What is the period during illness called? Typhoid fever - causes, symptoms, types, diagnosis and consequences. Entrance gates of infection
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What is typhoid fever?
Typhoid fever is an acute infectious disease with a predominant lesion gastrointestinal tract which is caused by bacteria of the genus Salmonella. Typhoid fever belongs to the category of anthroponotic diseases, which means that the causative agent of this pathology can only exist in the human body. Typhoid fever is a disease whose prevalence largely depends on socio-economic conditions. Thus, in the past, outbreaks of this disease occurred during periods of war, economic crisis and other social disasters.
Taking into account statistical data World Organization Healthcare, all countries of the world, depending on the prevalence of typhoid fever, are conventionally divided into several groups. The first group includes Canada, Belgium, Sweden and other countries with a high level of economic development. In these regions, there is no more than 1 annual case of this infection per 100,000 people. TO last group include countries such as Chile, Colombia, Peru. More than 30 cases per 100,000 people are reported annually in these countries.
In the territory Russian Federation Since 2007, the number of cases of typhoid fever has decreased significantly. If from 2003 to 2006 the annual number of patients varied from 150 to 180, then from 2007 to 2013 this figure did not exceed 80 people. In 2014, 14 patients were registered (13 adults and 1 child).
Causes of typhoid fever
Typhoid fever develops due to the penetration of pathogenic bacteria called salmonella into the body. There are two types of salmonella, including Salmonella enterica and Salmonella bongori. Each species is represented by various subspecies. The causative agent of typhoid fever is the bacterium Salmonella typhi, which belongs to the subspecies Salmonella enterica. This species also includes such serovars (subspecies) as Salmonella typhimurium, derby, paratyphi A and B. The causative agent of typhoid fever
The causative agent of typhoid fever is Salmonella typhi, a mobile rod with a complex antigenic structure. This is a fairly stable bacterium in the external environment, which persists for many months in water bodies, soil, vegetables and fruits, as well as in dairy products (in which salmonella can long time multiply). Bacteria can be killed with 96 percent ethyl alcohol or a 3 percent chloramine solution. The main characteristic of Salmonella is its complex antigenic structure. It is represented by somatic and flagellar antigen.Salmonella produces and secretes a strong endotoxin, which determines the clinical picture of the disease.
The antigenic structure of Salmonella includes:
- O-somatic antigen, is represented by a liposaccharide complex that is resistant to high temperatures;
- N-flagellar antigen, quickly deteriorating under the influence of high temperatures.
Transmission of typhoid fever
Typhoid fever is an infection with a fecal-oral transmission mechanism, which means that pathogenic bacteria enter the body primarily through the mouth. Infection can be through food or water. Salmonella persists in soil or water for a long time, which makes this route of infection the most common. Contact or household way infection is extremely rare, mainly in children. This can occur through direct contact with a source of infection (for example, a child may put a toy in his mouth that has been contaminated with salmonella).Once in the blood, salmonella leads to the development of bacteremia. Bacteremia refers to the circulation of bacteria in the blood (which is normally sterile). This process coincides with the appearance of the first symptoms of typhoid fever and the end of the incubation period. The more massive the bacteremia, the stronger and more pronounced the symptoms of the disease.
Pathogenesis of typhoid fever
Pathogenesis refers to the entire complex of mechanisms necessary for the development of the disease. In typhoid fever, pathogenesis occurs at several stages.The stages of the pathogenesis of typhoid fever are:
- penetration of salmonella into the gastrointestinal tract along with the source of infection (food, water);
- introduction of bacteria into the mucosa ileum;
- reproduction of Salmonella in solitary follicles and Peyer's patches, from where they migrate to the mesenteric lymph nodes;
- the development of inflammation in the mesenteric lymph nodes and an increase in the concentration of salmonella in them;
- release of bacteria into the blood and development of bacteremia;
- spread of bacteria through the bloodstream throughout all organs and tissues;
- the formation of foci of infection in the spleen, liver and other organs.
Thus, a vicious circle develops - bacteria enter the blood, where they die and release endotoxin, and are replaced by new salmonella from internal organs and lymph nodes. At the same time, endotoxin, having a strong neurotropic effect, determines the clinical picture of typhoid fever.
The effects of Salmonella endotoxin are:
- neurotoxic effect with damage to the central nervous system and the development of toxic encephalopathy;
- damage to nerve endings and autonomic ganglia, which leads to the development of ulcers on the intestinal mucosa;
- cardiotoxic effect, which manifests itself in dystrophic changes in the heart, which ultimately leads to the development of toxic myocarditis;
- disturbance of peripheral vascular tone, leading to a drop in blood pressure and the development of collapse;
- development of infectious-toxic shock, which is accompanied by a violation of water and electrolyte balance;
- kidney damage and the development of “shock kidney” syndrome.
Carriage for typhoid fever
The source of Salmonella typhus for healthy person in most cases it is a bacteria carrier. A carrier is someone who, while remaining practically healthy and not showing any signs of illness, excretes environment pathogenic bacteria. The discharge can last from several weeks to several decades. This phenomenon can be explained by several reasons. First of all, it can be a convalescent bacteria carrier, that is, a person recovering from an illness. During the recovery period, bacterial carriage can be either short-term or long-term. Short-term carriage is observed in dysentery or diphtheria (from 3 to 4 months). As for typhoid fever, in this case carriage lasts up to 10 years.The source of infection can also be patients with atypical forms of typhoid fever. In this case, the disease occurs without classic symptoms and is therefore not diagnosed in time. People with such forms of typhoid fever are treated on an outpatient basis (that is, at home) for a long time and remain not isolated from family members. In this case, infection can occur by consuming contaminated food or water. Dairy products pose a great danger, since bacteria can not only survive in them for a long time, but also multiply.
The population's susceptibility to typhoid fever is very high. In areas where an outbreak of typhoid fever is recorded, up to 50–60 percent of the total population may become ill.
Clinical picture of typhoid fever
There are several stages in the clinical picture of typhoid fever. Each of these stages (or periods) characterizes a specific mechanism of pathogenesis. For example, the incubation period corresponds to the period of dissemination of typhoid bacteria in the lymph nodes. The moment bacteria enter the bloodstream is accompanied by the appearance of the first symptoms and corresponds to the initial period of the disease. The periods (stages) of typhoid fever include:
- incubation period;
- initial period;
- period of the height of the disease;
- period of extinction of the main symptoms;
- recovery period.
