The fourth period is the period of convalescence. Periods of infectious diseases
Convalescence (from Late Latin reconvalescentia - recovery)
the period of recovery of a person or animal, characterized by the gradual disappearance of signs of illness and recovery normal life body. The boundaries of this period are arbitrary. Normalization of the function of individual organs begins at the height of the disease - in the so-called. acute period. R. can be quick or long-lasting; elimination of the underlying disease and restoration of the functions of the body as a whole does not always mean a complete return of the structure and functions of all systems and organs to the state that preceded the disease (for example, myocardial dystrophy remains after infections or post-influenza functional disorders nervous system). R. is usually accompanied by improved appetite and weight gain. During this period, restorative treatment and medical rehabilitation are especially important. With some infections (typhoid fever, dysentery) during the R. period, the release of the pathogen may continue, which determines the implementation of special anti-epidemic measures (discharge to work after laboratory examination, organization of a department for children - convalescents of dysentery).
Great Soviet Encyclopedia. - M.: Soviet Encyclopedia. 1969-1978 .
Synonyms:See what “Reconvalescence” is in other dictionaries:
- (lat.). Recovery. Dictionary foreign words, included in the Russian language. Chudinov A.N., 1910. RECONVALESCENCE recovery. A complete dictionary of foreign words that have come into use in the Russian language. Popov M., 1907 ... Dictionary of foreign words of the Russian language
Recovery Dictionary of Russian synonyms. convalescence noun, number of synonyms: 1 recovery (3) ASIS Dictionary of Synonyms ... Dictionary of synonyms
- (Late Latin reconvalescentia) period of recovery after an illness... Big Encyclopedic Dictionary
- (Late Latin reconvalescentia), the period of recovery after an illness. * * * RECONVALESCENCE RECONVALESCENCE (Late Latin reconvalescentia), the period of recovery after an illness... Encyclopedic Dictionary
- (reconvalescentia; re + lat. convalescentia recovery) see Recovery ... Large medical dictionary
I Reconvalescence (late Latin: reconvalescentia recovery) the process of restoring normal functioning of the body after an illness, see Infectious diseases. II Convalescence (reconvalescentia; Re + lat. convalescentia recovery) see ... Medical encyclopedia
- (Late Latin reconvaiescentia), the period of recovery after an illness... Natural science. Encyclopedic Dictionary Veterinary encyclopedic dictionary
The period of convalescence.
Feeling better. Regression of neurological and autonomic disorders. Long-term recovery muscle tone and bone formation. Radiographs show uneven compaction of growth zones.
Period residual effects: muscle hypotonia, residual skeletal changes.
Treatment
Diet. If possible natural feeding. Complementary foods should be introduced a month earlier. The amount of juice is doubled. Required Products - egg yolk, fish oil, caviar, butter, liver, meat.
Drug therapy
Vitamin D-3 (oil or alcohol solution). Therapeutic dose of vitamin D preparations. Stage I - 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 treatment) 400-500 IU/day, course 1 year.
Contraindications
Hypersensitivity to the components of the drug, hypervitaminosis D, increased level 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).
Directions for use and doses
- 1. Orally (1 drop contains about 500 IU of vitamin D 3).
- 2. Preventatively:
- - newborns from 4 weeks of life, full-term, with proper care and sufficient stay 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 health 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 ME (1-2 drops) per day.
Therapeutically:
Daily 3000-10,000 IU (6-20 drops) for 4-6 weeks, under close health monitoring and periodic urine testing.
If necessary, after a one-week break, you can repeat the course of treatment.
If vitamin D is intolerant, ultraviolet irradiation is prescribed for up to 20 sessions over 1-2 months, drug analogs (for example, alfacalcidol), calcium, potassium, magnesium supplements, and vitamin therapy. At muscle hypotonia- prozerin, ATP, massage, exercise therapy. Symptomatic therapy.
Complications
Persistent bone deformities. Pathological fractures. Osteomyelitis. Kidney failure. Renal tubular acidosis. Convulsive syndrome.
