Typhoid fever diagnosis treatment. Complications after infectious diseases

Typhoid fever is an acute anthroponotic infectious disease with a fecal-oral transmission mechanism, characterized by a cyclic course, intoxication, bacteremia, and ulcerative lesions of the lymphatic apparatus of the small intestine.

ICD code -10 A01.0. Typhoid fever.

Etiology (causes) of typhoid fever

Pathogen - Salmonella typhi, belongs to the genus Salmonella, serogroup D, family of intestinal bacteria Enterobacteriaceae.

S. typhi is rod-shaped with rounded ends, does not form spores or capsules, is motile, gram-negative, grows best 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 and is sensitive to heat: at 56°C it dies within 45–60 min, at 60°C after 30 min, and upon boiling in a few seconds (almost instantly at 100°C). 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.

Epidemiology

Typhoid fever belongs to the group of intestinal infections and typical anthroponoses.

Source of infection in typhoid fever - only a person - a patient or a bacterio-excretor, from whose body the causative agents of typhoid fever are excreted into the external environment, mainly with feces, less often with urine. With feces, the pathogen is excreted from the first days of the disease, but massive excretion begins after the seventh day, reaches a maximum at the height of the disease and decreases during the period of convalescence. In most cases, bacterial excretion lasts no more than 3 months (acute bacterial excretion), but in 3–5% chronic intestinal or, less commonly, urinary bacterial excretion is formed. Urinary carriers are the most dangerous in epidemiological terms due to massive bacterial excretion.

characteristic of typhoid fever fecal-oral transmission mechanism pathogen, which can be carried out by water, food and contact-household way. Transmission of the causative agent of typhoid fever through water, which prevailed in the past, plays a significant role at the present time. Water epidemics grow violently, but quickly end when they stop using the contaminated water source. If epidemics are associated with the consumption of water from a contaminated well, the diseases are usually focal in nature.

Sporadic diseases are currently often caused by the use of water from open reservoirs and technical water used in various industrial enterprises. There may be outbreaks associated with the use of foodstuffs in which typhoid bacteria can persist and multiply for a long time (milk). Infection can also occur by contact-household way, in which surrounding objects become transmission factors. Susceptibility to typhoid fever is significant.

The contagiousness index is 0.4. Most often, people aged 15 to 40 get sick.

After the disease, a stable, usually lifelong immunity is developed, however, in recent years, due to the antibiotic therapy of patients and its immunosuppressive effect, apparently, the intensity and duration of the acquired immunity have become less, as a result of which the frequency of repeated typhoid infections has increased.

Typhoid fever during epidemic spread is characterized by summer-autumn seasonality.

Measures to prevent typhoid fever

Specific

According to epidemiological indications (morbidity is higher than 25 per 100 thousand population).

of the population, travel to countries with a high incidence, constant contact with a bacteriocarrier under conditions conducive to infection) are vaccinated with typhoid alcohol dry vaccine♠ (Tifivak♠). The vaccine is used at the age of 15-55 years. It is administered subcutaneously at a dose of 0.5 ml, the second vaccination after 1 month at a dose of 1 ml, revaccination after 2 years at a dose of 1 ml. From the age of 3, the typhoid Vi-polysaccharide liquid vaccine♠ (Vianvac♠) is used at a dose of 0.5 ml subcutaneously once. Revaccination at the same dose after 3 years.

Non-specific

Non-specific prevention includes control over water supply, disinfection of drinking water, disinfection of wastewater, compliance with the rules for the preparation, storage and sale of food, personal hygiene, sanitary and educational work with the population, improvement of residential areas. Employees of food enterprises, children's institutions are examined upon admission to work in order to timely identify carriage (bacteriological examination of feces, RPHA with O- and Vi-diagnosticums).

An epidemiological survey is carried out in the focus of typhoid fever in order to identify the source of the pathogen and transmission factors. For each case of illness, an emergency notification is sent to the Sanitary and Epidemiological Supervision authorities. Patients are hospitalized. The final disinfection is carried out in the hearth. Contact persons are monitored for 21 days, they are examined for bacteriocarrier.

Employees of food and children's institutions, as well as children attending them, are not allowed into them until the results of the examination (bacteriological examination of feces, RPHA with Vi-antigen) are received.

The 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 entail 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 multiplies, fixes by solitary and group lymphoid follicles with further accumulation of the pathogen, which penetrates through the lymphatic vessels into the mesenteric lymph nodes. These processes are accompanied by inflammation of the lymphoid elements of the small, 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, CNS damage in the form of adynamia, lethargy, sleep disturbances, damage to the autonomic nervous system, characterized by pallor of the skin, a decrease in heart rate, intestinal paresis and stool retention . This period roughly corresponds to the first 5-7 days of illness. Inflammation of the lymphoid elements of the intestine reaches a maximum and is characterized as a cerebral swelling.

Bacteremia is accompanied by seeding of internal organs, primarily the liver, spleen, kidneys, bone marrow, and specific inflammatory granulomas are formed in them. This process is accompanied by an increase in intoxication and the appearance of new symptoms: hepatosplenomegaly, increased neurotoxicosis, and characteristic changes in the blood picture. At the same time, stimulation of phagocytosis, synthesis of bactericidal antibodies, specific sensitization of the body occur, the release of the pathogen into the environment through the bile and urinary system increases sharply. 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 trend towards a decrease in the intensity of bacteremia is noted. Organ lesions persist. In the intestine, necrotic masses are rejected and ulcers are formed, with the presence of which typical complications of typhoid fever are associated - perforation of ulcers with the development of peritonitis and intestinal bleeding. It should be emphasized that disturbances in the hemostasis system play a significant role in the development of bleeding.

On the 4th week, the intensity of bacteremia sharply decreases, phagocytosis is activated, granulomas in organs regress, intoxication decreases, and body temperature decreases. There is a cleansing of ulcers in the intestines and their scarring begins, 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 as a form of infectious process. At the same time, from the primary foci in the system of monocytic phagocytes, the pathogen penetrates into the blood, and then into the bile and urinary system with the formation of secondary foci. In these cases, chronic cholecystitis, pyelitis are possible.

Immunity in typhoid fever is long, but there are repeated cases of the disease after 20-30 years. In connection with the use of antibiotic therapy and insufficient strength of immunity, repeated cases of the disease occur at an earlier date.

Clinical picture (symptoms) of typhoid fever

The incubation period is from 3 to 21, more often 9–14 days, which depends on the dose of the infective infection, its virulence, the route of infection (shorter for food and longer for infection through water and direct contact) and the state of the macroorganism.

Classification

By the nature of the flow: - typical; - atypical (erased, abortive, outpatient; rare forms: pneumotyphoid, meningotif, nephrotif, colotif, typhoid gastroenteritis).

By duration: - acute; - with exacerbations and relapses.

According to the severity of the course: - light; - moderate; - heavy.

By the presence of complications: - uncomplicated; - complicated: - specific complications (intestinal bleeding, intestinal perforation, ITSH), - non-specific (pneumonia, mumps, cholecystitis, thrombophlebitis, otitis media, etc.).

The main symptoms of typhoid fever and the dynamics of their development

The initial period of typhoid fever characterized by gradual or acute development of intoxication syndrome. In the modern course, both options are almost equally common.

With a gradual increase in symptoms in the first days, patients note increased fatigue, increasing weakness, chilling, worsening headache, worsening or lack of appetite.

The body temperature rises in steps and reaches 39–40 °C by the 5–7th day of illness. With an acute onset, already in the first 2-3 days, all the symptoms of intoxication reach full development, i.e. the duration of the initial period is reduced, resulting in diagnostic errors and late hospitalization.

When examining patients in the initial period of the disease, some lethargy and adynamia attract attention. Patients are indifferent to the environment, they answer questions in monosyllables, not immediately. The face is pale or slightly hyperemic, sometimes slightly pasty. With a shorter incubation, a more rapid onset of the disease is more often noted.

Changes in the cardiovascular system in the initial period are characterized by relative bradycardia, arterial hypotension. Some patients report coughing or nasal congestion. Auscultatory over the lungs often listen to hard breathing and scattered dry rales, which indicates the development of diffuse bronchitis.

The tongue is usually thickened, with imprints of teeth on the lateral surfaces. The back of the tongue is covered with a massive grayish-white coating, the edges and tip are free from plaque, have a rich pink or red color. The pharynx is slightly hyperemic, sometimes there is an increase and hyperemia of the tonsils. The abdomen is moderately swollen.

Palpation in the right iliac region determines coarse, large-caliber rumbling in the caecum and small-caliber rumbling and pain along the terminal ileum, indicating the presence of ileitis. Determine the shortening of percussion sound in the ileocecal region (Padalka's symptom), which is due to hyperplasia, the presence of mesadenitis. This is also evidenced by the positive "cross" symptom of Sternberg. Stool with a tendency to constipation. By the end of the 1st week, the disease increases and the liver and spleen become available for palpation.

The hemogram in the first 2–3 days is characterized by moderate leukocytosis, and from the 4–5th day of the disease, leukopenia with a shift to the left is determined; their degree depends on the severity of the disease. In addition, aneosinophilia, relative lymphocytosis and thrombocytopenia are observed. ESR is moderately increased. These changes in the hemogram are a natural consequence of the specific effect of Salmonella typhoid toxins on the bone marrow and the accumulation of leukocytes in the lymphatic formations of the abdominal cavity. Note oliguria. Changes in the urogram are determined: proteinuria, microhematuria, cylindruria, which fit into the syndrome of "infectious-toxic kidney".

All symptoms of the disease reach their maximum development by the end of the first - the beginning of the second week, when the peak of the disease begins. This period lasts from several days to 2-3 weeks and is the most difficult for the patient. With the modern course, this period of the disease is much shorter and easier, it is characterized by an increase in intoxication and high fever, changes in the central nervous system. The patients are in a state of stupor. In severe cases, they do not orient themselves in place and time, they do not recognize others well, they are drowsy during the day and do not sleep at night, they do not complain about anything, sometimes they are delirious. These changes in the neuropsychic state characterize the typhoid status, which is rare in the modern course.

In some patients, in the second week of the disease, small ulcerations occur on the anterior palatine arches - Duguet's tonsillitis. The body temperature during this period is increased to 39-40 ° C and in the future it may have a constant or undulating character.

In 55–70% of patients with typhoid fever, on the 8–10th day of illness, a characteristic exanthema occurs on the skin - pinkish-red roseola with a diameter of 2–3 mm, located mainly on the skin of the abdomen and lower chest, and in cases of profuse rash covering the limbs . The rash is monomorphic; usually scarce; the number of elements rarely exceeds 6–8. Roseolas often rise slightly above the level of the skin (roseola elevata) and are clearly visible against its pale background. When the skin is pressed or stretched along the edges of the roseola, they disappear, after which they reappear, which indicates their inflammatory nature. In severe forms, the rash may become petechial. The duration of the existence of roseola is from 1 to 5 days, more often 3-4 days. After the disappearance of the rash, a barely noticeable pigmentation of the skin remains. The phenomenon of sprinkling is characteristic, which is associated with an undulating course of bacteremia. Roseola can also appear in the first days of the convalescence period at normal temperatures.

In some patients, a symptom of Filippovich is found - icteric staining of the skin of the palms and soles of the feet - endogenous carotene hyperchromia of the skin, which occurs due to the fact that the conversion of carotene to vitamin A is disturbed as a result of liver damage.

At the height of the disease, relative bradycardia persists, pulse dicrotia occurs, arterial and venous pressure decreases even more, auscultatory - deafness of heart sounds, a coarse systolic murmur is heard at the apex and base of the heart.

In patients with typhoid fever, a decrease in vascular tone is observed, and in 1.4% of patients - acute vascular insufficiency. Sudden tachycardia may indicate complications: intestinal bleeding, intestinal perforation, collapse - and has a poor prognostic value.

Changes in the respiratory organs in this period are expressed by the phenomena of bronchitis. Pneumonia is also possible, caused both by the causative agent of typhoid fever itself and by the accompanying microflora.

Changes in the digestive system at the height of the disease reach their maximum severity. The lips are dry, often covered with crusts, with cracks. The tongue is thickened, densely coated with a gray-brownish coating, the edges and tip of its bright red color with imprints of teeth ("typhoid", "fried" tongue). In severe cases, the tongue becomes dry and takes on a fulginous appearance due to the appearance of bleeding transverse cracks. Dryness of the tongue is a sign of damage to the autonomic nervous system. Belly swollen. Stool retention is noted, in some cases it is liquid, greenish in color, sometimes in the form of "pea soup". Rumbling and soreness on palpation of the ileocecal intestine, a positive symptom of Padalka, become distinct. The liver and spleen are enlarged. Sometimes there is cholecystitis, and in women it happens more often.

At the height of the disease, the amount of urine decreases. Determine proteinuria, microhematuria, cylindruria. There is bacteriuria, which sometimes leads to pyelitis and cystitis. In some cases, mastitis, orchitis, epididymitis, dysmenorrhea may develop, in pregnant women - premature birth or abortion.

During the height of the disease, such dangerous complications as perforation of typhoid ulcers and intestinal bleeding can occur, which occur respectively in 1–8% and 0.5–8% of patients with typhoid fever.

Disease resolution period does not exceed one week and is characterized by a decrease in temperature, which often acquires an amphibolic character before normalization, i.e. daily fluctuations reach 2.0–3.0 °С. Headache disappears, sleep normalizes, appetite improves, tongue is cleansed and moistened, diuresis increases.

With the modern course of typhoid fever, the temperature often decreases with a short lysis without an amphibolic stage. However, a normal temperature should not be taken as a sign of recovery. Weakness, increased irritability, mental lability, and weight loss persist for a long time. Subfebrile temperature is possible as a result of vegetative-endocrine disorders. In this period, there may be late complications: thrombophlebitis, cholecystitis.

Subsequently, the disturbed functions are restored, the body is freed from pathogens. This is a period of recovery, which is characterized by asthenovegetative syndrome within 2-4 weeks. During the recovery period, 3-5% of those who have had typhoid fever become chronic bacterial carriers.