Incubation period for typhoid fever
The incubation period is the period from the moment Salmonella enters the human body until the first symptoms appear. For typhoid fever, the incubation period usually lasts from 9 to 14 days. It can last up to 25 days. During this time, Salmonella that enter the body actively multiply in the ileal mucosa and lymph nodes. The moment the bacteria enter the bloodstream, the incubation period ends and the first signs of the disease appear.The duration of this period depends on the concentration of microbes that initially entered the body and on the route of infection. In case of food contamination, the incubation period is short - from 7 to 9 days, and the disease is highly severe. The water route of infection is characterized by a longer incubation period.
Period of onset of the disease
As a rule, the disease begins gradually. Even severe forms of typhoid fever are characterized by a gradual development of the clinical picture. Typhoid fever begins with the appearance of weakness, malaise, and a feeling of weakness. The temperature also rises, a moderate headache and chills appear. It appears that the person is coming down with a common cold. This state continues for a week. During this week, the headache intensifies, weakness and adynamia increase, appetite disappears, and stool retention is noted. By the end of 7–8 days, the temperature reaches its maximum of 40 degrees, which means the height of the disease. It is extremely rare that with the acute onset of the disease, all these symptoms develop within one to two days.The peak period for typhoid fever
Starts 7–8 days after the onset of the first symptoms. During this period, they are most pronounced general symptoms intoxication. Due to the neurotropic effect of endotoxin, encephalopathy develops, which is manifested by lethargy of patients. The patient's consciousness is clouded and confused (typhos means fog, which is where the name of the disease comes from), most often he lies in bed with eyes closed. Answers questions with difficulty, in monosyllables. The patient's skin is sharply pale, hot and dry. On examination, the lymph nodes are enlarged, the heart rate is low (bradycardia), and blood pressure is also reduced. The tongue is dry, covered with a brown coating (coated tongue), thickened, and teeth marks are visible along its edges. On the 8th – 9th day they appear specific symptoms typhoid fever - roseola rash, enteritis, toxic myocarditis.Period of extinction of the main symptoms
The period of extinction of the main symptoms begins from the moment the temperature decreases, the tongue clears, and the stool normalizes. All manifestations of general intoxication - headache, weakness, fatigue - go away. Body temperature begins to decrease, but still does not reach normal.Despite the reduction of symptoms, this period of the disease is very dangerous. It is at this moment that the disease can manifest itself again, that is, a relapse of typhoid fever is possible. Therefore, during the period of extinction of the main clinical symptoms the patient continues to remain in the hospital under constant supervision.
Recovery period
The recovery period for typhoid fever begins with normalization of body temperature. It lasts 2 weeks.Symptoms of typhoid fever
Typhoid fever is characterized by numerous clinical symptoms. The presence of certain signs of the disease depends on the shape and severity of the abdominal type. All symptoms can be mild, moderate or extremely severe. Also, symptoms may vary depending on the nature of the disease. Typhoid fever can occur cyclically and with periods of exacerbations (recurrent nature of the course). Symptoms of typhoid fever are:
- fever;
- rash;
- intestinal bleeding;
- damage to internal organs.
Fever due to typhoid fever
Fever during typhoid fever is a manifestation of a general intoxication syndrome. Fever develops in response to bacteremia. Having reached 39 - 40 degrees by the end of the week, the temperature continues to remain at this level for 2 - 3 weeks. Sometimes it can acquire a Botkin character, in which case the temperature occurs in waves. The decrease in fever occurs slowly and in stages, also with fluctuations between morning and evening temperatures.Typhoid fever rash
A specific manifestation of typhoid fever is a rash. It is caused by a violation of permeability blood vessels and saturation of the epidermis with blood elements. With typhoid fever, the rash is usually roseola, and the element of such a rash is roseola. Roseola is a round red spot, ranging in size from 1 to 5 millimeters. It does not peel off or create itching, and therefore does not cause discomfort to the patient. However, despite this, the period of rash itself is accompanied by a sharp rise in body temperature and a deterioration in the patient’s condition. The patient's consciousness becomes even more clouded, and he becomes sleepy, lethargic, and apathetic.With typhoid fever, the rash appears on the 8th – 9th day from the onset of the disease. It is localized on upper sections belly and chest. Sometimes elements of the rash can protrude above the skin level and acquire clear boundaries. Most often, the rash is mild and lasts from 3 to 5 days. It may disappear in just one or two days, but then it will appear again. At severe course disease, the rash becomes petechial-hemorrhagic in nature. In this case, the elements of the rash are saturated with blood, which indicates an unfavorable prognosis.
In rare cases, the rash characteristic of typhoid fever may be absent. The absence of a rash on the patient's body should not exclude the diagnosis of typhoid fever.
Intestinal bleeding in typhoid fever
In typhoid fever, due to specific damage to the gastrointestinal tract by Salmonella, signs of enteritis are revealed. On initial stages stool retention is noted, but already during the full-blown stage clinical manifestations there is enteric stool (that is, diarrhea). Some patients remain constipated.The abdomen of a patient with typhoid fever is swollen and painful on palpation. In moderate and severe cases, intestinal paresis develops, which is characterized by a complete absence of peristalsis. In this case, gases and intestinal contents accumulate in the intestinal lumen, making the abdomen tense and painful.
As a result of the specific effect of Salmonella endotoxin on nerve endings in the intestinal mucosa, trophic and vascular changes develop. They, in turn, lead to malnutrition of the intestinal mucous layer and the development of trophic ulcers. Trophic ulcers– these are those that develop as a result of impaired nutrition (trophism) of the mucous membrane. Ulcers go through several stages in their development.
The stages of development of ulcers are:
- first week– enlargement of lymphatic follicles of the intestinal mucosa;
- second week– necrosis (death) of enlarged formations;
- third week– rejection of necrotic (dead) masses and the formation in their place of small depressions, that is, ulcers;
- fourth week– stage of clean ulcers;
- fifth week– stage of healing of ulcers.