Hypervitaminosis D: loss of appetite, gastrointestinal disorders (lack of appetite, thirst, nausea, vomiting, constipation), headaches, muscle and joint pain, dry mouth, polyuria, depression, psychotic disorders, ataxia, stupor, weight loss , increased levels of calcium in the blood and/or urine, urolithiasis and tissue calcification ( blood vessels, heart, lungs and skin). Impaired renal function with proteinuria, hematouria and polyuria, increased loss potassium, hyposthenuria, nocturia and increased blood pressure. In severe cases - clouding of the cornea, swelling of the papilla optic nerve, inflammation of the iris, cataract. Cholestatic jaundice rarely develops.
Application
IN medical practice alcohol (0.5%) and oil (0.125%) solutions of the vitamin are used D2. A solution of ergocalciferol in oil is a transparent 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 place, protected from light, at a temperature not exceeding 10 ° C, in hermetically sealed, filled to the top orange glass bottles. Such storage conditions are necessary due to high reactivity. Air oxygen easily oxidizes calciferols, and light gradually decomposes them to form toxic products. Expiration date of all dosage forms 2 years.
The clinical picture 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 symptoms. The face is hyperemic, injection of scleral vessels. The rash appears earlier on days 6-7, is often profuse, and can be papular or morbilliform. Status typhozus is usually absent.
Paratyphoid B- also characterized by an acute onset, symptoms of gastroenteritis. The rash, as a rule, appears earlier, is abundant, polymorphic, and is localized on the trunk and limbs. Relapses and complications are rare.
Outcome of the disease in addition to recovery and liberation of the body from the causative agent of typhoid fever, the formation of bacterial carriage may occur (acute - up to 6 months, chronic - more than 6 months).
DIAGNOSTICS
1. To detect the pathogen, it is necessary to carry out cultures of blood, feces, urine, bile and, if indicated, bone marrow punctate.
2. Serological tests use the Widal reaction and RNGA, which must be repeated in the dynamics of the disease (increase in antibody titers).
3. To identify specific antigens, RAHA is used - the hemagglutination aggregate reaction.
4.Conduct general blood test(thrombocytopenia, leukopenia, relative lymphocytosis, aneosinophilia, accelerated ESR).
Differential diagnosis carried out 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 one - to a box in compliance with all anti-epidemic measures
2. strict bed rest until 10 days N temperature. Diet 4 abt(4 a - typhoid table.
2. Etiotropic therapy. cephalosporin antibacterial drugs, F torquinolone series(ciproflaxacin, tarivid, etc.)
3. Pathogenetic therapy:
· Detoxification therapy 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 (reopolyglucin, hemodez).
· For cardiac dysfunction and the development of myocarditis, therapy includes drugs such as Riboxin, cardiac glycosides in clinical doses.
· Symptomatic therapy. sedatives and hypnotics.
· Desensitization therapy(suprastin, diazolin, etc.) Antifungal drugs- reduce the possibility of developing candidiasis.
PREVENTION
Improvement of water supply sources, both centralized water supply systems and wells.
Treatment of wastewater discharged into open water bodies, especially effluents infectious diseases hospitals;
Elimination of sources of water pollution (latrines, garbage pits, landfills); boiling or pasteurization of milk, dairy products, including cottage cheese, ensuring sanitary maintenance of public catering places.
26) Yersiniosis.
Pseudotuberculosis (extraintestinal yersiniosis)– spicy infectious disease from the group of zoonoses with general intoxication, fever, scarlet-like rash, as well as damage to various organs and systems.
Etiology. The causative agent is Iersinia pseudotuberculosis - Gr-bacillus, in culture it is located in the form of long chains, does not form spores, has a capsule. Sensitive to dryness and exposure to sunlight. When heated to 60 o it dies after 30 minutes, when boiled - after 10. Conventional disinfection kills within 1 minute. A distinctive ability is the ability to grow at low temperatures. Based on surface AG, 8 serovars are distinguished; 1 and 3 are more common. It actively reproduces in boiled tap water and river water, and also multiplies and retains its properties at low temperatures. It has high invasive qualities and is able to penetrate natural barriers. Contains endotoxin, may form exotoxin.
