The period of recovery (reconvalescence). Period of residual effects: muscular hypotension, residual skeletal changes
The functions of the organs and systems of the body, disturbed during the three periods of the disease, gradually normalize. However, dysfunctions of the heart, liver, kidneys and other organs can be observed later and 2-4 years after the injury. Patients who have undergone burn disease are subject to follow-up.
Issues of blood transfusion, clinics and treatment of blood transfusion complications.
The history of blood transfusion has more than 3 centuries. Since the 17th century, attempts to transfuse human blood have most often ended in failure. A favorable outcome during this period could be purely accidental, since the issues of the interaction of the blood of the donor and the recipient were not studied at that time. In 1901, the Austrian Karl Landsteiner established that, depending on the presence of isoantigens in erythrocytes, and isoantibodies in plasma, all of humanity can be divided into 3 groups. In 1907, the Czech J. Jansky supplemented Landsteiner's data, highlighting the 4th group, and created a classification of blood groups, adopted since 1921 as an international one.
Blood groups.
For the occurrence of hemolytic post-transfusion reactions and incompatibility between the mother and fetus, the antigenic structure of the erythrocyte is primarily important. Antigens are substances of a protein nature that can cause the formation of antibodies in the body and react with them. In the human body, in addition to immune antibodies that are produced in response to an antigen entering it, there are natural antibodies that exist from the moment of birth and are determined by genetic traits inherited from parents. An example of natural antibodies are group isoagglutinins a and b. They are specific and react with the corresponding antigens - agglutinogens A and B. The temperature optimum of the reaction is +15 - +25 degrees C. All mankind, depending on the content of antigens (agglutinogens) A and B in erythrocytes, is divided into 4 groups:
group - does not contain antigens;
group - contains agglutinogen A;
group - contains agglutinogen B;
group - contains agglutinogens A and B.
The blood of these groups, in strict dependence on the presence or absence of group antigens A and B, which are called agglutinogens, contains group antibodies, which are otherwise called agglutinins (isoagglutinins, group agglutinins). The blood system remains stable in the absence of similar agglutinins and agglutinogens (antibodies and antigens) in it. In this case, their interaction does not occur, which is manifested by agglutination (gluing) and hemolysis (destruction) of erythrocytes. Thus, according to the serological properties of erythrocytes and plasma, 4 blood groups are distinguished.
group ab - there are no antigens (agglutinogens) in the blood.
group Ab - there are no antibodies and antigens of the same name in the blood.
group Ba - (agglutinins and agglutinogens).
group AB - there are no antibodies (agglutinins) in the blood.
The percentage of people with different blood types in different parts of the world is not the same. In the CIS countries, it is approximately as follows:
O(I gr.) 34%; A(II gr.) 38%; B (III gr.) 21%; AB (IV gr.) 8%.
Rh factor.
In 1937, Landsteiner and Wiener discovered the Rh factor (Rh - factor). In the course of experiments on rabbit immunization with erythrocytes of a rhesus monkey (Makakus rhesus), serum was obtained that agglutinated 85% of human erythrocyte samples, regardless of group affiliation. Thus, the presence in human erythrocytes of a substance of an antigenic nature, similar to that of the rhesus monkey, was established. It is called the Rh factor. People who have this factor in their blood began to be designated as "Rh-positive", those who did not have it - "Rh-negative". The Rh factor is contained in the blood of about 85% of people and, unlike agglutinogens (antigens) A and B, does not, as a rule, have natural antibodies. Antibodies against the Rh factor (anti-Rh) arise only due to the sensitization of a Rh-negative (without Rh factor) person by red blood cells containing the Rh factor. Antibodies can also appear in the blood of an Rh-negative pregnant woman in response to an Rh-positive fetus. Rh incompatibility (Rh-conflict) occurs in case of repeated contact of a sensitized person with the Rh factor (blood transfusion, pregnancy).
There are many other antigens in the blood. They are designated as systems MN, Kell, Duffy, Lewis, Lutheran, etc. Severe post-transfusion complications and hemolytic disease are extremely rare. Currently, antigens have been identified in leukocytes, platelets, and other protein structures with a total number of about 300 species.
The clinic of paratyphoid A and B resembles typhoid fever, however, their reliable recognition is possible only on the basis of data from bacteriological and serological studies.
Paratyphoid A often develops acutely with the appearance of catarrhal phenomena. The face is hyperemic, injection of scleral vessels. The rash occurs earlier by 6-7 days, often plentiful, may be papular, morbilliform. Status typhozus is usually absent.
Paratyphoid B- also characterized by acute onset, gastroenteritis phenomena. The rash, as a rule, appears earlier, profuse, polymorphic, localized on the trunk and extremities. Relapses and complications are rare.
The outcome of the disease in addition to recovery and release of the body from the causative agent of typhoid fever, there may be the formation of a bacteriocarrier (acute - up to 6 months, chronic - more than 6 months).
DIAGNOSTICS
1. To detect the pathogen, it is necessary to produce cultures of blood, feces, urine, bile and, according to indications, bone marrow punctate.
2. From serological tests, the Vidal reaction and RNGA are used, which must be repeated in the dynamics of the disease (increase in antibody titers).
