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What causes typhoid fever in adults?
Last reviewed: 06.07.2025
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Causes of typhoid fever
The cause of typhoid fever is Salmonella typhi, which belongs to the genus Salmonella, serogroup D, family of intestinal bacteria Enterobacteriaceae.
S. typhi is a rod-shaped organism with rounded ends, does not form spores or capsules, is mobile, gram-negative, and grows better on nutrient media containing bile. When it is destroyed, endotoxin is released. The antigenic structure of S. typhi is represented by O-, H-, and Vi-antigens, which determine the production of the corresponding agglutinins.
S. typhi survives relatively well at low temperatures, is sensitive to heating: at 56 °C it dies within 45-60 minutes, at 60 °C - after 30 minutes, when boiling - in a few seconds (at 100 °C almost instantly). A favorable environment for bacteria is food products (milk, sour cream, cottage cheese, minced meat, jelly), in which they not only survive, but are also capable of reproduction.
[ Pathogenesis of typhoid fever
The pathogenesis of typhoid fever is characterized by cyclicity and the development of certain pathophysiological and morphological changes. Infection occurs through the mouth, and the primary site of localization of pathogens is the digestive tract. It should be especially noted that infection does not always lead to the development of the disease. The pathogen can die in the stomach under the influence of the bactericidal properties of gastric juice and even in the lymphoid formations of the small intestine. Having overcome the gastric barrier, the pathogen enters the small intestine, where it reproduces, is fixed by solitary and group lymphoid follicles with further accumulation of the pathogen, which penetrates the mesenteric lymph nodes through the lymphatic vessels. These processes are accompanied by inflammation of the lymphoid elements of the small intestine, and often the proximal colon, lymphangitis and mesadenitis. They develop during the incubation period, at the end of which the pathogen breaks into the bloodstream and bacteremia develops, which becomes more intense every day. Under the influence of bactericidal blood systems, the pathogen is lysed, LPS is released and an intoxication syndrome develops, which is manifested by fever, damage to the central nervous system in the form of adynamia, lethargy, sleep disorders, damage to the autonomic nervous system, characterized by pale skin, decreased heart rate, intestinal paresis and stool retention. This period approximately corresponds to the first 5-7 days of the disease. Inflammation of the lymphoid elements of the intestine reaches its maximum and is characterized as cerebral swelling.
Bacteremia is accompanied by seeding of internal organs, primarily the liver, spleen, kidneys, bone marrow, where specific inflammatory granulomas are formed. This process is accompanied by increasing intoxication and the appearance of new symptoms: hepatosplenomegaly, increased neurotoxicosis, characteristic changes in the blood picture. Simultaneously, there is stimulation of phagocytosis, synthesis of bactericidal antibodies, specific sensitization of the body, and a sharp increase in the release of the pathogen into the environment through bile and the urinary system. Sensitization is manifested by the appearance of a rash, the elements of which are a focus of hyperergic inflammation at the site of accumulation of the pathogen in the vessels of the skin. Repeated penetration of the pathogen into the intestine causes a local anaphylactic reaction in the form of necrosis of lymphoid formations.
In the third week, a tendency toward a decrease in the intensity of bacteremia is noted. Organ lesions persist. In the intestine, necrotic masses are rejected and ulcers are formed, the presence of which is associated with typical complications of typhoid fever - perforation of ulcers with the development of peritonitis and intestinal bleeding. It should be emphasized that disorders in the hemostasis system play a significant role in the development of bleeding.
On the 4th week, the intensity of bacteremia decreases sharply, phagocytosis is activated, granulomas in the organs regress, intoxication decreases, and body temperature decreases. Ulcers in the intestines are cleared and begin to heal, the acute phase of the disease ends. However, due to the imperfection of phagocytosis, the pathogen can persist in the cells of the monocytic phagocyte system, which, with an insufficient level of immunity, leads to exacerbations and relapses of the disease, and in the presence of immunological deficiency - to chronic carriage, which in typhoid fever is considered a form of infectious process. In this case, the pathogen penetrates from the primary foci in the monocytic phagocyte system into the blood, and then into the bile and urinary system with the formation of secondary foci. In these cases, chronic cholecystitis and pyelitis are possible.
Immunity to typhoid fever is long-lasting, but there are repeated cases of the disease after 20-30 years. Due to the use of antibiotic therapy and insufficient strength of immunity, repeated cases of the disease occur at an earlier date.