Exacerbations and relapses. On the decline of the disease, but even before the temperature returns to normal, exacerbations are possible, characterized by a delay in the infectious process: fever and intoxication increase, fresh roseolas appear, and the spleen enlarges. Exacerbations are more often single, and with improper treatment and repeated. In conditions of antibiotic therapy and with the current course of the disease, exacerbations are rarely observed.

Relapses, or the return of the disease, occur already at normal temperature and the disappearance of intoxication. In modern conditions, the frequency of relapses has increased, which, apparently, can be associated with the use of chloramphenicol, which has a bacteriostatic effect, and especially glucocorticoids.

Precursors of relapse - subfebrile condition, preservation of hepatosplenomegaly, aneosinophilia, low level of antibodies. The clinical picture of recurrence, repeating the picture of typhoid fever, is still distinguished by a milder course, a faster rise in temperature, an early appearance of a rash, and less pronounced symptoms of general intoxication. Their duration is from one day to several weeks; two, three recurrences and more are possible.

Complications of typhoid fever

Intestinal bleeding often occurs at the end of the second and third weeks of illness. It can be profuse and insignificant, depending on the size of the ulcerated blood vessel, the state of blood clotting, thrombosis, blood pressure, etc. In some cases, it has the character of capillary bleeding from intestinal ulcers.

Some authors indicate that a transient increase in blood pressure, the disappearance of dicrotia of the pulse, increased heart rate, a critical drop in temperature, and diarrhea make one fear intestinal bleeding. Bleeding is promoted by flatulence and increased intestinal peristalsis.

A direct sign of bleeding is melena (tarry stools). Sometimes in the stool, the presence of scarlet blood is noted. General symptoms of internal bleeding are pallor of the skin, a drop in blood pressure, an increase in heart rate, a critical decrease in body temperature, which is accompanied by a clarification of consciousness, activation of the patient and creates the illusion that his condition has improved. With massive bleeding, hemorrhagic shock may develop, which has a serious prognosis. Due to a decrease in the volume of circulating blood due to the deposition of blood in the celiac vessels, patients are very sensitive to blood loss and general symptoms of bleeding may appear when blood loss is much less than in healthy people. The most dangerous bleeding from the colon. Bleeding can be single and repeated - up to six times or more, due to blood clotting disorders, it can last for several hours.

A more formidable complication is intestinal perforation, which occurs in 0.5–8% of patients. Observations indicate that there is no relationship between anatomical changes and the severity of intoxication, so it is difficult to predict the development of perforation. It most commonly occurs in the terminal ileum, approximately 20 to 40 cm from the ileocecal valve. Usually there is one (rarely two or three or more) perforated holes up to a two-ruble coin in size. Occasionally, perforation occurs in the large intestine, gallbladder, appendix, the lymphatic apparatus of which is actively involved in the inflammatory process. Perforations are usually single, but they occur three- and five-fold, and they occur more often in men.

Clinical manifestations of perforation - acute pain in the abdomen, localized in the epigastric region somewhat to the right of the midline, muscle tension in the abdominal press, a positive symptom of Shchetkin-Blumberg.

The pulse is frequent, of weak filling, the face turns pale, the skin is covered with cold sweat, breathing is quickened, in some cases severe collapse is noted. The most important clinical signs of intestinal perforation are pain, muscular protection, flatulence, and disappearance of peristalsis. Pain, especially “dagger”, is not always pronounced, especially in the presence of typhoid status, which is why doctors often make mistakes in making a diagnosis.

Important symptoms are flatulence with hiccups, vomiting, dysuria, and absence of hepatic dullness. Regardless of the intensity of pain in patients, local muscle stiffness in the right iliac region is determined, but as the process progresses, tension in the abdominal muscles becomes more common and pronounced.

Flatulence, increased peristalsis, and abdominal trauma contribute to intestinal perforation. The development of peritonitis is also possible with deep penetration of typhoid ulcers, with necrosis of the mesenteric lymph nodes, suppuration of the spleen infarction, typhoid salpingitis. Contribute to the development of intestinal bleeding and perforation late hospitalization and late started specific therapy.

The picture of perforation and peritonitis against the background of antibiotic therapy is often erased, so even mild abdominal pain should attract the attention of a doctor, and an increase in fever, intoxication, flatulence, tachycardia, blood leukocytosis, even in the absence of local symptoms, indicate the development of peritonitis.

In 0.5–0.7% of patients, as a rule, TSS develops during the peak of the disease.

The clinical picture of TSS is characterized by a sudden sharp deterioration, chills, hyperthermia, confusion, arterial hypotension, leuko- and neutropenia. The skin becomes pale, wet, cold, cyanosis, tachycardia increase, DN ("shock lung"), oliguria develop. In the blood, azotemia is noted (the concentration of urea and creatinine increases).

Mortality and causes of death

When treated with antibiotics, mortality is less than 1%, the main causes of death are peritonitis, TSS.

Diagnosis of typhoid fever

Diagnosis of typhoid fever is based on epidemiological, clinical and laboratory data.

Clinical diagnostics

Of the epidemiological data, contact with febrile patients, the use of undisinfected water, unwashed vegetables and fruits, unboiled milk and dairy products made from it and purchased from private individuals, food in public catering establishments with signs of sanitary problems, and a high incidence of intestinal infections at the place of stay are significant. sick. Of the clinical data, the most important are high fever, roseolous rash, weakness, a characteristic appearance of the tongue, flatulence, enlargement of the liver and spleen, stool retention, lethargy, sleep disturbance, headache, anorexia. All patients with fever of unknown origin should be examined on an outpatient basis for typhoid fever.

Specific and non-specific laboratory diagnostics

The most informative method is the isolation of the pathogen's blood culture.

A positive result can be obtained throughout the febrile period, but more often at the onset of the disease. Blood cultures should be performed for 2-3 days daily, the first time - preferably before the appointment of antimicrobials. Blood is taken in an amount of 10–20 ml and inoculated into 100–200 ml of Rappoport medium or bile broth, respectively. From the second week of illness until recovery, it is possible to isolate copro-, urine- and bilioculture, however, with a positive result of the study, the possibility of chronic carriage should be excluded. The study of bile is carried out on the tenth day after the normalization of body temperature. Crops of these substrates, as well as roseola scarificat, sputum, CSF are produced on selective media (bismuth sulfate agar, Ploskirev media, Endo and Levin agars). The preliminary result of a bacteriological study can be obtained in two days, the final result, including the determination of sensitivity to antibiotics and phage typing, in 4–5 days.

To confirm the diagnosis, RA (Vidal reaction) is also used, as well as a more sensitive and specific RNHA with H-, O- and Vi-antigen, which almost completely replaced the Vidal reaction. The study is carried out upon admission and after 7-10 days. A four-fold increase in the titer of O-antibodies or a titer of 1:200 and above is of diagnostic value. A positive reaction with the H-antigen indicates a previous illness or vaccination, with the Vi-antigen - a chronic typhoid carriage. In recent years, ELISA has also been used to diagnose typhoid fever.

Differential Diagnosis

Differential diagnosis is carried out with many diseases that occur with fever; more often with influenza, pneumonia, adenovirus infection, as well as with malaria, brucellosis, leptospirosis, ornithosis, rickettsiosis, trichinosis, a generalized form of yersiniosis, sepsis, miliary tuberculosis (Table 17-1).

Table 17-1. Differential diagnosis of typhoid fever

sign	Nosological form
	typhoid fever	flu	pneumonia	adenovirus infection	miliary tuberculosis	malaria
Seasonality	Summer-autumn	Winter	cold season	Autumn-winter	Absent	May–September
Chills	Rarely	Often	Often	not typical	Character-teren	Character-teren
Headache	Moderate	strong	Moderate	Weak	Moderate	strong
Algia	not typical	Expressed	Moderate	Possible	Possible	expression-wives
Duration of fever	4–6 days, 5–6 weeks	Up to 5–6 days	3–7 days	3–14 days	Long-term	Up to 3–4 weeks
Maximum fever (term)	2nd week	1–2 days	3rd–5th day	Indefined	Indefined	During an attack
Cough	Dry, sparse	Dry then productive	Dry then productive	Dry, productive	Dry	Not typical
Dyspnea	Not typical	Possible	characteristic	Not typical	Character-thorn	During an attack
Skin on the face	pale	Hyper-micable	Hyper-micable	Not changed	pale	Hyperactive during an attack
Conjunctiva, sclera	Not changed	Scleritis, conjunctivitis	conjunctival injection	membranous conjunctivitis	No characteristic changes	Scleritis, conjunctivitis
Lymph nodes	not enlarged	not enlarged	not enlarged	Enlarged	Possible poly-adenopathy	not enlarged
Physical data		Harsh breathing, occasional dry wheezing	Percussion sound shortening, moist rales, crepitus	Harsh breathing, dry wheezing	Harsh breathing, isolated dry and wet rales	Changes are not typical
Heart rate	Relative bradycardia	Relative bradycardia	Tachycardia	Changes are not typical	Tachycardia	Tachycardia
Hepato-spleno-megaly	typical	Not watching	Rarely	Often	Possible	Constantly
blood picture	Leuko- and neutropenia with a shift to the left, aneosinophilia, relative lymphocytosis	Leuko-singing, lymphocytosis	Neutrophilic leukocytosis with a shift to the left, an increase in ESR	non-specific	Non-specific	Anemia, leuco-singing

Indications for consulting other specialists

Consultation of the surgeon - with the development of intestinal bleeding or intestinal perforation.

Diagnosis example

A01.0. Typhoid fever, severe. Complication: intestinal bleeding.

Treatment for typhoid fever

Modern treatment of patients with typhoid fever is based on the complex use of etiotropic and pathogenetic therapy (Table 17-2).

Table 17-2. The scheme of treatment of patients with typhoid fever

The main directions of therapeutic measures	Preparations, schemes of application
diet therapy	The whole feverish period - table 4A, then 4, 2 and 13
Antibacterial therapy	Due to the wide spread of S. typhi strains resistant to chloramphenicol, ampicillin, co-trimoxazole, fluoroquinolones have become the drugs of choice: ciprofloxacin 0.5–0.75 g twice a day after meals; ofloxacin 0.2–0.4 g twice a day orally or intravenously; pefloxacin 0.4 g twice a day orally or intravenously. Highly effective ceftriaxone (alternative drug) 1.0–2.0 g IV once a day. Antibiotic therapy is carried out until the 10th day after the normalization of body temperature
Immunotherapy - according to indications (prolonged bacterial excretion, exacerbations, relapses)	Pentoxyl®, metacil, thymogen®, typhoid vaccine
Detoxification therapy - according to indications (typhoid status, arterial hypotension, hyperthermia and other manifestations of intoxication)	Intravenous Ringer's solution®, 5% glucose solution®, reopoliglyukin®, Reamberin®, etc.
Vitamin therapy, antioxidant therapy according to individual indications	Ascorbic acid - for 20-30 days, 0.05 g three times a day; cytochrome C - 5 ml intravenously, vitamin E 0.05-0.1 g / day, aevit® - 1 capsule (0.2 ml) three times a day, unithiol® - 0.25-0, 5 g daily or every other day

According to federal standards, the volume of medical care provided to patients with typhoid fever, the average duration of hospitalization for patients with mild form is 25 days, moderate - 30 days, severe - 45 days.

Therapy of patients with typhoid fever, in accordance with federal standards, is carried out in the following areas: antibacterial, detoxifying and plasma-substituting solutions, desensitizing agents, vitamin therapy, antispasmodics, biological products, symptomatic agents, amino acids, sugars and preparations for parenteral nutrition, hormones and their analogues (according to indications) (see Table 17-2).

Until the sixth or seventh day of normal temperature, the patient must observe bed rest, from the seventh to eighth day they are allowed to sit, and from the tenth to eleventh day of normal temperature, in the absence of contraindications, they are allowed to walk.

Patients are discharged from the hospital after clinical recovery, but not earlier than 21–23 days from the moment the temperature returns to normal and after receiving a double negative bacteriological examination of feces and urine and a single one of duodenal contents.

Forecast

In the pre-antibiotic period, mortality in typhoid fever was 3-20%, with modern therapy - 0.1-0.3%.

Clinical examination

Those who have been ill with typhoid fever, regardless of profession and employment after discharge from the hospital, are subject to dispensary observation in the KIZ polyclinic for 3 months. For timely detection of recurrence, convalescents are subjected to medical observation with thermometry once a week for the first 2 months and once every 2 weeks for the 3rd month.

In all those who have been ill with typhoid fever (except for workers in food enterprises and persons equated to them), during a 3-month dispensary observation, a single bacteriological examination of feces and urine is performed monthly, and by the end of the third month, bile culture and a Vi-hemagglutination reaction are additionally performed. Further, these persons are registered with the sanitary and epidemiological supervision authorities for two years. During this period, they have bacteriological examination of feces and urine twice a year, and at the end of the observation period - bile culture. If the results of bacteriological studies are negative, those who have been ill are removed from the register.

Convalescents of typhoid fever among employees of food enterprises and persons equated to them are not allowed to work in their specialty for a month after discharge from the hospital. At this time, in addition to medical supervision, it is necessary to carry out a five-fold bacteriological examination of feces and urine with an interval of 1–2 days, a single bile culture and a Vi-hemagglutination test.

Persons with a positive Vi-hemagglutination reaction are not allowed to work. They conduct an additional bacteriological examination of discharge at least five times and bile - once. Only with negative results of bacteriological examination and good health, such convalescents are allowed to work in their specialty.

Upon receipt of negative results, convalescents are allowed to work in food and equivalent institutions with a mandatory monthly bacteriological examination of feces and urine for a year and by the end of the third month - with bile culture and a Vi-hemagglutination test.

Subsequently, these persons are registered with the KIZ for 5 years with a quarterly bacteriological examination of feces and urine, and then throughout their entire working life they annually perform a bacteriological examination of feces and urine twice.

Chronic bacteriocarriers of typhoid microbes stay for life on the account of the sanitary-epidemiological supervision bodies and in the KIZ and are subjected to bacteriological examination and clinical examination twice a year.