3. To identify specific antigens, RAGA is used - the reaction of aggregate-hemagglutination.
4.Conduct general blood test(thrombocytopenia, leukopenia, relative lymphocytosis, aneosinophilia, accelerated ESR).
Differential Diagnosis performed with many infectious and non-communicable diseases. More often with yersiniosis, typhus, sepsis, tuberculosis, brucellosis, malaria, etc.
TREATMENT
1. hospitalization to a specialized department, and in the absence of such - to a box in compliance with all anti-epidemic measures
2.strict bed rest up to 10 days N temperature. Diet 4 abt(4a - typhoid table.
2. Etiotropic therapy. cephalosporin antibiotics, F torquinolone series(ciprofloxacin, tarivid, etc.)
3. Pathogenetic therapy:
· Detoxification therapy is carried out parenterally in a volume of 1200-2500 ml per day, depending on the severity of the disease. IN infusion therapy it is necessary to include glucose solutions, polarizing mixtures (trisol, quartasol, acesol), crystalloids, colloidal solutions (rheopolyglucin, hemodez).
In case of cardiac disorders, the development of myocarditis, therapy includes drugs such as Riboxin, cardiac glycosides in clinical doses.
· Symptomatic therapy . sedatives and hypnotics.
· Desensitizing therapy(suprastin, diazolin, etc.) Antifungal drugs- reduce the possibility of developing candidiasis.
PREVENTION
Improvement of water supply sources, both centralized water pipes and wells.
Treatment of wastewater discharged into open water, especially wastewater from infectious diseases hospitals;
Elimination of sources of water pollution (latrines, garbage pits, landfills); boiling or pasteurization of milk, dairy products, including cottage cheese, ensuring the sanitary maintenance of public catering places.
26) Yersiniosis.
Pseudotuberculosis (extraintestinal yersiniosis)- an acute infectious disease from the group of zoonoses with general intoxication, fever, scarlet fever-like rash, as well as damage to various organs and systems.
Etiology. The causative agent - Iersinia pseudotuberculosis - Gr-bacillus, in culture is located in the form of long chains, does not form spores, has a capsule. Sensitive to drying, exposure to sunlight. When heated to 60 about perishes after 30 minutes, when boiled - after 10. Conventional disinfection kills within 1 minute. Distinctive ability - the ability to grow at low temperatures. According to surface AG, 8 serovars are distinguished, 1 and 3 are more common. It actively multiplies in boiled tap and river water, and also multiplies and retains its properties at low temperatures. It has high invasive qualities, is able to penetrate through natural barriers. Contains endotoxin, can form exotoxin.
Epidemiology. Registered almost throughout the country. zoonotic infection. Source of infection- wild and domestic animals. Main tank- mouse-like rodents. They infect food stored in refrigerators and vegetable stores with secretions. Soil can also serve as a reservoir. Transmission route- alimentary; when using inf.food or water, not subjected to heat treatment. Both children and adults are susceptible to P.. Children under 6 months of age practically do not get sick, at the age of 7 months to 1 year - rarely. The disease is recorded throughout the year, maximum - February-March.
Pathogenesis. The causative agent with inf. food or water penetrates through the mouth (infection phase), overcomes the gastric barrier, enters the small intestine, where it is introduced into enterocytes or intercellular spaces of the intestinal wall (enteral phase). From the intestine, m / o penetrate into regional mesenteric l / y and cause lymphadenitis ( regional infection phase). The massive intake of the pathogen and its toxins from the primary localization sites into the blood leads to the development of the infection generalization phase. It corresponds to the appearance of clinical symptoms. Further progression is associated with the fixation of the pathogen by RES cells mainly in the liver and spleen ( parenchymal phase). This is followed by persistent fixation and elimination of the pathogen due to the activation of cellular factors of immune defense and the production of specific antibodies. There is a clinical recovery. The allergic component also plays a role in the pathogenesis, associated with the repeated entry of the pathogen into the circulation or the previous non-specific sensitization of the body (indicated by a high content of histamine, serotonin, arthralgia, al. rash, erythema nodosum).
Immunity. The duration of immunity has not been precisely established, but there are reasons to consider it persistent. Repeated - rare.
