Etiology and epidemiological features
Opportunistic bacteria act as the etiological factors. According to the classification, the most frequent pathogens are Bacillus cereus, clostridia (Clostridium perfringens, etc.), staphylococci (Staphylococcus aureus), halophilic vibrios, proteus, enterobacter, and klebsiellae. The ability of these microorganisms to cause poisoning strictly depends on the presence of extrachromosomal genetic elements encoding enterotoxin production.
The infection has a ubiquitous distribution. Transmission occurs via the enteral route through food. The main vehicles of transmission are meat and dairy products, salads, sauces, and confectioneries stored in violation of temperature conditions. This creates ideal conditions for the multiplication of microflora and the accumulation of toxins. People with purulent infections or bacterial carriers often serve as the reservoir. Susceptibility to enterotoxins is universal, and post-infectious antitoxic or antimicrobial immunity is not formed.
Pathogenesis features
The pathogenesis of bacterial foodborne intoxications is fundamentally different from other infectious diarrheas. Several key features of the development mechanism are distinguished:
- Minimal role of the microbial factor. Bacteria act merely as toxin producers and, as a rule, do not colonize the mucous membrane of the small intestine (an infectious process does not develop).
- Leading role of pre-formed toxins. Enterotoxins are produced in vitro (in food) and enter the body already in active form, easily overcoming the gastric acid barrier.
- Enhanced secretion. Toxins (both heat-labile and heat-stable) stimulate enterocyte enzyme systems (adenylate cyclase or guanylate cyclase), leading to massive release of water and electrolytes into the intestinal lumen.
- Absence of pronounced fever. Most enterotoxins act locally and are weak pyrogens.
- Systemic effects of heat-stable toxins. Unlike heat-labile ones, they are capable of penetrating into the systemic circulation and acting as superantigens, worsening the patient's condition.
- Short duration of the effect. The biological action of toxins is limited to 36–48 hours, which determines the rapid resolution of symptoms.
Clinical presentation and organ involvement
The disease debuts acutely with a short incubation period. The classical variant presents as gastroenteritis.
Main syndromes:
- Gastroenteritic: pronounced nausea, repeated vomiting, intense epigastric pain, frequent loose stools. The pain syndrome can be so severe that it deprives the patient of sleep.
- Dehydration: moderately pronounced signs of dehydration (dry mucous membranes, weakness, dizziness).
- Intoxication: body temperature is usually subfebrile.
Organ manifestations:
- Cardiovascular system: tendency toward arterial hypotension, normocardia, tachycardia, or relative bradycardia. In severe cases, hypovolemic shock is possible.
- Liver: in approximately 50% of cases at the peak of intoxication, benign hepatitis develops (6–8-fold increase in ALT activity, elevated direct bilirubin). Jaundice resolves within two weeks.
- Pancreas: parenchymal edema manifested by pain radiating to the back.
- Lymphatic system: painless peripheral and abdominal lymphadenopathy is possible.
Differential diagnosis
Diagnosis begins with the evaluation of clinical and epidemiological data, paying attention to the group character of the morbidity (consumption of a single dish by close contacts).
Differential diagnosis is carried out with the following pathologies:
- Rotavirus (RV) infection: differs by the absence of pathognomonic symptoms. Confirmation requires detecting the antigen in coprofiltrates (ELISA, RLA) or genetic material (PCR) during the first week of illness. Hepatosplenomegaly is atypical for RV.
- Amebiasis: differentiated by the presence of large vegetative forms of Entamoeba histolytica in stool, as well as by colonoscopy with biopsy of erosions and ulcers.
- Escherichioses and other acute intestinal infections: excluded on the basis of bacteriological and immunological studies.
Management tactics and laboratory tests
At the pre-hospital stage, it is extremely important to immediately initiate rehydration therapy and call an ambulance crew. Indications for hospitalization in an infectious diseases hospital are determined by the clinical and epidemiological situation and the severity of the condition.
Laboratory monitoring includes:
- Complete blood count (CBC) and urinalysis.
- Assessment of metabolic disorders: hematocrit, plasma electrolytes, acid-base balance (ABB).
- Determination of creatinine levels to assess renal function (the severity of renal impairment is directly proportional to the severity of the disease).
The main treatment method is pathogenetic therapy aimed at detoxification and restoration of water-electrolyte balance. Etiotropic therapy in typical bacterial foodborne intoxications and viral gastroenteritis is generally not used or is of secondary importance.
To remember the essence of foodborne toxicoinfections, recall the rule of the "Three Ts": Toxin in food, Small intestine (secretion), Thirty-six hours (short duration).
Class and exam questions
Does opportunistic flora cause an infectious process during food poisoning?
No, microorganisms act merely as toxin producers outside the body. The disease itself is caused by the action of pre-formed enterotoxins, without colonization of the intestinal mucosa.
Do the taste and odor of food change when bacterial enterotoxins accumulate in it?
No, the organoleptic properties of food products (taste, color, odor) remain unchanged, which increases the risk of mass group poisonings.
What is the main task of the physician at the pre-hospital stage?
Immediate initiation of pathogenetic rehydration therapy to correct the developing dehydration syndrome.
What else to study on this topic
- Mechanisms of development of hypovolemic and septic (toxic-infectious) shock
- Characteristics and properties of heat-stable enterotoxins as superantigens
- Criteria for assessing the severity of the course of bacterial foodborne intoxications
- Features of bacteriological and serological diagnosis using autostrains
- Principles of differential diagnosis with ulcerative colitis
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