Syndromes in infectious diseases

Intoxication syndrome and sepsis

The development of intoxication syndrome is associated with the formation of a primary focus followed by dissemination of microorganisms, their toxins, and tissue breakdown products into the systemic circulation. In severe courses of infections, such as toxic diphtheria (pathogen — Corynebacterium diphtheriae), damage to target organs is observed: the heart, adrenal glands, kidneys, and peripheral nervous system. Treatment requires strict bed rest and specific detoxification (administration of equine antitoxic serum, donor plasma).

The extreme variant of generalization is sepsis. In response to toxemia, immune cells (macrophages, monocytes, endothelial cells) massively release pro-inflammatory mediators—interleukins, tumor necrosis factor, prostaglandins. This triggers systemic inflammatory response syndrome (SIRS). Massive vascular endothelial damage, vasodilation, hypovolemia, and tissue ischemia occur. Activation of the coagulation cascade leads to DIC syndrome, and oxidative stress exacerbates hypoperfusion. The result is tissue hypoxia and multiple organ failure. Morphologically, "shock organs" develop: ischemic renal cortex, coalescing hemorrhages in the lungs, and foci of lobular necrosis in the liver.

Jaundice and hepatomegaly syndrome

Hepatocellular jaundice most commonly has a viral etiology. ELISA (antigen detection and IgM/IgG antibody differentiation to determine the stage) and PCR are used for verification. Acute viral hepatitis is usually secondary and resolves with adequate antibacterial therapy.

Special attention is required for infectious mononucleosis (EBV infection). The disease begins gradually. Hepatitis syndrome with moderate cytolysis occurs against the background of prolonged fever (up to 3–4 weeks) and acute tonsillitis. The leading feature is lymphoproliferative syndrome: symmetrical lymphadenopathy (especially submandibular and posterior cervical nodes) and hepatosplenomegaly syndrome with a predominance of splenomegaly. Blood tests reveal leukocytosis, a shift to the left towards lymphomonocytosis, and atypical mononuclear cells.

In the differential diagnosis of jaundice, it is important to consider leptospirosis. It is indicated by contact with rodents or swimming in fresh water bodies 2–4 weeks before the illness. Characteristic features include persistent fever during the icteric period and prominent myalgia syndrome (pain in the calf muscles). Leptospirosis is frequently complicated by acute kidney injury (decreased diuresis, rising urea and creatinine) and hemorrhagic syndrome.

Exanthematous and lymphadenopathic syndromes

The appearance of a rash is a classic sign of many cyclic infections. A prime example is rubella. Following virus entry and replication in regional lymph nodes, hematogenous dissemination (viremia) occurs. Damage to skin epithelial cells (exanthema) and the development of intoxication are immune-mediated in nature.

The clinical course of rubella is strictly cyclic. A distinctive feature of the prodromal period is the early appearance of lymphadenopathy, which persists and increases during the rash period. The exanthema itself is accompanied by catarrhal syndrome and oropharyngeal changes. When pregnant women are infected, the virus exhibits high teratogenic activity due to its endotheliotropism, necessitating specific diagnostic tactics.

Class and exam questions

What else to study on this topic

• Clinical classifications and criteria for septic syndrome
• Rules for the administration of equine antitoxic antidiphtheria serum
• Features of the course of rubella in pregnant women and the pathogenesis of its teratogenic effect
• Pathomorphology of septicopyemia and chronic sepsis
• Differential diagnosis of infectious and non-infectious jaundice

Other topics in the "Respiratory Infections" section

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