Clinic. The incubation period is from 3 to 18 days. Initial symptoms : begins acutely, body temperature up to 38-40. From the first days of illness, complaints of weakness, headache, insomnia, poor appetite, sometimes chills, muscle and joint pain. Some children at the onset of the disease have mild catarrhal phenomena (nasal congestion and cough). There may be pain when swallowing, a feeling of perspiration and soreness in the throat. Patients with pronounced initial symptoms may have dizziness, nausea, vomiting, abdominal pain, mainly in the right iliac region or in the epigastrium. May be liquid stool 2-3 r / d according to the type of enteritis. On examination: puffiness and hyperemia of the face, neck, pale nasolabial triangle. Hyperemia of the conjunctiva and injection of scleral vessels, less often - a hypertensive rash on the lips and wings of the nose. Hyperemia of the mucous membranes of the tonsils. The mucous membrane is edematous, enanthema is sometimes observed. The tongue in the initial period is densely coated with a grayish-white coating, from the 3rd day it begins to clear and becomes crimson, papillary. On the 3-4th day, the symptoms reach a maximum. Begins peak period- deterioration, higher temperature, severe symptoms of intoxication, damage to internal organs and skin changes. Some have a hood symptom - flushing of the face and neck with a cyanotic tint, a symptom of gloves - a delimited pink-cyanotic color of the hands, a symptom of socks - a delimited pink-bluish color of the feet. On the skin of the body rash; either dotted (reminiscent of scarlet fever) or spotted. Usually located in the lower abdomen axillary areas and on the sides of the body. Color from pale pink to bright red. The background of the skin may be hyperemic or unchanged. There is white persistent dermographism. Larger rashes are located around large joints, where they form continuous erythema. At long course or relapse - elements of erythema nodosum appear on the legs or buttocks. Pastia's symptoms (dark red color of skin folds), pinching, burning symptoms are usually positive. The rash lasts no more than 3-7 days, sometimes several hours. At the height of the disease noted arthralgia, there may be swelling and tenderness of the joints. Usually affects the wrist, interphalangeal, knee and ankle. Changes in the digestive organs: appetite is significantly reduced, nausea, infrequent vomiting, often - abdominal pain and upset stool. The abdomen is moderately swollen. Palpation can reveal soreness and rumbling in the right iliac region. Intestinal disorders - infrequently, a slight increase and thinning of the stool with a preserved fecal character. The liver and spleen are often enlarged. Changes in the CCC: relative bradycardia, muffled tones, sometimes systolic murmur, in severe cases - arrhythmia. BP moderately ↓. On the ECG - changes in the contractile function of the myocardium, conduction disturbances, extrasystole, ↓ T wave, lengthening of the ventricular complex. urinary system: possible pain in the lumbar region, ↓ diuresis.
Classification . By type: 1. Typical with a complete or partial combination of clinical symptoms (scarlet fever, abdominal, generalized, arthralgic, mixed and septic variants). 2. Typical with isolated syndrome(rarely). 3. Atypical (erased, subclinical, catarrhal). Severity: light, medium, heavy.
Flow . More often - a smooth flow. The total duration of the disease is not more than 1-1.5 months, but there may be exacerbations and relapses (they are easier, but the duration increases to 2-3 months). Chronic - rare. In some cases, after the rash - lamellar peeling on the hands and feet, pityriasis - on the back, chest and neck.
Diagnostics 1. OAM: albuminuria, microhematuria, cylindruria, pyuria. 2. UAC: leukocytosis, neutrophilia with P / I shift, monocytosis, eosinophilia, ESR. 3. Biochem.AK: direct bilirubin, activity of ALT, AST, F-1-FA and other hepatocellular enzymes. 4. Bakt. study: material for sowing - blood, sputum, feces, urine and swabs from the oropharynx. Inoculations on conventional nutrient media and enrichment media. Cultures of blood and swabs from the throat should be carried out in the 1st week of the disease, cultures of feces and urine - throughout the disease. 5. Serological studies: RA (most often; as AG - live reference cultures of pseudotube strains; diagnostic titer 1:80 and above; blood is taken at the beginning of the disease and at the end of 2-3 weeks), RP, RSK, RPGA, RTPGA, ELISA. For emergency diagnostics - PCR and immunofluorescence method.
Dif diagnostics . With scarlet fever, measles, enterovirus infection, rheumatism, vir.hepatitis, sepsis, typhoid-like diseases.
Treatment . Bed rest until the temperature normalizes and the symptoms of intoxication disappear. Nutrition is complete, without significant restrictions. Etiotropic treatment: levomecithin for 7-10 days. In the absence of effect or exacerbation after the abolition of levomecithin, a course of treatment with 3rd generation cephalosporins. In severe forms - 2 a / b, taking into account compatibility. With mild forms - a / b are not required. Detoxification therapy: intravenous reopoliglyukin, albumin, 10% glucose, enterosorbents: enterosgel, enterodez, etc. in severe cases - GCS at the rate of 1-2 mg of prednisolone per 1 kg of body weight per day in 3 divided doses for 5-7 days . Desensitizing therapy: antihistamines - suprastin, tavegil, diphenhydramine, etc. Drugs that stimulate immunogenesis: gepon, polyoxidonium, anaferon for children, etc. Posyndromic therapy.
Prevention . Rodent control. Proper storage of vegetables, fruits and other food products. Strict sanitary control of cooking technology, as well as the quality of water supply in rural areas. Anti-epidemic measures in the focus of infection are the same as in intestinal infections. After hospitalization of the patient, the final disinfection is carried out. Specific prophylaxis has not been developed.
Intestinal yersiniosis(enteritis caused by I. enterocolitica) is an acute infectious disease from the group of anthropozoonoses with symptoms of intoxication and a predominant lesion of the gastrointestinal tract, joints, less often other organs.
Etiology . The causative agent is I.enterocolitica. Gr - wand. Facultative aerobe, no capsule, does not form spores. It is undemanding to pit.sredam, grows well at low temperatures. According to biochemical properties, they are divided into 5 serovars (3 and 4 are more often found, less often - 2). According to O-AG - more than 30 serovars. It is sensitive to the action of physical and chemical factors, tolerates low temperatures well, while maintaining the ability to reproduce.
