The causative agent of the disease is a non-motile gram-negative meningococcus, characterized by great variability. Meningococcus is very unstable in the external environment: sensitive to drying, sun rays, cold, quickly dies when the temperature deviates from 37 ° C. The pathogenicity factor is a capsule that protects the microbe from absorption by phagocytes and from other unfavorable factors. The toxic properties of meningococcus are caused by endotoxin, which is a lipopolysaccharide, similar in chemical and biological properties to the endotoxins of enterobacteria, but superior to them in its potency by 5–10 times. According to antigenic properties, meningococcus is divided into 11 types (A, B, C, D, Z, X, Y, as well as non-agglutinating types 29E, 135, B0 and N). In Ukraine and Russia, there is a constant circulation of meningococci serogroup A, which periodically cause an increase in incidence, as well as strains B and C, which more often cause diseases in Western Europe. In typical cases, meningococcus in preparations looks like a fixed diplococcus, located intra- and extracellularly in pairs, similar to coffee beans, which is used as a preliminary diagnosis. Meningococcus grows on media with the addition of blood, serum or ascitic fluid, milk or yolk. The microbe is an aerobe; the optimal temperature for the proliferation of meningococcus is 36–37 °C with a slightly alkaline pH = 7.2–7.4.
Epidemiology
The reservoir and source of infection is a person sick with meningococcal infection or a healthy carrier of the bacteria. Especially dangerous from an epidemiological point of view are healthy carriers of meningococcus, who during periods of sporadic morbidity account for 1–2% of the total population. According to various sources, the ratio between patients and carriers can range from 1: 2000 to 1: 50,000. In 1–3% of cases of meningococcal infection, the source of infection is generalized forms, in 10–30% - patients with meningococcal nasopharyngitis, in 70–80 % are carriers of meningococcus. The duration of carriage is on average 11 days. The main transmission mechanism is airborne. The pathogen is released in environment from the nasopharynx when talking, coughing, sneezing. Transmission by contact is of no practical importance due to the instability of the pathogen. The most effective infection occurs at a distance of up to 50 cm from the source. Susceptibility to meningococcus is low and amounts to 0.5%. The concentration of the pathogen in the air, crowding of children, prolonged and close contact, and disturbances in temperature and humidity in the room are of great importance for infection. We observed a case when in winter, at the time of large admission of patients to infectious diseases hospital and in the absence of a free box in the emergency room, the young doctor went into the ambulance, where he examined a patient with meningococcal infection and filled out a medical history there. In total, the doctor was in the car for no more than 30 minutes. Five days later, this doctor fell ill with meningococcal infection and, despite the measures taken, died.
Cyclical increases in incidence are observed every 10–12 years, lasting up to 4–6 years. The beginning of the coming epidemic is expected in 2010–2011, but taking into account demographic processes in the CIS countries (migration and other factors), it may occur earlier. It is believed that the rise in incidence will be due to meningococcus serogroup A, which will be replaced by pathogens of serogroups B and C.
Children are especially susceptible to meningococcus, making up 50% of all cases under the age of 5 years. Winter-spring seasonality is typical (February - March), which is explained both by weather conditions (temperature fluctuations, humidity) and by the increased incidence of influenza and other acute respiratory infections.
Pathogenesis (what happens?) during Meningococcal meningitis
Contact of meningococcus on the mucous membranes of the nasopharynx and oropharynx does not yet mark the onset of the development of the disease. Only in 10–15% of cases does meningococcus enter the nasopharyngeal mucosa and lead to the development of nasopharyngitis. This is due to a number of protective factors and, above all, the bactericidal properties of the mucous membrane itself, the antagonistic properties of microorganisms located on the mucosa, the level of secretory IgA, IgG, C3-, C5-complement factors, and cellular protection factors. Of significant importance, of course, are the biological properties of the pathogen, primarily its virulence and the number of pili, which are a factor of adhesion to the mucous membrane of the nasopharynx and, possibly, to the tissues of the meninges. The main factors in the pathogenicity of meningococcus are the bacterial capsule, which protects microbes from being absorbed by phagocytes, and endotoxins, which are lipopolysaccharides and cause toxic manifestations. In addition, meningococci are able to secrete IgA proteases that break down IgA molecules, which protects them from the effects of antibodies. If local immunity is not impaired by previous viral diseases, hypothermia, stress and other unfavorable circumstances, then the outcome of meningococci entering the mucous membranes will be their death or healthy carriage. This is the outcome of meningococci getting into the mucous membranes of the upper respiratory tract healthy child observed in most cases. If local protective factors turn out to be untenable, then an inflammatory process with clinical manifestations of meningococcal nasopharyngitis develops at the site of introduction of meningococci. Obviously, in a number of cases, meningococci overcome local protective barriers and penetrate into the blood, primary bacteremia develops, which is manifested by the presence of single roseolous-papular or hemorrhagic exanthems, herpetic eruptions on the lips and wings of the nose, changes in the peripheral blood in the form of a band shift of the blood count to the left , high ESR, release of the pathogen from the blood. However, primary bacteremia is short-term in nature; it does not have enough, figuratively speaking, the fuse for the development of systemic reactions of the body, activation of “secondary pathogenetic mechanisms.” At the same time, the