Intestinal bleeding with typhoid fever usually occurs 3 to 4 weeks from the onset of the disease. An integral symptom of perforated intestinal ulcers is pain. The patient complains of sudden, acute pain.
Often the pain is localized in the lower abdomen on the right, but can also be diffuse. Pain syndrome accompanied by severe tension in the abdominal muscles, rapid breathing and a drop in blood pressure. Symptoms of ulcer perforation are pronounced in moderate forms of typhoid fever. This is explained by the fact that the patient’s consciousness in this case is not very clouded, and pain sensitivity remains. If intestinal bleeding begins against the background high temperature and the patient’s clouded consciousness, then his clinic is very worn out.
Upon examination, a pronounced protective tension of the abdominal muscles is revealed. The abdomen is dense and painful, movements of the abdominal wall during the act of breathing are barely noticeable or completely absent. Signs of peritoneal irritation appear, such as the Shchetkin-Blumberg symptom.
Damage to internal organs due to typhoid fever
After typhoid bacteria enter the bloodstream, they are carried through the bloodstream throughout the body to various organs and systems. So, along with the blood flow, they enter the liver, spleen, kidneys, and heart.Heart damage
Salmonella endotoxin leads to dystrophic changes in the heart with the development of toxic myocarditis. The term “myocarditis” means that the muscle layer of the heart is affected by the inflammatory process. This leads to the fact that the heart ceases to perform its basic functions. Normally, the main function of the heart is the “pump function”, which provides blood supply throughout the body. Due to damage to the muscle layer, the heart stops contracting effectively and pumping blood. Contractions become weak and muffled, which explains bradycardia (rare heartbeats), arterial hypotension (low blood pressure). When examining the patient, heart sounds are dull, weak, blood pressure is low, pulse is within 50 beats per minute.
The consequence of heart damage is hypoxia or oxygen starvation, water-electrolyte imbalance, hypovolemia (decreased circulating blood volume).
Kidney and lung damage
Against the background of hypovolemia, the syndrome of “shock kidney” and “shock lung” develops. Shock kidney is a condition in which all functions of the kidney are disrupted - filtration, secretion and excretion. Diuresis (daily volume of urine) with this complication decreases sharply, up to anuria. Due to impaired excretory function, metabolic products begin to accumulate in the body - creatinine, urea. This further aggravates the course of the disease and causes the development of infectious-toxic shock. Treatment of a shock kidney should be emergency and include measures to restore diuresis and remove toxic metabolic products.
Another consequence of hypovolemia is shock lung. With this syndrome, large amounts of fluid accumulate in the alveoli of the lungs. Thus, the lungs are filled not with air, but with water, which underlies pulmonary edema. It becomes difficult for the patient to breathe, and shortness of breath increases.
Typhus and typhoid fever
Typhoid fever is often confused with typhus, which is incorrect. Typhus is an acute infectious disease caused by bacteria of the genus Rickettsia. Unlike typhoid fever, this disease is not classified as intestinal infections. Typhus is characterized by predominant damage to the nervous and cardiovascular systems. This infection is transmitted mainly through lice, most often body lice and less often head lice. Infection occurs through the bites of these insects. Lice themselves become infected from sick people. Thus, body lice are carriers of infection.Once a louse has bitten a sick person, it can live for 30 to 45 days. A lice bite is very painful, causing a person to begin painfully scratching the bite site. By scratching the bite, he rubs lice feces into the skin, through which infection occurs. Rickettsia then enters the bloodstream and is spread throughout the body. The target for rickettsiae are endothelial cells, that is, structural elements of the vascular wall. Developing inside the vascular wall, rickettsiae destroy it, which leads to the destruction of blood vessels. Typhus is characterized by the phenomenon of vasculitis, that is, damage to the endothelial wall of blood vessels. This causes the development in the clinical picture of the disease of such symptoms as hemorrhages in the skin and mucous membranes, an enlarged spleen, and a decrease in blood pressure.
One more distinctive feature typhus is a lesion of the nervous system. The patient's consciousness is confused, and sometimes signs of meningism may develop. An extremely severe manifestation of typhus is typhoid status. During it, the patient experiences psychomotor agitation, memory disorders, and insomnia progresses. If the patient falls asleep, he will have nightmares. Sometimes delusions, hallucinations and other psychotic symptoms may develop.
Forms of typhoid fever
Sometimes typhoid fever may occur atypically, that is, not include specific symptoms. There are abortive and erased subclinical forms. The abortive form is characterized by the classic onset of the disease with a sharp and sudden disappearance of all symptoms. Initially, the disease develops as usual - the temperature rises, weakness and apathy develop. On days 2–3, gastrointestinal symptoms increase. However, on the 5th – 6th day from the onset of the disease, all symptoms suddenly disappear - the temperature drops sharply, the pain disappears, and recovery occurs. With erased and atypical forms of typhoid fever, many characteristic symptoms not expressed or completely absent. So, the temperature may not exceed 38 degrees, the abdominal pain is mild, and there is no rash at all.Consequences of typhoid fever
Typhoid fever refers to serious illnesses and often entails various negative consequences for the patient’s health. The cause of complications is the active activity of bacteria in the human body. The age of the patient is also an important factor, since most often the consequences are diagnosed in elderly people. The consequences of typhoid fever are divided into specific and nonspecific. Specific complications of typhoid fever
This category includes those consequences that are characteristic only of typhoid fever. The most important among the specific consequences of this disease is infectious-toxic shock. This condition develops at the height of the disease due to the massive entry into the blood of toxins that are secreted by typhoid bacteria. These toxins provoke vasospasm, resulting in impaired blood circulation.Toxins also contribute to increased release of adrenaline and other hormones into the blood, which increase vascular spasm. Blood ceases to perform its transport function, which leads to tissue ischemia (insufficient blood supply to tissues) and metabolic acidosis ( increased content acidic products in the blood). All this becomes the cause of degenerative (destructive) changes in organs and tissues, edema and other pathological conditions, which can lead to fatal outcome. Infectious-toxic shock begins with an increase in body temperature and develops in several stages.