Epidemiology . Widely spread. Often found in murine rodents, cattle, pigs, dogs, cats, isolated from dairy products, ice cream. Source of infection– human and animals, sick or carriers. Transmission route- alimentary, contact, maybe aerogenic. Diseases are registered all year round, outbreaks - from October to May with a peak in November and a decline in July-August. Preim.children are ill from 3 to 5 years.
Pathogenesis. When using inf.food, water or by contact. M/o passes through the stomach, is localized in the small intestine (frequent localization of the terminal section of the small intestine, appendix), where it begins to multiply. M / o takes root and destroys the epithelial cells of the intestinal mucosa. The infection spreads to regional l / y. At this stage, the disease often ends. In more severe cases, m / o enters the blood - a generalization of the process. Also, m\o is able to stay in l\u for a long time, causing relapses or transition to chronic form.
Clinical picture. The incubation period is 5-19 days, on average - 7-10. Allocate biliary-intestinal, abdominal form (pseudoappendicular, hepatitis), septic, articular forms, erythema nodosum.
Gastrointestinal form. Initial symptoms: begins acutely, T to 38-39. From the first days lethargy, weakness, ↓ appetite, headache, dizziness, nausea, repeated vomiting, abdominal pain. A constant symptom is diarrhea. Chair from 2-3 to 15 r / day. The feces are liquefied, often with an admixture of mucus and greenery, sometimes blood. In the coprogram: mucus, polymorphonuclear leukocytes, single erythrocytes, violation of the enzymatic function of the intestine. In the KLA: moderate leukocytosis with a shift of the formula to the left, ESR. Sometimes the disease begins with catarrhal phenomena in the form of a slight cough, runny nose, nasal congestion; chills, muscle pain, arthralgia are possible. In severe cases, there may be a picture of intestinal toxicosis and exsicosis, meningeal symptoms. peak period(after 1-5 days from the beginning): the abdomen is moderately swollen. On palpation - soreness and rumbling along the intestines, mainly in the region of the caecum and ileum. Sometimes the liver and spleen. Some patients have a polymorphic rash on the skin (punctate, maculopapular, hemorrhagic) with predominant localization around the joints, on the hands, feet (symptoms of gloves and socks). In some cases, recurrence of changes in the joints, myocarditis phenomena. The duration of the disease is 3-15 days.
Pseudoappendicular form. It occurs preim in children older than 5 years. It starts off sharp. Temperature up to 38-40. Complaints of headache, nausea, vomiting 1-2 times a day, anorexia. A constant and leading sign - pain in the abdomen - cramping, localized around the navel or in the right iliac region. On palpation - rumbling along the small intestine, diffuse or local pain in the right iliac region, sometimes - symptoms of peritoneal irritation. There may be short-term diarrhea or constipation, flying pains in the joints, mild catarrh of the upper respiratory tract. In the KLA: leukocytosis (8-25x10 9 /l) with a shift of the formula to the left, ESR) 10-40 mm/h). During surgery for an acute abdomen, catarrhal or gangrenous appendicitis is sometimes found, often mesadenitis, edema and inflammation of the terminal ileum.
Yersinia hepatitis. It begins acutely with pronounced signs of intoxication, body temperature, which does not decrease during the icteric period, ESR. Sometimes - short-term diarrhea, abdominal pain. In some, exanthema appears early. For 3-5 days - dark urine, discolored feces and jaundice. The liver is hardened and painful. The edge of the spleen is palpated. The activity of hepatocellular enzymes is low or ↓!!!
Knotty (nodose) form. Preferred in children over 10 years old. It begins acutely with symptoms of intoxication, body temperature. On the shins - rashes in the form of painful pink nodes with a cyanotic tint, which disappear after 2-3 weeks. Characterized by gastroenteritis, abdominal pain, sometimes - changes in the upper respiratory tract.
Articular form proceed according to the type of non-purulent polyarthritis and arthralgia. It is rare, predominantly in children older than 10 years. 5-20 days before the onset of arthritis, children have intestinal disorders that are accompanied by fever. The knee and elbow joints are more often involved, less often the small joints of the hands and feet. The joints are painful, swollen, the skin over them is hyperemic.
Septic (generalized) form. Occurs rarely. Acute septicemia. From the first days the temperature is up to 40 and above, it is hectic in nature. Drowsiness, weakness, anorexia, chills, headache, muscle and joint pain, weakness, pain when swallowing, nausea, vomiting, loose stools are noted. For 2-3 days, some patients develop a rash similar to that of rubella and scarlet fever. More often located around the joints, where it is maculopapular in nature. Quickly the liver, spleen, sometimes jaundice appears. Violations of the CCC and respiratory system are noted. In the KLA: ↓ hemoglobin, neutrophilic leukocytosis (16-25x10 9 / l), ESR 60-80 mm / h. In OAM: albuminuria, cylindruria, pyuria.
Intestinal yersiniosis in young children. At the age of 3 years, the gastrointestinal form is usually found in the form of gastroenteritis or gastroenterocolitis. They observe a higher prolonged fever, more pronounced intoxication (adynamia, periodic anxiety, convulsions, loss of consciousness, hemodynamic disorders), longer vomiting and stool disorders.
Diagnostics. Based on clinical and laboratory data. 1. PCR2. Bact method. most often allocated in the first 2-3 weeks, sometimes - within 4 months. 3. With articular and skin form– RA with live or killed culture and RNGA. Diagnostic titers of RA - 1:40-1:160, RNGA - 1:100-1:200.