development of clinically pronounced meningococcal nasopharyngitis is far from necessary. This is evidenced by the fact that in 70–80% of patients with generalized forms of meningococcal infection such a focus does not exist at all. The establishment of this phenomenon gave reason to believe that the mechanism of generalization of the pathological process during meningococcal infection lies in the formation of secondary foci of infection located in the endothelium of the capillaries. This is precisely what can explain such a massive contamination of the body with meningococci during the disease, manifested by the formation of a profuse hemorrhagic rash, adrenal insufficiency and, most importantly, the rapidity of development clinical symptoms toxicosis. Bacteremia and endotoxemia are accompanied by an increase in the blood of cytokines, eicosanoids and other biologically active substances, products of impaired metabolism, and organ-system disorders. In this case, conditions are created for the penetration of meningococci through the BBB into the subarachnoid space with the development of inflammation of the pia mater, and less often - inflammation of the brain and spinal cord. This is largely facilitated by the anatomical and physiological features of the mesodiencephalic region (abundant vascularization, significant permeability of the vessels of the interstitial medulla, proximity to the cerebrospinal fluid pathways). Sometimes penetration of meningococcus into the central nervous system is possible through the sheaths of nerve fibers and through the lymphatic tract passing through the ethmoid bone. Infection is also possible with traumatic brain injury and defects in the skull bones. We describe a case of recurrent meningococcal meningitis in a child who was cured only after reconstructive surgery for a ethmoid bone defect. We observed a case of a three-time relapse of meningococcal meningitis in a child with an epithelial tract, which was a malformation of the caudal end of the embryo behind the sacrum. After its excision, relapses of meningitis stopped. Recurrent meningitis caused by meningococcus and pneumococcus is possible with congenital defects of the complement system and deficiency of IgG subclasses.
The purulent inflammatory process can also spread along the membrane of the base of the brain to the medulla oblongata and spinal cord, cranial and spinal nerves.
Pathological anatomy
Morphological changes in purulent meningococcal meningitis are found in the pia mater, in the substance of the brain, the ependyma of the cerebral ventricles and the subependymal region. In the initial phase of inflammation, the pia mater is predominantly affected and the process is serous-purulent in nature, and later - purulent and purulent-fibrinous.
As the pathological process progresses, in addition to the pia mater, the substance of the brain is also affected as a result of the impact on brain tissue of both the meningococci themselves and their toxins. Damage to the ventricular ependyma, the presence of diffuse and focal hemorrhages, proliferation of granulation tissue, obstruction of the foramina of Magendie and Luschka, sclerotic changes in the perivascular fissures, degeneration of the arachnoid membrane and obliteration of the subarachnoid spaces lead to impaired outflow of cerebrospinal fluid and the development of internal hydrocephalus.
The substance and membranes of the spinal cord are naturally involved in the pathological process. The changes in them are not much different from those observed in the membranes of the brain. However, the clinical symptoms of these lesions are mild or absent. With severe lesions, a picture of myelitis develops.
Symptoms of Meningococcal meningitis
Incubation period meningococcal infection averages 2–7 days.
The clinical picture of purulent meningococcal meningitis consists of 3 syndromes: infectious-toxic, meningeal and hypertensive. The leading one is the infectious-toxic syndrome, since even before the development of meningitis, the patient may die from intoxication, and in children under the age of 1 year, all other syndromes may be absent or only slightly expressed. Meningococcal meningitis often begins acutely, violently, suddenly (often the child’s mother can indicate the hour of the onset of the disease). Less commonly, meningitis develops after nasopharyngitis or meningococcemia. Body temperature reaches 38–40 °C, chills appear, headache quickly increases, becomes painful, “bursting” in nature. Worried about dizziness, pain in the eyeballs, especially when they move. Appetite disappears, nausea occurs, repeated “fountain” vomiting appears, which does not bring relief to the patient, thirst torments. There is severe hyperesthesia to all types of stimuli - touch, bright light, loud sounds. Tendon hyperreflexia, trembling, twitching, flinching and other signs of convulsive readiness are characteristic; in some cases, tonic-clonic convulsions develop. Seizures in children of the first year of life are often the first and early symptom meningitis, while other symptoms, including stiffness of the neck muscles, do not have time to develop. Convulsive twitching at the onset of the disease in older children indicates the severity of the course and is considered a formidable symptom. In some patients, seizures may occur as a grand tonic-clonic seizure. Some children have an early disorder of consciousness: adynamia, lethargy, stunnedness, and sometimes complete loss of consciousness. Most older patients are characterized by motor restlessness, hallucinations, and delusions. Already from the first hours of the disease (after 10–12 hours), signs of damage to the meninges are noted: stiffness of the neck muscles, Brudzinsky’s, Kernig’s symptoms and others. By the end of the first day, a characteristic “coping dog” pose is observed. General muscle hypotonia is often detected. Tendon reflexes are increased, and there may be anisoreflexia. In severe intoxication, tendon reflexes may be absent, and skin reflexes (abdominal, cremasteric) are usually reduced. In this case, pathological Babinski reflexes and foot clonus are quite often observed. On the 3rd–4th day of illness, many children develop herpetic rashes on the face, less often on other areas of the skin, on the oral mucosa.