Epidemiology. It is registered almost throughout the country. Zoonotic infection. Source of infection– wild and domestic animals. Main tank- mouse-like rodents. They infect food products stored in refrigerators and vegetable stores with secretions. Soil can also be a reservoir. Transmission path– nutritional; when consuming infectious food or water that has not been subjected to heat treatment. Both children and adults are susceptible to P. Children under 6 months of age practically do not get sick; children aged 7 months to 1 year rarely get sick. The disease is recorded throughout the year, with a maximum of February-March.
Pathogenesis. The pathogen enters through the mouth with infectious food or water (infection phase), overcomes the gastric barrier, enters the small intestine, where it penetrates into enterocytes or intercellular spaces intestinal wall (enteral phase). From the intestine, mucous membranes penetrate into the regional mesenteric lymph nodes and cause lymphadenitis ( regional infection phase). The massive entry of the pathogen and its toxins from the sites of primary localization into the blood leads to the development of the generalization phase of the infection. It corresponds to the appearance clinical symptoms. Further progression is associated with fixation of the pathogen by RES cells mainly in the liver and spleen ( parenchymal phase). Next comes persistent fixation and elimination of the pathogen due to the activation of cellular immune defense factors and the production of specific antibodies. Clinical recovery occurs. Also in pathogenesis, the allergic component plays a role, associated with the re-entry of the pathogen into the circulation or previous nonspecific sensitization of the body (indicated by - high content histamine, serotonin, arthralgia, al.rash, erythema nodosum).
Immunity. The duration of immunity has not been precisely established, but there is reason to consider it durable. Repeated ones are rare.
Clinic. Incubation period– 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 have mild catarrhal symptoms (nasal congestion and cough) at the onset of the disease. There may be pain when swallowing, a feeling of soreness 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 loose stool 2-3 times per day according to enteritis type. Upon 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, and enanthema is sometimes observed. The tongue in the initial period is thickly covered with a grayish-white coating, from the 3rd day it begins to clear and becomes crimson and papillary. On the 3-4th day, symptoms reach their maximum. Begins peak period– deterioration of condition, higher temperature, severe symptoms of intoxication, damage to internal organs and skin changes. Some have a hood symptom - hyperemia of the face and neck with a cyanotic tint, a gloves symptom - a limited pink-bluish coloration of the hands, a socks symptom - a limited pink-bluish coloration of the feet. On the skin of the body - rash; either dotted (reminiscent of scarlet fever) or spotted. Usually localized in the lower abdomen, in the axillary areas and on the lateral surfaces of the body. Color ranges from pale pink to bright red. The skin background may be hyperemic or unchanged. There is white persistent dermographism. Larger rashes are located around large joints, where they form a continuous erythema. At long term or relapse - elements of erythema nodosum appear on the legs or buttocks. Pastia symptoms (dark red color skin folds), symptoms of a pinch or tourniquet are usually positive. The rash lasts no more than 3-7 days, sometimes several hours. At the height of the disease it is noted arthralgia, there may be swelling and tenderness of the joints. The wrist, interphalangeal, knee and ankle joints are usually affected. Changes in the digestive organs: appetite is significantly reduced, nausea, infrequent vomiting, often abdominal pain and upset stool. The abdomen is moderately distended. Palpation can reveal pain and rumbling in the right iliac region. Intestinal disorders– infrequently, slight increase and dilution of stools with retained fecal character. The liver and spleen are often enlarged. Changes to the SSS: relative bradycardia, muffled tones, sometimes systolic murmur, in severe cases – arrhythmia. BP is moderate ↓. ECG shows changes in myocardial contractile function, conduction disturbances, extrasystole, ↓ T wave, prolongation 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-like, abdominal, generalized, arthralgic, mixed and septic variants). 2. Typical with isolated syndrome (rare). 3. Atypical (erased, subclinical, catarrhal). By severity: light, medium-heavy, heavy.
Flow . More often – a smooth course. The total duration of the disease is no 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 a 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/N shift, monocytosis, eosinophilia, ESR. 3. Biokhim.AK: direct bilirubin, activity of ALT, AST, F-1-FA and other hepatocellular enzymes. 4. Bakt. study: material for culture - blood, sputum, feces, urine and oropharyngeal swabs. Inoculations on conventional growth media and enrichment media. Cultures of blood and throat swabs should be carried out in the 1st week of the disease, cultures of feces and urine - throughout the entire disease. 5. Serological studies: RA (most often; as an AG - live reference cultures of pseudotubular strains; diagnostic titer 1:80 and higher; 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.