The stages of infectious-toxic shock are:
- Early. The patient's consciousness remains clear, anxiety, motor restlessness, swelling of the face and upper half of the body may be observed. Breathing becomes rapid and blood pressure rises and falls in waves. In children, the early stage is usually accompanied by vomiting, diarrhea, and abdominal (upper) pain.
- Expressed. Anxiety and general excitement of the first stage are replaced by an apathetic state and motor retardation. The patient's skin becomes pale, cold and moist. Over time, hemorrhages may appear on the skin. The limbs take on a bluish tint. Temperature and blood pressure decrease, breathing and pulse become weak. The volume of urine decreases sharply. During this period, various pathologies of the kidneys and respiratory system develop.
- Decompensated. Arterial pressure and body temperature continues to fall. The patient suffers from convulsions, loss of consciousness or coma is possible. The skin becomes pronounced blue tint. There is no urination. Symptoms of dysfunction in all organs begin to appear.
Nonspecific complications of typhoid fever
This group includes diseases that can act as consequences not only of typhoid fever, but also of other diseases. Typhoid bacteria, in addition to the intestines, can affect other organs, causing inflammatory processes. The situation becomes more complicated when a secondary bacterial infection joins the primary inflammation.TO nonspecific consequences typhoid fever include:
- from the respiratory system– pneumonia (inflammation of lung tissue);
- from the side of blood vessels– thrombophlebitis (inflammation of the veins);
- from the side of the heart– myocarditis (inflammation of the heart muscle);
- from the kidneys– pyelitis (inflammation in the renal pelvis), pyelonephritis (inflammation of the kidney tissue);
- from the nervous system– peripheral neuritis (inflammation of the nerves), meningoencephalitis (inflammation of the brain and, in some cases, spinal cord followed by paralysis);
- from the musculoskeletal system– arthritis (inflammation of the joints), chondritis (inflammation cartilage tissue), periostitis (inflammation of the periosteum);
- from the outside genitourinary organs – cystitis (inflammation of the bladder), prostatitis (inflammation of the prostate).
Diagnosis of typhoid fever
Due to pronounced clinical signs diseases, doctors establish a preliminary diagnosis of typhoid fever even before the results laboratory research. Information about the epidemiological situation also helps to establish a preliminary diagnosis. The main symptoms, the presence of which raises suspicion of typhoid fever, are:
- dryness and pallor of the skin;
- elevated temperature;
- changes in the tongue - its enlargement, dryness and coating in the center with a coating;
- the appearance of a reddish rash on the body;
- dyspeptic disorders;
- manifestations of intoxication syndrome.
Tests for typhoid fever
Tests for typhoid fever are prescribed both to identify the causative agent of the disease and to determine the severity of the disease and monitor the effectiveness of treatment.The tests that are prescribed for the diagnosis of typhoid fever include:
- general clinical tests;
- bacteriological tests (cultures);
- serological tests.
Bacteriological studies help to detect the causative agent of typhoid fever in biological fluids of the body. TO serological studies are used to determine the antigens of the causative agent of typhoid fever in the human body. Serological tests are especially important in diagnosing bacterial carriage.
Tests for typhoid fever
General clinical tests for typhoid fever
General clinical tests for typhoid fever are prescribed from the moment the patient consults a doctor. Changes in tests are not specific to a given disease, but they help determine the condition of the patient’s body as a whole. The main tests are a hemogram and a general urinalysis.
Possible changes in the clinical blood test for typhoid fever are:
- moderate increase in leukocytes (white blood cells);
- leukopenia (decreased number of white blood cells);
- absence of eosinophils (a subtype of leukocytes);
- moderate increase in the number of lymphocytes (a subtype of anucleate leukocytes);
- moderate acceleration of erythrocyte sedimentation.
Possible changes in a general urine test for typhoid fever are:
- presence of protein;
- high levels of red blood cells (RBCs);
- high cylinder level.
Cultures for typhoid fever
Early specific diagnostics Typhoid fever begins with bacteriological studies based on cultures. Various biological fluids of the body act as material for sowing.Biological fluids that are used for culture for typhoid fever include:
- blood;
- urine;
- feces;
- content duodenum(bile);
To make a diagnosis, collection of biological fluids should be carried out before the start of etiotropic therapy.
Blood culture
At early diagnosis For typhoid fever, they most often resort to blood culture, in which the pathogen is easily detected even during the incubation period. It is best to take blood samples during periods of increased body temperature. If you start antibacterial therapy blood is drawn immediately before the next dose of the drug is administered. Up to 20 milliliters of blood are inoculated onto special liquid nutrient media. The most commonly used blood culture medium for typhoid fever is Rappoport's medium, which consists of a bile-based broth with the addition of glucose and a special dye. The nutrient medium with blood is placed in an incubator with a temperature of 37 degrees Celsius for 10 days. Laboratory technicians check the cultures every day for signs of growth of bacterial colonies - turbidity of the liquid, change in its color. If there is no growth at the end of ten days, the test result is negative. If signs of colony growth are detected, seeding is carried out on solid media in Petri dishes. New crops are again incubated at 37 degrees Celsius for 24 hours. As a result, bacterial colonies grow on the surface of a dense medium, which must be identified using a series of biochemical tests. In parallel with this, the sensitivity of bacteria to various antibacterial drugs. The final blood culture results are obtained after four days.
Urine culture
Urine testing to identify the causative agent of typhoid fever can be carried out throughout the entire period of the disease. Considering the fact that the pathogen is excreted in the urine inconsistently and for a short time, urine cultures should be repeated every 5 to 7 days. Collected urine must be delivered to the laboratory for culture no later than two hours from the moment of collection. The longer the material is stored, the greater the chance of the pathogen dying off or other bacteria growing. Uroculture is obtained by the same method of seeding and incubation as blood culture.
Sowing feces
Stool cultures to diagnose typhoid fever are performed starting from the second week of illness. Stool is collected using a sterile spatula, wire loop or spoon. A sterile container is used to transport the material. In the laboratory, coproculture is prepared by inoculating feces on solid nutrient media and incubating at 37 degrees Celsius for 18 to 24 hours.