In severe forms of meningitis, possible involvement in the process cranial nerves. Damage to the oculomotor nerves (III, IV, VI pairs) is manifested by strabismus, ptosis upper eyelid, sometimes anisocoria; in case of defeat facial nerve(VII pair) facial asymmetry occurs. The identification of hearing disorders requires close attention, especially in young children, which can occur from the first days of the disease, and disorders auditory analyzer possible at various levels and can lead to partial or complete deafness. The II, IX, X pairs of cranial nerves are rarely affected. Severe manifestations of meningococcal meningitis include the appearance of signs of edema-swelling of the brain, which are manifested by attacks of psychomotor agitation, followed by a stuporous state followed by a transition to a coma.
A significant role in the clinical diagnosis of meningococcal meningitis is played by its frequent combination with a hemorrhagic-necrotic rash, which appears on the skin and mucous membranes in 70–90% of children in the first hours of generalization of the infection. The mechanism of its occurrence is the development of thrombovasculitis of the skin capillaries
with subsequent formation of local necrosis. The rash appears 4–6 hours after the onset of the disease, and the earlier the rash appears, the more severe the disease. A typical meningococcal rash has various sizes - from small petechiae to larger ecchymoses, stellate, irregular in shape, with necrosis in the center, sometimes extensive (5-15 cm in diameter) hemorrhages, dense to the touch, protrudes above the surface of the skin. Subsequently, areas of necrosis are rejected and defects are formed, in place of which scars remain during recovery. In exceptional cases, it is possible to develop gangrene of the nail phalanges, fingers, toes, ears. Hemorrhagic rash is usually localized on the buttocks, thighs, legs, eyelids and sclera, less often on upper limbs. But the rash can be of a different nature - roseolous, papular, erythematous, herpetic along the way trigeminal nerve(top and underlip, nose).
In past years, for meningococcemia it was characteristic lesion joints, which was observed in almost 50% of cases, and the choroid, which was observed in 11%
cases. Currently, joints are rarely affected, with small joints most often affected: metacarpals, wrists, and occasionally larger ones can be affected. Children hold their fingers spread out, react to touch by crying, the joints themselves look swollen, and the skin over them is hyperemic. However, the outcome of arthritis is favorable and no special treatment is required.
Lesions of the choroid (rusty eye syndrome) in the form of iridochoroiditis (uveitis) are also extremely rare at present (1.8%).
Complications. The most serious and common complications in young people are acute edema and swelling of the brain, infectious-toxic shock.
Acute edema and swelling of the brain occur more often at the end of the first - beginning of the second day of illness. Against the background of a rapid course of meningitis with sharp signs of intoxication, cerebral disorders and psychomotor agitation, the patient experiences loss of consciousness. Patients do not respond to strong stimuli. General clonic-tonic convulsions appear and increase. There is a fading of corneal reflexes, narrowing of the pupils and a sluggish reaction to light. Bradycardia quickly gives way to tachycardia. Blood pressure is initially labile, with a tendency to significantly decrease, in terminal stage- high, up to 150/90-180/110 mm Hg. Art. Shortness of breath quickly increases to 50-60 breaths per minute, breathing becomes noisy, shallow, with the participation of auxiliary muscles, then arrhythmic. Meningeal symptoms fade, increased cerebrospinal fluid pressure decreases. Involuntary bowel movements and urination are noted. Pulmonary edema develops and hemiparesis occurs. Death occurs when breathing stops as a result of paralysis of the respiratory center; cardiac activity can continue for another 5-10 minutes.