Differential diagnostics . With scarlet fever, measles, enterovirus infection, rheumatism, viral hepatitis, sepsis, typhus-like diseases.
Treatment . Bed rest until the temperature normalizes and the symptoms of intoxication disappear. The food is complete, without significant restrictions. Etiotropic treatment: levomecithin for 7-10 days. In the absence of effect or in case of exacerbation after discontinuation of levomecithin, a course of treatment with 3rd generation cephalosporins. For severe forms - 2 a/b, taking into account compatibility. For mild forms, a/b is not required. Detoxification therapy: intravenous rheopolyglucin, albumin, 10% glucose, enterosorbents: enterosgel, enterodesis, etc. in severe cases - GCS at the rate of 1-2 mg of prednisolone per 1 kg of body weight per day in 3 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 vegetables, fruits and other food products. Strict sanitary control of food preparation technology, as well as the quality of water supply in rural areas. Anti-epidemic measures at the source of infection are the same as for intestinal infections. After hospitalization of the patient, final disinfection is carried out. Specific prevention 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 primary damage to the gastrointestinal tract, joints, and less often other organs.
Etiology . The causative agent is I. enterocolitica. Gr-stick. Facultative aerobe, no capsule, does not form spores. Undemanding to growing media, grows well at low temperatures. Based on their biochemical properties, they are divided into 5 serovars (3 and 4 are more often found, less often 2). According to O-AG, there are more than 30 serovars. Sensitive to the effects of physical and chemical factors, tolerates well low temperatures, maintaining the ability to reproduce.
Epidemiology . Widespread. Often found in mouse-like rodents, large cattle, pigs, dogs, cats, isolated from dairy products, ice cream. Source of infection– humans and animals, patients or carriers. Transmission path– nutritional, 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. Mostly children from 3 to 5 years old are affected.
Pathogenesis. When consuming infectious food, water or by contact. M\o passes through the stomach, is localized in the small intestine (often localized in the terminal section small intestine, appendix), where it begins to reproduce. M/O penetrates and destroys epithelial cells of the intestinal mucosa. The infection spreads to regional lymph nodes. At this stage, the disease often ends. In more severe cases, m\o enters the blood - generalization of the process. M\o is also capable of remaining in the l\u for a long time, causing relapses or transition to a chronic form.
Clinical picture . The incubation period is 5-19 days, on average 7-10. There are gastrointestinal, abdominal forms (pseudoappendicular, hepatitis), septic, articular forms, erythema nodosum.
Gastrointestinal form. Initial symptoms: begins acutely, T up to 38-39. From the first days lethargy, weakness, ↓ appetite, headache, dizziness, nausea, repeated vomiting, abdominal pain. Persistent symptom– diarrhea. Chair from 2-3 to 15 r/day. The stool is liquefied, often mixed with mucus and greens, and sometimes blood. In the coprogram: mucus, polymorphonuclear leukocytes, single erythrocytes, impaired intestinal enzymatic function. In the CBC: moderate leukocytosis with a shift to the left, ESR. Sometimes the disease begins with catarrhal symptoms in the form of slight cough, runny nose, nasal congestion; possible chills, muscle pain, arthralgia. In severe cases, there may be a picture of intestinal toxicosis and exicosis, meningeal symptoms. High period(1-5 days from the beginning): the abdomen is moderately swollen. On palpation - pain and rumbling along the intestine, mainly in the area of the cecum and ileum. Sometimes the liver and spleen. Some patients have a polymorphic rash on the skin (punctate, maculopapular, hemorrhagic) with a primary localization around the joints, on the hands, feet (symptoms of gloves and socks). In some cases - inflammation in the joints, the phenomenon of myocarditis. The duration of the disease is 3-15 days.
