What causes typhoid fever in adults?
Last reviewed: 23.04.2024
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
Causes of typhoid fever
The cause of typhoid fever is Salmonella typhi, which belongs to the genus Salmonella, the serological group D, to the enterobacteriaceae family of intestinal bacteria.
S. Typhi has the shape of a rod with rounded ends, spores and capsules do not form, mobile, gram-negative, better grows 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 is relatively well preserved at low temperatures, sensitive to heating: at 56 ° C it dies within 45-60 minutes, at 60 ° C after 30 minutes, at boiling in a few seconds (at 100 ° C almost instantaneously). A favorable environment for bacteria - food products (milk, sour cream, cottage cheese, minced meat, jelly), in which they are not only preserved, but also capable of reproduction.
[Pathogenesis of typhoid fever
The pathogenesis of typhoid fever is characterized by the cyclicity and development of certain pathophysiological and morphological changes. Infection occurs through the mouth, and the primary site of localization of pathogens is the digestive tract. Particularly it should be noted that infection does not always lead to the development of the disease. The causative agent may die in the stomach under the influence of the bactericidal properties of the gastric juice and even in the lymphoid formations of the small intestine. Overcoming the gastric barrier, the pathogen enters the small intestine, where its multiplication occurs, fixation by solitary and group lymphoid follicles with further accumulation of the pathogen, which penetrates the lymphatic vessels into the mesenteric lymph nodes. These processes are accompanied by inflammation of the lymphoid elements of the thin, and often proximal part of the large intestine, lymphangitis and mesadenitis. They develop during the incubation period, at the end of which the causative agent breaks into the bloodstream and bacteremia develops, which becomes more intense with each passing day. Under the influence of bactericidal blood systems, the pathogen lyses the pathogen, releases LPS and develops an intoxication syndrome, which is manifested by fever, CNS damage in the form of adynamia, inhibition, sleep disorders, vegetative nervous system damage characterized by pale skin, decreased heart rate, bowel paresis and stool retention . This period roughly corresponds to the first 5-7 days of the disease. Inflammation of the lymphoid elements of the intestine reaches a maximum and is characterized as a cerebral swelling.
Bacteremia accompanies the seeding of internal organs, especially the liver, spleen, kidneys, bone marrow, in which specific inflammatory granulomas are formed. This process is accompanied by an increase in intoxication and the appearance of new symptoms: hepatosplenomegaly, increased neurotoxicosis, characteristic changes in the blood picture. At the same time, phagocytosis stimulates, the synthesis of bactericidal antibodies, a specific sensitization of the organism, sharply increases excretion into the environment through bile and urinary system. Sensitization is manifested by the appearance of a rash, the elements of which are the focus of hyperergic inflammation in the place of aggravation 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 to decrease the intensity of bacteremia is noted. Organ damage remains. In the intestine, necrotic masses are rejected and ulcers are formed, with the presence of which typical typhoid fever complications are associated with perforation of ulcers with the development of peritonitis and intestinal bleeding. It should be emphasized that violations in the hemostatic system play an important role in the development of bleeding.
At week 4, the intensity of bacteremia sharply decreases, phagocytosis is activated, granulomas in organs regress, intoxication decreases, body temperature decreases. Purification of ulcers in the intestine occurs and their scarring begins, the acute phase of the disease ends. However, due to the imperfection of phagocytosis, the causative agent can persist in the cells of the monocytic phagocyte system, which, with insufficient level of immunity, leads to exacerbations and relapses of the disease, and in the presence of immunological insufficiency, to chronic carrier, which in typhoid fever is considered a form of the infectious process. In this case, from the primary foci in the system of monocytic phagocytes, the causative agent penetrates into the blood, and then into the bile and urinary system with the formation of secondary foci. In these cases chronic cholecystitis, pyelitis, is possible.
Immunity with typhoid fever is long, but there are repeated cases of the disease in 20-30 years. In connection with the use of antibiotic therapy and the lack of immunity, repeated cases of the disease occur at an earlier time.