Convalescents of typhoid fever are on the same register and are subject to a similar examination, in whom typhoid microbes were isolated from bile during their stay in the hospital. Chronic bacteria carriers, as well as persons living with them, are suspended from work at food industry, catering and trade enterprises, in medical, sanatorium and resort institutions, pharmacies, etc.

Reminder for patients

Rational employment of convalescents is recommended for 2-3 months with exemption from hard physical labor, sports, business trips. Diet food for a period of 2-3 months with the exception of spicy foods, alcohol, animal fats, compliance with the diet and personal hygiene rules.

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Typhoid fever (typhus abdominalis) is an acute infectious disease characterized by damage to the lymphatic apparatus of the intestine (mainly the small intestine), severe intoxication, bacteremia, enlargement of the liver and spleen, often with a roseolous rash. According to clinical manifestations and pathogenesis, it is similar to the infectious disease paratyphoid A and B (paratyphus abdominalis A et B).

Etiology

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The causative agent of typhoid fever- bacteria Salmonella typhi,

Genus - Salmonella,
Serological group - D,
Family - Enterobacteriaceae (intestinal bacteria)

Morphology. The shape is short sticks measuring (0.5–0.8) x (1.5–3) µm with rounded ends. There are filtering and L forms. They have flagella located peritracheally due to which they are mobile.
Spores and capsules do not form.

Antigenic structure.
Somatic (thermostable) O antigen lipopolysaccharide-protein complex, identical to endotoxin,
- Flagella (thermolabile) H antigen superficial, shell, capsular
— Somatic thermolabile Viantigen, which is located more superficially on the O antigen.
Bacteria that are antigenically complete and include O-, H- and Vi-antigens are released only at the height of the disease, and during the period of convalescence the Vi-antigen is lost. Vi-antigen is also lost during subculturing in the laboratory.

toxin formation
When bacteria are destroyed, endotoxins are formed that cause general intoxication of the body (bacteremia and toxinemia phase).
The resulting endotoxins have pronounced neurotropic properties. They affect the central nervous system (CNS), in severe cases they can cause status typhosus. The autonomic nervous system is also affected, leading to the appearance of symptoms of vagotonia (the predominance of the tone of the parasympathetic nervous system over the tone of its sympathetic part). Endotoxins contribute to the development of trophic disorders, flatulence, and abdominal pain.

Stability in the external environment
In soil and water, depending on environmental conditions, typhoid bacteria remain alive from several days to several months, sometimes up to a year. Food products (minced meat, jelly, sour cream, milk, cottage cheese) are a favorable environment in which they not only remain, but can also multiply. Typhoid bacteria tolerate low temperatures well, but die when heated (after 30 minutes at 60°C, almost instantly at 100°C). Disinfectants at normal concentrations kill typhoid pathogens within minutes.

Pathogenicity for animals. Typhoid fever only affects humans.

Epidemiology

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source of infection typhoid is only a person - sick or carrier. In the external environment, pathogens are excreted along with saliva, urine and feces. After the 7th day of the disease, a massive excretion of bacteria from the patient's body begins and reaches a maximum at the height of the disease, decreases during the period of convalescence. In most cases, the isolation of typhoid bacteria is completed within 3 months (acute bacterial excretion). Sometimes the excretion of bacteria continues for life (chronic bacterial excretion). Chronic carriers (bacteria excretors) are the main sources of typhoid infection.

For typhoid fever characteristically seasonal, summer autumn, increased incidence.
The most frequently ill people aged 15–45, predominantly men.

mechanism of infection. Typhoid fever is characterized by a fecal-oral infection mechanism, which is carried out by contact, water and food transmission routes of infection.

contact mechanism - non-compliance with the rules of personal hygiene in direct contact with patients and with objects of its use.
water mechanism - the use of contaminated water: from open reservoirs, from a polluted well, industrial water, etc. Water epidemics develop rapidly and quickly fade away after the cessation of use of a contaminated water source.
food mechanism — eating contaminated food. Insects, in particular flies, play a special role in food contamination.

Immunity. Innate immunity to infections caused by typhoid pathogens does not exist. After the transfer of infection, stable immunity is maintained, but cases of repeated diseases are known.

Pathogenesis and pathological anatomical picture

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Phase of infection (invasion). When it enters the mouth and overcomes the protective barriers of the upper digestive tract, typhoid bacteria enter the small intestine.

Phase of bacteremia and toxinemia. As a result of a violation of the permeability of the hematolymphatic barrier, bacteria enter the bloodstream, bacteremia develops, which coincides with the onset of the febrile period of the disease. When some of the bacteria die under the influence of the bactericidal properties of the blood and due to phagocytosis by the cells of the macrophage system, endotoxins are released, causing general intoxication of the body. Possessing pronounced neurotropic properties, they have a damaging effect on the central nervous system and, in severe cases, can cause status typhosus. The defeat of the autonomic nervous system leads to the appearance of symptoms of vagotonia, the development of flatulence, abdominal pain, and trophic disorders.

Phase of parenchymal dissemination. Part of the bacteria circulating in the blood is absorbed by SMF cells, but they remain viable and multiply in them. Corresponding clinical signs appear - damage to internal organs and exanthemia.

excretory allergic phase. From the moment the infection develops, a protective reaction of the body appears, contributing to the release from pathogens. In this process, an important role belongs to specific antibodies (agglutinins, opsonins, precipitins, bacteriolysins, complement binding, antiendotoxins), and the phagocytic activity of macrophages also increases.

In the process of freeing the body from typhoid bacteria, it is essential to increase the function of the excretory systems: the liver, kidneys, intestinal glands (intestinal crypts, or Lieberkün's glands). Starting from the 8th–9th day of illness, the bacteria, together with bile, are secreted into the intestinal lumen and partially excreted from the body. The remaining bacteria are introduced into the primary sensitized group and solitary lymphatic follicles of the distal small intestine. The rapid development of the necrotic process in them is explained by an allergic reaction, which manifests itself in the form of hyperergic inflammation.

Isolation of the pathogen from the body can also occur with urine, sweat, saliva, breast milk. A significant increase in the excretion of bacteria from the body, the accumulation of specific antibodies, an increase in the phagocytic activity of cells of the macrophage system indicate the formation of immunity and the restoration of physiological balance.

Disease relapses. From localized foci, typhoid bacteria can break into the bloodstream with subsequent generalization of the infectious process in the form of relapses of the disease. Of essential importance in the occurrence of relapses is the insufficient intensity of the emerging immunity due to the use of antibiotics, which, by weakening the antigenic irritation, help to reduce the production of specific antibodies.
In typhoid fever, prolonged bacterial excretion is often observed. Currently, it is considered as a chronic form of typhoid infection, in which the pathogen persists in the cells of the SMF. At the heart of the formation of typhoid carriage lies the imperfection of the immune system. Chronic carriers were found to be deficient in macroglobulin O antibodies (IgM). It is known that this class of immunoglobulins plays an important role in the formation of antityphoid immunity.

The main pathomorphological changes in typhoid and paratyphoid diseases are observed in the lymphoid tissue of the ileum. The regularity and cyclicity of the development of these changes in the intestine served as the basis for the allocation of five pathomorphological periods. They are conditional, since they do not always fully correspond to the clinical periods and severity of the disease.

brain swelling period. The first period corresponds to approximately the 1st week of illness and is characterized by a significant swelling of the lymphoid tissue of the small intestine. Group and solitary lymphatic follicles increase in size and protrude above the level of the mucous membrane.

period of necrosis. On the 2nd week, necrotization of the central parts of the swollen lymphatic formations begins. Their surface becomes dirty gray or greenish yellow.

Period of ulceration. On the 3rd week, rejection of necrotic elements of the lymphoid tissue and the formation of ulcers occur. This exposes the deep layers of the mucosa and submucosa. By the beginning of the 4th week of the disease, the rejection of necrotic tissues ends and the fourth period begins.

The period of "clean ulcers". In the area of group and solitary lymphatic follicles, ulcers are formed with a clean, smooth bottom and slightly swollen edges, located along the ileum.

Healing period. The fifth period, corresponding to about the 5th week of the disease, is characterized by healing of ulcers without constricting cicatricial changes, but with slight slate-gray pigmentation.

Specific pathological changes

Specific for typhoid fever are hyperplastic processes in the reticular stroma of group and solitary lymphatic follicles. In addition to hyperplasia, typhoid granulomas (“typhomas”) are formed, consisting of macrophages in the form of large, so-called typhoid cells with massive light cytoplasm and light nuclei. They are found in the appendix, colon, lymph nodes of the mesentery, in the liver, spleen, bone marrow, less often in the lymphoid tissue of the pharynx, alveoli, meninges.

Liver in typhoid fever, it is enlarged, swollen, dull on the cut, yellowish in color. Microscopic examination reveals specific granulomas with foci of necrosis, protein and fat, degeneration of hepatocytes.
The spleen is enlarged due to blood supply and inflammatory proliferation of reticular cells with the formation of typhoid granulomas, the development of splenic infarcts with their subsequent suppuration is possible.

in the kidneys- cloudy swelling. Sometimes there may be necrotizing nephrosis, hemorrhagic or embolic nephritis, and inflammatory processes in the pelvis, ureters, and bladder.

pneumonia in typhoid fever in most cases due to secondary infection, but there are also specific typhoid pneumonia with the formation of typical granulomas ("pneumotyphoid").

Roseolous rash in typhoid fever, it appears as a result of productive inflammatory changes in the surface layers of the skin along the course of the blood and lymphatic vessels. In the scrapings of roseola, typhoparatyphoid bacteria are found.

Degenerative changes are often found in the heart muscle and nerve ganglia.. The same changes are observed in the ganglion cells of the nodes of the sympathetic nervous system, autonomic plexuses. Characterized by waxy (Zenker's) necrosis of the rectus abdominis muscles.

There are no significant differences in the pathoanatomical picture observed in typhoid fever and paratyphoid fever.

Clinical picture (Symptoms) of typhoid fever

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Incubation duration The period for typhoid fever ranges from 7 to 25 days, more often 9–14 days.

By the nature of the flow distinguish

typical course and
atypical course of typhoid fever.

Typical shapes The course of the disease is cyclical.

There are four periods of the disease:

initial period,
peak period,
resolution period and
recovery period.

Atypical forms the course of the disease proceeds with the absence of a number of characteristic signs of typhoid fever.

Atypical include abortive and erased forms of the disease.

According to the severity of clinical manifestations are distinguished

light,
moderate and
severe form of typhoid fever.

According to the features of the flow diseases distinguish

complicated and
unexplained typhoid fever.

Typical form of typhoid fever

The initial period of the disease

It is characterized by gradual or acute development of intoxication syndrome. In the past, the variant of the gradual development of symptoms of intoxication prevailed, at present both variants occur with almost equal frequency.
With the gradual development of symptoms of the disease in the first days, patients note increased fatigue, increasing weakness, chilling, increasing headache, loss or lack of appetite.

The body temperature, rising daily in steps, reaches 39–40 °C by the 5th–7th day of illness. By this time, all the phenomena of intoxication are growing, significant weakness, adynamia develop, headache becomes persistent, sleep is disturbed, anorexia, constipation, and flatulence occur. Sometimes with errors in the diet, diarrhea is observed. The chair is rarely more than 2-4 times a day.

With acute onset disease in the first 2-3 days, all symptoms of intoxication reach full development.
When examining patients in the initial period of the disease, some lethargy and adynamia attract attention. Patients are indifferent to the environment, they answer questions in monosyllables, not immediately. The face is pale or slightly hyperemic, sometimes slightly pasty.

In the study of the cardiovascular system, relative bradycardia is noted, sometimes dicrotia of the pulse. Arterial pressure is reduced. Over the lungs, vesicular breathing with a hard tone and scattered dry rales are often heard, which indicates the development of diffuse bronchitis.

Digestive system naturally involved in the pathological process, and changes in its organs are of great diagnostic value. The tongue is usually thickened, with imprints of teeth on the lateral surfaces. The back of the tongue is covered with a grayish-white coating, the edges and tip are free from plaque, have a rich pink or red color. The pharynx is slightly hyperemic, sometimes there is an increase and hyperemia of the tonsils. The abdomen is moderately swollen due to flatulence.

On palpation in the right iliac region, coarse, large-caliber rumbling in the caecum and small-caliber rumbling and pain along the terminal ileum are determined, indicating the presence of ileitis.

With percussion there is a shortening of percussion sound in the ileocecal region (Padalka's symptom), which is due to hyperplasia of the inflammatory lymph nodes of the mesentery. This is also evidenced by the positive "cross" symptom of Sternberg.

By the end of the 1st week of illness enlargement of the liver and spleen is revealed.

In the hemogram after a short-term (in the first 2-3 days) moderate leukocytosis, from the 4th-5th day of illness, leukopenia with a shift of the leukocyte formula to the left, aneosinophilia, relative lymphocytosis and thrombocytopenia are noted. ESR moderately increased. Changes in the hemogram are a natural consequence of the effects of typhoid bacteria toxins on the bone marrow.

Changes in the urogram often fit into the syndrome of an infectious toxic kidney: proteinuria, microhematuria, cylindruria.

period of illness

By the end of the 1st - the beginning of the 2nd week, the period of the peak of the disease begins, when all the symptoms reach their maximum development. It lasts 1-2 weeks. The body temperature, having risen to 39-40 ° C, may subsequently have a constant character (Wunderlich type) or be of a multi-wave character (Botkin type), the temperature curve may also have one wave - a curve of the "inclined plane" type (according to Kildyushevsky).

During this period of illness, headache and insomnia often become excruciating. Status typhosus develops, characterized by severe weakness, adynamia, apathy, impaired consciousness from stupor to stupor or coma. Perhaps the development of infectious delirium.

On the 8th–10th day of illness, a characteristic exanthema appears on the skin. It is detected in 55-70% of patients with typhoid fever and is localized mainly on the skin of the abdomen and lower chest. The rash, as a rule, is scanty, the number of its elements rarely exceeds 6–8, is roseolous in nature, monomorphic. Roseolas have the appearance of pink spots of a rounded shape, with clear contours, with a diameter of about 3 mm. Often they rise slightly above the level of the skin (roseola elevanta) and are clearly visible against its pale background.

