What causes typhoid fever?

Causes of typhoid fever

The typhoid rod, or Salmonella typhi, belongs to the family of enterobacteria, gram-negative, spores and capsules do not form, mobile, grows well on ordinary nutrient media, especially with the addition of bile, facultative anaerobic.

The pathogenicity of typhoid bacteria determines endotoxin, as well as "aggression enzymes": hyaluronidase, fibrinolysin, lecithinase, hemolysin, hemothoxin, catalase, etc., secreted by bacteria during colonization and death.

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Pathogenesis of typhoid fever

The entrance gate of the infection is the gastrointestinal tract. Through the mouth, stomach and duodenum the pathogen reaches the lower part of the small intestine, where the primary colonization takes place. Intruding into the lymphoid formations of the intestine - solitary follicles and Peyer's plaques, and then into the mesenteric and retroperitoneal lymph nodes, the typhoid sticks multiply, which corresponds to the incubation period.

At the end of the incubation period of typhoid fever, the causative agent from regional lymph nodes bursts into the circulatory system in large numbers - bacteremia and endotoxinemia occur , which is the beginning of clinical manifestations of the disease. There is a fever and an infectious-toxic syndrome. When bacteremia occurs hematogenous invasion of the pathogen into different organs, primarily in the liver, spleen, bone marrow, where there are secondary foci of inflammation with the formation of typhoid granulomas. From the tissue foci, the pathogen re-enters the bloodstream, strengthening and supporting bacteremia, and in case of death, endotoxinemia. In the liver and gall bladder, microorganisms find favorable conditions for existence and reproduction. Standing out with bile in the intestine, they re-enter the previously sensitized lymphatic formations and cause them hyperergic inflammation with characteristic phases of morphological changes and a violation of the function of the digestive tract (flatulence, constipation, diarrhea syndrome, impaired cavitary and membrane digestion, absorption, etc.). ).

Mass death of typhoid bacteria in the body and accumulation of endotoxin lead to the development of general toxic syndrome. Endotoxin acts primarily on the cardiovascular and nervous systems. The toxic effect on the central nervous system manifests itself as a "typhoid status", and on the cardiovascular system - pronounced hemodynamic disorders in various organs and tissues.

Bacteremia and hemodynamic disorders in the organs of the abdominal cavity contribute to the onset of hepatolienal syndrome. As a result of the interaction of typhoid bacteria that have been hematogenously infiltrated into the lymphatic cracks of the skin, with the specific antibodies formed (the 8th to the 10th day of the disease), a typical for typhoid fever is a rose-yellow rash.

Prolonged and uneven intake of microorganisms and endotoxin from the primary (intestine) and secondary inflammation into the blood causes a prolonged and undulating fever.

Toxic effects on the bone marrow of endotoxin, the emergence of miliary foci of inflammation and necrosis are manifested by leukopenia, neutropenia, aneosinophilia, relative lymphocytosis or nuclear shift to the left in the peripheral blood.

In the development of diarrheal syndrome (enteritis) arising from the early days of typhoid fever in young children, local inflammatory process in the intestine, hemodynamic disorders, toxic damage of the solar and celiac nerves have a certain significance, which leads to circulatory collapse, intestinal motility disorder, digestive processes and the absorption of not only food ingredients, but also water and electrolytes. Great importance in the development of diarrheal syndrome in children with typhoid fever is given to cyclic nucleotides and prostaglandins, which regulate intestinal function, acting as the mediator of most hormones, and take an active part in the processes of absorption of water and electrolytes in the intestine.