Serological examination for typhoid fever
Serological tests for the diagnosis of typhoid fever reveal special antigens and antibodies in the patient's blood. There are several main antigens that are detected when testing a patient's blood.The main antigens that are found in the blood of a patient with typhoid fever are:
- O-antigen;
- H-antigen;
- Vi-antigen.
Antibodies are special proteins that are produced immune system human to neutralize pathogen antigens. High levels of antibodies indicate the formation of stable immunity to the pathogen, which is observed during the recovery period or during bacterial carriage. Antigens and antibodies are determined in the patient’s blood using special serological reactions.
Serological examination reactions for typhoid fever include:
- Vidal reaction;
- reaction indirect hemagglutination;
- fluorescent antibody reactions.
Vidal reaction for typhoid fever
The Widal reaction is a direct agglutination (gluing) reaction, which allows one to determine the presence of O-antigen in the patient’s serum. This reaction is widely used in the diagnosis of typhoid fever, but it is not specific, giving false-positive results due to the recognition of other types of Salmonella. For the Widal reaction, 2–3 milliliters of venous blood is required, usually from the cubital vein. The blood is left for some time in the test tube until it completely clots. The serum formed on the surface is sucked out with a sterile syringe and placed in another tube. The agglutination reaction consists of a step-by-step dilution of the patient's serum to a ratio of 1 to 800 and the addition of a special diagnosticum (antibodies to the desired antigens).The steps of the Widal reaction are:
- filling a number of test tubes with 1 milliliter of saline solution;
- adding 1 milliliter of serum to the first test tube and obtaining a dilution of 1 to 50;
- sucking 1 milliliter from the first test tube with a pipette and adding it to the second test tube - a dilution of 1 to 100 is obtained;
- repeat the manipulations until solutions are obtained in a ratio of 1 to 800;
- adding a special diagnosticum to each test tube;
- two-hour incubation at 37 degrees Celsius;
- subsequent maintenance of the tubes at room temperature during the day.
Indirect hemagglutination reaction
The indirect hemagglutination reaction is more specific and sensitive for the diagnosis of typhoid fever. With its help, all three main antigens of the pathogen are determined. Red blood cells sensitized to Salmonella antigens serve as diagnostic agents. The reaction technique is similar to the Widal reaction technique, however, dilutions start from 1 to 10. Hemagglutination manifests itself in the form of the formation of a red precipitate at the bottom of the test tube, similar to an inverted umbrella. A reaction is considered positive when a precipitate forms in a test tube with a dilution of 1 to 40 or more. In subsequent tests after 5 and 10 days, antibody titers increase 2–3 times, especially O-antibodies. An increase in the titer of Vi- and H-antibodies is observed in patients during the recovery period. Their levels may also be high in carriers.
Fluorescent antibody reactions
From the first days of the disease, the pathogen can be identified using fluorescent antibody reactions. These reactions involve the detection of pathogen antigens using antibodies marked with fluorescent substances. “Marked” antibodies are added to biological diagnostic material (blood, feces, urine) and studied using special microscopes. When an antibody binds to a pathogen antigen, a glow is visible under the microscope. Preliminary reaction results are ready within one hour, and final results are ready in 10–20 hours. Fluorescent antibody reactions are quite specific and highly sensitive, but are rarely used in the diagnosis of typhoid fever.
Infectious diseases have certain periods, or phases.
● Incubation (hidden) period - the time when the infection enters the body and goes through its development cycle, including reproduction. The duration of the period depends on the characteristics of the pathogen. At this time, there are still no subjective sensations of illness, but reactions between the infection and the body are already occurring, mobilization protective forces body, changes in homeostasis, increased oxidative processes in tissues, allergies and hypersensitivity increase.
● Prodromal, or initial period of the disease. The first unclear symptoms of the disease are characteristic: malaise, often chills, headache, minor muscle and joint pain. Inflammatory changes and moderate hyperplasia of the lymph nodes and spleen often occur in the area of the entrance gate. The duration of this period is 1–2 days. Upon reaching top level hyperergy sets in next period.
● Period of main manifestations of the disease. The symptoms of a specific infectious disease and characteristic morphological changes are clearly expressed. This period has the following stages.
The stage of increasing manifestations of the disease.
The stage of height, or maximum severity of symptoms.
The stage of extinction of the manifestations of the disease. This period already reflects the beginning of hypoergy, indicating that the body has managed to limit the infection to some extent and in the area of its localization the specificity and intensity of the infection is most clearly manifested. During this period, the disease can occur without complications or with complications, and the patient’s death may occur. If this does not happen, the disease progresses to the next period.
The period of the main manifestations of the disease reflects the beginning of a decrease in reactivity, indicating that the body has managed to localize the infection to some extent. In the area of its localization, the specificity of the infection is most clearly manifested. During this period, complications may develop, even the death of the patient. If this does not happen, the next period of illness begins.
● The period of extinction of the disease is the gradual disappearance of clinical symptoms, normalization of temperature and the beginning of reparative processes.
● The period of convalescence (recovery) can have different durations depending on the form of the disease, its course, and the patient’s condition. Often clinical recovery does not coincide with full restoration morphological damage, the latter often lasting longer.
Recovery can be complete when all impaired functions are restored and incomplete if there are residual effects (for example, after polio). In addition, after clinical recovery, carriage of infectious agents occurs, which is obviously associated with insufficient immunity of the convalescent, improper treatment or other reasons. Carriage of pathogens of a number of diseases is possible for years (for example, in those who have suffered from malaria) and even throughout their lives (in those who have suffered from typhoid fever). The carriage of infectious agents is of great epidemiological importance, since carriers who are not aware of the release of microorganisms by them can become an unwitting source of infection to others, and sometimes - a source of epidemic.
In the development of the disease, four periods (stages) are usually distinguished: latent, prodromal, the period of the height of the disease and the outcome, or the period of the end of the disease. Such periodization developed in the past during the clinical analysis of acute infectious diseases (typhoid fever, scarlet fever, etc.). Other diseases (cardiovascular, endocrine, tumors) develop according to different patterns, and therefore the given periodization is not very applicable to them. A.D. Ado distinguishes three stages of disease development: the onset, the stage of the disease itself, and the outcome.
