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What causes typhoid fever?
Last reviewed: 06.07.2025
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Causes of typhoid fever
Typhoid bacillus, or Salmonella typhi, belongs to the family of enterobacteria, is gram-negative, does not form spores or capsules, is mobile, grows well on conventional nutrient media, especially with the addition of bile, and is a facultative anaerobe.
The pathogenicity of typhoid bacteria is determined by endotoxin, as well as “aggressive enzymes”: hyaluronidase, fibrinolysin, lecithinase, hemolysin, hemotoxin, catalase, etc., secreted by bacteria during the process of colonization and death.
[ Pathogenesis of typhoid fever
The gastrointestinal tract serves as the entry point for the infection. Through the mouth, stomach and duodenum, the pathogen reaches the lower part of the small intestine, where primary colonization occurs. Penetrating into the lymphoid formations of the intestine - solitary follicles and Peyer's patches, and then into the mesenteric and retroperitoneal lymph nodes, typhoid bacilli multiply, which corresponds to the incubation period.
At the end of the incubation period of typhoid fever, the pathogen breaks into the bloodstream in large quantities from the regional lymph nodes - bacteremia and endotoxinemia occur, which marks the beginning of the clinical manifestations of the disease. Fever and infectious-toxic syndrome occur. With bacteremia, the pathogen is hematogenously carried to various organs, primarily to the liver, spleen, bone marrow, where secondary foci of inflammation occur with the formation of typhoid granulomas. From tissue foci, the pathogen re-enters the bloodstream, increasing and maintaining bacteremia, and in case of death - endotoxinemia. In the liver and gallbladder, microorganisms find favorable conditions for existence and reproduction. Secreted with bile into the intestine, they are re-introduced into previously sensitized lymphatic formations and cause hyperergic inflammation in them with characteristic phases of morphological changes and dysfunction of the gastrointestinal tract (flatulence, constipation, diarrhea syndrome, dysfunction of cavity 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 primarily affects the cardiovascular and nervous systems. Toxic effects on the central nervous system are manifested by "typhoid status", and on the cardiovascular system - by pronounced hemodynamic disorders in various organs and tissues.
Bacteremia and hemodynamic disturbances in the abdominal organs contribute to the development of hepatosplenic syndrome. As a result of the interaction of typhoid bacteria, introduced hematogenously into the lymphatic clefts of the skin, with the specific antibodies formed (8-10th day of illness), a roseola rash typical of typhoid fever appears.
The prolonged and uneven flow of microorganisms and endotoxin from the primary (intestine) and secondary foci of inflammation into the blood causes a prolonged and wave-like fever.
The toxic effect of endotoxin on the bone marrow, the occurrence of miliary foci of inflammation and necrosis are manifested by leukopenia, neutropenia, aneosinophilia, relative lymphocytosis or a nuclear shift to the left in the peripheral blood.
In the development of diarrheal syndrome (enteritis), which occurs from the first days of typhoid fever in young children, a certain role is played by the local inflammatory process in the intestine, hemodynamic disorders, toxic damage to the solar and splanchnic nerves, which leads to circulatory collapse, impaired intestinal motility, digestion processes and 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 a mediator of most hormones, and take an active part in the processes of absorption of water and electrolytes in the intestine.