When pressing or stretching the skin along the edges of the roseola, it disappears, after which it appears again. Each element of the rash lasts 1-5 days, usually 3-4 days. After the disappearance of the rash, a barely noticeable pigmentation of the skin remains. New roseolas may form against the background of fading old ones (the phenomenon of "sprinkling"), which is associated with an undulating course of bacteremia.

In some patients, icteric staining of the skin of the palms and soles is found - carotene hyperchromia of the skin (Philippovich's symptom), which occurs as a result of a violation of carotene metabolism due to liver damage.

At the height of the disease, relative bradycardia, pulse dicrotia persist, and blood pressure decreases even more. Damage to the heart muscle is manifested by a moderate shift of the boundaries of cardiac dullness to the left, deafness of the heart sounds, and a coarse systolic murmur heard at the apex and at the base of the heart.

Above the lungs, vesicular breathing with a hard tone and scattered dry rales continue to be heard. In some cases, symptoms of focal pneumonia occur, caused both by the causative agent of typhoid fever itself and by the accompanying microflora.

Symptoms of damage to the digestive system in the midst of the disease reach their maximum development. The lips of patients are dry, often covered with crusts. The tongue is thickened, densely coated with a gray-brownish coating, the edges and tip of its bright red color, with imprints of teeth ("typhoid", "fried" tongue).

In seriously ill patients the tongue becomes dry and takes on a fulginous appearance, the abdomen is swollen due to flatulence, stools - constipation is possible, in some cases liquid, stools in the form of pea soup and with a peculiar sour smell. Rumbling and pain on palpation of the ileocecal intestine become distinct, positive symptoms of Padalka and Sternberg persist.

Liver enlarged, well accessible to palpation, its edge is even, slightly rounded, sometimes painful, the consistency is doughy. The spleen is enlarged, usually accessible to palpation.

At the height of the disease, the amount of urine excreted decreases. Proteinuria, microhematuria, cylindruria are determined. There is bacteriuria, which sometimes leads to inflammation of the mucous membrane of the renal pelvis and bladder.

During this period of the disease, such dangerous complications as perforation of typhoid ulcers and intestinal bleeding can occur. In some cases, due to severe intoxication and dangerous complications, death can occur.

Disease resolution period

Body temperature decreases, and often before normalization it begins to fluctuate, acquiring an amphibolic character (differences between morning and evening temperatures reach 2–2.5 ° C). The headache stops, sleep normalizes, appetite improves, the tongue is moistened, plaque disappears from it, diuresis increases. The duration of the period of resolution of the disease, as a rule, does not exceed 1 week.

convalescence period

The disturbed functions of the body are restored, and it is released from the pathogens of typhus. For this period, asthenovegetative syndrome is typical, which persists for 2–4 weeks and depends on the severity of the disease. Among survivors of typhoid fever, 3–5% of patients become chronic typhoid bacterio-excretors.

Relapses

On average, 7-9% of patients. They often occur on the 2nd–3rd week of normal temperature, but may also occur at a later date (1–2 months), regardless of the form and severity of the disease. They are single and multiple.

The duration of fever during relapse can range from 1–3 days to 2–3 weeks. In the pre-relapse period, subfebrile condition is noted, the cleansing of the tongue from plaque slows down, the liver and spleen remain enlarged, and the hemogram shows changes inherent in the peak of the disease. Clinically, relapses of typhoid fever are similar to the first wave of the disease and differ only in a more rapid rise in temperature, early onset of a rash, a shorter duration of fever, and usually a milder course.

Atypical forms of typhoid fever

abortion form. It has many similarities with the typical course of the disease, but the clinical picture does not reach full development. The temperature quickly (after 7–10 days) and often drops critically, other symptoms of intoxication disappear, and recovery occurs.

Erased form(“ambulatory typhus”, “mild typhus”). Intoxication is expressed slightly. The temperature is subfebrile, its duration is no more than 5-7 days (sometimes 2-3 days). Exanthema rarely occurs. Changes in internal organs are weakly expressed. Patients are usually able to work.

Complications

Sometimes the disease occurs with a predominance of symptoms of damage to individual organs and systems: lungs, meninges, caecum (the so-called pneumotyphoid, meningotif, colotif).
In typhoid fever, complications can be conditionally divided into specific, caused by the pathogenic influence of the pathogen and its toxin, as well as non-specific, caused by concomitant microflora.

Specific complications of typhoid fever. The most important for the outcome of the disease are intestinal bleeding, perforative peritonitis and infectious toxic shock.

Intestinal bleeding, which occurs in 1-2% of patients, worsens the prognosis and is more often observed at the 3rd week of illness, sometimes after a decrease in temperature. It is caused by an arrosion of a vessel (vein or artery) at the bottom of a typhoid ulcer. Bleeding can also be diffuse, capillary in nature. In the mechanism of its development, a decrease in blood clotting and a slowdown in thrombus formation are important. Depending on the rate of evacuation of the contents of the intestine and the massiveness of bleeding, the stool of patients becomes tarry (melena), contains blood clots or fresh blood.

Minor bleeding usually does not affect the patient's condition. They are detected when examining the stool or using the Gregersen reaction many hours after the onset. With massive bleeding, body temperature suddenly drops to normal or subnormal, thirst arises, the pulse quickens, and blood pressure drops. A small bleeding with timely treatment ends safely. Massive bleeding can lead to the development of hemorrhagic shock, which always has a serious prognosis.

Perforative peritonitis as a result of perforation of an intestinal ulcer is a dangerous complication of typhoid fever. It develops on the 2nd–4th week of illness, sometimes after the temperature normalizes. It occurs in 0.5–1.5% of patients and can be observed not only in severe, but sometimes in mild cases of the disease. Most often, perforation of the ulcer occurs in the ileum at a distance of 25–30 cm from the place where it passes into the caecum. Perforation is facilitated by flatulence, increased peristalsis, sudden movements, severe cough, rough palpation of the abdomen, and diet violations.

The clinical picture of typhoid perforative peritonitis has a number of features that must be taken into account in the diagnosis. The presence of status typhosus may mask the symptoms of perforation. The main symptom of perforation - a sudden sharp pain - is often absent, so the appearance of even slight pain in the abdomen should attract the attention of a doctor. Another leading symptom of developing peritonitis - contraction of the muscles of the abdominal wall - in patients with clouding of consciousness may be the only one. Not a constant, but an important sign of perforation is a positive Shchetkin-Blumberg symptom.

Bowel perforation is sometimes accompanied by severe collapse. A few hours after perforation, a pronounced picture of peritonitis develops. Facies hyppocratica appears, vomiting, persistent hiccups, bloating and severe diffuse pain in the abdomen join. Hepatic dullness disappears. However, these symptoms develop too late. The patient can be saved if surgery is performed within the first 6 hours after perforation. With a later operation, the prognosis is almost hopeless.

Infectious-toxic shock develops, as a rule, during the height of the disease and occurs in 0.5-0.7% of patients. Its occurrence is due to the massive intake of typhoid bacteria and their toxins into the blood. The development of shock is based not so much on the toxic effect itself, but on the manifestation of a violent immune conflict as a result of the intake of bacterial antigens, the formation of immune complexes, complement fixation, the reaction of plasma cells, a sharp depletion of the mononuclear phagocyte system, heparin and histaminemia.

In the clinical picture of the disease, infectious toxic shock is preceded by symptoms of hyperthermia and neurotoxicosis. With its development, a sharp decrease in body temperature, increased sweating, tachycardia, tachypnea, a drop in blood pressure, oliguria, and further anuria are observed.

Nonspecific complications of typhoid fever

This group of complications includes pneumonia, thrombophlebitis, meningitis, pyelitis, mumps, stomatitis, etc.

Forecast

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In uncomplicated typhoid fever, the prognosis is favorable. With the development of complications, it is worse and can be unfavorable (especially with perforated peritonitis). Mortality is 0.1–0.3%.

Typhoid Diagnosis

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In typhoid fever and paratyphoid, diagnosis is most important in the first 5-7 days of illness. This is due to the epidemiological requirements due to the high contagiousness of the patient in the following days of illness, and is also dictated by the clinical and pathogenetic features of the disease.

In the recognition of typhoid and paratyphoid diseases, both clinical epidemiological and laboratory data are of great importance. In laboratory diagnostics, bacteriological and serological research methods are used, which are carried out taking into account the period of the infectious process.
At the 1-2nd week of the disease, the pathogen is easiest to isolate from the blood, from the 2-3rd week - from feces and urine, during the entire disease - from the duodenal contents (duodenal sounding is contraindicated in the acute period of the disease, biliculture is isolated during the convalescence period) . It is possible to isolate the pathogen by sowing scrapings of roseola, bone marrow, pus, exudates, sputum.
The detection of bacteria in the blood is always an indicator of an acute illness, a sign that absolutely confirms the diagnosis of typhoid fever. The presence of the pathogen in the faeces may be the result of a disease or a bacteriocarrier. In these cases, in the presence of clinical signs, the issue is resolved in favor of acute typhoid fever, in their absence - in favor of the bacteriocarrier.
Blood cultures for blood culture isolation can be carried out from the 1st day of illness and throughout the entire febrile period. Sterile 5–10 ml of blood is taken from a vein and inoculated into a vial with 50–100 ml of 10–20% bile broth or Rappoport medium. When sowing blood on a nutrient medium, it is necessary to maintain a ratio between blood and medium of 1:10; with a smaller volume of nutrient medium, blood can have a bactericidal effect on the pathogen microorganism.
To obtain myeloculture, you can use the bone marrow obtained by puncture. When isolating L forms of bacteria from the blood and bone marrow, special penicillin serum media are used. To obtain scat, bili- and urine cultures, Ploskirev's medium is used.
A specific antigen in the blood, bone marrow and other test materials is also detected by immunofluorescent and enzyme immunoassay methods. These methods are highly sensitive and can be used for rapid diagnosis of epidemic outbreaks of typhoid fever.
For serological diagnosis of typhoid fever and paratyphoid A and B from the 5th–7th day of the disease, RNHA with erythrocyte diagnosticums (O, H, Vi antigens) is mainly used. A reaction in a titer of 1:200 or more is considered positive. In the study of paired sera taken in the dynamics of the disease in the RNGA, a fourfold or greater increase in antibody titer to the pathogens of typhoid and paratyphoid is considered diagnostically significant. RNHA with Vi antigen is used to detect bacteria carriers. Widely used in the past, the Vidal reaction is gradually losing its diagnostic value. Of great importance is the observance of hygiene, skin care and oral cavity.
In the febrile period and within a week after the normal temperature is established, patients are given mechanically and chemically the most sparing food for the intestines, at the same time, the food should be sufficiently high in calories and should not cause putrefactive and fermentation processes (diet No. 4 and 46. With recovery No. 4c , No. 2).

Antibiotic treatment must be carried out during the entire febrile period and the first 10 days after the temperature returns to normal.
The most effective in typhoid fever is the use of chloramphenicol. Assign Levomycetin inside 0.5-0.75 g 4 times a day. In case of frequent vomiting, chloramphenicol succinate soluble is prescribed intramuscularly or intravenously. The adult dose is 3-4 g per day (50 mg/kg).
The use of antibiotics does not guarantee against recurrence of the disease and the formation of chronic bacteriocarrier.
When treated with levomycetin, as a rule, relapses occur at a later date (on the 18th–25th day of normal temperature) and are characterized by a milder course than relapses in untreated patients. In case of recurrence of the disease, levomycetin is prescribed again in the same doses.
Levomycetin does not have a positive effect in chronic bacteriocarrier.
The use of Ampicillin at a dose of 1 g 4-6 times a day gives a good effect in the acute period of the disease and in some cases of acute bacterial excretion.

When the causative agents of typhoid fever are resistant to antibiotics, nitrofuran or sulfanilamide preparations are used.

Antibacterial therapy is combined with drugs that increase the reactivity of the body to prevent relapses and form a chronic bacteriocarrier. Non-steroidal anabolics (potassium orotate, methyluracil) are used from the means that increase the nonspecific resistance of the body.

For detoxification of the body, 5% glucose solution, Ringer's solution, reopoliglyukin, gemodez are prescribed intravenously. Corticosteroids, which are used only in severe cases of the disease, also have a positive effect.

For intestinal bleeding strict bed rest is required in the supine position for 12–24 hours. Cold is prescribed on the stomach, food intake is prohibited for 10–12 hours, the volume of liquid drunk by the patient is reduced to 500 ml. In the future, you can assign small portions of mucous decoctions, juices, jelly, jelly, meat or fish broth. From the 2nd day, the diet is gradually expanded. For minor bleeding, calcium chloride, vitamins C and K, hypertonic sodium chloride solution (5-10 ml in a vein), gelatinol, plasma and other blood products are used. In the fight against massive bleeding in infusion therapy with a substitution purpose, significant amounts of blood (1-2 l), polyionic solutions (Acesol, Trisol, Quartasol, Laktasol, etc.), colloidal solutions (rheopoliglyukin, polyglukin , gelatinol, etc.) and corticosteroids.

Perforation of the intestinal wall urgent surgical intervention is indicated.

In the treatment of infectious toxic shock use the method of controlled hemodilution with the introduction of rheologically active and complexing drugs (colloids) - hemodez, rheopolyglucin, gelatinol, crystalloid polyionic solutions in combination with the introduction of vasoactive drugs (for example, dopamine or dopamine), massive doses of glucocorticosteroids. In order to increase the antiaggregation effect of crystalloid solutions, proteolysis inhibitors - contrical (trasilol, tzalol) are added to them, in some cases spontaneous fibrinolysis activators (magnesium salts, nicotinic acid) are used.

Prevention

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Measures to combat typhoid and paratyphoid diseases should be aimed at neutralizing the sources of infection, suppressing transmission routes, and increasing the body's immunity.

