Chapter 25. Childhood infections

Purulent infections are caused by gram-positive cocci, especially staphylococci and streptococci. They have many virulence factors and are able to cause purulent inflammation in various organs and tissues.

Scarlet fever. Etiology. It is an infectious disease caused by group A β-hemolytic streptococcus. The disease develops in children aged 3-15 years. Airborne transmission route. The source of infection is a person affected by any streptococcal infection. The entry of infection is usually through the mucous membrane of the pharynx, tonsils, much less often the surface of wounds, burns, and the uterine cavity.

Clinical picture. According to its severity scarlet fever can be mild, moderate or severe. When the entry of infection is in the wound area or in the uterine cavity, atypical scarlatina develops after birth.

Pathogenesis. The main changes are observed in the entry area of infection, where a primary affect occurs in the form of purulonecrotic inflammation of the oral cavity and pharynx. Acute hyperemia of the mucosa is characteristic: “flaming oropha­rynx”, raspberry tongue (fig. 25.1). The pathogen spreads through the lymphatic pathways, causing lymphangitis and regional lymphadenitis (primary infectious complex). When absorbed into the blood, the toxin causes vasculitis with acute hyperemia of the skin and a punctate scarlatinous rash, first on the skin of the face, with the exception of the nasolabial triangle, then the neck, trunk and extremities (fig. 25.2). At the same time, general intoxication with high fever, sensitization of the body to streptococcus and altered antigens of destroyed tissues increases. Cross-reacting antibodies are produced.

Fig. 25.1. Scarlet fever. Raspberry-colored tongue

Fig. 25.2. Scarlet fever rash against the background of significant skin hyperemia

Pathology. Sore throat of scarlet fever (scarlatina anginosa) first arises as catarrhal inflammation, but by the end of the first day, it turns into catarrhal-purulent and pyo­lonecrotic inflammation. When necrotized tissues are rejected, the tonsillar lesions become ulcerous-necrotic. The basis of the scarlatinous rash is vasculitis of small vessels in the form of their sharp hyperemia, stasis of erythrocytes, sludges.

Perivascular formation of lympho-macrophage infiltrates, especially in the dermis, leads to necrosis of the epidermis. Intoxication in combination with vasculitis leads to adipose and albuminous degeneration of the myocardium and liver, brain edema, damage to the autonomic nervous system. Sometimes, hemorrhages develop in the adrenal glands. When the rash subsides, lamellar desquamation of the epidermis occurs, especially on the skin of the hands and foots.

Complications. From the end of the 1st week of the disease, possible developments are pharyngeal abscess, neck phlegmons with the spread of purulent exudate into the interpleural space, otitis, temporal bone osteomyelitis, brain abscess, purulent me­ningitis and sepsis. Autoimmune disorders due to sensitization of the body peak in the 2nd and 3rd week of the disease. Endomyocarditis and glomerulonephritis develop, which are based on the cross-reaction of antibodies. Immune complex glomerulonephritis is an expression of the DTH reaction after attenuation of inflammation of the oropharynx. In many cases, it is productive intracapillary glomerulonephritis, sometimes taking a chronic course.

Measles is one of the most common diseases of children and adolescents, which is often epidemic.

Etiology. The causative agent of measles is an RNA virus from the family of paramyxoviruses, which binds the complement, produces hemagglutination and hemolysis. The source of infection is a diseased person, the route of transmission is airborne. The port of entry of the infection is the mucous membranes of the upper airway, sometimes the conjunctiva of the eyes.

Pathogenesis. The incubation period begins with virus invading the epithelium of the mucous membranes of the upper airway, where it replicates. Then the virus enters regional lymph nodes, after 2-3 days - the blood (primary viremia). The virus invades lymphocytes, leucocytes, monocytes. By the end of the 1st week of the di­sease, secondary viremia develops when the epithelium of the mucosa of all airways is damaged with the development of serocatharral inflammation. Intoxication and fever develop in the prodromal period; the measles rash develops in 4-5 days. At this time, an immune response develops involving NK cells, cTL, and plasma cells synthesizing antibodies. This contributes to a decrease in the ITH response, the development of anergy and immunodeficiency.

Pathology. 1-2 days before the appearance of the rash on the mucosa of the cheeks, lips, gingivae, sometimes conjunctiva, enanthema develops represented by small whi­tish spots surrounded by a slightly swollen reddish halo. The enanthema in the area of the buccal mucosa near the molar teeth is called Koplik spots, which have diagnostic significance in measles (fig. 25.3). First, hyperemia, edema, lymphohistiocytic infiltration, vacuolization and necrosis, and then epithelial desquamation are detected micro­scopically in the foci of the enanthema. Giant epithelial cells typical of morbilli are visible. A rash on the skin (eczanthema) of spotted papular nature is characte­ris­tic, arising first behind the ears, then on the face, neck, trunk and extremities.

Fig. 25.3. Measles. Koplik spots on the buccal mucosa

In the areas of rashes, one can see
hyperemia of microvessels, perivascular infiltration with lymphocytes and histiocytes, diapedic hemorrhages with the formation of hemosi­de­rin. In the epidermis, vacuolization, giant epithelial cells are observed. Follicle hyperplasia occurs in the lymph nodes, giant Warthin-Finkeldey polykaryocytes are found in them.