Pseudoappendicular form. Preim occurs in children over 5 years of age. It starts off sharp. Temperature up to 38-40. Complaints of headache, nausea, vomiting 1-2 times a day, anorexia. The constant and leading symptom is abdominal pain - 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, intermittent pain in the joints, and mild catarrh of the upper respiratory tract. In the CBC: leukocytosis (8-25x10 9 /l) with a shift of the formula to the left, ESR) 10-40 mm/h). During surgery for acute abdomen sometimes found catarrhal or gangrenous appendicitis, often - mesadenitis, swelling and inflammation of the final ileum.
Yersinia hepatitis. Starts sharply with pronounced signs intoxication, body temperature, which does not decrease in icteric period, ESR. Sometimes - short-term diarrhea, abdominal pain. Some have early dates exanthema appears. On days 3-5 - dark urine, discolored feces and jaundice. The liver is hard and painful. The edge of the spleen is palpated. The activity of hepatocellular enzymes is low or ↓!!!
Nodular (nodose) form. Preferably for children over 10 years old. It begins acutely with symptoms of intoxication and body temperature. On the legs there are rashes in the form of painful pink nodules with a cyanotic tint, which disappear after 2-3 weeks. Gastroenteritis, abdominal pain, and sometimes changes in the upper respiratory tract are typical.
Articular shape proceeds as non-purulent polyarthritis and arthralgia. It is rare, mainly in children over 10 years old. 5-20 days before the onset of arthritis, children experience intestinal disorders, which are accompanied by fever. More often the knee and elbow joints are involved, less often - small joints hands and feet. The joints are painful, swollen, the skin over them is hyperemic.
Septic (generalized) form. Rarely seen. Acute septicemia. From the first days the temperature reaches 40 and above and is hectic in nature. Drowsiness, adynamia, anorexia, chills, headache, pain in muscles and joints, weakness, pain when swallowing, nausea, vomiting, loose stools are noted. On days 2-3, some patients develop a rash similar to that of rubella and scarlet fever. Most often located around the joints, where it is maculopapular in nature. Rapidly the liver, spleen, sometimes jaundice appears. Violations of the cardiovascular system and respiratory system are noted. In the CBC: ↓ hemoglobin, neutrophilic leukocytosis (16-25x10 9 /l), ESR 60-80 mm/h. In OAM: albuminuria, cylindruria, pyuria.
Colonic yersiniosis in young children. At the age of up to 3 years, the gastrointestinal form, such as gastroenteritis or gastroenterocolitis, usually occurs. Observe higher prolonged fever, more pronounced intoxication (adynamia, periodic restlessness, convulsions, loss of consciousness, hemodynamic disorders), longer vomiting and stool disorders.
Diagnostics. Based on clinical and laboratory data. 1. PCR2. Bakt.method. most often released in the first 2-3 weeks, sometimes within 4 months. 3. For articular and cutaneous form – RA with live or killed culture and RNGA. Diagnostic titers RA – 1:40-1:160, RNGA – 1:100-1:200.
Diff. Diagnostics. With scarlet fever, measles, enterovirus infection, rheumatism, sepsis, typhoid-like diseases.
Treatment. WITH mild form-Houses. For gastrointestinal and abdominal problems, an appropriate diet is prescribed. Enterosorbents are prescribed: enterosgel, enterodes, etc. Causal therapy: chloramphenicol and 3rd generation cephalosporins. For moderate and severe forms, additional symptomatic therapy is prescribed: detoxification, rehydration measures, antihistamines, vitamins, diet. In case of septic form, 2 a\b (orally and parenterally) and GCS are prescribed. For arthritis and knotty forms a\b are ineffective, antirheumatic drugs and corticosteroids are prescribed, etc. For appendicitis, abscesses, osteomyelitis - surgical intervention.
Prevention. The same as with kish.inf. + the same measures as for pseudotuberculosis.
27) Cholera. Etiology. Epidemiology. Pathogenesis. Clinic. Diagnostics and differential diagnosis. Treatment. Prevention.
(type Vibrio cholerae.) - acute intestinal, life-threatening sapronotic infection. Characterized by a fecal-oral mechanism of infection, damage small intestine, watery diarrhea, vomiting, quick loss 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: curved rod with a fairly long flagellum. Gr (-), easily stained with aniline dyes. Can form L-forms.