Dif. Diagnostics. With scarlet fever, measles, enterovirus inf, rheumatism, sepsis, typhoid-like diseases.
Treatment. WITH mild form-Houses. In case of gastrointestinal, abdominal, an appropriate diet is prescribed. Enterosorbents are prescribed: enterosgel, enterodez, etc. Etiotropic therapy: chloramphenicol and cephalosporins of the 3rd generation. With moderate and severe forms, symptomatic therapy is additionally prescribed: detoxification, rehydration measures, antihistamines, vitamins, and diet. In the septic form, 2 a/b (oral and parenteral) and GCS are prescribed. In arthritis and nodular forms, a\b are ineffective, antirheumatic drugs and corticosteroids, etc. are prescribed. In case of appendicitis, abscesses, osteomyelitis - surgical intervention.
Prevention. The same as with kish.inf. + the same measures as in case of pseudotuberculosis.
27) Cholera. Etiology. Epidemiology. Pathogenesis. Clinic. Diagnosis and differential diagnosis. Treatment. Prevention.
(type Vibrio cholerae.) - acute intestinal, life-threatening sapronous infection. It is characterized by the fecal-oral mechanism of infection, damage to the small intestine, watery diarrhea, vomiting, rapid loss of body fluids and electrolytes with the development of varying degrees of dehydration up to hypovolemic shock and death.
Endemic foci are located in Africa, Latin. America, India and Southeast Asia.
Etiology
There are 3 types of pathogens
Morphology: a curved stick with a fairly long flagellum. Gr (-), stain well with aniline dyes. Can form L-shapes.
Agave, Inaba, Gikoshima.
Vibrios secrete exotoxin - cholerogen - the most important pathogenetic factor.
When microbial bodies are destroyed, endotoxins are released.
The 3rd component of toxicity is the permeability factor. A group of enzymes that increase the permeability of the vascular wall cell membranes and contribute to the action of cholerogen.
Stability in the external environment is high.
In open water pools, they remain for several months, in wet feces - they remain as much as possible up to 250 days.
Can be stored in direct sunlight for up to 8 hours.
Epidemiology
There are 3 types of pathogens
V. cholerae asiaticae (causative agent of classical cholera),
V. cholerae eltor (the causative agent of El Tor cholera)
Serovar O139 (Bengal) (the causative agent of cholera in Southeast Asia).
They differ in biochemical properties.
Morphology: curved stick with a fairly long flagellum. Spores and capsules do not form. Gr (-), stain well with aniline dyes. Can form L-shapes.
Growth features: obligate aerobes, the optimal environment is alkaline (pH 7.6 -9.0). On liquid media, they grow in the form of a gray or bluish film. They are characterized by very fast reproduction.
Antigenic structure: they have a flagellar H-antigen (common for all vibrios) and a somatic thermostable O-antigen. The causative agents of cholera belong to the O-1 serogroup.
Depending on the properties of the O-antigen, 3 serovars are distinguished: Agave, Inaba, Gikoshima.
Pathogenesis
The mechanism of infection is fecal-oral.
Ways of distribution - water, alimentary, contact-household.
Most frequent way infection - water (drinking, washing vegetables, fruits, vegetables, bathing).
Infection of mollusks, fish, shrimps, frogs should be indicated. In these organisms, vibrio persists for a long time. Eating them without heat treatment increases the risk of developing the disease.
Seasonality - summer-autumn. During this period, more fluids are consumed, bathing. Increased fluid intake also leads to a decrease in concentration of hydrochloric acid in gastric juice.
Clinical picture Incubation period
It lasts from several hours to 5 days, more often 24-48 hours. The severity of the disease varies - from erased, subclinical forms to severe conditions with severe dehydration and death within 24-48 hours.
For a typical clinical picture cholera is characterized by 3 degrees of flow.
Features of cholera in children
Severe current.
· Early development and severity of dehydration.
More often develops a violation of the central nervous system: lethargy, disturbed. Consciousness stupor and coma.
Convulsions are more common.
Increased tendency to hypokalemia.
Increase in body temperature.
Degrees of dehydration in children
I degree -< 2 % первоначальной массы тела;
II degree - 3-5% of the initial body weight;
III degree - 6-8% of the initial body weight;
IV degree -> 8% of the initial body weight.
Complications
Hypovolemic shock
Acute renal failure: oliguria, anuria
CNS dysfunction: convulsions, coma
Diagnostics
· History: endemic area, known epidemic.
The clinical picture.
The purpose of the diagnosis: indication of Vibrio cholerae in feces and / or vomit, water, determination of agglutinins and vibriocidal antibodies in paired blood sera of patients
Diagnostic technique.
Inoculation of bacteriological material (feces, vomit, water) on thiosulfate-citrate-bile-salt-sucrose agar (eng. TCBS), as well as 1% alkaline peptone water; subsequent transfer to the second peptone water and seeding on plates with alkaline agar.
· Isolation of pure culture, identification.
· Study of the biochemical properties of the selected culture - the ability to decompose certain carbohydrates, the so-called. "series of sugars" - sucrose, arabinose, mannitol.
· Agglutination reaction with specific sera.