Of great importance in the prevention of typhoid fever are early diagnosis, timely isolation and provisional hospitalization of the patient, effective therapy with complete release of the body from the pathogen.
In the recovery period, at intervals of 5 days, a three-time control bacteriological examination of feces and urine and a single examination of bile are carried out. If a pathogen is detected in the feces, urine or bile, the convalescent is subjected to intensive treatment in a hospital, depending on the comorbidity and reactivity of the body.
Extraction of a bacterioexcretor is possible only with the permission of the epidemiologist. After discharge, all convalescents are subject to dispensary observation with a systematic examination for the timely detection of a recurrence of the disease and the formation of a chronic bacteriocarrier. The duration and intensity of laboratory examination of recovered patients depend on their professional affiliation. Those who have been ill are registered at the center of sanitary and epidemiological surveillance for 2 years, and people working at food enterprises - 6 years.
In order to prevent the spread of the pathogen in the outbreak, current disinfection is carried out before the hospitalization of the patient or the bacterioexcretor. After hospitalization, the final disinfection is carried out in the outbreak.
For persons in contact with patients, medical observation is established for 21 days with daily thermometry. A single, and according to indications, a double bacteriological examination of feces and urine is carried out. In those who have previously been ill with typhoid fever, as well as in persons suffering from diseases of the liver and biliary tract, duodenal contents are cultured and a blood test is performed in RNHA with erythrocyte Vi antigen. Specific prophylaxis in the focus includes the appointment of a bacteriophage to all contacts.
Specific prophylaxis of typhoid fever is carried out according to epidemic indications. In territories unfavorable for typhoid fever, vaccination is carried out for the entire population, starting from children of 7 years of age. Specific prophylaxis is also indicated for persons belonging to risk groups: workers of treatment facilities, employees of infectious diseases hospitals and bacteriological laboratories. Vaccination is also carried out for people traveling to countries in Africa and Asia with a high incidence of typhoid fever. In Russia, for active immunization against typhoid fever, inactivated vaccines are used: typhoid alcohol dry vaccine; typhoid alcohol vaccine enriched with Vi antigen; vaccine typhoid U1 polysaccharide liquid. In response to the introduction of vaccines, immunity develops in 1–2 weeks. Immunity to infection persists for 2 years.
Some countries also use live typhoid vaccine. It is expected to create a conjugate vaccine against typhoid fever, which would be suitable for administration, including children of the first 2 years of life.

Acute cyclic intestinal infection caused by Salmonella typhi bacteria. The course of typhoid fever is accompanied by fever, general intoxication, roseolous rashes on the skin, a pathological increase in the size of the liver and spleen, and damage to the lymphatic system of the lower small intestine.

The causative agent of typhoid fever is Salmonella typhi. This is a bacterium of the species Salmonella enterica, subspecies enterica, serovar typhi. Like other Salmonella, it grows on normal nutrient media, but thrives especially on media containing bile. The optimal growth conditions are called a temperature of 37 ° C, and an acidity of pH = 7.2-7.4. To the environment, typhoid-paratyphoid salmonellae are relatively stable, they tolerate low temperatures well for several months. The survival of these pathogens in water depends on the conditions: in running water they persist for several days, in tap water for up to 3 months, and in silt of wells for up to 6 months. They are very well preserved in food products, namely in milk, cheese, sour cream, minced meat, vegetable salads, where they are capable of reproduction and with which they often enter the human body.

Salmonella typhi dies under the influence of high temperature - within 1 hour at 50 ° C, within half an hour at 60 ° C and instantly when boiled. Direct sunlight also has a detrimental effect on them. Conventional disinfectants cause their death in a few minutes.

The causative agents of typhoid and paratyphoid diseases, like other salmonella, are characterized by a wide range of enzymes that increase their aggressiveness (hyaluronidase, fibrinolysin, lecithin aza, hemolysin, etc.). Many properties of typhoid and paratyphoid bacilli (for example, virulence, agglutinability, lisability) are capable of changing under the influence of antibiotics, bacteriophages, and other factors unfavorable for bacteria. It is noteworthy that in the course of the disease in one patient, the properties of the pathogen change.

Causes of typhoid fever are explained by its anthroponotic nature, that is, the source of infection is always a sick person or a carrier of these microbes. The mechanism of transmission of infection is fecal-oral:

chronic bacterionosia, in particular those whose activities are associated with food, water supply sources;
the feces of a sick person contain millions of microbes - the so-called urinary carriers are considered the most dangerous, since the act of urination is often not accompanied by sufficient hygiene;
household contact route of transmission - through contaminated hands (direct route of transmission), dishes, linen, door handles (indirect route);
contaminated water due to faecal contamination of water supplies - outbreaks are explosive
food - mainly when consuming infected milk, dairy products, products with cream, ice cream, butter, mainly in the warm season; infection of finished food products occurs when sanitary norms and rules for processing raw materials, storage, transportation, and sale of finished food products are violated;
transmission of infection involving insects, such as flies - they turn out to be a mechanical carrier of microbes on products consumed without heat treatment;

When 10 and microbial bodies enter the body, the disease develops in 25% of those infected, 105 - 50%, 108 - 100%. Since patients with severe typhoid-paratyphoid diseases are mainly identified and hospitalized, they are less likely to become a source of infection - usually only for those who deal with them or directly surround them.

Typhoid-paratyphoid diseases are characterized by summer-autumn seasonality, this period accounts for up to 75% of all cases. The seasonal increase in the incidence is due not only to a simplified mechanism of infection transmission, but also to the following factors:

a decrease in the reactivity of the body under the influence of excessive insolation,
swimming in open water,
eating large amounts of carbohydrates
violation of water metabolism,
decrease in the barrier function of the stomach,
decrease in bactericidal properties of blood,
increased migration of the population in summer (tourism, recreation by the sea, etc.),
consumption of unboiled milk, unwashed berries, fruits, vegetables.

The transferred disease, if the carriage has not formed, contributes to the emergence of long-term sterile immunity.

The pathogenesis of the abdominal type includes several stages. In the penetration phase pathogens enter the alimentary canal through the mouth. Due to their high resistance to the acidic environment of the stomach, they freely enter the lymphatic formations: Peyer's patches and solitary follicles of the small intestine, which serve as a barrier to other infections. Contribute to such a deep penetration of their stomach surgery, alcoholism with the formation of stable achlorhydria, the use of antacids, H2-hietamin receptor blockers or proton memory inhibitors. Sometimes microbes can even get into the lymphatic formations of the mouth of the throat.

Typhoid-paratyphoid bacilli can easily penetrate into lymphoid cells and multiply there, while bacteria do not penetrate into the cytoplasm of immune lymphocytes obtained from the peripheral blood of vaccinated people and chronic carriers, but are located around the lymphocytes. Microbes multiply in these lymphatic formations, accumulate in sufficient quantities and enter the next protective barrier - the mesenteric lymph nodes, resulting in their hyperplasia, the formation of granulomas.

Into the breakthrough phase microbes in the bloodstream appear clinical signs of the disease:

gradual excitation of the thermoregulatory center with an increase in typical cases of body temperature to febrile numbers during the first 3-5 days of illness;
general intoxication manifestations;
redistribution of blood - its accumulation in the vessels of internal organs with the appearance of some of their edema and a simultaneous decrease in blood flow in the vessels of the skin;
weakening of salivation, which subsequently leads to problems in the oral cavity;
retention of stool, urination may be due to the stimulating effect of endotoxin on the sympathetic part at the level of autonomic nodes of the abdominal cavity;
a decrease in intestinal motility is also associated with the severity of mesadenitis;
the work of the bone marrow is suppressed, causing a decrease in the level of leukocytes, neutrophils and platelets.

Occurs almost simultaneously parenchymal diffusion- microbes are carried to various organs and tissues, secondary foci of inflammation and granulomas are formed there. As a result, there are manifestations of damage to certain organs, which can distort the typical clinical picture (pneumonia, nephritis, meningitis).

Pathogen elimination phase from the body begins approximately from the second week of clinical symptoms. The microbe is excreted in urine and bile. Pathogens enter the intestines in large quantities from the gallbladder, where they can multiply and accumulate. Prior to this, as a result of the ingress of pathogens of typhoid-paratyphoid infections into the lymphatic apparatus of the small intestine during the incubation period, sensitization of antigens to them occurs. The process of repeated "passage" of microbes through the intestines is accompanied by a number of sequentially occurring morphological changes:

1st week - "brain-like swelling" of the lymphatic apparatus of the intestine as a reaction to repeated exposure to pathogens;
2 weeks - the formation of local necrosis in the area of the follicles; necrosis can spread deep into, sometimes reaching the muscle layer and even the peritoneum;
3 week - rejection of necrotic masses and the formation of ulcers. If at the same time the wall of the blood vessel is damaged, bleeding is possible, with the formation of deep ulcers, intestinal perforations may occur;
4 weeks - complete cleansing of ulcers; bleeding, perforation are also possible;
5th week - healing of ulcers without the formation of scars, strictures.

There are several periods during the course of the disease:

elementary- gradual onset, increased body temperature, general weakness, increased fatigue, a feeling of fatigue, worsening appetite, sleep disturbance. Paleness of the skin develops. Spasm of superficial vessels and their expansion in the internal organs lead to a gradual increase in the liver and spleen. Blood pressure drops, bradycardia occurs. Sometimes there may be coughing, especially when changing the position of the body from horizontal to vertical, which is due to squeezing of the vessels of the lungs. Due to slow blood flow and vasodilation of the central nervous system, cerebral edema (toxic encephalopathy) develops, due to which the headache becomes constant, annoying, and intensifies in the afternoon. There is a violation of the sleep formula - drowsiness develops during the day and insomnia at night. Strong general weakness makes the patient stay in bed, he gradually loses interest in the environment, reluctantly answers questions, the reaction is slow. The initial period lasts 4-7 days and ends when the body temperature reaches a maximum.
peak period- without treatment lasts 2-3 weeks. The fever acquires a permanent character at the level of 39-40 ° C without chills. Intoxication increases to a maximum, sometimes very pronounced, to typhoid status. In a severe course, the patient develops confusion ("fuzziness"), he is restless, completely disoriented in space, delirious. The face is amimic. Sometimes there are hallucinations, aggressiveness. The signs developed at the initial stage acquire the maximum manifestation. Arterial pressure can decrease significantly, relative bradycardia can turn into absolute. Heart sounds are muffled, systolic murmur at the apex is possible. A small number of physically developed individuals may develop dicrotia of the pulse (feeling of an additional pulse beat immediately after the main one). Weakened breathing, single dry rales are heard over the lungs. The skin of the trunk and face is very pale, dry to the touch due to high body temperature. The tongue is thickened, at first it is covered with a white coating, except for the edges and the tip, so the impressions of the teeth along the edges are clearly visible. From the 2nd week, in the absence of oral care, it becomes covered with a black coating ("fulginous tongue"). Characteristic flatulence, enlarged liver and spleen, constipation. With percussion of the right iliac region, a noticeable shortening of the percussion sound is manifested. On the skin of half of the patients, a roseolous rash may appear with typical localization: the lateral surfaces of the abdomen, the lower part of the chest, sometimes the forearms, and the lower back. The elements of the rash are pink-red or pale pink spots with clear contours, which disappear when pressed, but reappear. A rash with a hemorrhagic component is a sign of a very severe course of the disease.
regression period of the disease and the period of convalescence - the body temperature decreases both politically and critically, the symptoms gradually disappear. Prolonged low-grade fever during convalescence is often a harbinger of an exacerbation of the disease.

Not always, all the periods described above are clearly traced. The clinical course of typhoid and paratyphoid diseases has undergone a certain transformation over the past decades, which is explained by cardinal changes in living conditions and the significant use of antibiotics. More often, an acute onset of the disease is recorded with a rapid increase in body temperature and its critical decrease, a short febrile period, mild manifestations of intoxication, the rapid appearance of a rash with a very small amount of roseola; mild forms of the disease are more common. Early use of antibiotics in most cases significantly reduces the duration of typhoid-paratyphoid diseases, sometimes literally "breaks" their course.

In addition to the usual cyclic course, typhoid fever may differ:

exacerbations;
relapses.

An exacerbation is suspected if, against the background of a decrease in body temperature to subfebrile numbers and a significant improvement in the patient's well-being, a high fever occurs for several days, followed by the appearance of all leading clinical symptoms. Now the cause of exacerbations is most often the early cancellation of the antibiotic or a decrease in its dose.

Relapses can occur at any time after the normalization of body temperature, but more often at the 2-3rd week, that is, soon after the antibiotic is discontinued. However, later relapses are also described - 1-2 months after normalization of body temperature. With relapses, typical clinical signs of typhoid or paratyphoid fever also appear from the first days.

Features of paratyphoid A note:

much more often than with typhoid fever (more than half of the patients), the disease begins acutely;
often in the first days, patients show signs of damage to the respiratory tract (tickle, sore throat, slight cough);
the skin and conjunctiva are often hyperemic, often there are signs of pharyngitis;
the rash appears earlier (in most patients - already on the 5-7th day of illness); it is more often papular, sometimes morbilliform; abundant, located not only on the trunk, but also on the flexion surfaces of the arms;
constipation and stool disorders in the initial period of the disease occur with the same frequency;
chills, sweating are often observed.

Features of paratyphoid B include:

shorter than with typhoid fever and paratyphoid A, the incubation period;
the onset in most cases is acute, sudden, with moderate nausea and vomiting, stool disorders;
often in the initial period there are chills, sweating;
fever is usually short-term (1-5 days), of a different nature - subfebrile, undulating;
due to the short duration of the course, the rash may be absent, but sometimes appears on the 4-5th day; may be abundant, polymorphic.

How to treat typhoid fever?

Treatment for typhoid fever is etiotropic in nature, that is, it is aimed at eliminating the pathogen. Treatment is prescribed as soon as possible after typhus is suspected. The patient needs hospitalization. It is important to establish the epidemiology of the infection in order to stop its spread.

The main antibacterial agent is (chloramphenicol), to which the microbes circulating in our country are still sensitive. It is prescribed orally at 0.75-1.0 grams 4 times a day during the entire febrile period and up to the 10th day of normal body temperature. Parenteral administration of chloramphenicol should be used for typhoid status or certain complications (meningotitis) due to poor penetration of the drug into the lymphatic formations of the intestine during this route of administration.