Latent period(in relation to infectious diseases - incubation) lasts from the moment of exposure to the cause until the appearance of the first clinical signs of the disease. This period can be short, as with the action of chemical warfare agents, and very long, as with leprosy (several years). During this period, the body’s defenses are mobilized, aimed at compensating possible violations, to destroy pathogenic agents or to remove them from the body. It is important to know the features of the latent period when carrying out preventive measures (isolation in case of infection), as well as for treatment, which is often effective only in this period (rabies).
Prodromal period- this is the period of time from the first signs of the disease to the full manifestation of its symptoms. Sometimes this period manifests itself clearly ( lobar pneumonia, dysentery), in other cases it is characterized by the presence of weak but clear signs of the disease. With mountain sickness, for example, this is causeless fun (euphoria), with measles - Velsky - Koplik - Filatov spots, etc. All this is important for differential diagnosis. At the same time, identifying the prodromal period in many chronic diseases is often difficult.
Period of pronounced manifestations, or the height of the disease, is characterized by the full development of the clinical picture: convulsions with insufficiency of the parathyroid glands, leukopenia with radiation sickness, a typical triad (hyperglycemia, glycosuria, polyuria) with diabetes mellitus. The duration of this period for a number of diseases (lobar pneumonia, measles) is determined relatively easily. At chronic diseases with their slow progress, the change of periods is elusive. In diseases such as tuberculosis and syphilis, the asymptomatic course of the process alternates with its exacerbation, and new exacerbations are sometimes noticeably different from the primary manifestations of the disease.
Outcome of the disease. The following outcomes of the disease are observed: recovery (complete and incomplete), relapse, transition to a chronic form, death.
Recovery- a process that leads to the elimination of disorders caused by the disease and the restoration of normal relations between the body and the environment, in humans - primarily to the restoration of working capacity.
Recovery can be complete or incomplete. Full recovery is a condition in which all traces of the disease disappear and the body completely restores its adaptive capabilities. Recovery does not always mean returning to your original state. As a result of the disease, changes in various systems, including the immune system, may appear and persist in the future.
In case of incomplete recovery the consequences of the disease are expressed. They remain for a long time or even forever (fusion of the pleura, narrowing of the mitral orifice). The difference between complete and incomplete recovery is relative. Recovery can be almost complete, despite a persistent anatomical defect (for example, the absence of one kidney, if the second fully compensates for its function). One should not think that recovery begins after the previous stages of the disease have passed. The healing process begins from the moment the disease occurs.
The idea of recovery mechanisms is formed on the basis general position that illness is the unity of two opposing phenomena - the actual pathological and the protective-compensatory. The predominance of one of them decides the outcome of the disease. Recovery occurs when the complex of adaptive reactions is strong enough to compensate for possible disturbances. Recovery mechanisms are divided into urgent (emergency) and long-term. Urgent ones include such reflex protective reactions as changes in respiratory rate and heart rate, the release of adrenaline and glucocorticoids during stress reactions, as well as all those mechanisms that are aimed at maintaining the constancy of the internal environment (pH, blood glucose, blood pressure, etc.). d.). Long-term reactions develop somewhat later and last throughout the disease. This is primarily the inclusion of backup capabilities of functional systems. Diabetes mellitus does not occur when even 3/4 of the pancreatic islets are lost. A person can live with one lung, one kidney. A healthy heart can perform five times more work under stress than at rest.
Enhanced function increases not only as a result of the inclusion of previously non-working structural and functional units of organs (for example, nephrons), but also as a result of an increase in the intensity of their work, which in turn causes activation of plastic processes and an increase in organ mass (hypertrophy) to a level when the load for each functioning unit does not exceed normal.
The activation of compensatory mechanisms, as well as the cessation of their activity, depends primarily on the nervous system. P.K. Anokhin formulated the idea of functional systems that specifically compensate for a functional defect caused by damage. These functional systems are formed and operate according to certain principles:
Signaling of a violation that has occurred, leading to the activation of appropriate compensatory mechanisms.
Progressive mobilization of spare compensatory mechanisms.
Reverse afferentation about the successive stages of restoration of impaired functions.
The formation in the central nervous system of such a combination of excitations that determines the successful restoration of functions in a peripheral organ.
Assessing the adequacy and strength of final compensation over time.
The collapse of the system as unnecessary.
The sequence of stages of compensation can be traced using the example of lameness when one leg is damaged:
signaling of imbalance from the vestibulocochlear organ;
restructuring the work of motor centers and muscle groups in order to maintain balance and the ability to move;
caused by a stable anatomical defect, constant combinations of afferentations entering the higher parts of the central nervous system, and the formation of temporary connections that provide optimal compensation, i.e., the ability to walk with minimal lameness.
Relapse- a new manifestation of the disease after its apparent or incomplete cessation, for example, the resumption of attacks of malaria after a more or less long interval. Recurrences of pneumonia, colitis, etc. are observed.
Transition to chronic form means that the disease progresses slowly, with long periods of remission (months and even years). This course of the disease is determined by the virulence of the pathogen and mainly by the reactivity of the body. Thus, in old age, many diseases become chronic (chronic pneumonia, chronic colitis).
Terminal states- the gradual cessation of life even with seemingly instantaneous death. This means that death is a process, and in this process several stages (terminal states) can be distinguished: preagony, agony, clinical and biological death.
Preagonia can be of varying duration (hours, days). During this period, shortness of breath, a decrease in blood pressure (up to 7.8 kPa - 60 mm Hg and below), and tachycardia are observed. The person experiences a blackout of consciousness. Gradually the pre-agony turns into agony.
Agony(from the Greek agon - fight) is characterized by a gradual shutdown of all body functions and at the same time extreme tension of protective mechanisms that are already losing their expediency (convulsions, terminal breathing). The duration of the agony is 2 - 4 minutes, sometimes more.
Clinical death is a condition when everything visible signs lives have already disappeared (breathing and heart function have stopped, but metabolism, although minimal, still continues). At this stage, life can be restored. That is why the stage clinical death attracts special attention from clinicians and experimenters.
Biological death is characterized by irreversible changes in the body.
Experiments on animals, primarily on dogs, made it possible to study in detail the functional, biochemical and morphological changes at all stages of dying.