· Detection of Vibrio cholerae DNA by PCR, which also allows identification of belonging to pathogenic strains and serogroups O1 and O139.
Differential Diagnosis
Salmonellosis
Dysentery Sonne
Gastroenteritis due to Escherichia coli
Viral diarrhea (rotaviruses)
Poisoning poisonous mushrooms
Poisoning by organophosphorus pesticides
Botulism
Before initiating competent treatment of cholera,
F to establish the degree of dehydration and loss of electrolytes;
F select appropriate solutions;
F choose the way of their introduction;
F determine the rhythm of administration and the number of solutions, by stages;
F set the total required amount of fluids;
F to check the correct hydration, which is the criterion for the effectiveness of the treatment.
Hospitalization required. Cases require reporting to WHO.
At the first stage - pathogenetic therapy: replenishment of fluid loss - rehydration, is performed in two stages:
I. Primary rehydration - depending on the degree of dehydration (in a person 70 kg, 4th degree of dehydration (10%) - 7 liters are poured.)
II. Correction of ongoing losses (those that already occur in the clinic).
Primary rehydration is carried out by intravenous injection of fluid into 2-3 veins. Trisol solution is used
It is necessary to heat these solutions to a temperature of 37 degrees.
Etiotropic treatment: It is carried out with antibacterial drugs of the group tetracycline.(accelerate the cleansing of vibrios)
Tetracycline 0.3-0.5 g q / o 6 hours (3-5 days) or
Levomycetin 0.5 h / s 6 h (5 days).
If they are not tolerated - Furazolidone 0.1 x 6 r / day (5 days).
Pathogenetic treatment: Principles of pathogenetic therapy of patients with cholera:
1. restoration of the BCC;
2. restoration of the electrolyte balance of the blood;
Polyionic solutions: Quartasol, disol, acesol, trisol, lactasol
Oral rehydration: "Glucosol" ("Regidron"): NaCl-3.5 g + Na bicarbonate - 2.5 g + KCl - 1.5 g + glucose - 20 g + 1 liter of drinking water.
Potassium orotate, Panangin:
1 t x 3 r / day (in the absence of vomiting).
It is carried out in two stages:
1. Replenishment of lost fluid - rehydration (in the amount corresponding to the initial deficit in body weight).
2. Correction of ongoing water and electrolyte losses.
Can be administered orally or parenterally. The choice of route of administration depends on the severity of the disease, the degree of dehydration, and the presence of vomiting. Intravenous jet administration of solutions is absolutely indicated for patients with III and IV degree dehydration.
For initial intravenous rehydration, Ringer's solution. Hypokalemia + potassium.
Comparative characteristics of the electrolyte composition of cholera stool and Ringer's solution (mml/L)
Prevention
Nonspecific: increased sanitary and hygienic requirements; consumption of acidic foods (lemons, vinegar, etc.)
Specific: Corpuscular cholera vaccine (CVD 103-HgR vaccine - consists of attenuated live oral genetically modified strains of V. cholerae O1 (CVD 103-HgR). A single dose of the vaccine provides protection against V. cholerae at a high level (95%). After three months after the vaccine, protection against V. Cholerae El Tor was at the level of 65%.
(stimulates antimicrobial immunity). Vaccinate once parenterally, certain contingents of the population from 7 years of age. Revaccinate after 1 year.
CARRIED OUT ACCORDING TO EPID INDICATIONS!
Forecasting
With timely and adequate treatment, the prognosis is favorable. Ability to work is fully restored within approximately 30 days. In the absence of adequate medical care, the likelihood of a quick death is high.
Botulism.
- acute food poisoning that develops as a result of ingestion of botulinum toxin in the human body. Botulism is characterized by damage to the nervous system as a result of blocking acetylcholine receptors of nerve fibers with botulinum toxin, manifested in the form of muscle paralysis and paresis.
Exciter characteristic
Botulinum toxin produces a bacterium Clostridium botulinum – gram-positive spore-forming bacillus, obligate anaerobe. Unfavorable environmental conditions are experienced in the form of spores. Clostridia spores can remain in a dried state for many years and decades, developing into vegetative forms when they get into optimal conditions for life: temperature 35 C, lack of oxygen. Boiling kills the vegetative forms of the pathogen after five minutes, the temperature of 80 ° C is maintained for half an hour. Spores can survive in boiling water for more than half an hour and are inactivated only in an autoclave. Botulinum toxin is easily destroyed during boiling, but is able to be well preserved in brines, canned food and foods rich in various spices. At the same time, the presence of botulinum toxin does not change the taste of the products. Botulinum toxin is one of the most powerful toxic biological substances.
Reservoir and source of Clostridium botulism is the soil, as well as wild and some domestic (pigs, horses) animals, birds (mainly waterfowl), rodents. Clostridia carrier animals are usually not harmed, the pathogen is excreted with feces, bacteria enter the soil and water, animal feed. The contamination of environmental objects with clostridia is also possible during the decomposition of the corpses of animals and birds suffering from botulism.
The disease is transmitted by the fecal-oral mechanism by food. The most common cause of botulism is the use of home-canned foods contaminated with spores of the pathogen: vegetables, mushrooms, meat products and salted fish.
