What is the name of the convalescence period. Periods and Complications of Infectious Disease. Chronic course of the disease

1. Incubation

2. Preicteric with the following options - dyspeptic, asthenovegetative, polyarthralgic, mixed, influenza-like, without manifestations.

3. The peak period, signs - hyperenzymemia without jaundice, with jaundice, hepatomegaly, sometimes hepatosplenomegaly, endogenous intoxication.

4. The period of convalescence.

5. Outcomes - biliary dyskinesia, protracted hepatitis, chronicity of the disease with outcomes in cirrhosis or cirrhosis-cancer (hepatocellular carcinoma).

In the acute period of viral hepatitis, especially with hepatitis B, hepatitis B + D, the development of acute hepatic encephalopathy (OPE) is possible.

OPE periods:

1. Precom I

2. Precommittee II

3. Coma I (shallow coma)

4. Coma II (deep coma, suppression of all body functions).

The clinical picture of all viral hepatitis is largely similar and differs in percentage terms in the severity of the course of the disease and its outcome. For hepatitis A and E, a predominantly cyclical benign course with complete recovery is characteristic, and with hepatitis B, C and D, moderate and severe course, protracted and chronic forms of the disease, and deaths are often observed.

It is not always easy to assess the severity of viral hepatitis correctly and in a timely manner, since clinical manifestations sometimes, even in cases that end in death, are mild and only in the period of complete decompensation of liver function symptoms appear, indicating a particular severity of the course of the disease. Clinical criteria of severity in viral hepatitis are often subjective, and the indicators of functional tests do not always accurately and fully reflect the degree of damage to the hepatic parenchyma.

When assessing the severity of the disease, the severity of intoxication and jaundice, an increase in the size of the liver and spleen, weight loss, the level of bilirubin in the blood serum, the activity of aminotransferases, and the prothrombin index are taken into account. The most reliable assessment of the severity of the disease is possible during the height of the disease.

In this case, the duration of the incubation period should be taken into account. The shorter it is, the more severe the disease progresses. Pay attention to the nature and duration of the preicteric period. Severe intoxication, polyarthralgia, a pronounced dyspeptic symptom complex are characteristic of fulminant and severe forms of viral hepatitis. Prolonged intense jaundice, hypotension, bradycardia, alternating with tachycardia, lethargy, nausea, low-grade fever, decreased urine output indicate a severe or malignant course of viral hepatitis with an uncertain prognosis.

In a mild course of viral hepatitis, the concentration of total bilirubin in the blood serum is 20-80 μmol / l according to the Jendrashik method, the prothrombin index corresponds to normal values; with a moderate course, the total bilirubin rises to 80-160 μmol / L, the prothrombin index does not change significantly; in severe cases, the concentration of bilirubin is more than 160 μmol / l, the prothrombin index, the level of total protein, fibrin, albumin decrease, and the indicators of the blood coagulation system change.



Acute viral hepatitis occurs mainly cyclically. The incubation period for acute hepatitis A is on average 15-30 days, for acute hepatitis B - 30-180 days. The preicteric (initial) period can proceed according to the following options: 1) dyspeptic - patients complain of lack of appetite, nausea, sometimes vomiting, low-grade fever, the duration of this period is 3-7 days; 2) asthenovegetative - patients complain of weakness, headache, general malaise, loss of appetite, body temperature - subfebrile or normal; 3) flu-like - patients complain of headache, muscle pain, weakness, loss of appetite, body temperature - 37.5-39 ° C, and in some cases 39-40 ° C; the duration of the 2nd and 3rd variants of the preicteric period is 5-10 days. 4) the polyarthralgic variant is observed mainly in acute hepatitis B, as well as C. Patients complain of joint pain, sometimes muscle pain, weakness, loss of appetite are observed. The duration of this period is 7-14 days. 5) a mixed version of the onset of the disease is manifested most often by signs of several syndromes.



In some patients, the disease may begin without signs of intoxication.

With the appearance of clear signs of liver damage - the height of the disease - the state of health in most patients improves. The temperature normalizes, the urine darkens, the sclera becomes subicterous, jaundice gradually increases, the feces become discolored. The further course of the disease depends on the degree of damage to the liver virus, which determines the severity of the disease. With a mild course of viral hepatitis, jaundice increases within 3-5 days, remains at the same level for 1 week, then completely disappears by 15-16 days. Already at the end of 1-2 weeks of the icteric period, the urine brightens, the feces turn yellowish-brown.

With a moderate and severe course of the disease, the icteric staining of the sclera, skin is more intense, a longer icteric period (20-45 days). On the part of the cardiovascular system, hypotension is observed, in most patients - bradycardia, deafness of heart sounds. In 80-90% of patients, the liver increases in size, its surface is smooth, the edge is rounded, moderately painful. In 30-40% of patients, the spleen is palpable. In the severe course of acute viral hepatitis, some patients experience bloating due to indigestion (signs of damage to the pancreas, gastric secretory glands and impaired biocinosis of the gastrointestinal tract). Some patients with severe viral hepatitis may have mild ascites. In some patients, itching is noted - the so-called cholestatic variant of the course of the disease.

On the part of the central nervous system, some patients experience certain changes. Already with a mild course of acute viral hepatitis, mood changes, weakness, lethargy, and sleep disturbances may occur. With the increase in the severity of the disease, these phenomena are more common, their severity is more distinct.

In severe cases, there are clear cerebral disorders caused by significant dystrophic changes in the liver, endogenous intoxication and increased activity of LPO processes, as well as the accumulation of their intermediate products.

In the period of convalescence, there is a reverse development of the symptoms of the disease, the normalization of biochemical parameters.

The preliminary diagnosis of acute viral hepatitis is established on the basis of the epidemiological history, data on the development of the disease, the clinical picture, taking into account the characteristics of the transmission routes, the duration of the incubation period, the presence of a preicteric period, typical subjective and objective signs, taking into account the patient's age.

The diagnosis is confirmed by routine and special laboratory tests.

In the general analysis of blood in patients with viral hepatitis, lymphocytosis is observed with moderate anemia and leukopenia in severe cases. ESR is slightly reduced. Urobilin and bile pigments are found in urine, in feces - during the peak period - especially with moderate and severe forms of the disease, stercobilin cannot be detected.

In the blood serum throughout the entire icteric period, an increased content of total bilirubin is found, mainly due to its direct fraction. The ratio between its direct and indirect fractions is 3: 1. In all patients, already in the preicteric period of the disease, throughout the entire icteric period and in the period of early convalescence, an increased activity of ALT, AsAT enzymes is observed, indicating the presence of cytolytic processes in the liver. In patients with acute hepatitis, there is an increase in the thymol test, a decrease in the concentration of total protein, which indicates a reduced protein-synthetic function of the liver. In viral hepatitis, there are violations of the indicators of the coagulation and anticoagulation system of the blood, depending on the period and severity of the disease. With the help of these indicators (electrocoagulograms, thrombocytograms, biochemical tests), one can judge the severity of the disease, the phase and degree of DIC.

