ongoing losses (monitoring every 2–4 hours).

Tactics depend on the degree of dehydration:

• Grade I (up to 3% of body weight): oral administration.
• Grade II (4–6%): intravenous 40–65 ml/kg in the first 15–20 min (rate 80–90 ml/min), followed by drip infusion.
• Grade III (7–9%): intravenous rapid bolus 70–100 ml/kg (rate 100–130 ml/min), followed by drip infusion.
• Grade IV (10% and above): intravenous rapid bolus 100–120 ml/kg at a rate of 150 ml/min for 1–1.5 hours, then drip infusion for up to 3–5 days.

Lactosol solution is used for infusions. Etiotropic therapy includes fluoroquinolones (ciprofloxacin), tetracyclines (doxycycline), or nitrofurans (furazolidone) for 5 days. Discharge of convalescents and vibrio carriers is possible only after 3 consecutive negative stool cultures and one negative bile culture.

Yersiniosis: pathogenesis and forms

Upon alimentary transmission, Yersinia overcome gastrointestinal barriers thanks to enzymatic activity and motility. Adhesion and colonization occur in the small and large intestine.

Invasion into the epithelium occurs via M cells with subsequent translocation into lymphoid formations (Peyer's patches, solitary follicles). Endotoxin release causes the development of general toxic syndrome and the gastroenterocolitic variant of the disease.

With incomplete phagocytosis, the pathogen spreads lymphogenically to the mesenteric lymph nodes, where foci of granulomatous inflammation form (zone of necrosis, reticulum cells, areas of purulent melting). This forms the basis of the abdominal form, manifested by terminal ileitis, acute appendicitis, or mesenteric lymphadenitis.

Insufficiency of the lymphatic apparatus leads to the development of the generalized form (hepatitis, pyelonephritis, meningitis, sepsis) with microabscess formation in internal organs and hepatosplenomegaly. Secondary focal forms (arthritis, erythema nodosum) are possible, caused by antigenic mimicry and sensitization.

Class and exam questions

What else to study on this topic

• Pathomorphological changes in abdominal organs in yersiniosis
• Follow-up dispensary observation schedules for vibrio carriers and cholera convalescents
• Mechanisms of development of secondary focal forms in infectious diseases
• Compositions of polyionic crystalloid solutions for rehydration therapy

Other topics in the "Acute Intestinal Infections" section

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