Infectious-toxic shock occurs against the background of a rapid course of meningococcemia. In patients with high fever and severe hemorrhagic syndrome body temperature drops critically to normal or subnormal numbers. In the first hours, patients are fully conscious. Characterized by severe hyperesthesia and general agitation. The skin is pale. The pulse is frequent, barely perceptible. Blood pressure drops rapidly. Cyanosis and shortness of breath increase. Urination stops ( renal failure). Excitement gives way to prostration, convulsions occur. Without intensive treatment, death can occur within 6-60 hours from the moment the first signs of shock appear. Under conditions of environmental and professional stress in young people, infectious-toxic shock occurs, as a rule, in combination with acute edema and swelling of the brain. Against the background of severe intoxication and cerebral disorders, hemorrhagic rashes and disturbances in cardiovascular activity appear. The skin is pale, cyanosis of the lips and nail phalanges. Tachycardia increases, blood pressure rapidly decreases. Signs of general cerebral disorders increase sharply, breathing quickens to 40 or more per minute, complete loss of consciousness occurs, general clonicotonic convulsions occur, corneal reflexes fade, the pupils narrow and almost do not react to light. Anuria occurs. Death occurs 18-22 hours after the first signs of combined complications appear.
Features of central nervous system damage in other forms of meningococcal infection
The clinical features of meningococcal meningitis include its combination with meningococcemia, the development of serous meningitis, purulent meningitis with liquor hypotension, Waterhouse-Friderichsen syndrome, as well as the development of complications in the form of infectious-toxic shock, meningoencephalitis and ependymatitis.
Meningococcal meningitis in combination with meningococcemia
The combination of meningococcal meningitis with meningococcemia is the most common form of the disease. This is due to the fact that its development is based on common mechanisms, the main one of which is the generalized spread of meningococcus in the body with damage to many organs and systems. The disease occurs, as a rule, in moderate or severe forms and is characterized by typical manifestations in the form of infectious-toxic, meningeal, hypertension syndromes and the development of a characteristic hemorrhagic-necrotic rash. At the same time, the mixed form is more “understandable” for the doctor, since the classic onset of meningococcal infection in the form of a stellate hemorrhagic rash with necrosis in the center occurs several hours, or even a day earlier than symptoms of damage to the meninges appear, and at the same time indicates and on the etiology of purulent meningitis, which allows the doctor, without waiting for the results of bacteriological studies, to justify and without hesitation carry out the early prescription of penicillin, cefotaxime, chloramphenicol, ceftriaxone and other antibiotics. Apparently, it is active therapy without waiting and doubt that explains the faster and more complete sanitation of the cerebrospinal fluid in mixed forms of meningococcal infection compared to isolated meningitis and meningoencephalitis.
Serous meningitis
In practice, the doctor has to deal with the fact that clinical and laboratory signs of meningococcal meningitis (namely the presence of pronounced infectious-toxic and meningeal syndromes, characteristic stellate hemorrhagic with necrosis in the center of the rash, significant changes in the peripheral blood - neutrophilic leukocytosis, shift of the blood count to the left , increased ESR, aneosinophilia) are combined with changes in the cerebrospinal fluid, typical of serous meningitis; those. with a significant increase in pressure, mixed pleocytosis or with a predominance of lymphocytes, increased protein content, decreased glucose. In these cases, despite the evidence of a bacterial purulent infection as an etiological factor, the results of a study of the cerebrospinal fluid (pleocytosis with a predominance of lymphocytes) force the doctor to diagnose serous meningitis and treat it as purulent. It should be emphasized important detail: the absolute majority of such patients are hospitalized on the first day and they are prescribed adequate antibacterial therapy, which, as is believed, does not allow the development of purulent inflammation(V.I. Pokrovsky et al., 1987).
Clinical features of serous meningococcal meningitis include the presence of a prodrome in the form of acute nasopharyngitis; in the rapid, within 5–10 days, disappearance of the clinical manifestations of meningitis and in the sanitization of the cerebrospinal fluid by the 7–10th day of illness. However, in some patients, despite intensive antibacterial therapy, transformation of serous meningitis into purulent meningitis is possible with a corresponding worsening of the clinical picture of the disease and changes in the picture of peripheral blood and cerebrospinal fluid parameters corresponding to a purulent inflammatory process.
Waterhouse-Friderichsen syndrome
The development of adrenal insufficiency to one degree or another is characteristic of any acute infectious process. However, specific and deep damage to the adrenal glands, leading to death, is characteristic of meningococcal infection. However, Waterhouse-Friderichsen syndrome extremely rarely develops with meningococcal meningitis.