Agawa, Inaba, Gikoshima.
Vibrios secrete an exotoxin - cholerogens - the most important pathogenetic factor.
When microbial bodies are destroyed, endotoxins are released.
The third component of toxicity is the permeability factor. A group of enzymes that help increase permeability vascular wall cell membranes and contribute to the action of cholerogens.
Stability in the external environment is high.
In open water pools they last for several months, in wet feces they last up to 250 days.
On direct sunlight can last up to 8 hours.
Epidemiology
There are 3 types of pathogens
V. cholerae asiaticae (causative agent of classical cholera),
V. cholerae eltor (El Tor cholera causative agent)
Serovar O139 (Bengal) (the causative agent of cholera in Southeast Asia).
They differ in biochemical properties.
Morphology: curved rod with a rather long flagellum. They do not form spores or capsules. Gr (-), stain well with aniline dyes. Can form L-forms.
Growth characteristics: obligate aerobes, optimal environment - 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 rapid reproduction.
Antigenic structure: they have a flagellar H-antigen (common to all vibrios) and a somatic thermostable O-antigen. The causative agents of cholera belong to serogroup O-1.
Depending on the properties of the O-antigen, 3 serovars are distinguished: Agawa, Inaba, Gikoshima.
Pathogenesis
The mechanism of infection is fecal-oral.
Distribution routes: water, alimentary, contact and household.
Most frequent path infection - water (drinking, washing vegetables, fruits, vegetables, bathing).
Infection of shellfish, fish, shrimp, and frogs should be noted. Vibrio persists in these organisms long time. Eating them without heat treatment increases the risk of developing the disease.
Seasonality - summer-autumn. During this period, more fluids and bathing are consumed. Increased fluid intake also leads to a decrease in the concentration of hydrochloric acid in gastric juice.
Clinical picture Incubation period
Lasts from several hours to 5 days, usually 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.
The typical clinical picture of cholera is characterized by 3 degrees of progression.
Features of cholera in children
· Severe course.
· Early development and severity of dehydration.
· CNS disorders develop more often: lethargy, disturbances. Consciousness stupor and coma.
· Convulsions are more common.
· Increased tendency to hypokalemia.
· Increased body temperature.
Degrees of dehydration in children
I degree -< 2 % первоначальной массы тела;
II degree -3-5% of initial body weight;
III degree - 6-8% of initial body weight;
IV degree - > 8% of initial body weight.
Complications
Hypovolemic shock
Acute renal failure: oliguria, anuria
Dysfunction of the central nervous system: convulsions, coma
Diagnostics
· History: endemic area, known epidemic.
· Clinical picture.
Purpose of 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.
· Sowing of bacteriological material (stool, vomit, water) on thiosulfate-citrate-bile-salt-sucrose agar (eng. TCBS), as well as 1% alkaline peptone water; subsequent transfer to a second peptone water and sowing onto alkaline agar plates.
· Isolation of pure culture, identification.
· Study of the biochemical properties of the isolated culture - the ability to decompose certain carbohydrates, the so-called. “a number of sugars” - sucrose, arabinose, mannitol.
· Agglutination reaction with specific sera.
· Vibrio cholerae DNA detection PCR method, which also allows you to identify belonging to pathogenic strains and serogroups O1 and O139.
Differential diagnosis
· Salmonellosis
Sonne's dysentery
Gastroenteritis caused by coli
· Viral diarrhea (rotaviruses)
Poisoning poisonous mushrooms
Organophosphorus pesticide poisoning
Botulism
Before starting competent treatment for cholera, it is necessary
F establish the degree of dehydration and loss of electrolytes;
F select appropriate solutions;
F choose the route of their introduction;
F determine the rhythm of administration and the amount of solutions in stages;
F set the total required amount of liquids;
F check proper hydration, which is a criterion for the effectiveness of treatment.
Hospitalization is required. Cases of the disease require reporting to WHO.
At the first stage - pathogenetic therapy: replenishment of fluid loss - rehydration, performed in two stages:
I. Primary rehydration - depending on the degree of dehydration (in a person 70 kg, degree 4 dehydration (10%) - 7 liters are transfused)
II. Correction of ongoing losses (those that already occur in the clinic).
Primary rehydration is carried out by intravenous administration of fluid into 2-3 veins. Use Trisol solution
It is necessary to heat these solutions to a temperature of 37 degrees.