A prerequisite for the reproduction of clostridia in products and the accumulation of botulinum toxin is the lack of air access (tightly closed canned food).
In some cases, infection of wounds and abscesses with spores is likely, which contributes to the development of wound botulism. Botulinum toxin can be absorbed into the blood, both from the digestive system and from the mucous membranes of the respiratory tract and eyes.
Humans are highly susceptible to botulism, even small doses of the toxin contribute to the development of the clinical picture, but most often its concentration is insufficient to form an antitoxic immune response.
When poisoning with botulinum toxin from canned foods, cases of family damage are not uncommon. Currently, cases of the disease are becoming more frequent due to the spread of home canning. Botulism most often affects people from age group 20-25 years old.
Symptoms of botulism
The incubation period of botulism rarely exceeds a day, most often being several hours (4-6). However, sometimes it can take up to a week and 10 days. Therefore, observation of all people who ate the same food with the patient lasts up to 10 days.
In the initial period of the disease, nonspecific prodromal symptoms may be noted. Depending on the predominant syndrome, gastroenterological, ocular variants are distinguished, as well as the clinical form in the form of acute respiratory failure.
The gastroenterological variant is the most common and proceeds according to the type food poisoning, with epigastric pain, nausea and vomiting, diarrhea. The severity of enteral symptoms is moderate, however, there is dry skin that does not correspond to the general loss of fluid, and often patients complain of a disorder in swallowing food (“lump in the throat”).
The initial period of botulism, which occurs in the ophthalmic variant, is characterized by visual disturbances: blurring, flickering of "flies", loss of clarity and decreased visual acuity. Sometimes there is acute farsightedness.
The most dangerous variant of the initial period of botulism is acute respiratory failure (suddenly developing and progressive shortness of breath, spreading cyanosis, cardiac arrhythmias). It develops extremely quickly and is fatal after 3-4 hours.
Clinical picture botulism at the height of the disease is quite specific and is characterized by the development of paresis and paralysis of various muscle groups.
Patients have symmetrical ophthalmoplegia (the pupil is stably dilated, there is strabismus, usually converging, vertical nystagmus, omission of the eyelid). Dysphagia (swallowing disorder) is associated with progressive paresis of the muscles of the pharynx. If initially patients experience discomfort and difficulty swallowing solid food, then with the development of the disease it becomes impossible to swallow liquids.
Speech disorders develop through four stages in succession. First, the timbre of the voice changes, hoarseness occurs as a result of insufficient moisture in the mucous membrane of the vocal cords. In the future, due to paresis of the muscles of the tongue, dysarthria (“porridge in the mouth”) appears, the voice becomes nasal (paresis of the muscles of the palatine curtain) and disappears completely after the development of paresis of the vocal cords. As a result of a disorder of the innervation of the muscles of the larynx, the cough impulse is lost. Patients can suffocate if mucus and liquid enter the respiratory tract.
Botulinum toxin contributes to paralysis and paresis of mimic muscles, causing facial asymmetry, dysmimia. In general, it is noted general weakness, unsteady gait. Due to paresis of the intestinal muscles, constipation develops.
Fever is not characteristic of botulism, in rare cases subfebrile condition is possible. The state of cardiac activity is characterized by increased heart rate, some increase in peripheral arterial pressure. Disorders of sensitivity, loss of consciousness are not typical.
Complications of botulism
The most dangerous complication of botulism is the development of acute respiratory failure, respiratory arrest due to paralysis of the respiratory muscles or asphyxia. respiratory tract. Such complications can lead to death.
Due to the development of congestion in the lungs, botulism can provoke secondary pneumonia. Currently, there is data on the likelihood of complications of infection with myocarditis.
Diagnosis of botulism
With the development of neurological
The period of convalescence
It is characterized by the disappearance of signs of active rickets: the elimination of neurological and autonomic disorders(restoration of sleep, reduction of sweating, improvement or normalization of static functions, formation of new conditioned reflexes), reduction of muscle hypotension, improvement of well-being and general condition of the child. The severity of bone deformities gradually decreases. On radiographs - pathognomonic changes for this period in the form of uneven compaction of growth zones, osteosclerosis (along with persistent osteoporosis).
Period of residual effects
It is usually diagnosed at the age of 2-3 years, when the child no longer has clinical manifestations of active rickets, and the biochemical parameters are normal, but are clearly present. pronounced signs previous illness. Long-term preservation of reversible changes is possible - hypotension of muscles, looseness of joints and ligaments. The deformities of the tubular bones disappear with time (there may be a change in the axis of the lower extremities, "rachitic" flat feet). Deformations of flat bones decrease, but often persist during later life (frontal and parietal tubercles, flattening of the occiput, malocclusion, deformities of the chest, pelvic bones, etc.). It is impossible not to emphasize the significance of the negative long-term consequences of the transferred rickets - both at the individual and at the population level. For example, pelvic deformities are fraught with forced necessity delivery by caesarean section in the future, flat feet - a long-term pain syndrome and mediated damage to the spine and joints throughout life. A variety of orthodontic pathologies require long-term, traumatic, expensive correction; pronounced deformities of the lower extremities, chest, and skull bones are essential cosmetic defect, leading to psychological discomfort of the patient (especially a teenager), can disrupt the work internal organs(located in the chest cavity). It has been proven that transferred to early age rickets predisposes in the future to the violation of the formation of peak bone mass, the development of osteoporosis and other disorders of bone mineralization in older age.