In the diagnosis and differential diagnosis of viral hepatitis, instrumental research methods are widely used - ultrasound, cholangiography, computed tomography.

For the purpose of specific diagnostics, ELISA reactions, radioimmunoassay and their various combinations are used. With the help of these methods, specific antigens and antibodies to the antigens of all currently known hepatitis viruses are detected in the blood of patients. Detection of antibodies in the Ig M class indicates an acute illness. The detected antibodies in the Ig G class indicate a protracted or chronic course of viral hepatitis or a previous infectious process, or a past illness, vaccinations.

With the help of the polymerase chain reaction in the blood of patients, DNA or RNA of hepatitis viruses can be detected, which confirms the diagnosis.

Differential diagnosis of acute viral hepatitis should be carried out with diseases such as leptospirosis, yersiniosis, mononucleosis, malaria, mechanical and hemolytic jaundice, toxic hepatosis. In this case, one should take into account the peculiarities of the clinical picture of these diseases, the possibilities of modern specific and instrumental diagnostics.

When making a clinical diagnosis, the type of virus that caused the disease, the severity and course of viral hepatitis should be noted.

Leptospirosis is characterized by an acute onset of the disease, often with chills, continued fever during the height of the disease and jaundice, muscle pain, especially in the calf, hemorrhagic syndrome. In the blood, leukocytosis with neutrophilia and a shift of the formula to the left is detected, an accelerated ESR is observed. The activity of ALT, ASAT is moderately increased, the ratio of direct and indirect bilirubin is 1: 1. In the blood serum, the concentration of urea and residual nitrogen increases. Bilirubin is constantly found in the feces, the reaction to occult blood is often positive, the feces are not discolored. Erythrocytes, leukocytes in large numbers, granular, waxy cylinders are found in urine. Diuresis is reduced, up to anuria. Azotemic coma is possible. The final recognition of the disease is confirmed by the detection of leptospira in the urine sediment or blood serum and an increase in antibodies in the blood serum of patients in the reaction of agglutination-lysis with a specific leptospirosis antigen.

In generalized forms of yersiniosis, jaundice can also be observed, however, it is accompanied by fever, metastatic foci in other organs, tissues, leukocytosis with neutrophilia, accelerated ESR. Exacerbations and relapses of the disease are possible. The diagnosis is confirmed by serological methods with a specific yersiniosis antigen.

The visceral form of mononucleosis is characterized by lymphadenopathy, fever at the height of jaundice, and a serious condition. In the blood, wide-plasma lymphocytes (virocytes) are found in an increased amount.

In malaria, there is a clear alternation of attacks of apyrexia with chills, alternating with a feeling of heat and sweating, often a painful, enlarged spleen is found. Hemolytic anemia occurs in the blood, and various forms of Plasmodium malaria are found in a thick drop of blood and a smear. The indirect fraction of bilirubin prevails in the blood serum.

With obstructive jaundice, ultrasound can detect stones in the gallbladder and bile ducts, dilatation of the bile ducts, an increase in the size of the head of the pancreas and other components that cause obstructive jaundice. Most patients may have a moderate increase in the activity of ALT, AST, leukocytosis, accelerated ESR.

Hemolytic jaundice is characterized by anemia, accelerated ESR, an increase in total bilirubin due to its indirect fraction. Stercobilin is always present in the feces.

Differential diagnosis of acute viral hepatitis with hepatosis is difficult and requires thoughtful and painstaking work from the doctor. In this case, a fully-fledged anamnesis is essential.

Outcomes of the disease. Acute viral hepatitis most often results in complete recovery. Some patients after acute hepatitis may develop cholecystitis, cholangitis, pancreatitis, biliary dyskinesia. In 5-10% of patients, a protracted course with periodic exacerbations can be observed, due to prolonged persistence of the virus. In such cases, the development of chronic hepatitis is possible, which is typical for hepatitis B and C and, as a result, can lead to cirrhosis of the liver or hepatocellular carcinoma.

The most formidable outcome of viral hepatitis is acute or subacute massive liver necrosis, in which the clinical picture of acute or subacute hepatic encephalopathy develops. Acute viral hepatitis is characterized by acute hepatic encephalopathy.

The mechanism of development of acute or subacute liver necrosis is extremely complex and poorly understood. As a result of the intense multiplication of the virus in hepatocytes, an excessive accumulation of reactive oxygen species occurs, which in turn leads to depletion of the functional capacity of the antioxidant system. This leads to an increase in LPO processes, destruction of the structure of cell membranes of the hepatocyte and its intracellular structures, accumulation of toxic peroxides, ammonia in tissues and blood, inactivation of many enzyme systems of the cell. Additional channels appear in cell membranes, natural channels are destroyed, the receptor sensitivity of the cell decreases, which leads to irreversible disturbances in enzymatic reactions, dissociation of phosphorylation processes, the release of lysosomal proteases, leading to the complete destruction of hepatocytes.

With this destruction of hepatocytes, all liver functions are inhibited. First of all, pigment metabolism is disturbed. In the blood of patients, there is an intense increase in bilirubin to extremely high numbers. In peripheral blood, the concentration of LPO products increases several times, indicating a high intensity of formation of fatty acid radicals in membrane structures. The activity of all AOS components is depleted. The synthetic function of the liver is impaired. Defective proteins, fibrin degradation products appear in the blood, the level of total blood protein and its fractions decreases. The synthesis of the components of the blood coagulation system is disrupted, which leads to the development of "consumption coagulopathy" (the third phase of DIC) and bleeding, sometimes massive, leading to the death of patients. The cycle of urea synthesis and ammonia utilization is disrupted, which leads to the accumulation of these products in the blood and profound pathological changes in the central nervous system.

As a result of the suppression of the functions of the gastrointestinal tract and the development of dysbiosis in the intestine, fermentation processes are activated, such highly toxic products as indole, skatole, ammonia and others are accumulated and absorbed into the blood. Passing with the blood flow through the liver, they are not activated and are brought into the central nervous system, causing signs of encephalopathy. Reactive oxygen species circulating in high concentrations in the blood, intercellular fluid and tissues of the brain substance contribute to the destruction of myelin and other cellular structures, increase the binding of poisons circulating in the blood by the cells of the nervous tissue, enhancing the manifestations of encephalopathy.

Water-electrolyte, carbohydrate, protein, fat metabolism, and the exchange of vitamins are disturbed. There is a complete "imbalance" of metabolism, metabolic acidosis increases, which in 2/3 of cases is the direct cause of death. 1/3 of patients die from massive bleeding.

Clinic and methods for predicting acute hepatic encephalopathy (PE). The term "acute hepatic encephalopathy" denotes the unconscious state of the patient with impaired reflex activity, seizures, disorders of vital functions as a result of deep inhibition of the cerebral cortex with spread to the subcortex and underlying parts of the central nervous system. This is a sharp inhibition of neuropsychic activity, characterized by impaired movements, sensitivity, reflexes and lack of reactions to various stimuli.

