Antibacterial therapy for acute intestinal infections

Clinical syndromes and topical diagnosis of botulism

The disease is characterized by an acute onset. Depending on the epidemiological history, a foodborne form (associated with the consumption of dried fish, canned goods, and vacuum-packed products) and a wound form (occurring upon wound infection, for example, upon contact with manure and the use of occlusive dressings or ointment compresses) are distinguished.

The leading features in the clinical picture are specific neurological syndromes developing against the background of clear consciousness:

• Ophthalmoplegic syndrome: manifests as bilateral ptosis, pronounced mydriasis (wide pupils with sluggish pupillary light reflex), and anisocoria. Patients complain of visual impairment, inability to tell time on a clock, diplopia, and divergent strabismus (strabismus divergens). Impairment of accommodation and convergence is characteristic (for example, a sudden need for stronger plus lenses).
• Bulbar syndrome: includes choking when swallowing liquid food (dysphagia), a sensation of a "lump" in the throat, decreased gag reflex, nasal voice (dysphonia), and difficulty protruding the tongue.
• Myasthenic syndrome: progressive general weakness, rapid fatigue, unsteady gait (ataxia).
• Gastrointestinal paresis: pronounced dryness of the oral mucosa (not corresponding to actual fluid losses), moderate abdominal distension, flatulence, and lack of stool.
• Acute respiratory failure syndrome: develops by the hypercapnic type. It manifests as a feeling of air hunger, decreased chest excursion, tachypnea upon the slightest exertion (up to 36 respiratory movements per minute), and shallow breathing. Objectively, tachycardia at normal body temperature, arterial hypertension, and facial hyperemia are recorded.

Management tactics for severe forms of toxicoinfection

Suspicion of a severe form of botulism arises when the disease progresses rapidly, for example, when bulbar syndrome develops by the end of the first day. The presence of signs of swallowing and breathing disorders is an absolute indication for emergency hospitalization of the patient in the intensive care unit of an infectious diseases hospital.

Complex intensive care includes:

1. Mechanical ventilation (MV) in case of increasing respiratory failure.
2. Gastric and intestinal tube lavage to remove toxin residues.
3. Administration of specific antitoxin serum.
4. Parenteral detoxification.

It is extremely important to initiate non-specific and specific detoxification before receiving the results of laboratory confirmation of the diagnosis. For laboratory diagnostics proper (mouse neutralization test for botulinum toxin, ELISA), the material must be collected before serum administration and delivered to the laboratory strictly under cold chain conditions.

Pathogenesis and complications of intestinal amebiasis

The incubation period for amoebic infection ranges from 1 week to 2–3 months. The pathological process in the intestine begins with local changes: phenomena of epithelial cytolysis and tissue necrosis increase. This leads to the formation of deep ulcers and severe microcirculation disorders.

The course of intestinal amebiasis can be accompanied by serious complications:

• Development of pancolitis: indicates a severe course of the invasion.
• Intoxication syndrome: usually mild to moderate. It is caused by the absorption into the systemic bloodstream of biologically active substances formed during the decomposition of necrotic areas of the intestinal wall.
• Ameboma formation: proliferation of specific granulation tissue, which leads to local thickening and induration of the intestinal wall. Amebomas are capable of narrowing the intestinal lumen up to its complete obturation.
• Surgical complications: deep ulcers can cause intestinal perforation, which naturally leads to peritonitis and the subsequent development of severe adhesions.

Extraintestinal forms and immune response

In addition to intestinal involvement (acute amoebic dysentery, non-dysenteric colitis), extraintestinal and cutaneous amebiasis are distinguished.

The pathogenesis of extraintestinal forms is based on hematogenous dissemination of the pathogen via the portal and inferior vena cava systems. Amoebas settle in internal organs, causing the development of abscesses. Most often, the target is the right lobe of the liver, less commonly the lungs. In some cases, the brain, kidneys, pancreas, and pericardium are affected. A formidable complication is the formation of a subphrenic liver abscess, which can provoke purulent melting of the diaphragm resulting in purulent pleurisy.

Cutaneous amebiasis occurs secondarily: the discharge of pathogens with liquid stools leads to contamination of the perineal skin, where specific erosions and ulcers subsequently form.

Body defense factors in amebiasis include macrophage activity, the production of secretory IgA and lymphokines directly in the colon, as well as the formation of systemic humoral antibodies (they persist during the convalescence period for a year or more).

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Method for performing the botulinum toxin neutralization test in mice
• Differential diagnosis of wound and foodborne botulism
• Mechanisms of intestinal ameboma formation and surgical management
• The role of secretory IgA and macrophages in local immunity of the large intestine

Other topics in the "Acute Intestinal Infections" section

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