Dying represents the disintegration of the integrity of the organism. It ceases to be a self-regulating system. In this case, the systems that unite the body into a single whole are first destroyed, primarily the nervous system. In the same time lower levels regulations are preserved to some extent. In turn, there is a certain order of dying of various parts of the nervous system. The cortex is most sensitive to hypoxia big brain. In case of asphyxia or acute blood loss, activation of neurons is first observed. In this regard, motor agitation occurs, breathing and heart rate increase, and blood pressure increases. Then inhibition occurs in the cortex, which has a protective significance, since for some time it can save cells from death. With further dying, the process of excitation, and then inhibition and exhaustion, spreads lower, to the stem part of the brain and to the reticular pharmacy. These phylogenetically more ancient parts of the brain are the most resistant to oxygen starvation (the centers of the medulla oblongata can tolerate hypoxia for 40 minutes).
Changes in other organs and systems occur in the same sequence. With fatal blood loss, for example, within the first minute breathing sharply deepens and becomes more frequent. Then its rhythm is disrupted, the breaths become either very deep or superficial. Finally, the excitation of the respiratory center reaches a maximum, which is manifested by especially deep breathing, which has a pronounced inspiratory character. After this, breathing weakens or even stops. This terminal pause lasts 30–60 s. Then breathing temporarily resumes, acquiring the character of rare, first deep, and then increasingly shallow sighs. Together with the respiratory center, the vasomotor center is activated. Vascular tone increases, heart contractions intensify, but soon stop and vascular tone decreases.
It is important to note that after the heart stops working, the system that generates excitation continues to function for quite a long time. On the ECG, biocurrents are observed within 30 - 60 minutes after the disappearance of the pulse.
In the process of dying, characteristic metabolic changes occur, mainly due to ever-deepening oxygen starvation. Oxidative metabolic pathways are blocked, and the body obtains energy through glycolysis. The inclusion of this ancient type of metabolism has a compensatory value, but its low efficiency inevitably leads to decompensation, aggravated by acidosis. Clinical death occurs. Breathing and blood circulation stop, reflexes disappear, but metabolism, although at a very low level, still continues. This is enough to maintain the “minimal life” of nerve cells. This is precisely what explains the reversibility of the process of clinical death, i.e., revival is possible during this period.
The question of the time period during which resuscitation is possible and advisable is very important. After all, revival is justified only if mental activity is restored. V. A. Negovsky and other researchers argue that positive results can be achieved no later than 5 - 6 minutes after the onset of clinical death. If the dying process continues for a long time, leading to depletion of creatine phosphate and ATP reserves, then the period of clinical death is even shorter. On the contrary, with hypothermia, revival is possible even an hour after the onset of clinical death. In the laboratory of N. N. Sirotinin, it was shown that a dog can be revived 20 minutes after death as a result of bleeding, followed by a complete restoration of mental activity. It should, however, be borne in mind that hypoxia causes greater changes in the human brain than in the brain of animals.
Resuscitation, or revitalization, of the body includes a number of measures that are aimed primarily at restoring blood circulation and breathing: cardiac massage, artificial ventilation, cardiac defibrillation. The latter event requires the availability of appropriate equipment and can be carried out under special conditions.
Etiology. The concept of the causes and conditions of the disease.
Classification of causes of diseases. The role of heredity and constitution in the occurrence and development of the disease.
A disease is a state of the body in which normal functioning and the ability to maintain self-regulation are disrupted, life expectancy decreases, which is caused by a limitation of functional and energetic capabilities as opposed to pathogenic causes.
The nomenclature of diseases includes a wide list of names of existing nosological forms that are used in medicine to uniformly designate pathological conditions. To this day, this list of diseases has not been completed. Any specificity infectious disease
lies in its cyclical nature. The following sequential periods of the disease are distinguished: incubation, initial, peak of the disease and recovery. Each of them has its own characteristics.
This stage is also called incubation. This is a period of hidden, not clinically manifested development: from the moment when the pathogenic agent has an impact on the body until the development of the first symptoms of the disease. A feature of this stage is an ever-increasing decrease in the body’s ability to prevent pathogenic effects; adaptive mechanisms no longer work so effectively. During this period, no significant symptoms are observed, but if a person performs stress tests, individual signs may appear.
The incubation period of the disease lasts from several minutes to several months, and sometimes even years. It all depends on the body’s resistance to the influence of the pathogenic agent, on how much it is able to overcome the resulting disturbances with the help of protective devices. Only after exposure to strong poisons does almost instantaneous poisoning occur (no longer than a few minutes). If the latent period is established in time, this will greatly facilitate the prevention and control of the disease.
What other periods of illness exist?
Precursor stage
Another name for this stage is prodromal. It is observed from the moment of the first manifestations and continues until the development of the usual clinical picture. The prodrome stage is a natural result of the insufficient efficiency of adaptation processes, the main function of which is to normalize the homeostasis of the body at a time when the causes of the disease are active.
On at this stage The first subjective and objective nonspecific signs appear: fast fatiguability, malaise, painful sensations in muscles and joints, irritability, decreased appetite, discomfort, headaches, fever, sometimes chills, etc. Let's consider the remaining periods of the disease.
Stage of severe disease
During the stage of pronounced manifestations, or height, the general and local symptoms. If it goes unfavorably, various kinds of complications may arise (for example, coma with diabetes mellitus). At the same time, at this stage of development, adaptive mechanisms still continue to operate, although they are no longer so effective as to independently stop the disease.
During this acute period of the disease, the main symptoms develop, while some diseases have a more or less definite duration of course (especially infectious ones), while others, especially chronic ones, do not have this property.
The following forms of diseases are observed:
Exact dates cannot be established, since everything depends on the specifics of the pathology, the intensity and time of exposure of the pathogenic agent to the body, and the endurance of the person himself.
The main periods of the disease are considered. But there is also a stage of recovery or other options for the outcome of the pathology.
There are the following options for ending the disease: recovery (incomplete and complete), relapse, remission, complication, development into chronic disease, death.