Hepatic coma is an endogenous coma caused by endogenous intoxication as a result of loss of function and liver decay.

Currently, there are many different classifications of OPE that characterize one or another stage of complication. EAT. Tareev, A.F. Bluger proposed to distinguish between three stages of the OPE - precom 1, precom 2 and 3 - actually to whom.

Precoma 1 is characterized by intermittent disturbance of consciousness, instability of mood, depression, reduced ability to orientate, mild tremor, and sleep inversion. Patients are irritable, sometimes euphoric. They are worried about bouts of melancholy, doom, a premonition of death. Fainting, short-term loss of consciousness, dizziness, hiccups, nausea, vomiting may occur. The jaundice increases. Bradycardia is replaced by tachycardia. Tendon reflexes are increased. This state lasts from several hours to 1-2 days with the transition to the second stage.

In the second stage of precoma, consciousness is more and more disturbed, memory lapses are characteristic, alternating with attacks of psychomotor and sensory arousal up to delirium. Upon awakening, there is no orientation in time, space and action. Tendon reflexes are high. Deafness of heart sounds, tachycardia, hypotension are observed. The breathing rhythm is periodically disturbed. The size of the liver begins to shrink. One third of patients have nosebleeds, gastrointestinal, uterine and other bleeding. Diuresis decreases. The abdomen is swollen, intestinal motility is reduced. This state lasts 12 hours - 2 days.

At the 3rd stage - the coma itself - there is a complete loss of consciousness and the disappearance of reflexes, first tendon, then corneal and, last of all, pupillary. Abnormal Babinsky reflexes, clonus of the feet, muscle rigidity of the limbs, hyperkinesis, convulsive syndrome, and then complete areflexia may occur. Severe tachycardia, hypotension, and disturbance of the respiratory rhythm are observed. The abdomen is swollen, intestinal motility is reduced, in some patients free fluid is found in the abdominal cavity, the liver is reduced in size. There is a significant decrease in urine output up to anuria. Soon (6 hours - day), patients die from massive bleeding or with symptoms of profound metabolic disorders with symptoms of severe metabolic acidosis.

Some clinicians adhere to a different classification of hepatic coma, which provides for the following stages of its development: precoma-1, precoma-2, coma-1, coma-2. Precoma-1 is a period of harbingers. Precoma-2 - in the clinic of the disease there are clear clinical signs of encephalopathy. Coma-1 - a period of excitement with loss of consciousness. Coma-2 - deep loss of consciousness, areflexia, respiratory rhythm disturbance, reduction in the size of the liver, bleeding, anuria.

PEE prediction is possible several days before the appearance of the harbingers of this formidable complication. In order to predict OPE, seriously ill patients should daily examine the state of the coagulation and anticoagulant systems of the blood using the method of electrocoagulography, which makes it possible to obtain a graphical record of the entire process of blood coagulation and fibrinolysis within 20 minutes.

We have developed a new method for assessing the indicators of various phases of coagulation by the degree of retraction of the blood clot and the time of maximum retraction. A simple formula for calculating the blood clot retraction index (IRKS) is proposed:

t is the duration of the maximum retraction of the blood clot, sec;

h is the height of the oscillatory movements of the recorder, mm.

For a severe course of viral hepatitis, a decrease in IRKS is characteristic. Patients in whom it is equal to 32 conventional units. the coagulogram should be examined daily, and their condition should be regarded as a threat of coma. With IRKS equal to 9 conventional units. in patients, there are harbingers of coma. With its further development, the value of IRKS decreases to 0. In case of improvement of the general condition of the patient, IRKS increases.

This method can also be used to assess the effectiveness of the therapy.

The commonly used prothrombin index is not an early predictive test. With its help, it is possible only to document an already developing and clinically diagnosed coma. The outcomes of OPE are most often unfavorable. In case of recovery, but improper management of patients in the period of early convalescence, those who have recovered develop early cirrhosis of the liver.

With early prediction of PEE at preclinical stages and correct management of patients, recovery occurs, or PEE does not occur.

Treatment. All patients with acute viral hepatitis during the period of acute clinical manifestations must comply with bed rest.

For the entire period of acute clinical manifestations and early convalescence, patients are prescribed table No. 5 according to Pevzner. It is forbidden to eat anything fried, fatty and spicy. Alcoholic drinks are strictly contraindicated. From meat products recommend white boiled chicken meat, veal, rabbit boiled meat. Patients are shown fresh boiled fish. From the first courses, lean vegetable soups, pea, rice, buckwheat soups should be recommended. From the second courses are shown mashed potatoes, rice, buckwheat, oatmeal, seasoned with butter (20-30g). Boiled sausages should be included in the diet. From dairy products, milk, cottage cheese, kefir, lean mild cheeses should be recommended. Patients are shown salads of fresh vegetables without onions, seasoned with refined sunflower oil (olive, corn, Provencal), vinaigrette. Compotes, jelly from fresh and canned fruits and berries, table mineral waters, rosehip decoction, lemon tea should be widely recommended. Patients can eat fresh apples, pears, plums, cherries, pomegranates, watermelons, cucumbers, tomatoes.

In hepatitis A and E, which are characterized by an acute, cyclic course, the appointment of antiviral agents is not indicated. It is advisable to use them in cases of a progressive (protracted) course of acute hepatitis B and D against the background of a high activity of the pathological process with indicators of replication of pathogens and in all cases of acute hepatitis C, given the high probability of chronicity. Patients are prescribed alpha-interferon, in particular its recombinant (intron A, roferon A, pegintron, pegasys) and native (wellferon, human leukocyte interferon) drugs. There is no unanimous opinion regarding the interferon therapy regimen for acute viral hepatitis. Most often, drugs are prescribed 3-5 million IU 3 times a week (or every other day) for 3-6 months. With this method of therapy, the percentage of chronicity decreases by about 5 times in hepatitis B and 3 times in hepatitis C. Synthetic nucleosides (famciclovir, lamivudine, ribavirin, trivorin), protease inhibitors (invirase, crixivan) can also be used for etiotropic treatment. In recent years, inducers of endogenous interferon have been effectively used - neovir, cycloferon, amiksin, kagocel, etc. Amiksin is prescribed to patients at 0.125 g 2 days in a row a week, for 5 weeks. In addition, leukinferon, interleukin-1, interldeukin-2 (roncoleukin), thymus preparations (thymalin, thymogen, T-activin), thymopoietins (glutoxim) can be recommended.

The above drugs are also indicated for severe acute hepatitis B with the threat of acute liver failure.

In the presence of intoxication, patients are prescribed detoxification intravenous therapy for 3-5 days. For this purpose, a 5% glucose solution 200.0-400.0 is injected into the vein; reosorbilact 200.0-400.0; 5% solution of ascorbic acid 10.0-15.0; acesol and chlorosalt 200.0-400.0.

