186. Measles: etiology, pathogenesis, morphological characteristics, complications, causes of death.

187. Typhoid fever: etiology, pathogenesis, characteristics of intestinal changes and their outcomes.

Typhoid fever is an acute infectious disease from the group of intestinal infections, a typical anthroponosis.

Etiology:

Typhoid fever is caused by the typhoid bacillus (Salmonella typhi). The source of infection is a sick person or a bacillus carrier, whose secretions (feces, urine, sweat) contain microorganisms. Infection occurs parenterally.

Pathogenesis:

In the lower part of the small intestine, bacteria multiply and secrete endotoxins.

Through the lymphatic pathways, they enter the group lymphatic follicles (Peyer's plaques) and solitary follicles, and then into the regional lymph nodes.

The pathogen enters the bloodstream. (Bacteremia expressed during the 1st week of the disease-hemoculture).

Secreted with bile into the lumen of the small intestine, bacteria cause a hyperergic reaction in sensitized group lymphatic and solitary follicles.

Characteristics of intestinal changes:

Local changes in typhoid fever occur in the mucous membrane and lymphatic apparatus — the group lymphatic and solitary follicles of the intestine. They go through 5 stages (periods) — cerebral swelling, necrosis, ulceration, the stage of clean ulcers and healing. Each stage lasts an average of 1 week of the disease.

In the stage of cerebral swelling, the group follicles are enlarged, protrude above the surface of the mucous membrane, furrows and convolutions are visible on their surface, which resembles the surface of the brain. On the cut, they are gray-red, juicy. The basis of cerebral swelling is the proliferation of monocytes, histiocytes and reticular cells, which displace lymphocytes. These cells go beyond the group follicles and mucous membrane, penetrate into the muscle layer and sometimes reach the serous cover. Many of the proliferating cells, especially monocytes, turn into macrophages (large cells with light cytoplasm), phagocytic typhoid rods — typhoid cells that form clusters, or typhoid granulomas.

The basis of the stage of necrosis of group follicles is necrosis of typhoid granulomas. Necrosis begins in the surface layers of the group follicles, gradually deepening and sometimes reaching the muscle layer and even the peritoneum. Demarcation inflammation occurs around necrotic masses. The dead tissue is inhibited by bile and acquires a greenish color. The same changes are observed in solitary follicles. In intramural nerve ganglia, dystrophy of nerve cells and fibers is noted.

The transition to the stage of ulcer formation is associated with sequestration and rejection of necrotic masses. First of all, "dirty" ulcers appear in the inferior section of the ileum, then in the overlying sections. At this stage, there is a danger of intra—intestinal bleeding, less often - perforation of the intestinal wall.

In the stage of "clean" ulcers, they change their appearance: they are located along the lumen of the intestine, the edges are smooth, slightly rounded, the bottom is clean, formed by a muscular layer, less often by a serous membrane. At this stage, there is a great danger of perforation of the intestinal wall.

The healing stage of ulcers ends with the formation of delicate scars in their place; the lymphoid tissue of the intestine is partially or completely restored, only slight pigmentation remains.

Outcomes: Recovery, relapses, chronic carriage, death (posthemorrhagic anemia, peritonitis, pneumonia, shock).