Periods of infectious diseases. Convalescence period
· Period of convalescence
It is characterized by the disappearance of signs of active rickets: the elimination of neurological and autonomic disorders (restoration of sleep, decreased sweating, improvement or normalization of static functions, the formation of new conditioned reflexes), a decrease in muscle hypotonia, improving the well-being and general condition of the child. The severity of bone deformities gradually decreases. Radiographs show changes pathognomonic 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 biochemical parameters correspond to the norm, but there are clearly expressed signs of a previously suffered disease. Long-term persistence of reversible changes is possible - muscle hypotonia, looseness of joints and ligaments. Deformations of the tubular bones disappear over time (a change in the axis may remain lower limbs, “rickets” flat feet). Deformations of flat bones decrease, but often persist throughout subsequent life (frontal and parietal tuberosities, flattening of the occiput, malocclusion, deformations of the chest, pelvic bones, etc.). It is impossible not to emphasize the significance of the negative long-term consequences of rickets - both at the individual and population levels. For example, pelvic deformities are fraught with the forced need for delivery by cesarean section in the future, flat feet - long-term pain syndrome and indirect 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 serve as a significant cosmetic defect leading to psychological discomfort patient (especially a teenager), may interfere with work internal organs(located in chest cavity). It has been proven that rickets suffered at an early age predisposes in the future to impaired 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, three degrees of rickets are distinguished:
I degree (mild) - mild signs of rickets from the nervous and skeletal systems (increased sweating, anxiety, slight softening of the skull bones, mild “rosary”);
II degree (moderate) - moderately severe disorders of the nervous, bone, muscle and hematopoietic systems. Possible enlargement of 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 second degree develops 1.5 - 2 months from the onset of the disease, in premature infants - somewhat earlier. In full-term infants, the diagnosis of stage II rickets can be made no earlier than 4 to 5 months of life. Children become inactive, lethargic, muscle hypotension and anemia appear. With rickets of degree II, bone damage in two or three parts of the skeleton is characteristic;
III degree (severe) - significant impairments from 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 bone curvature, severe dysfunction of the autonomic nervous system;
- - subacute - slow development with the growth of defective bone tissue (hyperplasia of osteoid tissue);
- - recurrent - characterized by alternating improvement and exacerbation of the disease.
Currently, mild rickets with a subacute course predominates, with a predominance of skeletal system phenomena of osteoid hyperplasia.
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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. Infusion therapy must include glucose solutions, polarizing mixtures (trisol, quartasol, acesol), crystalloids, colloid 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 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 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-like rash, as well as damage 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 multiplies in boiled tap 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 of the 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 of 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 the 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 levels of histamine, serotonin, arthralgia, 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. 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 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. There may be loose stools 2-3 times a day, of the 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. It is 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. With a long course or relapse, elements appear on the legs or buttocks erythema nodosum. Pastia symptoms (dark red color of skin folds), pinch symptoms, tourniquet symptoms 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. Blood pressure 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 the rash there is lamellar peeling on the hands and feet, and pityriasis-like peeling 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, typhoid-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 levomecitin, a course of treatment with 3rd generation cephalosporins. At 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 of 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 . Widely spread. Often found in mouse-like rodents, cattle, pigs, dogs, cats, and isolated from dairy products and ice cream. Source of infection– humans and animals, patients or carriers. Transmission path– nutritional, contact, maybe aerogenic. Diseases are recorded all year round, outbreaks occur 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 contact. M\o passes through the stomach, is localized in the small intestine (often localized in the terminal section of the small intestine, the appendix), where it begins to multiply. 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. The gastrointestinal tract is isolated abdominal shape(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. A constant symptom is 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 a slight cough, runny nose, and 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 an acute abdomen, catarrhal or gangrenous appendicitis is sometimes discovered, and often mesadenitis, swelling 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, and ESR. Sometimes - short-term diarrhea, abdominal pain. Some people develop exanthema early on. On days 3-5 – dark urine, discolored stool 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 – the small joints of the 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. Higher prolonged fever, more severe intoxication (adynamia, periodic restlessness, convulsions, loss of consciousness, hemodynamic disorders), longer vomiting and stool disorders are observed.
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 forms– 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 a light form - at home. 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 nodular 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. It is characterized by a fecal-oral mechanism of infection, damage to the small intestine, watery diarrhea, vomiting, rapid loss of fluid and electrolytes by the body 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 the permeability of the vascular wall of 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.
In direct sunlight they 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. In these organisms, the 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 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 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.
· Detection of Vibrio cholerae DNA by PCR, which also allows one to identify belonging to pathogenic strains and serogroups O1 and O139.
Differential diagnosis
· Salmonellosis
Sonne's dysentery
Gastroenteritis caused by Escherichia coli
· Viral diarrhea (rotaviruses)
Poisoning poisonous mushrooms
Organophosphorus pesticide poisoning
· Botulism
Before competent treatment of cholera is initiated, 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 general required amount liquids;
F check for proper hydration, which is a criterion for the effectiveness of treatment.
Hospitalization is required. Cases 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 administration of solutions is absolutely indicated for patients with degree III and IV 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; 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, the likelihood of rapid death is high.