The beginning of this clinical form typical for meningococcal infection: suddenly, indicating the exact time of onset of the disease. Body temperature, which rises to 38.5–39.5 °C, is combined with signs of intoxication in the form of headache, nausea, lethargy, and skin hyperesthesia. The severity of these symptoms, as a rule, does not cause any particular concern either to parents, or to local doctors, or to emergency doctors who took the child to the hospital. The most significant and important thing for them is the appearance first on the lower extremities, buttocks, and then on the torso of a stellate hemorrhagic rash; sometimes in some elements of the rash emerging foci of necrosis were observed. Changes from the side of cardio-vascular system were manifested by a rapid decrease in blood pressure, sharp tachycardia, and thread-like pulse. Breathing became more frequent, often intermittent, and urine output decreased or was absent. Changes in the central nervous system increased from somnolence to coma and were accompanied by further disturbances in various organs and systems. Total cyanosis of the skin, cold sticky sweat, a further decrease in systolic and diastolic pressure, which often reached zero, and body temperature up to 36.6 °C and below were noted. On the part of the respiratory organs, shortness of breath was noted, the percussion sound was boxy, and moist rales of various sizes were heard on both sides. Heart sounds were muffled and high tachycardia was detected. There was no diuresis. During lumbar puncture, fluid flowed out under high blood pressure, transparent; neutrophilic pleocytosis was moderate or absent; an increase in protein levels was noted. Changes in the cerebrospinal fluid largely depended on the timing of the puncture. If hours passed from the moment of illness, then the composition of the cerebrospinal fluid corresponded to the above; if a day or more, then the changes corresponded to those with purulent meningitis. It should be especially emphasized that this clinical form of meningococcal infection is characterized by high mortality (80–100%).
Diagnosis of Meningococcal meningitis
Main diagnostic criteria for meningococcal meningitis
1. Epidemiological history - winter-spring seasonality, contact with a patient with any form of meningococcal infection or a healthy carrier of meningococcus, airborne transmission, predominant incidence in young children.
2. Typically acute, sudden onset with a rapidly progressing and pronounced general toxic syndrome.
3. Characterized by high fever with chills, bursting headache, repeated vomiting, and severe hyperesthesia.
4. Meningeal syndrome is characterized by the completeness of the entire symptom complex and often occurs with the development of edema-swelling of the brain and a disorder of consciousness.
5. In 70–90% of cases of meningitis, the appearance of a hemorrhagic rash ranging in size from petechiae to larger ecchymoses, sometimes extensive (5–15 cm), irregular, stellate in shape with necrosis in the center with predominant localization on the buttocks, lower extremities, torso, arms is natural. , face, eyelids.
6. Characterized by pronounced inflammatory changes in blood and cerebrospinal fluid tests.
7. Microscopy of cerebrospinal fluid smears, a thick drop of blood, and mucous discharge from the nose makes it possible to detect gram-negative diplococci located predominantly intracellularly, which suggests the meningococcal nature of the disease.
8. During bacteriological examination of mucus from the nasopharynx, blood, and cerebrospinal fluid, meningococcus is isolated, which confirms the etiological diagnosis.
Laboratory diagnostics
General blood analysis. In the analysis of peripheral blood, leukocytosis is determined within the range of 15–25 x 109/l with neutrophilia, a shift of the formula to the left to young and myelocytes, increased ESR, aneosinophilia. There are indications in the literature that in relatively mild forms of meningococcal meningitis, a blood test may be normal. This seems unlikely to us and requires re-checking the quality of the performed general blood test and clarifying the diagnosis.
Study of cerebrospinal fluid. Lumbar puncture is performed under sterile conditions. Liquor is collected into 3 sterile tubes (minimum 1 cm3): tube No. 1 - for biochemical studies (determining the amount of protein and glucose); test tube No. 2 - for bacteriological studies and test tube No. 3 - for cytological studies (cell counting). All tubes are delivered to the laboratory no later than 2 hours after collection. CSF is cloudy, whitish in color, with high pleocytosis it resembles diluted milk, flows out under increased pressure, neutrophilic pleocytosis reaches several hundred or thousand cells in 1 μl, the protein content is increased, glucose is decreased. During a puncture performed on the first day of the disease, the cerebrospinal fluid may still be transparent, pleocytosis may be moderate and of a mixed nature. With late diagnosis (after the 3rd–5th day of illness) or with a hypotensive form of meningitis, the cerebrospinal fluid may not flow out, but “stand” in the needle. In the first case, this is due to increased viscosity and the beginning of the organization of pus with the loss of fibrin threads, in the second - the absence of cerebrospinal fluid pressure. In these cases, it should be aspirated with a syringe.
Bacterioscopic examination. Material from the nasopharynx, cerebrospinal fluid, skin scrapings taken at the border of necrotic and healthy areas, blood smears (thick drop), as well as punctures of rash elements in patients with meningococcal meningitis are examined. In all biological samples, gram-negative cocci or diplococci located extra- and intracellularly are looked for. Bacteroscopic detection of diplococci is not an etiological confirmation of the diagnosis, but only indirectly indicates the presence of meningococcal infection.