Fluoroquinolones are the second-line drugs in the treatment of typhoid fever:

or
- inside of 0.4 g 2 times a day for 7-14 days.

In the event of certain complications, typhoid status, these drugs can be prescribed parenterally.

However, now for the countries of Eastern Europe, WHO recommends starting treatment with the above-mentioned fluoroquinolones - first-line drugs (in case of complications, administer them parenterally), but as second-line drugs (i.e., with resistance or intolerance to first-line drugs) in uncomplicated cases inside apply:

- 0.5 g on the 1st day, 0.25 g on the 2nd-5th days;
- 0.75-1.0 g per day for 7-10 days;
cefixime - 0.2 g 2 times a day for 14 days.

In complicated cases, with typhoid status, second-line drugs for these regions are:

- 1.0-2.0 g every 4-6 hours parenterally;
- 2 g 4 times a day;
- 1-2 g 2 times a day.

For the treatment of a patient who has become infected in a region with multidrug-resistant typhoid-paratyphoid pathogens (South and East Asia), WHO recommends in uncomplicated cases as a first-line drug to prescribe cefixime (0.2 g 2 times a day for 14 days) in combination with ciprofloxacin or ofloxacin (0.2-0.4 g 2 times a day for 7-14 days), and as a second-line drug - azithromycin (0.5 g 1 time per day orally for 10 days) .

In complicated cases, first-line drugs in these regions include ceftriaxone (1-2 g 2 times a day or defotaxime 2 g 4 times a day) in a mandatory combination with ciprofloxacin or ofloxacin (0.2-0.4 g 2 times a day for 7-14 days parenterally). As second-line drugs in this region, it is recommended to prescribe (1-2 g 3-4 times a day) or imipine together with dilastin (0.5-1.0 g every 6 hours) in combination with ciprofloxacin or ofloxadine (0 ,2-0.4 g 2 times a day for 14 days) or (0.4 g per day for 7-14 days), or (0.5 g per day for 7-14 days). All second-line drugs are administered parenterally.

It is necessary to dynamically evaluate the effectiveness of the drug. In the case of using levomycetin, the effect indicating the sensitivity of pathogens should be assessed on the 4th day of using the drug, with all other antibiotics - on the 2nd day. If insensitivity is suspected, a quick replacement of the antibacterial agent is needed. According to the WHO recommendations, the appearance of an exacerbation or recurrence of a typhoid-paratyphoid infection does not require the replacement of an antibacterial drug that previously had an effect, but encourages the search for other causes that led to an inappropriate course of the disease.

All patients are prescribed strict bed rest during the entire febrile period and another 5 days after normalization of body temperature. In case of non-compliance with the regimen before this period, the occurrence of such complications as collapses, bleeding, perforations is very likely. Patients need to be constantly monitored, cared for (regular treatment of the oral cavity, skin), with constipation - lactulose preparations, cleansing enemas. Diet No. 1 is prescribed from the first day, its gradual expansion is possible only after normalization of body temperature, but not earlier than the 5th week of illness. Food should contain a sufficient amount of vitamins and potassium salts. You can not consume carbonated mineral water, rosehip infusion, choleretic herbs.

In the presence of toxicosis in patients, the use of detoxification therapy is important. If the required amount of liquid (up to 40 ml/kg of body weight per day) cannot be provided orally, including with food, intravenous balanced polyionic solutions can be prescribed (in order to compensate for water and electrolyte disorders), glucose-salt mixtures, mixtures of salts and others. carbohydrates, 5-10% glucose solutions, reopoliglyukin.

Prolonged use of antibiotics can be the cause of the development of candidiasis, dysbiosis. Therefore, throughout the course of antibiotic therapy, patients should receive either other antifungal drugs and agents that correct the intestinal microflora.

In the event of intestinal bleeding, cold is urgently prescribed on the stomach, special diets, antihemorrhagic agents, if necessary, transfusion of erythrocyte, platelet mass, cryoprecipitate. If within 2 days conservative treatment of intestinal bleeding does not give an effect, surgical intervention is necessary to repair bleeding ulcers. As a rule, the last 70 cm of the small intestine, where such ulcers are concentrated, are subject to revision.

What diseases can be associated

Chronic carriage as a result of an acute form of typhoid-paratyphoid infection should be considered a kind of chronic form of the course, because in this category of people throughout life there are short-term cases of fever with a short appearance of the pathogen in the blood. In chronic bacterial carriers, the gallbladder, kidneys, and bone marrow are a common site of pathogen localization. Contribute to this or, the presence of urinary, etc. Such persons make up 3-6% of all patients. After removal of the gallbladder in "bilious" carriers, Salmonella is often eliminated from the body.

In addition, typhoid fever provokes the following complications

intestinal bleeding- develops in 25% of patients with typhoid fever and in 7-10% of patients with paratyphoid fever, but the degree of blood loss is different; in most patients, bleeding is not clinically pronounced, and therefore is diagnosed only by examining feces for occult blood; in a certain number of cases, bleeding leads to pronounced hemodynamic changes (tachycardia, an even greater decrease in blood pressure), a sudden decrease in body temperature, sometimes below 37 ° C, which is noticeable in the temperature sheet; such massive bleeding is observed with numerous intestinal ulcers;
bowel perforation- occurs more often in the 3rd week; the perforation site is usually not large in size, covered by the peritoneum, due to which, unlike the perforation of gastric and duodenal ulcers, which are accompanied by dagger pain, pain during typhoid-paratyphoid perforations is usually absent and appears only with the development of diffuse peritonitis. Therefore, the patient and medical staff must constantly be vigilant. If the patient has any unusual sensations in the right iliac region, the detection of abdominal wall resistance there, positive symptoms of peritoneal irritation, these signs should potentially be regarded as suspicions of intestinal perforation. Rarely, peritonitis may result from mesenteric lymph node necrosis.

Other complications of typhoid fever should include any clinically pronounced signs of infectious lesions of certain organs - piyevmotif, meningotif, myocarditis, nephrotif, osteomyelitis and others.

Treatment of typhoid fever at home

Treatment for typhoid fever contraindicated at home for two reasons:

firstly, the disease requires constant medical monitoring and repeated diagnostic procedures, which is more convenient and efficient in a hospital setting;
secondly, the disease is infectious in nature and poses a danger to persons in contact with the patient.

The patient is discharged from the hospital on the 21st day of normal temperature, given that it goes down as soon as possible with adequately selected treatment.

Be sure to conduct a control examination before discharge: 2 days after the antibiotic is discontinued, stool and urine cultures are prescribed for 3 days in a row and bile cultures (biliculture) once. With negative results of cultures of feces, urine and biliculture, the patient is discharged.

Subsequently, at home, it is important to lead a healthy lifestyle with a balanced diet and the exclusion of bad habits. Personal hygiene items used by patients before the disease must be sanitized or destroyed.

What drugs are used to treat typhoid fever?

First line drugs:

- inside of 0.75-1.0 grams 4 times a day during the entire febrile period and up to the 10th day of normal body temperature;
- inside of 0.2-0.4 g 2 times a day for 7-14 days;
- inside of 0.4 g 2 times a day for 7-14 days;
- inside of 0.2-0.4 g 2 times a day for 7-14 days.

Second-line drugs in uncomplicated cases:

- inside 0.5 g on the 1st day, 0.25 g on the 2-5th day;
- inside, 0.75-1.0 g per day for 7-10 days;
Cefixime - inside 0.2 g 2 times a day for 14 days.

Second-line drugs in complicated cases:

- parenterally 1.0-2.0 g every 4-6 hours;
- inside 2 g 4 times a day;
- inside 1-2 g 2 times a day.

Typhoid brought from the southern regions is susceptible to the following medicines:

- parenterally 1-2 g 3-4 times a day;
Imipinem - parenterally 0.5-1.0 grams every 6 hours;
- inside of 0.2-0.4 g 2 times a day for 7-14 days;
- inside of 0.2-0.4 g 2 times a day for 7-14 days;
- parenterally, 0.4 g per day for 7-14 days;
- parenterally, 0.5 g per day for 7-14 days.

Treatment of typhoid fever with folk methods

The use of folk remedies in typhoid fever treatment is not able to provide a sufficient antibacterial effect, therefore it can be used for other purposes, but at the final stage of treatment. Herbal preparations recommended for use have a bactericidal, immuno-strengthening, anti-inflammatory effect, help to relieve pain and restore the function of the liver and gastrointestinal tract. Any prescription should be discussed with the attending physician and used with his consent, and not as part of self-treatment.

In the treatment of typhoid fever folk remedies are used:

burnet roots- 1 tbsp. l. crushed roots pour 1 cup boiling water, boil for 30 minutes, cool, strain and take 1 tbsp. l. 5-6 times a day;
currant juice- freshly squeezed 100 ml 2-3 times a day;
herbal collection- combine 4 parts of the roots of Rhodiola rosea and lure high, brown rose hips, 3 parts of blood-red hawthorn and leaves of nettle dioica, 2 parts of St. John's wort; 2 tbsp collection, pour 200 ml of water, boil for 15 minutes, strain, take 1/3 and 1/2 cup of broth 2-3 times a day;
melissa and mountaineer- combine 2 parts of lemon balm and 5 parts of highlander; 1 tbsp place the collection in a thermos, pour a glass of boiling water, strain after 10 hours; take 2-3 glasses during the day.

Treatment of typhoid during pregnancy

Treatment for typhoid fever during pregnancy is a difficult task, since the doctor's goal is not to harm the health of the woman and her fetus, but at the same time to select sufficiently effective drugs.

personal hygiene (especially clean hands),
prevention of contamination of food, water, household items,
compliance with the conditions of preparation and storage of food.

According to the indications (most often an outbreak of typhoid-paratyphoid disease in a separate territory, travel to areas unfavorable for these infections), vaccinations are carried out with a complex trivaccine TAB at a dose of 0.5 ml subcutaneously (three times with intervals between injections of 10 days). After vaccination, immunity lasts up to 10 years. In the territory where an increase in the incidence is recorded, revaccination is carried out every 3 years.

Travelers to endemic countries are advised to avoid consuming raw fruits or vegetables that may have been soaked in dirty water; in addition, they should not drink plain water, but only bottled from well-known manufacturers or, at worst, boiled.

If pregnant women have an elevated temperature of unclear origin, it is recommended to conduct a blood test for the Vidal, Weil-Felix reaction and for the presence of Obermeyer's spirochete. With typhoid fever, the percentage of premature termination of pregnancy is high (up to 80%), and in most cases it occurs at the 2-3rd week of the disease. The course of the birth act does not change significantly. The course of the disease itself under the influence of pregnancy is often more protracted.

Which doctors to contact if you have typhoid fever

The beginning of diagnostic procedures occurs with an assessment of epidemiological criteria - fever, pallor of the face and skin of the body, a tendency to bradycardia and hypotension, a tendency to inhibition of the nervous system, a violation of the sleep formula, an annoying headache, changes in language, and bloating.

In the general analysis of blood, leukopenia with lymphocytosis, aneosinophilia, in severe cases - thrombocytopenia, moderate hypoplastic anemia are characteristic of the peak period of typhoid-paratyphoid diseases. Even in the absence of signs of bleeding in 20-25% of patients, the reaction to occult blood from the 3rd week becomes positive. In the case of complications, there are signs of acute posthemorrhagic anemia with intestinal bleeding, with perforation - leukocytosis and neutrophilia. Other changes in laboratory and instrumental parameters correspond to those organ complications that arose during typhoid-paratyphoid disease.

A positive bacteriological culture of feces, urine, bile is not a confirmation of the severity of the process, but makes it possible to first diagnose a possible bacteriocarrier. Sowing of bile taken during duodenal sounding can be carried out exclusively during the period of convalescence, because during the height of the disease, this diagnostic technique can lead to undesirable complications - intestinal bleeding, to a greater extent to perforation.

In the leading countries of the world, PCR diagnostics is used to diagnose typhoid.

The serological method is applicable to confirm the diagnosis from the 2nd week of the disease; studies must be carried out in dynamics at intervals of 5-7 days:

RA (Vidal reaction) - diagnostic titer - not less than 1,200, in the future, an increase in titer is possible;
RIGA - more specific, becomes positive on the 6-7th day;

The information is for educational purposes only. Do not self-medicate; For all questions regarding the definition of the disease and how to treat it, contact your doctor. EUROLAB is not responsible for the consequences caused by the use of the information posted on the portal.

Typhoid fever(typhoid fever - English, Abdominaltyphus - German, abdominale fievre - French) - an acute infectious disease caused by salmonella (Salmonella typhi), characterized by fever, symptoms of general intoxication, bacteremia, enlargement of the liver and spleen, enteritis and peculiar morphological changes in the lymphatic intestinal apparatus.

The causative agent of typhoid fever (S. typhi) belongs to the family Enterobacteriaceae, genus Salmonella, species Salmonella enterica, subspecies enterica, serovar typhi and morphologically does not differ from other Salmonella. It is a Gram-negative motile bacillus with peritrichous flagella, does not form spores or capsules, and grows well on ordinary nutrient media. It differs biochemically from other Salmonella in that it ferments glucose without gas production and slows down the release of hydrogen sulfide. The antigenic structure of S. typhi is characterized by the presence of a somatic O (9, 12, Vi) complex and a flagellar antigen H (d). Depending on the amount and location of the Vi antigen, there are 3 types of cultures:

1) the V-form contains the Vi-antigen covering the O-complex, the colonies of such cultures are opaque and are not agglutinated by the O-serum;
2) the W-form does not contain Vi-antigen, the colonies are transparent, the culture is well agglutinated by O-serum;
3) The VW-form has a nested arrangement of the Vi-antigen and is agglutinated by O- and Vi-sera.