Depending on the severity of the clinical picture, there are three degrees of rickets:
I degree (mild) - mild signs of rickets from the nervous and skeletal systems (excessive sweating, anxiety, slight softening of the skull bones, mild "rosary");
II degree (moderate) - moderately severe disorders of the nervous, bone, muscle and hematopoietic systems. Perhaps an increase in the liver, spleen, anemia. The general condition of the child is noticeably disturbed, functional disorders appear in the respiratory, cardiovascular and digestive systems. Rickets of the II degree develops after 1.5 - 2 months from the onset of the disease, in premature babies - a little earlier. In full-term children, the diagnosis of rickets of the II degree can be made no earlier than 4-5 months of life. Children become inactive, lethargic, muscular hypotonia and anemia appear. With rickets of the II degree, damage to the bones in two or three sections of the skeleton is characteristic;
III degree (severe) - significant disorders of the nervous system (lethargy, decreased motor activity), bone deformities, decreased muscle tone, loose joints, enlarged liver and spleen, functional disorders of the cardiovascular, respiratory and digestive systems, hematopoiesis.
The course of rickets can be:
- - acute rapid development with osteomalacia (osteoporosis) and curvature of the bones, severe dysfunction of the autonomic nervous system;
- - subacute - slow development with proliferation of defective bone tissue (hyperplasia of osteoid tissue);
- - relapsing - characterized by a change in improvement and exacerbation of the disease.
Currently dominated rickets mild degrees from subacute course, dominated by skeletal system manifestations of osteoid hyperplasia.
convalescence period.
Feeling better. Regression of neurological and autonomic disorders. Long-term restoration of muscle tone and bone formation. On radiographs - uneven compaction of growth zones.
The period of residual effects: muscular hypotension, residual changes in the skeleton.
Treatment
Diet. Breastfeeding whenever possible. Complementary foods should be introduced a month earlier. The amount of juice is doubled. Mandatory products - egg yolk, fish oil, caviar, butter, liver, meat.
Drug therapy
Vitamin D-3 (oil or alcohol solution). Therapeutic dose of vitamin D preparations. I degree - 1000-1500 IU / day, course 30 days. II degree - 2000-3500 IU / day, course 30 days. III degree - 3500-5000 IU / day, course 45 days. Prophylactic dose (after completion of the course of treatment) 400-500 IU / day, course 1 year.
Contraindications
Hypersensitivity to the components of the drug, hypervitaminosis D, increased levels of calcium in the blood and urine, calcium kidney stones, sarcoidosis, renal failure. Children up to the fourth week of life (due to the possibility of hypersensitivity to benzyl alcohol).
Dosage and administration
- 1. Orally (1 drop contains about 500 IU of vitamin D 3).
- 2. Preventively:
- - newborns from 4 weeks of life, full-term, with proper care and sufficient exposure to fresh air, as well as children under 2-3 years old: 500-1000 ME (1-2 drops) per day;
- - premature babies, twins, babies in poor living conditions - from 4 weeks of life 1000-1500 ME (2-3 drops) per day. In summer, you can limit the dose to 500 IU (1 drop) per day;
- - adults prophylactically: 500-1000 IU (1-2 drops) per day.
Therapeutically:
Daily 3,000-10,000 IU (6-20 drops) for 4-6 weeks, under close medical supervision and with periodic urinalysis.
As needed, after one week break, you can repeat the course of treatment.
In case of vitamin D intolerance, UVR is prescribed for up to 20 sessions within 1-2 months, drug analogues (for example, alfacalcidol), calcium, potassium, magnesium preparations, vitamin therapy. With muscular hypotension - prozerin, ATP, massage, exercise therapy. Symptomatic therapy.
Complications
Persistent bone deformities. pathological fractures. Osteomyelitis. Renal failure. Renal tubular acidosis. Convulsive syndrome.
Hypervitaminosis D: loss of appetite, disorders of the gastrointestinal tract (lack of appetite, thirst, nausea, vomiting, constipation,), headache, muscle and joint pain, dry mouth, polyuria, depression, psychotic disorders, ataxia, stupor, weight loss , increased levels of calcium in the blood and (or) in the urine, urolithiasis and tissue calcification ( blood vessels, heart, lungs and skin). Impaired renal function with proteinuria, hematuria and polyuria, increased loss of potassium, hypostenuria, nocturia and increased blood pressure. In severe cases - clouding of the cornea, swelling of the papilla of the optic nerve, inflammation of the iris, cataracts. Rarely develops cholestatic jaundice.
Application
In medical practice, alcohol (0.5%) and oil (0.125%) solutions of vitamin D2. A solution of ergocalciferol in oil is a clear oily liquid from light yellow to dark yellow. In addition, calciferols are found in such dosage forms as oral drops, capsules, and tablets.
Storage
The drug is stored in a dry, dark place at a temperature not exceeding 10 ° C, in hermetically sealed, filled to the brim with orange glass bottles. Such storage conditions are necessary due to the high reactivity. Air oxygen easily oxidizes calciferols, and light gradually decomposes them to the formation of toxic products. The shelf life of all dosage forms is 2 years.
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