Bacteriological research cerebrospinal fluid, blood, urine, mucus from the nasopharynx, and in case of an unfavorable outcome - cadaveric material. To isolate the culture of meningococci, the material is inoculated on solid and semi-liquid nutrient media containing serum, blood or ascitic fluid (20% agar and chocolate agar, blood is inoculated on 0.1% agar).
Serological studies. By using serological studies determine the presence of specific antibodies in the blood serum in the indirect hemagglutination reaction and the minimum concentration of meningococcal toxin in the blood and urine of patients in the counter immunoelectrophoresis reaction. Blood, urine, and CSF can be used for quantitative immunoelectrophoresis reactions to detect capsular antigens of living and dead meningococci.
Molecular genetic research with the identification of DNA fragments specific to meningococcus is promising.
Diagnosis and differential diagnosis. Diagnosis is based on clinical and epidemiological data. Among the most important clinical signs include: acute onset of the disease, severe symptoms general intoxication - heat body, chills, lack of appetite, sleep disturbances, pain in the eyeballs, muscles of the whole body, stupor or agitation: increasing meningeal syndrome - headache, general hyperesthesia, nausea, vomiting, changes in abdominal, tendon and periosteal reflexes, stiffness of the neck muscles, symptoms Kernig, Brudzinsky. Considering the fulminant course of meningococcal infection, the optimal time for diagnosis should be considered the first 12 hours from the onset of the disease. Rational treatment started within these periods leads to complete recovery of patients. However, it should be taken into account that in the first hours of the disease some supporting meningeal symptoms (stiffness of the neck muscles, Kernig's sign, etc.) may be absent. In a hospital setting, lumbar puncture is of particular diagnostic importance. The cerebrospinal fluid pressure is increased. By the end of the first day of the disease, as a rule, it is already cloudy, cell-protein dissociation is observed, globulin reactions (Pandey, Nonne-Appelt) are sharply positive. The content of sugar and chlorides in the liquor decreases. In the peripheral blood - high leukocytosis with a shift of neutrophils to the left, from the second day - a sharp increase in ESR. Bacteriological studies of cerebrospinal fluid, blood, scrapings from hemorrhagic elements of the rash, mucus from the nasopharynx, as well as detection of the growth of anti-meningococcal antibodies in the blood serum are necessary. However, negative results of bacteriological tests for meningococcus in no way exclude the diagnosis of meningococcal infection if the disease occurs clinically in a typical form. Against the background of an epidemic outbreak, a clinical and epidemiological diagnosis is also possible in the case of mild forms of meningitis.
Differential diagnosis carried out with meningitis caused by various bacterial flora: pneumococci, Haemophilus influenzae, staphylococci, streptococci, fungi, etc. Meningococcemia must be distinguished from measles, rubella, Henoch-Schönlein disease, etc.
Treatment of Meningococcal meningitis
Early and adequate therapy can save the patient’s life and determine a favorable social and labor prognosis. In the acute period of the disease it is carried out complex therapy, including the prescription of etiotropic and pathogenetic drugs.
In etiotropic therapy, the drug of choice is benzylpenicillin, which is prescribed at the rate of 200 thousand units/kg of patient’s body weight per day. The drug is administered intramuscularly at intervals of 4 hours (you can alternate intramuscular and intravenous administration penicillin). Required condition The use of benzylpenicillin in these doses is the simultaneous administration of agents that improve its penetration through the blood-brain barrier. Optimal is the simultaneous administration of caffeine sodium benzoate (in a single dose of 4-5 mg/kg), Lasix (0.3-0.6 mg/kg) and isotonic solutions of sodium chloride or glucose (15-20 ml/kg). These drugs are administered intravenously at intervals of 8 hours. The duration of therapy is usually 6-7 days. Reducing the dose of penicillin, as well as discontinuing these pathogenetic agents, during treatment is unacceptable. The indication for discontinuation is a decrease in cytosis in the cerebrospinal fluid below 100 cells in 1 μl with a clear predominance of lymphocytes. Reserve antibiotics are chloramphenicol succinate, kanamycin sulfate and rifampicin. These drugs can be used in case of individual intolerance to penicillin, lack of therapeutic effect when using it, or for follow-up treatment of patients. Levomycetin-succinate is used 1.0-1.5 g intravenously or intramuscularly after 8 hours, rifampicin - 0.6 g orally after 8 hours (to improve absorption, take acidinpepsin or 0.5 g ascorbic acid in 100 ml of water). The use of a new ampoule form of rifampicin for parenteral administration is likely to be promising. In conditions of a dry, hot climate and mountainous desert areas, especially if patients are underweight, therapy has some features, which are associated with a more severe course of the infection and a more frequent development of combined complications in the form of infectious-toxic shock against the background of dehydration in combination with edema and swelling of the brain. In this case, firstly, therapy is aimed primarily at ensuring sufficient tissue perfusion, rehydration and detoxification. For this purpose, intravenous administration of 500 ml is prescribed. isotonic solution sodium chloride (5% glucose solution, Ringer's solution) with simultaneous use of prednisolone at a dose of 120 mg (intravenously) and 5-10 ml of 5% ascorbic acid solution. In cases of sudden fall blood pressure additionally, 1 ml of 1% mesatone solution in 500 ml of isotonic sodium chloride solution is injected intravenously. Experience has shown the inappropriateness of using colloidal solutions (hemodez, polyglucin, rheopolyglucin, etc.) due to the risk of developing acute heart failure and pulmonary edema (especially when large quantities of these solutions are administered - up to 1 liter or more).