The causative agents of typhoid fever are divided into 78 stable phages according to their sensitivity to typical bacteriophages. Phage typing is a convenient label for establishing an epidemiological relationship between diseases and identifying the source of infection. Typhoid bacteria are capable of L-transformation, which may be the result of the evolutionary adaptation of the pathogen to survive in an immune organism. S. typhi is moderately stable in the environment - in soil, water can persist up to 1-5 months, in feces - up to 25 days, on linen - up to 2 weeks, on food - from several days to weeks, especially for a long time - in milk , minced meat, vegetable salads, where at temperatures above 18 ° C they are able to multiply. When heated, they quickly die. Disinfectants (lysol, chloramine, phenol, sublimate) in normal concentrations kill the pathogen within a few minutes.

Epidemiology. Typhoid fever refers to intestinal anthroponoses. Humans are the only source and reservoir of infection. The source of infection is most often chronic bacterial carriers of the causative agent of typhoid fever, which, while remaining practically healthy, secrete salmonella for a long time (years and even decades). Persons with mild and atypical forms of the disease are also dangerous, as they are not always isolated in a timely manner, visit public places, continue to perform official duties, including at food and water supply facilities.

The mechanism of transmission of pathogens is fecal-oral, i.e. Humans become infected by ingesting contaminated water or food. Contact-household transmission of S. typhi is rare, mainly among children. Water outbreaks occur when water sources are polluted with sewage, technical malfunctions of plumbing, sewer systems and structures, as well as due to violations of the water treatment regime. The danger of food contamination lies in the fact that in some products (milk, cold meats) typhoid salmonella can persist and even multiply. The risk of disease in these cases increases due to the large infectious dose of the pathogen.

The disease occurs in all climatic zones and parts of the world. However, it is more common in countries with a hot climate and a low level of sanitary and communal facilities for the population.

Pathogenesis. Developed back in 1924-1934. Sh. Ashar and V. Laverne, the phase theory of the pathogenesis of typhoid fever has generally been preserved to this day. On its basis, the following links of pathogenesis are distinguished: the introduction of the pathogen into the body, the development of lymphadenitis, bacteremia, intoxication, parenchymal diffusion, the release of the pathogen from the body, the formation of immunity and the restoration of homeostasis. The above scheme is conditional, since it has been experimentally proven that, for example, the penetration of pathogens into the blood occurs already within the first two phases. Therefore, it is more correct to speak of interdependent and often coinciding in time links in the pathogenesis of typhoid fever.

For the occurrence of the disease, a certain infectious dose of pathogenic microbes must enter the gastrointestinal tract. In studies on volunteers, American authors found that it ranges from 10 million to 1 billion microbial cells. The introduction of the pathogen occurs in the small intestine, from the lumen of which Salmonella penetrate into solitary follicles and Peyer's patches, causing lymphangitis. Then the microbes enter the mesenteric lymph nodes, where they multiply, and, breaking through the lymphatic barrier, enter the blood through the thoracic duct. There is bacteremia, which coincides with the first clinical signs of typhoid fever. As a result of the bactericidal action of blood, some of the microbes die with the release of endotoxin. The same process occurs in the lymph nodes. Endotoxin circulating in the blood causes intoxication of the body of varying intensity.

Endotoxin has a pronounced neurotropic effect with toxic damage to the nerve centers and the development of inhibition processes in them. Clinically, this is characterized by infectious-toxic encephalopathy, which manifests itself in a kind of lethargy of patients, clouding of consciousness. In the severe course of the disease, it is most pronounced and is called the typhoid state (status typhosus). Endotoxin also acts on the sympathetic nerve endings of the celiac nerve (at the site of excretion) and on the autonomic ganglia, which leads to trophic and vascular disorders in the mucous membrane and lymphatic formations of the small intestine. As a result, there are intestinal ulcers, flatulence, and sometimes diarrhea. In favor of a similar mechanism for the occurrence of ulcerative lesions of the small intestine in typhoid fever is evidenced by the formation of ulcers similar in morphology in experimental animals with the introduction of typhoid endotoxin into the abdominal vegetative nodes [Kazantsev A.P., Matkovsky V.S., 1985]. S. typhi endotoxin also affects the bone marrow, which is manifested by leukopenia.

Endotoxin damage to the myocardium causes its degenerative changes, and in more severe cases, toxic myocarditis. In a severe course of the disease, an infectious-toxic shock may develop. In this case, there is a violation of the tone of peripheral vessels (arterioles and sphincters of postcapillary venules). There is a deposition of blood in the peripheral channel, the exit of its liquid part into the extravasal space. First, relative and then absolute hypovolemia develops with a decrease in venous flow to the heart. Hypoxia, metabolic acidosis, and water and electrolyte imbalances are on the rise. The course and prognosis of infectious-toxic shock are largely determined by cardiovascular insufficiency, damage to the kidneys ("shock kidney"), lungs ("shock lung") and liver. In conditions of prolonged typhoid endotoxemia, the kallikreinkinin system is activated, which can contribute to the development of toxic shock, hemodynamic disorders, functional and morphological changes in internal organs, and hemostasis disorders in typhoid fever.

Therefore, endotoxin intoxication plays a leading role in the pathogenesis of typhoid fever. However, the causative agent itself is of great importance. Salmonella typhoid is carried by the bloodstream throughout the body and is fixed in various organs ("parenchymal diffusion by microbes"), where they are captured by elements of the mononuclear-phagocytic system (MPS). Depending on the functional state of MFS, microbes in the organs either die or cause various focal lesions (meningitis, osteomyelitis, pyelitis, pneumonia, abscesses).

Simultaneously with the dissemination of Salmonella, cleansing of the body begins by removing the pathogen by various excretory organs (kidneys, digestive glands of the intestine, salivary, sweat glands, liver).

Most intensively, bacteria are excreted through the liver, where most of them die, and the rest are excreted with bile into the intestinal lumen. Some of them are excreted with feces into the external environment, and some are again introduced into the lymphoid formations of the small intestine. The hypothesis related to this fact about the allergic genesis of the formation of ulcers of the small intestine now seems unlikely, since typhoid fever is not characterized by pronounced allergic reactions, and intestinal changes can be explained by the toxic effect of endotoxin both on peripheral vegetative nodes and endings, and directly on the lymphatic formations of the intestine.

Protective reactions of the body in typhoid fever develop from the onset of the infectious process. Already on the 4-5th day of illness, specific antibodies related to IgM can be detected in the blood. By the 2-3rd week of the disease, specific immunogenesis reaches its highest development (IgM O-antibodies predominate). At the same time, IgG antibodies appear, the titer of which subsequently increases, and IgM antibodies decrease. The formation of cellular immunity is induced by Salmonella typhoid antigens to a lesser extent than humoral, which is a consequence of a deep deficiency of the total pool of T-cells and T-helpers, as well as a moderate decrease in T-suppressors.

The cyclic course of typhoid fever can be manifested by five periods of pathogenetic changes in the small intestine, sometimes the large intestine is also affected. The first period (1st week of illness) is characterized by a significant swelling of group lymphatic follicles; the second (2nd week) is accompanied by necrosis of these formations. During the third period, rejection of necrotic masses and the formation of ulcers occur. The fourth (3-4 weeks) is called the period of pure ulcers. In the fifth period (weeks 5-6), ulcers heal. When treated with antibiotics, pathogenetic changes in the intestines can develop already against the background of normalization of body temperature.

Post-infectious immunity in typhoid fever is strictly specific and can persist for a long time (15-20 years). However, at present, there are observations of repeated typhoid infections at relatively short intervals (1.5-2 years), which is most often associated with a violation of immunogenesis as a result of antibiotic therapy.

Symptoms and course. The clinical classification of typhoid fever implies its division depending on the clinical forms - typical, atypical (abortive, erased); severity - mild, moderate, severe; the nature of the course - cyclic, recurrent; the presence of complications - uncomplicated, complicated.

The incubation period lasts most often 9-14 days (minimum - 7 days, maximum - 25 days), which depends on the number of microbes that have entered the body. When patients are infected with a large dose of the pathogen (with food outbreaks), the incubation period is usually short, and the disease is more severe than with the water route of infection.

During the course of the disease, the following periods are distinguished:

elementary;
the height of the disease;
extinction of the main clinical manifestations;
recovery.

In typical cases of typhoid fever, the disease begins gradually, sometimes it is even difficult to establish the day of onset of the disease. Patients develop severe general weakness, fatigue, weakness, moderate headache, there may be slight chills. Every day these phenomena intensify, the body temperature rises and by the 4-7th day of illness it reaches a maximum. Intoxication increases, headache and adynamia increase, appetite decreases or disappears, sleep is disturbed (drowsiness during the day, insomnia at night). The chair is usually delayed, flatulence appears. By the 7-9th day, the disease reaches its full development.

When examining a patient in the initial period of the disease, symptoms of general intoxication are predominantly detected without clear signs of organ damage. Inhibition of patients is observed, they are inactive, prefer to lie with their eyes closed, they do not answer questions immediately, in monosyllables. The face is pale, rarely slightly hyperemic, conjunctivitis and herpetic rash usually do not occur. The skin is dry, hot. In some cases, hyperemia of the mucous membrane of the pharynx is possible. Peripheral lymph nodes are usually not enlarged, although some patients have enlargement and tenderness of the posterior cervical and axillary lymph nodes. Relative bradycardia is characteristic, some patients experience dicrotia of the pulse, muffled heart sounds (or only I tone at the top). Arterial pressure goes down.

Dispersed dry rales are heard over the lungs, which is regarded as a manifestation of specific typhoid bronchitis. Pneumonia during this period is detected in rare cases. The tongue is usually dry, covered with a grayish-brown coating, thickened (there are teeth marks along the edges), the tip and edges of the tongue are free from plaque. The abdomen is moderately swollen. Sometimes there is a shortening of the percussion sound in the right iliac region (Padalka's symptom). On palpation, a rough rumbling of the caecum and an increase in pain sensitivity are determined here. From the 3-5th day of illness, the spleen enlarges, and by the end of the 1st week, an enlarged liver can be detected. Sometimes typhoid fever begins in the form of acute gastroenteritis or enteritis without severe general intoxication, when in the first days nausea, vomiting, loose stools without pathological impurities, diffuse pains in the abdomen, and subsequently characteristic symptoms of the disease appear.

By the 7-8th day of the disease, the peak period begins, when a number of characteristic signs appear that facilitate clinical diagnosis. A significant increase in intoxication is manifested in a sharp lethargy of patients, clouding of consciousness (infectious-toxic encephalopathy).

A characteristic roseolous exanthema appears on the skin. There are usually few elements of the rash, they are localized on the skin of the upper abdomen and lower chest. Roseolas are monomorphic with clear boundaries, slightly rise above the level of the skin (roseola elevata). Elements exist from several hours to 3-5 days. In place of roseola, a barely noticeable pigmentation remains. During the febrile period, fresh roseola may appear. In severe forms of the disease, hemorrhagic impregnation of the elements of the rash is possible, which is an unfavorable prognostic sign. Relative bradycardia and dicrotia of the pulse persist, blood pressure decreases even more. Heart sounds become muffled. Approximately 1/3 of patients develop myocardial dystrophy, and in some cases specific infectious-toxic myocarditis may occur. During this period, against the background of bronchitis, pneumonia can develop. It can be caused both by the pathogen itself and by the attached secondary flora, more often coccal. Changes in the digestive system become even more pronounced. The tongue is dry, cracked, with imprints of teeth, covered with a dense dirty-brown or brown coating (fuliginous tongue), the edges and tip of the tongue are free from plaque. The abdomen is significantly swollen, in some patients the stool is delayed, in the majority there is diarrhea (stool of an enteric nature). Rumbling and pain on palpation in the ileocecal region, as well as Padalka's symptom, are more clearly identified. The liver and spleen in this period are always enlarged.

In the period of extinction of the main clinical manifestations, the body temperature lytically decreases, and then normalizes. The phenomena of general intoxication, headache decrease and subsequently disappear. Appetite appears, the tongue is cleared, the size of the liver and spleen decreases.

The period of convalescence begins after the normalization of body temperature and lasts 2-3 weeks, depending on the severity of the disease. As a rule, increased fatigue and vascular lability persist at this time.

In addition to typical clinical forms, atypical forms of typhoid fever can be observed. These include abortive and erased clinical forms. Abortive forms of the disease are characterized by the onset and deployment of more or less characteristic signs of the disease, but with a rapid (after 5-7 days, sometimes after 2-3 days), often critical, decrease in temperature, disappearance of symptoms and transition to the stage of recovery. Erased forms include cases of typhoid fever with short-term subfebrile fever, mild symptoms of intoxication and the absence of many characteristic signs. Body temperature throughout the disease does not exceed 38oC, intoxication is insignificant, there is no bradycardia, flatulence, no rash.

According to established ideas, the hemogram in typhoid fever is characterized by short-term, in the first 2-3 days, moderate leukocytosis, which is replaced by leukopenia with a shift of the leukocyte formula to the left, an- or hypoeosinophilia, and relative lymphocytosis. ESR is often moderately increased. Leukocytosis in the early days usually remains undetected.

At present, the clinical picture of typhoid fever has changed significantly, which is to some extent explained by the frequent use of antibiotics and preventive vaccinations against typhoid and paratyphoid diseases. Mild forms of typhoid fever have become more frequent, in which the phenomena of general intoxication are weakly expressed, many symptoms of the classical course of the disease are absent. The fever lasts only 5-7 days (sometimes 2-3 days) even without the use of antibiotics. The acute onset of the disease is more common (in 60-80% of patients), as well as an increase in lymph nodes. Difficulties in diagnosis are also presented by atypical current cases, for example, typhoid fever with a clinical picture of acute gastroenteritis and short-term fever (1-3 days). During the period of convalescence against the background of normal body temperature, complications may occur in the form of perforation of an intestinal ulcer; such patients are admitted to surgical hospitals. The results of laboratory tests have also changed. So, almost half of the patients have normocytosis, eosinophils remain in the blood, serological reactions may remain negative throughout the disease.

Paratyphoid A and B are acute infectious diseases caused by salmonella and proceeding like typhoid fever.