Throughout the icteric period, enterosorbents are prescribed inside. Starting from the first day of the disease and until the complete normalization of the activity of aminotransferases, patients should receive natural antioxidants inside, such as infusion of astragalus woolly and others.

With the threat of OPE, patients should be prescribed drip intravenous administration of saline and colloidal solutions in a total volume of 1200-2400 ml per day. The introduction of solutions is carried out 2 times a day (morning and evening) into the subclavian vein through a catheter. Rheosorbilact 400.0 is prescribed; acesol - 400.0; 4% glutargin solution - 50 ml, 5% ascorbic acid solution - 20.0; 5% glucose solution - 400.0; whistle-blowing albumin - 400.0-500.0; cocarboxylase, ATP, trasylol or gordox 100,000-200,000 U, or contrycal, aminocaproic acid, heptral (800 mg per day).

When bleeding occurs, hemostatic therapy is prescribed, adequate to the losses. For this purpose, you can use aminocaproic acid, vikasol, blood plasma, whole blood, erythrocyte suspension, fibrinogen.

Patients are shown cleansing enemas.

With psychomotor agitation, patients are fixed to the bed, seduxen or sodium oxybutyrate is injected.

With reduced diuresis, mannitol, mannitol, and aminophylline should be administered intravenously.

When organizing and conducting a complex of therapeutic measures, it should be remembered that the effectiveness of treatment largely depends on the quality of patient care, therefore, specially trained personnel should work in the intensive care unit, who are familiar with the methods of intensive therapy and resuscitation, as well as methods of care and service for patients with hepatic coma. ...

It should also be remembered that an OPE recognized at the preclinical stages and correctly conducted treatment will save the patient's life.

Dispensary observation of convalescents is carried out by the KIZ doctor at district polyclinics for viral hepatitis A and E for 3 months, for hepatitis B and C - for 6 months.

In the case when the recovery of hepatocytes is delayed (indicators of aminotransferase activity are increased), the observation is prolonged until complete recovery.

Incubation period (latent) occurs from the moment the pathogen is introduced into the body and lasts until the first clinical signs of the disease appear. Its duration can be different: with flu, salmonellosis, PTI, it is measured in hours, and with viral hepatitis B or rabies - for months. The duration of the incubation period depends on the virulence of the pathogen and the reactivity of the patient's body.

Prodromal or precursor period begins with the appearance of the first symptoms of the disease, has no specific features and is similar in many infectious diseases. It is characterized by the following signs: malaise, weakness, fever, headache, weakness, sleep disorder. Therefore, diagnosis during this period is difficult. The duration of the prodromal period is different, more often it lasts 1-3 days.

The peak period characterized by the full development of the clinical picture inherent in this disease. For example, jaundice - with viral hepatitis, rash - with measles, scarlet fever, chickenpox, typhoid fever. Its duration is from several days (influenza, measles) to several weeks and months (typhoid fever, malaria, brucellosis). During the peak period, there is an immunological restructuring of the body, the production and circulation of specific antibodies in the blood.

Convalescence period(convalescence) begins from the moment of extinction of clinical symptoms and is accompanied by the restoration of impaired body functions. The duration of the recovery period varies depending on the form of the disease, the severity of the course, the reactivity of the body, the effectiveness of treatment, and a number of other factors.

The outcome of an infectious disease, in addition to recovery, may be a relapse (return of the disease), chronicity (transition from an acute to a chronic form), the formation of a carrier of bacteria, and death.

According to the severity of the course, infectious diseases are divided into mild, moderate and severe forms.

With a mild course, the symptoms of the disease are not pronounced sharply. For forms of moderate severity, typical symptoms of the disease, a short course and a favorable outcome are characteristic. The severe form is accompanied by pronounced clinical symptoms, a prolonged course, and often the presence of complications.



In the course of the disease, complications may develop. Specific complications are caused by the causative agents of this disease (for example, perforation of ulcers in typhoid fever; myocarditis in diphtheria, hepatic coma in viral hepatitis). The cause of nonspecific complications is the activation of autoflora or endogenous infection with other pathogens.

The concept of the epidemic process,

Epidemic focus

Epidemiology (from the gr. Epidemia - "general disease") - the science of the patterns of occurrence, spread of infectious diseases, prevention and control measures. The object of study of epidemiology is the epidemic process.

Epidemic process- this is a continuous chain of successively emerging and interconnected infectious conditions due to the continuous interaction of its three main links: 1 - the source of the causative agent of the infection, 2 - the mechanism of transmission of pathogens, 3 - the susceptible organism. The epidemic process manifests itself in the form of epidemic foci with one or more cases of disease or carriage.

Epidemic focus this is the location of the source of infection with its surrounding territory, within the limits in which it is capable of transmitting an infectious principle to others in a given specific situation and with a given infection.

Source of infection - the first link in the epidemic process. The source of causative agents of infectious diseases is the human or animal organism, in which this pathogen has found a habitat, reproduction and from which it is released viable into the external environment. The source of infection can be a sick person, bacterio, virus carrier, convalescent, animals and birds.

From the source of infection, through appropriate transmission mechanisms, the pathogen enters the susceptible organism.

Pathogen transmission mechanism is the second link in the epidemiological process, while the pathogen from the infected organism enters the susceptible organism. In the process of evolution, pathogenic microorganisms have developed the ability to enter the body through certain organs and tissues, which are called the entrance gate of infection. After introduction, the pathogen is localized in certain organs or systems. Depending on the entrance gate and the localization of the pathogen in the body, the following main mechanisms of transmission of infectious diseases are distinguished.

Fecal-oral transmission mechanism. The pathogen enters a healthy body through the mouth; it is localized in the human gastrointestinal tract; excreted from the body with feces. The fecal-oral mechanism is realized by water, food and household routes. The transmission factors are water, food, contaminated hands, soil, household items, flies. A person becomes infected with intestinal infections when drinking infected water, using it for household purposes or when swimming in polluted water bodies; when consuming infected milk and dairy products, eggs, meat and meat products, unwashed vegetables and fruits.

Aerogenic(aspiration) transmission mechanism. Infection occurs when the infected air is inhaled. The pathogen is localized on the mucous membranes of the upper respiratory tract; excreted with exhaled air, phlegm, mucus, when coughing, sneezing, talking. The aerogenic transmission mechanism is realized by airborne droplets and airborne dust routes; transmission factors are infected air, household items (books, toys, dishes, linen).

Transmission transmission mechanism... The pathogen is in the blood. The natural route of transmission occurs through blood-sucking insects (lice, mosquitoes, fleas, ticks, mosquitoes); artificial - during transfusion of blood and blood products, parenteral interventions through medical instruments.

Contact transmission mechanism occurs when the pathogen is localized on the skin and mucous membranes. Infection occurs through direct contact with a sick person or his personal belongings (clothes, shoes, hairbrush) and household items (bedding, shared toilet and bath).