Etiotropic treatment: Carried out antibacterial drugs groups tetracycline.(accelerates the cleansing of vibrios)
Tetracycline 0.3-0.5 g w/w 6 hours (3-5 days) or
Levomycetin 0.5 h/w 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 bcc;
2. recovery electrolyte balance 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 times a day (in the absence of vomiting).
It is carried out in two stages:
1. Replenishment of lost fluid - rehydration (in a volume corresponding to the initial body weight deficit).
2. Correction of ongoing losses of water and electrolytes.
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 injection solutions are absolutely indicated for patients with degree III and IV dehydration.
For initial intravenous rehydration, Ringer's solution. Hypokalemia + potassium.
Comparative characteristics electrolyte composition of cholera stool and Ringer's solution (mml/L)
Prevention
Nonspecific: increased sanitary and hygienic requirements; eating 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 for high level(95%). Three months after taking the vaccine, protection against V. Cholerae El Tor was 65%.
(stimulates antimicrobial immunity). The vaccine is administered once parenterally to certain populations from the age of 7 years. Revaccinate after 1 year.
CARRIED OUT ACCORDING TO epidemiological indications!
Forecasting
With timely and adequate treatment, the prognosis is favorable. Working capacity is fully restored within approximately 30 days. In the absence of adequate medical care there is a high probability of rapid death.
Botulism.
- acute food toxic infection that develops as a result of botulinum toxin entering the human body. Botulism is characterized by damage to the nervous system as a result of botulinum toxin blocking acetylcholine receptors of nerve fibers, manifested in the form of muscle paralysis and paresis.
Characteristics of the pathogen
Botulinum toxin produced by bacteria Clostridium botulinum – gram-positive spore-forming rod, 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 exposed to optimal conditions for life: temperature 35 C, lack of oxygen. Boiling kills vegetative forms of the pathogen in five minutes; the bacteria can withstand a temperature of 80 C for half an hour. Spores can remain viable in boiling water for more than half an hour and are only inactivated in an autoclave. Botulinum toxin is easily destroyed during boiling, but can be preserved well in brines, canned food and food products, rich in various spices. However, 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 clostridia Botulism is found in soil, as well as wild and some domestic (pigs, horses) animals, birds (mainly waterfowl), and rodents. Animal carriers of clostridia are usually not harmed; the pathogen is excreted in feces, and the bacteria enter the soil, water, and animal feed. Contamination of environmental objects with clostridia is also possible during the decomposition of the corpses of animals and birds sick with botulism.
The disease is transmitted through the fecal-oral mechanism through food. The most common cause of botulism is the consumption of home-canned foods contaminated with spores of the pathogen: vegetables, mushrooms, meat products and salted fish.
Required condition For the proliferation of clostridia in products and the accumulation of botulinum toxin, there is a lack of air access (tightly closed canned food).
In some cases, infection of wounds and ulcers with spores is likely, which contributes to the development of wound botulism. Botulinum toxin can be absorbed into the blood, both from digestive system, and from the mucous membranes of the respiratory tract and eyes.
People 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 reaction.
In case of poisoning with botulinum toxin from canned food Cases of family defeat 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.
Symptoms of botulism
The incubation period of botulism rarely exceeds a day, most often amounting to 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 continues for up to 10 days.
In the initial period of the disease, nonspecific prodromal symptoms may be observed. Depending on the predominant syndrome, gastroenterological and 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 occurs as a foodborne illness, with epigastric pain, nausea and vomiting, and diarrhea. The severity of enteral symptoms is moderate, however, there is dry skin that is inappropriate for the general loss of fluid, and patients often complain of difficulty swallowing food (“lump in the throat”).
The initial period of botulism, which occurs in the ocular variant, is characterized by visual disturbances: blurring, flickering “floaters”, loss of clarity and decreased visual acuity. Sometimes acute farsightedness occurs.
The most dangerous option downstream initial period Botulism is acute respiratory failure (suddenly developing and progressive shortness of breath, spreading cyanosis, heart rhythm disturbances). It develops extremely quickly and can be 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 various groups muscles.