Full recovery
It consists in the formation of effective adaptive reactions and processes that successfully eliminate the cause and/or pathogenic consequences of the disease, restoring the body’s self-regulation in full. However, there is no guarantee that the body will return to its pre-disease state. After recovery, qualitatively and quantitatively different vital signs appear, new functional systems are formed, metabolic activity and immunobiological surveillance systems change, and many other adaptive changes also develop. This is influenced by the main periods of the disease.
Incomplete recovery is characteristic of the body in cases where residual symptoms of the disease and individual deviations from the norm persist.
Relapse
Relapse - re-intensification or re-development signs of the disease after they have already been eliminated or weakened. Symptoms are similar to those of the primary disease, but may differ in some cases. Relapse occurs most often due to the causes that caused the initial episode of illness, a decrease in the effectiveness of adaptive mechanisms, or the body’s ability to resist any factors. This is typical during periods of infectious diseases.
Remission
Remission is a stage of the disease that is characterized by temporary mitigation (incomplete, followed by relapse) or elimination (complete) of symptoms. Most often, this period occurs as a consequence or feature of the causes of the disease or is associated with changes in the patient, as well as with treatment that does not allow a complete recovery.
Complication
Complication is a process that develops against the background of the disease, but is not necessarily characteristic of it. Most often, complications arise as a result of the indirect action of the causes of the disease or associated with the components of the process of its occurrence (for example, with an ulcer, perforation of the intestinal or stomach walls can occur).
Death
If the disease develops unfavorably, it is likely to develop into a chronic disease, which is protracted, as well as such a period of development of the disease as the death of the patient, when the body is not able to adapt to new conditions, is exhausted, and further existence becomes impossible.
The direct cause of death is cardiac arrest, which can be caused either by its damage or by disruption of the brain centers responsible for regulating the functions of the cardiovascular system. Another reason is respiratory arrest, which occurs when the respiratory center located in the medulla oblongata caused by anemia, hemorrhage, swelling or exposure to poisons such as cyanide, morphine, etc.
Stages
Death includes the following stages:
- preagony;
- terminal pause;
- agony;
- clinical death;
- biological death.
The first four stages, subject to timely medical measures, can be reversible.
Agony is characterized by disturbances in the mechanisms of the central nervous system and changes in all body functions important for life: breathing, heart activity, lowering the temperature, relaxing the sphincters. Often the patient loses consciousness. This condition lasts from several hours to two to three days.
The next stage after agony is clinical death, and it is fundamentally reversible. Signs: cessation of breathing, blood circulation and heartbeat. This period lasts 3-6 minutes during normothermia, but can be extended to 15-25 minutes during hypothermia. Its duration depends on the degree of hypoxia of neurons located in the cerebral cortex.
In case of clinical death, it is necessary to carry out the following:
- artificial ventilation;
- restoration of blood circulation and cardiac activity, including cardiac massage, if necessary - defibrillation, starting artificial circulation using oxygenated blood;
- correction of the acid-base state and restoration of ionic balance;
- improving the state of the body's self-regulation and microcirculation system.
After the body can be revived, it remains for some time in an unstable post-resuscitation state, which includes the following stages:
- temporary regulation of the body’s vital functions;
- transient destabilization;
- normalization of life and recovery.
Biological death is the cessation of human life that is irreversible. Complete revitalization of the body is no longer possible, but the possibility of resuming the functioning of some organs remains. Thus, although the stages of the disease are conditional, this classification is used quite widely.
We looked at the main periods of the disease.
Each acute infectious disease occurs cyclically with alternating periods.
I – incubation, or incubation period.
II – prodromal period (precursor stage).
III – the period of height, or development, of the disease.
IV – period of convalescence (recovery).
Incubation period– this is the time from the moment the infection enters the body until the first symptoms of the disease appear. The duration of this period varies widely - from several hours (influenza, botulism) to several months (rabies, viral hepatitis B) and even years (with slow infections). For many infectious diseases, the incubation period averages 1–3 weeks. The duration of this stage depends on a number of factors. First of all, it depends on the virulence and number of pathogens that have entered the body. The greater the virulence and number of pathogens, the shorter the incubation period. Also important is the state of the human body, its immunity, protective factors and susceptibility to this infectious disease. During incubation period bacteria multiply intensively in the tropic organ. There are no symptoms of the disease yet, but the pathogen is already circulating in the bloodstream, and characteristic metabolic and immunological disorders are observed.
Prodromal period– appearance of the first clinical symptoms and signs of an infectious disease (fever, general weakness, malaise, headache, chilling, weakness). During this period, children sleep poorly, refuse to eat, are lethargic, and do not want to play or participate in games. All of the above symptoms occur in many diseases. Therefore, making a diagnosis in the prodromal period is extremely difficult. Manifestations uncharacteristic for this infection may also occur, for example, unstable stool with viral hepatitis, influenza, measles-like rash with chicken pox. Symptoms of the precursor period develop in response to the circulation of toxins in the blood as the body’s first nonspecific reaction to the introduction of a pathogen. The intensity and duration of the prodromal period depend on the causative agent of the disease, on the severity of clinical symptoms, and on the rate of development of inflammatory processes. Most often, this period lasts for 1–4 days, but can be reduced to several hours or increased to 5–10 days. It may be completely absent in hypertoxic forms of infectious diseases.
High period. Characterized by the maximum severity of general (nonspecific) signs and the appearance of symptoms typical of this disease (icteric discoloration of the skin, mucous membranes and sclera, skin rashes, stool instability and tenesmus, etc.), which develop in a certain sequence. The period of development of the disease also has a different duration - from several days (influenza, measles) to several weeks (typhoid fever, brucellosis, viral hepatitis). Sometimes during the peak period three phases can be distinguished: growth, height and decline. In the rising phase, the restructuring of the immune response to infection continues, which is expressed in the production of specific antibodies to this pathogen. Then they begin to circulate freely in the blood of a sick person - the end of the peak stage and the beginning of the fading of the process.
Period of convalescence (recovery)– gradual extinction of all signs of the disease, restoration of the structure and functions of the affected organs and systems. After an illness, there may be residual effects (so-called post-infectious asthenia), expressed in weakness, increased fatigue, sweating, headache, dizziness and other symptoms. During the period of convalescence, children develop a special sensitivity to both reinfection and superinfection, which leads to various complications