To relieve predominantly hypertonic dehydration, the use of isotonic crystalloid solutions is preferable. In this case, the speed and duration of perfusion, the total amount of administered fluid, glucocorticoids, and pressor amines are regulated depending on the level of blood pressure and diuresis. Regular auscultation of the lungs is necessary (danger of pulmonary edema!).
In the initial phase of shock, intravenous administration of 10-20 thousand units of heparin is mandatory to prevent intravascular coagulation syndrome.
The second important feature of the treatment of patients with severe forms of the disease is the justified, rational prescription of etiotropic drugs. The use of penicillin, especially in massive doses - 32-40 million units per day, leads to a sharp deterioration in the condition of patients due to deepening shock and is tactically erroneous. In these cases, it is advisable to begin etiotropic therapy with the administration of chloramphenicol-succinate 1.5 g every 8 hours parenterally, until the patient is brought out of shock. The complex of therapeutic measures necessarily includes constant oxygen therapy (including hyperbaric oxygenation), regional cerebral hypothermia (ice packs to the head and large main vessels), administration of cardiac glycosides, potassium preparations, antihypoxants (sodium hydroxybutyrate, seduxen). After the patient has been brought out of shock, if signs of edema and swelling of the brain persist, therapy is continued, which involves intensifying dehydration and detoxification measures (a complex of diuretics, the introduction of glucocorticoids, antipyretics, and, if necessary, a lytic mixture) under the mandatory control of the injected and excreted fluid, electrolyte and acid-base body balance. In some cases, the use of sorption methods of detoxification (hemo- and plasma sorption) may be successful.
In the period of early convalescence, immediately after discontinuation of etiotropic drugs, the following are prescribed:
- drugs that improve microcirculation in the vessels of the brain (trental or emoxipine 2 tablets 3 times a day or doxium up to 0.25 g 3 times a day for 3 weeks);
- drugs with “nootropic” action, normalizing the processes of tissue metabolism of the brain (pantogam 1 tablet 3 times or piracetam 2 capsules 3 times or aminalon 2 tablets 3 times a day for 6 weeks);
- after completion of treatment with drugs that improve microcirculation, adaptogenic agents are prescribed (from the 4th week of rehabilitation treatment): pantocrine 30-40 drops 2 times a day or Leuzea 30-40 drops 2 times a day or Eleutherococcus 30-40 drops 2 times a day for 3 weeks.
Throughout the entire period of rehabilitation treatment, patients receive multivitamins (undevit, hexavit), calcium glycerophosphate 0.5 g 2 times a day and glutamic acid 1 g 2 times a day. For prolonged sanitation of the cerebrospinal fluid (more than 30 days from the start of treatment), aloe is prescribed 1 ml subcutaneously daily for 10 days or pyrogenal intramuscularly every other day (doses must be selected individually - the initial dose is 25-50 MTD, then the dose that causes an increase in body temperature is set up to 37.5-38.0°C, and its administration is repeated until the temperature rise stops, after which the dose is gradually increased by 25-50 MTD; the course of treatment consists of 10 injections.
Forecast at timely treatment in most cases favorable. Lethal outcomes are possible with the development of infectious-toxic shock and edema and swelling of the brain. Such severe organic lesions as hydrocephalus, dementia and mental retardation, amaurosis, have become rare. Residual effects are more common and more pronounced in individuals whose treatment was started late in the disease. Mainly functional disorders of neuropsychic activity are noted (asthenic syndrome, delayed rate of mental development).
Prevention of Meningococcal meningitis
Patients with generalized forms of infection are hospitalized; patients with nasopharyngitis with a bacteriologically confirmed diagnosis are also hospitalized or isolated at home. Children who have had contact with patients are allowed into the team after a medical examination and a one-time bacteriological examination of nasopharyngeal mucus. Convalescents are allowed into preschool and educational institutions, as well as other groups, after a single bacteriological examination of nasopharyngeal mucus, carried out no earlier than 5 days after discharge from the hospital or completion of treatment of a patient with nasopharyngitis at home.