Transplacental (vertical) transmission mechanism. The pathogen is transmitted from the mother to the fetus through the placenta or during childbirth (when the fetus passes through the birth canal).

Receptive organism- the third link in the epidemic process. The susceptibility of people to infectious diseases depends on the body's immunological reactivity. The larger the immune layer (people who have had this infection or vaccinated), the less susceptibility of the population to this infection. Turning off one of the links in the epidemic chain allows you to eliminate the focus of infection.

Specificity of infection

Each infectious disease is caused by a specific pathogen. However, infections (for example, purulent-inflammatory processes) caused by various microbes are known. On the other hand, one pathogen (for example, streptococcus) can cause various lesions.

Contagiousness(infectiousness) determines the ability of a pathogen to be transmitted from one person to another and the rate at which it spreads in a susceptible population. For a quantitative assessment of contagiousness, an index of contagiousness is proposed - the percentage of people who have been ill in the population for a certain period (for example, the incidence of influenza in a certain city for 1 year).

The development of a specific infectious disease is limited in time, accompanied by a cyclical process and a change in clinical periods.

1. Incubation period- this is the time elapsed from the moment the microorganism enters the macroorganism until the first clinical signs of the disease appear. Usually, the incubation period is typical only for exogenous infections. During this period, the pathogen multiplies, there is an accumulation of both the pathogen and the toxins secreted by it up to a certain threshold value, beyond which the body begins to respond with clinically expressed reactions.

The duration of the incubation period can vary from hours and days to several years and depends mainly on the type of pathogen. For example, with intestinal infections, the incubation period is not long - from several hours to several days. With other infections (flu, chickenpox, whooping cough) - from several weeks to several months. But there are also infections in which the incubation period lasts several years: leprosy, HIV infection, tuberculosis. During this period, cell adhesion occurs and, as a rule, pathogens are not detected.

2. Prodromal period- or the "stage of precursors". Its duration does not exceed 24-48 hours.

During this period, the pathogen is colonized on sensitive cells of the body. During this period, the first precursors of the disease appear (the temperature rises, appetite and performance decrease, etc.), microorganisms form enzymes and toxins, which lead to local and generalized effects on the body. With such diseases as typhoid fever, smallpox, measles, the prodromal period is very characteristic and then already in this period the doctor can make a preliminary diagnosis. During this period, as a rule, the pathogen is not detected, except for whooping cough and measles.

3. The period of development of the disease- during this period, there is an intensive reproduction of the pathogen, the manifestation of all its properties, the clinical manifestations characteristic of this pathogen are manifested as much as possible (yellowing of the skin with hepatitis, the appearance of a characteristic rash with rubella, etc.).


In a clinically pronounced phase, one can distinguish:

Stages of increasing symptoms (stadium werementum),

Flourishing disease (stadium acme)

Extinction of manifestations (stadium decrementum).

During this period, a protective reaction of the macroorganism is formed in response to the pathogenic action of the pathogen, the duration of this period is also different and depends on the type of pathogen. For example, tuberculosis, brucellosis lasts a long time, several years - they are called chronic infections. For most infections, this period is the most contagious. At the height of the disease, a sick person releases a lot of microbes into the environment.

The period of clinical manifestations ends with the recovery or death of the patient. Death can occur with infections such as meningitis, influenza, plague, etc. The severity of the clinical course of the disease can be different. The disease can occur in severe or mild... And sometimes the clinical picture may be generally atypical for this infection. Such forms of the disease are called atypical, or erased. In this case, it is difficult to make a diagnosis, and then microbiological research methods are used.

4. Convalescence period(convalescence) - how the final period of an infectious disease can be rapid (a crisis) or slow (lysis), and also be characterized by a transition to a chronic state. In favorable cases, clinical manifestations usually disappear faster than normalization of morphological disorders of organs and tissues and complete removal of the pathogen from the body. Recovery may be complete or be accompanied by the development of complications (for example, from the central nervous system, musculoskeletal system, or cardiovascular system). The period of final removal of the infectious agent can be delayed and for some infections (for example, typhoid fever) it can take weeks.

During this period, pathogens die, class G and A immunoglobulins build up. During this period, bacterial carriers can develop: antigens can remain in the body, which will circulate throughout the body for a long time. The recovery period is accompanied by a decrease in temperature, restoration of working capacity, and an increase in appetite. During this period, microbes are excreted from the patient's body (with urine, feces, sputum). The duration of the period for the isolation of microbes is not the same for different infections. For example, with chickenpox, anthrax, patients are freed from the pathogen when the clinical manifestations of the disease disappear. In other diseases, this period lasts 2-3 weeks.

The infectious process does not always go through all stages and may end in the early stages of the disease. For example, if a person is vaccinated against a particular disease, then there may not be a period of development of the disease. In any period of an infectious disease, but especially during its height, it is possible complications: specific and non-specific.

Specific- these are complications caused by the causative agent of this disease and are a consequence of the unusual severity of functional and morphological changes in the patient's body (for example, enlargement of the tonsils with staphylococcal sore throat or perforation of intestinal ulcers with typhoid fever).

Non-specific- these are complications caused by microorganisms of another type, as a rule, opportunistic, which are nonspecific for this disease (for example, the development of purulent otitis media in a patient with measles).

A separate medical science is engaged in the study of the conditions for the occurrence of infectious diseases and the mechanisms of transmission of their pathogens, as well as the development of measures for their prevention - epidemiology.

Almost any epidemic process includes three interrelated components:

1) source of infection;

2) the mechanism, ways and factors of transmission of the pathogen;

3) a susceptible organism or collective.

The absence of one of the components interrupts the course of the epidemic process.

Sources of infection (pathogen)

Various animate and inanimate objects of the external environment containing and preserving pathogenic microorganisms are denoted by the term reservoirs of infection, but their role in human morbidity is far from the same. For most human infections, the main reservoir and source is a sick person, including those in the incubation period (early carriers) and at the stages of convalescence, or asymptomatic (contact) microcarriers. In accordance with the source of infection, the following types of infectious diseases are distinguished.

Sporadic morbidity[from the Greek. sporadikos, diffuse] - the usual incidence of a particular infection in a particular region for a certain period (usually a year). As a rule, the number of patients does not exceed ten cases per 100,000 population.

Epidemic[from the Greek. epi-, over, + demos, people].

In some cases, the normal incidence of a particular infection over a given period is sharply higher than the sporadic incidence. In such cases, an epidemic outbreak occurs, and when several regions are involved in the process, an epidemic occurs.

Pandemic... In rare situations, the incidence of a particular infection for a certain period sharply exceeds the level of epidemics. At the same time, the incidence is not limited to a particular country or mainland, the disease practically covers the entire planet. Fortunately, such "super-epidemics", or pandemics [from the Greek. pan-, general, + demos, people], causes a very limited range of pathogens (eg influenza virus).

In accordance with the prevalence, infectious diseases also secrete ubiquitous (ubiquitous) and endemic infections detected in certain, often small areas.