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 foods 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 the 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 cases of botulinum toxin poisoning from canned foods, cases of familial damage are common. Currently, cases of the disease are becoming more frequent due to the spread of home canning. Most often, people from the age group of 20-25 years get sick with botulism.
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 a 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 of “floaters”, loss of clarity and decreased visual acuity. Sometimes acute farsightedness occurs.
The most dangerous variant of the initial period of 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, and hoarseness occurs as a result of insufficient moisture in the mucous membrane of the 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 it is noted general weakness, 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 and a slight increase in peripheral blood pressure. Sensitivity disorders and 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 of the 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
The period of convalescence.
Feeling better. Regression of neurological and autonomic disorders. Long-term restoration of muscle tone and bone formation. Radiographs show uneven compaction of growth zones.
Period of residual effects: muscle hypotonia, residual skeletal changes.
Treatment
Diet. Breastfeeding whenever possible. Complementary foods should be introduced a month earlier. The amount of juice is doubled. Mandatory products are 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 exposure to fresh air, as well as children under 2-3 years old: 500-1000 IU (1-2 drops) per day;
- - premature children, twins, infants in poor living conditions - from 4 weeks of life 1000-1500 IU (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. For muscle hypotension - proserin, 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 calcium levels 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 potassium loss, 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. The shelf life of all dosage forms is 2 years.
RECONVALESCENT(from Latin convalesco - coming to a healthy state) - recovering, convalescence - recovery. The term R. should be understood as such a period of clinical recovery when obvious signs the diseases have ended, but not yet full recovery the previous state of the body. Recovery is a conditional concept, since with many therapeutic or surgical treatments. b-yah recovery is only relative. Thus, after operations, the dead parts are usually only partially regenerated, scars form, and the loss of a paired organ entails a vicarious enhanced function of the other. In the clinic, the term convalescence is used only when the restoration of the body’s previous state is expected, for example. for the postpartum period and ch. arr. for cases of recovery after infectious diseases(for convalescence after childbirth, see Postpartum period). Reconvalescence after infectious diseases has its own characteristics and requires special study, because sometimes for a long time in the absence of visible manifestations the disease actually remains in the body whole line long-term disorders of various organs (nervous, of cardio-vascular system, muscles, psyche, etc.) and often the causative agent of the infectious disease itself remains in the body (see. Bacillary carriage). Of particular importance both for the person recovering and for those around him is the period of convalescence after typhus, cholera, dysentery, scarlet fever, diphtheria and cerebrospinal meningitis. The period of convalescence after typhoid fever lasts on average from 4 to 6 weeks. At this time, the patient needs a careful diet and protection from intense physical and mental activity. Wedge, the manifestations of the transferred b-nor are expressed in adynamia, lability of cardiovascular activity, instability of the gastrointestinal tract. tract (frequent constipation), rapid mental fatigue. For at least 2 weeks from the day the rate drops, relapses of typhoid fever are possible and therefore, until the expiration of this period, the typhoid convalescent should be in bed. and comply careful diet"In approximately 5% of cases, the patient is a carrier of the bacilli, excreting the typhoid bacillus in feces or urine. The basis of bacilli excretion is most often pathological changes in the gallbladder and kidneys, usually accompanied by catarrhal phenomena in them and sometimes causing only insignificant symptoms in these organs objective and subjective phenomena. These organs in typhoid R. for a long time In general, they can be unstable and, in case of exacerbation of the process, give cholecystitis, pyelitis and cystitis. R. after dysentery or cholera also requires a special regime and observation. On the one hand, he is also often a bacilli excretor, and on the other hand, after suffering bacilli for a long time, sometimes measured in months, he himself is susceptible to intestinal disorders that require a careful diet. - With regard to typhus, the period of convalescence is often may drag on instead of the usual 2-4 weeks to several (3 to 5) months, since histopathological processes in the body after the disappearance of fever may not only not go away, but even progress during the period of convalescence. At this time, R.’s psyche may change in the form of capricious mood swings, weakening of memory and thinking abilities (see. Infectious psychoses), Sometimes there may be pain in the limbs, general weakness, speech disorder and changes in the cardiovascular system. "09 . Carriage of bacilli in diphtheria R. can last for a very long time (see. Bacillus carriage, Diphtheria). For treatment, regimen and prevention, see Diphtheria. Scarlet R. (see Scarlet fever) often needs medical supervision for many months, especially in cases where scarlet fever occurred with complications in the kidneys (glomerulonephritis) or in the heart (myocarditis, endocarditis). Often such R. - after scarlet fever nephritis, having already fully a good urine test, after several months, can reveal leached red blood cells and casts in the urine. Therefore, hygienic and nutritional regimes are mandatory for it for a long time, sometimes measured in months. With regard to R., epidemic cerebrospinal meningitis requires especially careful observation. On the one hand, they can give very late relapses - 3 or even 4 weeks after full recovery, on the other hand, they, often being carriers of infection, can infect others and cause entire epidemic outbreaks. The period of convalescence from other infectious diseases also requires special attention from the doctor and adherence to a strict regime from the patients (see the corresponding Words).P. Galtsov.