Paratyphoid A is caused by Salmonella enterica subs. enterica serovar paratyphi A, paratyphoid B - Salmonella enterica subs. enterica serovar paratyphi B. Like typhoid bacteria, they contain O- and H-antigens, but do not have Vi-antigens, have the same morphological properties, and are divided into phage types. Sources of infection in paratyphoid A are sick people and bacteria carriers, and in paratyphoid B, they can also be animals (cattle, pigs, poultry). Pathogenetic and pathological-anatomical disorders in paratyphoid A and B are the same as in typhoid fever.

Paratyphoid A and B are very similar in their clinical features and have some clinical features. It is practically possible to differentiate them from each other and from typhoid fever only bacteriologically - by isolating the pathogen. Only some signs of paratyphoid fever are noted, which distinguish them from typhoid fever.

Paratyphoid A. It is less common than typhoid fever and paratyphoid B. More often it occurs in the form of moderate diseases, but it can also give severe forms of the disease. In the initial period, there is hyperemia of the face, injection of blood vessels of the sclera, herpetic rash on the lips, runny nose, cough. The rash appears early - already on the 4-7th day of illness, it can be polymorphic (roseolous, macular, maculo-papular and even petechial). The main method of confirming the diagnosis is bacteriological. The Vidal reaction is usually negative throughout the illness (in some cases positive at very low titers). Complications and relapses are currently observed somewhat less frequently than with typhoid fever.

Paratyphoid B. Clinically, paratyphoid B is milder than typhoid fever, although there are also severe forms with purulent septic complications. The disease often begins suddenly with the phenomena of acute gastroenteritis, and only then symptoms similar to the clinical manifestations of typhoid fever join. The temperature curve is characterized by a large diurnal range, often wavy. The rash appears on the 4-6th day of illness, roseolous, but more abundant than in typhoid fever. The diagnosis is confirmed by the isolation of the pathogen, however, serological tests can also be used, especially when they are set in dynamics.

The origin of the name - typhoid fever, goes back to ancient times, this disease was known hundreds of years before our era. The term "typhus" used to hide all diseases that were accompanied by clouding of consciousness or insanity. A little later, this infection was classified as a “dangerous” disease, which was associated with the peculiarities of its manifestation, since the symptoms resemble a combination of several diseases at the same time. But today the situation has changed dramatically for the better, although even now this infection cannot be called mild or non-dangerous.

What is typhoid fever and why does it occur? How does the disease manifest itself today and how often does it occur in the modern world? What is the causative agent of this infection and how is it transmitted? What are the phases of the disease and what are the symptoms at different stages of its development? How is typhoid fever tolerated and are complications possible or after it? How is this disease treated and what preventive measures should be observed? All these questions will be answered below.

What is typhoid fever

Despite the fact that this infection has existed since the appearance of life on the planet, scientists constantly learned something new about it.

Typhoid fever is an anthroponotic infection, that is, its source is a sick person who is contagious at almost any stage of the disease.
A person is contagious for a long time, starting from the end of the first week after infection, and the period of bacterial excretion of the pathogen itself lasts about three months.
Adolescents and adults from 15 to 45 years of age are more likely to suffer from typhoid fever, who become infected mainly by water. Infants may encounter the pathogen contained in mother's milk.
Mortality from the disease has always been high. What is the current mortality rate for typhoid fever? - it does not exceed 1% of all recovered patients and is more often associated with complications.
A past infection provides 100% immune protection for only a few years. After this time, with a sharp decrease in immunity, you can re-infect.
The number of cases is decreasing from year to year, if in 2000 the total number of patients with typhoid fever worldwide was within a few million, then today in some countries there are no more than a few hundred. In Russia, the number of cases per year does not exceed a hundred people.

Now typhoid fever is not as terrible as its many complications.

The causative agent of typhoid fever

There are a number of features that can help you learn more about bacteria.

The causative agent of typhoid fever is very mobile. It does not form spores and capsules, but it can be converted into L-forms - this is a temporary cell-free state of the bacterium, which makes it resistant in the human body, including many drugs.
The stick itself is unstable to the action of antiseptics and dies upon contact with alcohol and conventional chlorine-containing solutions.
Bacteria persist in the external environment for a long time - they can stay in water for up to several months, and multiply rapidly in milk, sour cream and jelly.
A feature of the causative agent of typhoid fever is the ability to multiply in the cells of the lymphatic system, causing their death.
The typhoid bacillus tolerates low temperatures well, but when boiled, it quickly dies.

Bacteria have flagella, so they are well mobile, but they grow better on media containing bile. This explains the defeat of the biliary tract and the bacteriocarrier, when a person, years after the disease, is found to have causative agents of typhoid fever in the gallbladder or digestive system.

Causes and ways of transmission of typhoid fever

The main transmission mechanism is fecal-oral, that is, through the oral cavity. But there are several ways of transmission of typhoid fever, among which there are the most important and permissible.

The source of infection in typhoid fever is only a person. It does not matter if it is a patient in the acute phase of the disease, a carrier of bacteria, or someone who has an exacerbated chronic infection. All of them are in the category of especially dangerous for the disease. Susceptibility to the disease is high, so people become infected very quickly.

The pathogenesis of typhoid fever

How a bacterium behaves in the human body depends on the characteristics of its structure. The infectious agent has three important antigens or proteins, which are the cause of the destructive action in the human body. Even when the bacterium dies, a toxin is released that acts further.

The entrance gate of typhoid fever is the oral cavity. But the pathogen easily passes all the defense systems of the body on its way to the intestines. Of course, an insignificant part of the bacteria dies, but this does not make a person feel better.

The causative agent stops in the initial section of the intestine, is fixed to its cells and penetrates into the deeper layers of the lymphatic system. There are multiple formations in the intestine - follicles or accumulations of lymphoid tissue. It is she who makes up a significant part of human immunity, which is often forgotten.

The first blow falls on the immune system, because having penetrated into the lymph nodes, the typhoid bacillus begins to multiply intensively and causes local inflammation. The lymph nodes are the first to be affected in typhoid fever. At this time, there are still no specific manifestations of the disease.

Then the pathogen enters the bloodstream, which is associated with a violation of barrier systems. The conditional second phase of the disease begins - bacteremia. The human body begins to fight, so some of the bacteria die. During their death, endotoxin is released, which contributes to further inflammation. Endotoxin is neurotropic, that is, the nervous system is also involved in the inflammatory process.

Later, typhoid bacteria infect the internal organs, and it was at this time that, in order to get rid of the pathogen, the body tries to bring it out by all available methods: with bile into the intestinal lumen, with urine and feces.

Classification of typhoid fever

The severity of the infection can be mild, moderate and severe, which is determined by the manifestations of the disease. According to its course, typhoid fever is classified into typical and atypical.

A typical infection proceeds cyclically and includes 4 main phases in the development of typhoid fever:

initial phase;
peak period;
resolution of the disease;
recovery phase.

The atypical course of typhoid fever is rare and proceeds relatively favorably. This is an abortive and erased form of the disease.

The disease is also divided into complicated and uncomplicated.

Symptoms at different periods of the disease

Each period of development of typhoid fever proceeds with certain symptoms, has its own characteristics.

First phase of typhoid fever

The incubation period is the most dangerous, in terms of the spread of infection. Indeed, at the moment the pathogen appears in the blood and penetrates into all internal organs, a person is already contagious to others.

The incubation period for typhoid fever is 9 to 14 days. But it can fluctuate within other limits - from a week to 25 days.

The initial period of the disease is long. At this time, the person is concerned about the following symptoms.

Approximately after 7 days, the first period of initial manifestations of typhoid fever ends and the time of increase in symptoms and the height of the disease begins.

Second phase of typhoid fever

The disease does not proceed in waves, but rather with an increase in the main manifestations. During the height of the disease, the symptoms intensify and new ones join, because the causative agent of typhoid fever is in the blood, and the toxin released as a result of its partial destruction affects more and more systems. Changes in the nervous system join the initial clinical manifestations. This period lasts about two weeks.

What signs of typhoid fever can be noted at this stage?

This period is the most dangerous because of the numerous severe symptoms and complications of typhoid fever. In the best case, it passes in 9-10 days.

Resolution and convalescence periods

The next stage of typhoid fever is the resolution of the disease, which lasts about a week. General well-being improves a lot, but gradually.

The temperature drops, but in a special way, the difference between morning and evening sometimes fluctuates within 2.5 ºC.
Sleep is normalized.
The action of the toxin is reduced, so the headaches in typhoid fever also gradually subside.
Appetite improves, kidney function is restored.

The recovery period is the most anticipated after all the manifestations of typhoid fever. But this is a long stage in the development of the disease. For at least two weeks, a person is still worried about some weakness, only gradually the body gets rid of the pathogen, and the functions of all organs are fully restored. The maximum adaptation of the body takes about a month.

Despite timely and properly selected treatment, 3–5% of patients may experience a relapse of the disease. In the third week after the phase of typhoid fever has subsided, the temperature begins to rise slowly, and recovery does not occur. At the same time, the liver and spleen are still enlarged and inflamed, the rash appears earlier, and recurrent typhoid fever is much easier. Another feature is its short course.

Typhoid fever in children follows the same scenario as in adults, with the same clinical manifestations. But mostly school-age children get sick. At an early age in children, the disease proceeds atypically with an acute onset.

Complications of typhoid fever

The desired outcome of any infectious disease is complete recovery. But in the case of typhoid fever, this option is not always the case. The disease is dangerous for its numerous and severe complications. As for this ailment, they occur not only after the subsidence of the disease itself, but also during the active manifestation of one of the periods.

Complications of typhoid fever are possible as follows.

Sometimes during the development of the disease itself, inflammation of one or another organ predominates - the membranes of the brain, lungs, caecum (they are called meningotifus, pneumotyphoid fever, and so on by the presence of inflammation in a certain system).
The second group of complications is the non-specific consequences of typhoid fever, which develop due to the weakness of the immune system after the infection: bronchitis and pneumonia, meningitis, thrombophlebitis, inflammation of the kidney tissue.
Specific complications of typhoid fever are more severe processes, one of them is intestinal bleeding, which occurs in 2% of cases and often manifests itself in the third week, can be local or diffuse (in all departments), occurs due to the weakness of the vascular walls in the affected areas, as well as due to a decrease in blood clotting and a tendency to thrombosis. A small amount of bleeding will have little effect on a person's condition, but a strong one can cause shock.
Perforative peritonitis is an undesirable complication of typhoid fever, when, due to the weakness of the intestinal wall, its membrane breaks through and all the contents enter the abdominal cavity. This is facilitated by sudden movements, increased peristalsis and flatulence. Peritonitis develops in 1.5% of cases and approximately in the second week after the onset of the disease.
During the peak of typhoid fever, no more than 1% of diseases are complicated by infectious-toxic shock, which occurs due to the presence of a large number of bacteria and their toxins in the human body, during its development there is a sharp decrease in temperature, blood pressure drops, sweating increases, and the amount of urine excreted decreases.

Diagnostics

Diagnosis of typhoid fever does not always begin from the moment of taking the tests. An important role in the diagnosis is played by the area of the infection and the manifestation of the disease. Until the pathogen is identified, the typical clinical manifestations of typhoid fever can help doctors. The problem is that the disease in recent years does not always proceed with a classic picture, and in the case of vaccination, symptoms are rare.

Then blood tests are the basis of diagnosis. How is typhoid fever tested? You can conduct a study from the first day of illness and the entire febrile period. For bacteriological seeding on media, blood is taken from the cubital vein under sterile conditions from 5 to 15 ml. After that, in the next few minutes, it is inoculated into vials with 50–100 ml of bile broth. The result is evaluated a few hours or days after taking. But this study has its drawbacks:

if you take blood for typhoid fever and do not keep its concentration with the medium 1:10, then the blood cells will inactivate or defeat the microorganism and the analysis will be meaningless;
in the case when a person was vaccinated against an infection, cells of the causative agent of typhoid fever remain in the blood - there will be a false positive analysis;
in all those who have been ill or who are bacterial carriers, bacteria can also be detected.

To finally determine the diagnosis, serological tests for typhoid fever are carried out. This is the definition of the titer of antibodies to the pathogen in human blood. Do mainly RA and RPGA. A titer of 1:200 is considered positive.

With Vidal's reaction to typhoid fever, the first study is carried out on the 5-7th day from the onset of the disease. Then the same is done at 3-4 weeks. There is an increase in the titer by 2, 3 or more times (1:400, 1:800). Such a study is gradually losing its significance, as other methods help to quickly determine the diagnosis.

The pathogen can also be found in urine, feces, sweat, and rashes.

Treatment for typhoid fever

Regardless of the severity of typhoid fever, it should be treated only in a hospital setting. Patients do not just feel bad, they are carriers of the infection, so they are isolated from others as much as possible.

What principles of treatment should be observed?

According to the clinical guidelines for typhoid fever, patients need a special diet - as sparing as possible during the febrile period with a gradual expansion at the time of recovery. A person needs to be provided with peace and good hygienic conditions.
To relieve symptoms of intoxication and support the body, plasma-substituting solutions, glucose and Ringer's solution are used.
The main treatment for typhoid fever is a long-term prescription of antibiotics, and in the case of a bacteriocarrier, antibacterial drugs are prescribed for a period of several months.
In case of a severe course of the infection, hormonal preparations are prescribed.

Prevention of typhoid fever

For the purpose of general prevention of typhoid fever, compliance with sanitary and hygienic standards is monitored when water is taken from open sources for use in everyday life. Public catering enterprises and the food industry are monitored for their compliance with the sanitary regime.

Personal prevention includes the refusal to swim in unfamiliar water bodies, hygiene, washing raw vegetables and fruits, heat treatment of meat and milk.

In the foci of infection, it is disinfected, as well as the isolation of sick people.

Vaccination is also used for prevention. First of all, vaccinations are given in areas where outbreaks of typhoid fever are often recorded. In other countries - according to epidemic indications.

What is special about typhoid fever? - its long course and diverse manifestations. Numerous symptoms with damage not only to the intestines, but also to the immune system, the nervous system are characteristic of this infection. Therefore, typhoid fever does not need to be treated on its own, the most correct help is a timely visit to a doctor.