According to the frequency of cases, there are:

- crisis infections- incidence of more than 100 cases per 100,000 population (for example, HIV infection);

- massive infections- the incidence is 100 cases per 100,000 population (for example, ARVI);

- common preventable infections- incidence is 20-100 cases per 100,000 population (eg measles);

- common uncontrollable infections- the incidence is less than 20 cases per 100,000 population (for example, anaerobic gas infections);

- sporadic infections- the incidence is isolated cases per 100,000 population (for example, rickettsioses).

The causative agents of ubiquitous infections are ubiquitous. Endemic pathogens cause endemics[from the Greek. en-, in, + -demos, people]. As a criterion of the epidemic process, endemic does not reflect its intensity, but indicates the incidence in a particular region.

There are true and statistical endemics:

- True endemics determine the natural conditions of the region (the presence of sources of infection, specific vectors and reservoirs for the preservation of the pathogen outside the human body). Therefore, true endemics are also known as natural focal infections.

Concept statistical endemic also used in relation to ubiquitous infections common in various natural conditions (for example, typhoid fever). Their frequency is determined not so much by climatic as socio-economic factors(eg water supply deficiencies). In addition, the concept of social endemic is also applied to non-infectious diseases, for example, endemic goiter, fluorosis, etc.

Natural focal infections- a special group of diseases that have evolutionary foci in nature. A natural focus is a biotope on the territory of a specific geographical landscape, inhabited by animals, the species or interspecific differences of which ensure the circulation of the pathogen due to its transmission from one animal to another, usually through blood-sucking arthropod vectors.

Natural focal infections are divided into endemic zoonoses, the range of which is associated with the range of animals - hosts and vectors (for example, tick-borne encephalitis), and endemic metaxenoses associated with the range of animals, the passage through the body of which is an important condition for the spread of the disease (for example, yellow fever). When a person appears at a certain time in the outbreak, the carriers can infect him with a natural focal disease. This is how zoonotic infections become anthropozoonotic.

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From the moment the pathogen enters the body until the clinical manifestation of the symptoms of the disease, a certain time passes, which is called the incubation (latent) period. Its duration is different. With some diseases (flu, botulism), it takes hours, with others (rabies, viral hepatitis B) - weeks or even months, with slow infections - months and years. For most infectious diseases, the incubation period is 1-3 weeks.

Duration of the incubation period due to several factors. To some extent, it is associated with virulence and the infectious dose of the pathogen. The incubation period is the shorter, the higher the virulence and the higher the dose of the pathogen.

For the spread of the microorganism, its reproduction, and the production of toxic substances by it, a certain time is required. However, the main role belongs to the reactivity of the macroorganism, which determines not only the possibility of an infectious disease, but also the intensity and pace of its development.

From the beginning of the incubation period, physiological functions change in the body. Having reached a certain level, they are expressed in the form of clinical symptoms.

Prodromal period, or the period of precursors of the disease

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With the appearance of the first clinical signs of the disease, the prodromal period, or the period of the precursors of the disease, begins.

Symptoms of it(malaise, headache, fatigue, sleep disturbances, decreased appetite, sometimes a slight increase in body temperature) are characteristic of many infectious diseases, and therefore the establishment of a diagnosis during this period causes great difficulties.

An exception is measles: detection in the prodromal period of a pathognomonic symptom (Belsky - Filatov - Koplik spots) allows to establish an accurate and final nosological diagnosis.

The duration of the onset of symptoms usually does not exceed 2-4 days.

The height of the disease

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The peak period has a different duration - from several days (with measles, flu) to several weeks (with typhoid fever, viral hepatitis, brucellosis).

During the peak period, the symptoms characteristic of this infectious form are most pronounced.

The period of extinction of the disease

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The height of the disease is replaced by a period of extinction of clinical manifestations, which is replaced by a period of recovery (convalescence).

The period of recovery (convalescence) of the disease.

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The duration of the recovery period varies widely and depends on the form of the disease, the severity of the course, the effectiveness of therapy and many other reasons.

Recovery can be complete, when all functions impaired as a result of the disease are restored, or incomplete, if residual (residual) phenomena persist.

Complications of the infectious process

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In any period of the disease, complications are possible - specific and nonspecific.

Complications are specific. caused by the causative agent of this disease and are a consequence of the unusual severity of the typical clinical picture and morphofunctional manifestations of infection (perforation of an intestinal ulcer with typhoid fever, hepatic coma with viral hepatitis) or atypical localization of tissue damage (salmonella endocarditis).

Complications caused by other types of microorganisms are not specific to this disease. Of exceptional importance in the clinic of infectious diseases are life-threatening complications that require urgent intervention, intensive observation and intensive therapy. These include hepatic coma (viral hepatitis), acute renal failure (malaria, leptospirosis, hemorrhagic fever with renal syndrome, meningococcal infection), pulmonary edema (influenza), cerebral edema (fulminant hepatitis, meningitis), and shock.

In infectious practice, the following types of shock are encountered:

  • circulatory (infectious-toxic, toxic-infectious),
  • hypovolemic,
  • hemorrhagic,
  • anaphylactic.

1. Infection - the sum of biological reactions by which the macroorganism responds to the introduction of a microbial (infectious) agent, which causes a violation of the constancy of the internal environment (homeostasis).

Similar processes caused by the simplest, are called invasions.

The complex process of interaction between microorganisms and their products, on the one hand, cells, tissues and human organs, on the other, is characterized by an extremely wide variety of its manifestation. The pathogenetic and clinical manifestations of this interaction between microorganisms and a macroorganism are designated by the term infectious disease (disease).

In other words, the concepts "infectious disease" and "infection" are absolutely not equivalent, the disease is only one of the manifestations of the infection. Although even in the specialized medical literature, the term "infection" is now widely used to denote the corresponding infectious diseases.

For example, in the expressions "intestinal infections", "airborne S infections", "sexually transmitted infections".

Infectious diseases continue to wreak havoc on humanity. They came out on top among other diseases, accounting for 70% of all human diseases.

In recent years, 38 new infections have been registered - the so-called emergent diseases, including HIV, hemorrhagic fevers, Legionnaires' disease, viral hepatitis, prion diseases; moreover, in 40% of cases these are nosological forms that were previously considered non-infectious.

Features of infectious diseasesare as follows:

Their etiological factor is a microbial agent;

They are transmitted from sick to healthy;

They leave behind one or another degree of immunity;

They are characterized by a cyclical flow;

They have a number of common syndromes.