Patients have symmetrical ophthalmoplegia (the pupil is stably dilated, there is strabismus, usually converging, vertical nystagmus, drooping eyelid). Dysphagia (swallowing disorder) is associated with progressive paresis of the pharyngeal muscles. If initially patients experience discomfort and difficulty swallowing solid food, then as the disease progresses, swallowing liquids also becomes impossible.
Speech disorders develop through four successive stages. First, the timbre of the voice changes, hoarseness occurs as a result of insufficient moisture of the mucous membrane vocal cords. Subsequently, due to paresis of the tongue muscles, dysarthria (“porridge in the mouth”) appears, the voice becomes nasal (paresis of the muscles of the velum) 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 promotes paralysis and paresis of facial muscles, causing facial asymmetry and dysmymia. In general, there is general weakness and unsteady gait. Due to paresis of the intestinal muscles, constipation develops.
Fever is not typical for botulism, but in rare cases low-grade fever is possible. The state of cardiac activity is characterized by increased heart rate, a slight increase in peripheral blood pressure. Sensitivity disorders and loss of consciousness are not typical.
Complications of botulism
The most dangerous complication botulism - development of acute respiratory failure, respiratory arrest due to paralysis of the respiratory muscles or asphyxia respiratory tract. Such complications can be fatal.
Due to development stagnation in the lungs, botulism can provoke secondary pneumonia. Currently, there is evidence of the likelihood of complications of infection with myocarditis.
Diagnosis of botulism
Due to the development of neurological
Recovery - special condition of the body, occurring after the end of any disease process and continuing until normal nutrition and activity of all organs are completely restored. In mild diseases, this condition occurs completely unnoticed, almost coinciding with the end of the disease. However, the longer the disease lasts and the more important for the body the disturbances it causes in the activity of various organs, the more important the recovery period becomes.
Features of the recovery process
Recovering woman (photo by Monty)
Recovery is characterized, first of all, by different frequency. For example, the consequences that occur from heavy blood loss in the peripheral areas of the body (extremities) are eliminated relatively easily and quickly, while a stroke causes a recovery period that often lasts several months. Recovery after relatively dangerous disease, such as lobar pneumonia, sometimes occurs within a few days, while relatively harmless gastric catarrh may require several months to restore normal digestion and nutrition. Happy ending typical shape typhoid fever, a healthy state occurs after 2-3 weeks. After surgical illnesses or major operations, the recovery period - often very long - is determined by the course of those local processes that underlie the disease process or operation.
Private arrangements and instructions needed for convalescents regarding their diet, furnishings, clothing, activities, etc., when various diseases are considered in a particular description of these diseases. Here it is necessary to dwell only on the social and hygienic significance that represents the contingent of those recovering in a given population or in a given social group.
Recovery in social settings
Those who are recovering, due to the state of their health, cannot yet return to their usual way of life, but no longer require the forms of care that were applied to them during the period of illness. People recovering from many contagious diseases retain the ability to transmit the infection for quite a long time. healthy people, such as, for example, those recovering from smallpox, measles, scarlet fever, and therefore, like the sick, should be isolated for some time from the healthy and other convalescents. Care for those recovering is carried out in various ways. In families, with home treatment, the doctor examining the patient continues to monitor the progress of recovery. In hospitals, they often detain convalescents on a general hospital basis until they fully regain strength and health, and sometimes they are transferred to special wards with special staff and special organization.
Institutional basis of the process
In some countries, very special institutions are common, designated specifically for the placement of convalescents. Special institutions for convalescents, which are not connected with hospitals, originate from France, where the first such institution, established on a charitable basis, arose back in 1640 for women and girls leaving the Hotel-Dieu hospital. In 1855, public convalescent homes arose in Paris, namely Asyle de Vincenne for men (with 525 beds) and Asyle de Vesiret for women (350 beds). At the end of the 19th century, such shelters were common in England, where there were more than 150 of them, together with private ones. In the Russian Empire, there have long been some methods of caring for convalescents, the so-called “weak teams” in the troops, in essence, shelters for convalescents.