2. According to these features any infectious disease has certain clinical stages (periods) of its course, expressed in varying degrees:

incubation period- the period from the moment the infectious agent enters the human body until the first precursors of the disease appear. The causative agent during this period is usually not released into the environment, and the patient does not pose an epidemiological hazard to others;

prodromal period - the manifestation of the first nonspecific symptoms of the disease, characteristic of the general intoxication of the macroorganism with the products of the vital activity of microorganisms and the possible action of bacterial endotoxins released upon the death of the pathogen; they are also not released into the environment (although with measles or whooping cough, the patient during this period is already epidemiologically dangerous for others);

the height of the disease- manifestation of specific symptoms of the disease. In the presence of a characteristic symptom complex in this period of development of the disease, clinicians call such a manifestation of the disease overt infection and in cases where the disease during this period proceeds without pronounced symptoms, - asymptomatic infection. This period of development of an infectious disease, as a rule, is accompanied by the release of the pathogen from the body, as a result of which the patient presents an epidemiological danger to others; period of outcomes. V this periodpossible:

relapse of the disease - return of clinical manifestations of the disease without re-infection due to pathogens remaining in the body;

superinfection - infection of a macroorganism with the same pathogen until recovery. If this occurs after recovery, it will be called reinfection as it occurs as a result of a new infection with the same pathogen (as is often the case with influenza, dysentery, gonorrhea);

. bacteriocarrier, or rather microbearer,- Carriage of the causative agent of any infectious disease without clinical manifestations;

complete recovery (convalescence) - during this period, pathogens are also excreted from the human body in large quantities, and the routes of excretion depend on the localization of the infectious process. For example, with a respiratory infection - from the nasopharynx and oral cavity with saliva and mucus; with intestinal infections - with feces and urine, with purulent-inflammatory diseases - with pus;

death. It should be remembered that the corpses of infectious patients are subject to mandatory disinfection, since they represent a certain epidemiological danger due to the high content of a microbial agent in them.

In the doctrine of infection, there is also the concept persistence (infection): microorganisms enter the human body and can exist in it without manifesting themselves for a sufficiently long time.

This happens with the herpes virus and very often with the pathogen

tuberculosis and HIV infection.

The differencecarriage of bacteriafrom persistence:

- when carriage, a person releases the pathogen into the environment and is dangerous to others;

during persistence, the infected person does not release the microorganism into the environment, therefore, not dangerous to others in an epidemiological respect.

In addition to the above terms, there is also the concept "infectious process" - This is the body's response to the penetration and circulation of the microbial agent in it.

From the definition of "infection" it becomes obvious and factors necessary for its emergence and development:

pathogen microorganism;

- susceptible macroorganism;

- the external environment in which they interact.

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Incubation period the disease is calculated from the moment the pathogen enters the body (it would be more correct to say - from the moment the pathogen overcomes the body's defense systems) to the clinical manifestation of the symptoms of a particular disease.

The duration of the incubation period for various diseases varies within a fairly wide range - from several hours (influenza, botulism) to several weeks, months (viral hepatitis B, AIDS, rabies), and even years with slow infections. For most infectious diseases, the incubation period is 1 to 3 weeks.

The duration of the incubation period is influenced by:

  • the virulence of the infection (the higher it is, the shorter the period);
  • the infectious dose of the pathogen (the larger it is, the shorter the period);
  • the reactivity of the macroorganism, on which the very possibility of the occurrence of the disease depends, as well as the intensity and pace of its development.

The incubation period is followed by pro-normal period, which begins from the moment the first clinical signs of the disease appear:

  • headache;
  • malaise;
  • sleep disorder;
  • decreased appetite;
  • possible increase in body temperature.

Since the first clinical signs of many infectious diseases are similar, it is not always possible to reliably establish an accurate diagnosis in the prodnormal period of the disease. An exception is measles, which manifests itself in the prodnormal period by the spots of Belsky-Filatov-Koplik, which makes it possible to establish a reliable nosological diagnosis.

Within 2-4 days there is period of onset of symptoms diseases followed by peak period disease, depending on the specific pathogen (several days with measles; several weeks with viral hepatitis).

During the peak period, the symptoms characteristic of this infection are most pronounced.

At the end of the height of the disease begins extinction period clinical manifestations, alternating period of convalescence(recovery). The length of the recovery period varies widely and depends on many factors:

  • forms of the disease;
  • the severity of the course of the disease;
  • the effectiveness of treatment;
  • the age of the patient;
  • the presence of concomitant diseases;
  • the general condition of the body.

Recovery can be complete (impaired body functions are fully restored) or incomplete (residual symptoms of the disease remain).

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Clinical stages of an infectious disease

In accordance with these characteristics, any infectious disease has certain clinical stages (periods) of its course, expressed in varying degrees :

  • incubation period - the period from the moment the infectious agent enters the human body until the first precursors of the disease appear. The causative agent during this period is usually not released into the environment and the patient does not pose an epidemiological danger to others;
  • prodromal period the manifestation of the first nonspecific symptoms of the disease, characteristic of the general intoxication of the macroorganism with the products of the vital activity of microorganisms, as well as the possible action of bacterial endotoxins released upon the death of the pathogen, are also not released into the environment, although, for example, with measles or whooping cough, the patient during this period is already epidemiologically dangerous for others ;
  • the height of the disease manifestation of specific symptoms of the disease.

Development stages, signs of an infectious disease

Wherein in the presence of in this period of development of the disease characteristic symptom complex clinicians call this manifestation of the disease overt infection , and in cases where the disease during this period proceeds without severe symptoms, — asymptomatic infection ... This period of development of an infectious disease, as a rule, is accompanied by the release of the pathogen from the body, as a result of which the patient presents an epidemiological danger to others;

  • period of outcomes; during this period may come :
  • relapse of the disease return of clinical manifestations of the disease without re-infection, due to pathogens remaining in the body;
  • superinfection infection of a macroorganism with the same pathogen until recovery. However, if this occurs after recovery, then it is called reinfection , since it occurs as a result of a new infection with the same pathogen, as is often the case with influenza, dysentery, gonorrhea;
  • bacteriocarrier , or rather, microbearer carrier of the pathogen any infectious disease without clinical manifestations;
  • complete recovery (convalescence) in this period pathogens are also excreted from the body a person in large quantities, and the way of excretion depends on the localization of the infectious process. For example, with a respiratory infection - from the nasopharynx and oral cavity with saliva and mucus; with intestinal infections - with feces and urine, with purulent-inflammatory diseases - with pus;
  • death , it should be remembered that corpses infectious patients are subject to mandatory disinfection, since they represent a certain epidemiological danger due to the high content of a microbial agent in them.

In the doctrine of infection there is also such a thing as persistence (infection) microorganisms enter the body a person and can exist in him, not showing myself for quite a long time, as it happens, for example, with the herpes virus, and very often with the causative agent of tuberculosis and HIV infection.

The difference carriage of bacteria from persistence consists in the fact that during carriage, a person releases the pathogen into the environment and is dangerous to others, and during persistence, an infected person does not release a microorganism into the environment, therefore, it is not epidemiologically dangerous to others.

In addition to the above terms, there is also such a concept as " infectious process". This is the collective response to the penetration and circulation of a microbial agent in it. From the definition of the concept of" infection "the factors necessary for its occurrence and development become obvious. This is a microorganism-pathogen, a susceptible macroorganism, the external environment in which they interact.

Question 21. Ways of transmission of infections

Infection entrance gate

For the occurrence and development of an infectious disease are of great importance:

  • infectious dose - the minimum number of microbial cells that can cause an infectious disease;
  • entrance gate of infection body tissues through which the microorganism enters the macroorganism.

Infection entrance gate often determine the localization of the pathogen in the human body, as well as the pathogenetic and clinical features of an infectious disease. For some microorganisms, there are strictly defined entrance gates (measles virus, influenza - the upper respiratory tract, enterobacteria - the gastrointestinal tract). For other microorganisms entrance gate can be different, and they cause diseases that are different in their clinical manifestations. For example, staphylococci, streptococci, proteas, when they get on the mucous membrane of the upper respiratory tract, cause bronchitis, pneumonia, and when they get on the mucous membrane of the urethra, purulent urethritis.

Entrance gate infections can determine the clinical form of the disease, like this occurs with anthrax :

  • skin,
  • pulmonary,
  • intestinal form.

Accordingly, they are caused by the penetration of microorganisms into the body through the skin, mucous membranes of the upper respiratory tract or the gastrointestinal tract.

Transmission routes

The concept of "entrance gate of infection" is very closely related to the concept of transmission routes causative agents of infectious diseases. In this case, the same microorganism - the pathogen can enter the macroorganism in different ways, causing different clinical forms of the disease - the same anthrax pathogen, for example.

On the other hand, it depends on the transmission path which nosological form diseases can be caused by a pathogenic microorganism - for example, when ingested airborne by streptococci cause sore throat, and contact-household- streptoderma (purulent-inflammatory disease of the skin).

Isolation of this or that transmission routes infectious diseases is rather arbitrary, but nevertheless, the following are distinguished among them:

  • airborne - it is typical for chickenpox, tuberculosis, whooping cough, flu;
  • fecal-oral , which is sometimes distinguished water - characteristic, for example, of cholera, and alimentary - typical, for example, for dysentery;
  • transmission path - associated with the transmission of the pathogen through the bites of blood-sucking insects (tick-borne encephalitis, lice and lousy typhus);
  • contact-household, which, in turn, is divided into:
  • direct contact - (from source to host) - including sexually transmitted diseases, including HIV infection;
  • indirect contact (through an intermediate object) - these can be hands (for wound infections, intestinal infections) or various objects, including those for medical purposes (for purulent-inflammatory diseases and parenteral hepatitis).

Recently, as a separate, very often stand out artificial(artifactual) the path of spread of infectious diseases, connected, first of all, with medical manipulations... Moreover, it can simulate as transmissible(parenteral and especially intravenous injections) and contact-household transmission path (various kinds of laboratory examinations using medical devices - bronchoscopes, cystoscopes, etc.).

In accordance with the predominance of a particular transmission route - according to the epidemiological principle - all infectious diseases are divided into :

  • intestinal;
  • airborne, or respiratory;
  • transmission;
  • skin infections.

The existing one is close to this classification. clinical classification infectious diseases depending on the affected organ system. Allocate :

  • intestinal infections
  • respiratory infections,
  • meningoencephalitis,
  • hepatitis,
  • infections of the genitourinary tract (urogenital),
  • skin infections.

By biological nature of the pathogen, all infectious diseases are divided into :

  • bacterial infections;
  • viral infections;
  • fungal infections;
  • protozoal infections.

By the number of pathogens that cause an infectious disease, they are divided into :

  • monoinfection;
  • mixed(associated)- mixed infection.

It is necessary to distinguish from the latter secondary infection, in which to the main, the original already developed. Another, caused by a new pathogen, joins, although in some cases the secondary infection may, in its importance for the patient, exceed, and significantly, the primary infection.

By the duration of the course of infectious diseases are divided into :

  • sharp;
  • chronic.

By the origin of the pathogen, infectious diseases are divided into :

  • exogenous;
  • endogenous, including autoinfection.

Exogenous infection Is an infection caused by microorganisms, coming from the environment with food, water, air, soil, secretions of a sick person or micro-carrier.

Endogenous infection- an infection caused by microorganisms - representatives of their own normal microflora person. It often occurs against the background of a person's immunodeficiency state.

Autoinfection- a kind of endogenous infection that occurs as a result of self-reproduction by transfer of the pathogen from one biotope to another... For example, from the mouth or nose with the hands of the patient himself to the wound surface.

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periods of infectious diseases

Incubation period (latent) - occurs from the moment of infection and lasts until the first clinical signs appear.

For some infections, it takes hours, weeks, months, and even years. The duration of the incubation period depends on the reactivity of the human body, the dose and virulence of the pathogen.... Most infectious diseases have an incubation period of 1 to 3 weeks.

Features of the stages and periods of infectious diseases

Prodromal period, or the period of precursors - during this period, non-specific signs are characteristic: malaise, fever, headache, sleep disorders... Therefore, diagnosis during this period is difficult. Sometimes during this period, characteristic signs (rash, redness, spots) may appear that help early diagnosis. Lasts 1 to 3 days. And also many infectious diseases can proceed without a precursor period..

After an increase in clinical symptoms occurs and the disease passes at the stage of the peak of clinical manifestations , which is characterized by all symptom complexes including specific signs - jaundice with viral hepatitis, rash with measles, scarlet fever, typhoid fever.

The height of the disease is changing a period of extinction of symptoms, that is, recovery with the restoration of the disturbed internal environment of the body, with the participation of defense mechanisms. The duration of the recovery period varies depending on the form of the disease, the severity of the course, the body's defenses.

The outcome of an infectious disease can be a transition to a chronic form, disability, and the formation of bacterial carriers. Death is possible.

According to the severity of the current: severe, moderate, mild.

Severe form characterized by pronounced symptoms, prolonged course, the presence of complications.

For medium severity pronounced clinical symptoms, a short course and usually a favorable outcome are typical.

With an easy course the symptoms of the disease are mild. There may be fulminant forms of the disease, which are very difficult, with the rapid development of clinical symptoms, are often fatal. The difference in the form of the severity of the disease requires a different approach to the appointment and dosage of drugs.

With the flow: acute, subacute and chronic.

In the case of a decrease in the body's defenses, complications may arise such as: myocarditis with diphtheria, vascular thrombosis with typhus. Often there is a complication associated with the activation of microbes in the patient's body. These complications include pneumonia, otitis media, abscesses.

Infectious diseases caused by one type of microorganism - monoinfection; caused by several types of microbes - mixed infections.

Distinguish from mixed infection secondary infection when another one joins an already developed infectious disease. Repeated illness with the same infectious disease is called reinfection(malaria, dysentery). The return of the symptoms of the disease as a result of the weakening of the body's defenses is called relapse(typhoid fever).

See infectious process

Saenko I.A.

  1. Belousova A.K., Dunaitseva V.N. Nursing in infectious diseases with a course of HIV infection and epidemiology. Series ‘Secondary vocational education’. Rostov n / a: Phoenix, 2004.