In children's institutions, when a patient is identified after hospitalization, medical observation is established, bacteriological examinations are carried out, admission of new children is stopped, and normal immunoglobulin is administered to children aged 1 to 7 years. Identified carriers are isolated and treated with chloramphenicol or ampicillin. According to indications, vaccination is carried out with a polysaccharide vaccine of serogroups A and C.
Vaccination.
A feature of outbreaks of meningococcal infection is the appearance of secondary cases of the disease several weeks after the first case. This makes it possible to establish the etiology and use vaccines from bacterial antigens of the appropriate serotypes at the very beginning of the epidemic.
Currently, mono (A), di (A+C) and polyvalent meningococcal vaccines are produced, which have high protective activity and low reactogenicity. In the Russian Federation, a mono-A vaccine is produced, and A and C vaccines are also registered (G.N. Gabrichevsky Research Institute of Epidemiology, Russia and Pasteur Merrier Connaught, France). The vaccine produced in the USA contains antigens of 4 serogroups: A, C, Y and W-135.
It should be borne in mind that the component of the vaccine from serogroup A antigens is immunogenic in children 3 months and older, the component from serogroup C antigens is immunogenic in children starting from 18 months of age. To control epidemics caused by serogroup A, children under 18 months of age are vaccinated twice at 3-month intervals. If children are under 18 months. When a 4-valent vaccine is administered, an immune response is obtained predominantly to bacteria of serogroup A.
The duration of immunity has not been precisely established, but it is at least 3 years in children vaccinated over the age of 2 years. Adverse reactions are rare and local in nature.
Routine immunization against meningococcal disease is not carried out, with the exception of children and adults from high-risk groups. In the United States, all military personnel are being vaccinated.
The immune response of adults to meningococcal vaccines is characterized by a rapid increase in antibody titers, peaking after 2-3 weeks, and then decreasing by 50% over 3 years. However, even after this period, the level of antibodies remains sufficient for several years. However, the immune response to C-polysaccharide is less stable than to A-polysaccharide. Therefore, repeated immunization with a group C vaccine in children under 18 months of age. does not provide a booster response, but occurs when a group A vaccine is administered. Therefore, 2 vaccinations with a group A vaccine provide protection for children from 3 months of age.
Also registered in Russia meningococcal vaccine against serogroup B (Republic of Cuba), which is constructed on the basis of (envelope) capsular proteins of bacteria of serogroup B and polysaccharide of bacteria of group C. This vaccine has shown effectiveness in different countries from 50 to 80%. However, this vaccine has shown little effectiveness in children, and the duration of immunity is relatively short.
Clinical trials of an experimental vaccine designed to prevent type A bacterial meningitis are planned. It was created as part of the international Meningitis Vaccine Project program, which is supervised by the World Health Organization. It is expected that the new vaccine will reliably protect young children from meningococcal infection and induce longer-lasting immunity than other drugs of similar action.
In addition, according to representatives of the Meningitis Trust, it has developed prototype a vaccine that is effective against a strain of group B meningococci for which no drugs have yet been developed. Trials have also shown that the vaccine is effective against septicemia - a blood poisoning that is often associated with the disease - and meningitis type C. The vaccine was developed by a research team at the Center for Applied Microbiology and Research, located near Salisbury in Wiltshire, Great Britain. It is made using the harmless bacterium Neisseria Lactamica, which lives on the mucous membranes of the nose and throat of 10% of children and adults.
Chief children's phthisiatricians visited school No. 72 in St. Petersburg to study the reasons why 11 schoolchildren felt weak and dizzy after they were tested for tuberculosis on Monday, February 18
Vaccinations are the only way to protect yourself from a deadly infection 18.02.2019
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Liquor (cerebrospinal or cerebrospinal fluid, CSF) - biological fluid necessary for the functioning of the central nervous system. Its research is one of the most important types of laboratory research. It consists of a preanalytical stage (preparation of the subject, collection of material and its delivery to the laboratory), analytical (the actual implementation of the study) and postanalytical (decoding the result obtained). Only the correct execution of all manipulations at each of these stages determines the quality of the analysis.
Cerebrospinal fluid (CSF) is formed in the choroid plexuses of the ventricles of the brain. In an adult, 110-160 ml of cerebrospinal fluid circulate simultaneously in the subarchnoid spaces and in the ventricles of the brain, and 50-70 ml in the spinal canal. CSF is formed continuously at a rate of 0.2-0.8 ml/min, which depends on intracranial pressure. per day healthy person 350-1150 ml of cerebrospinal fluid is formed.
Liquor is obtained by puncture of the spinal canal, more often - lumbar puncture - in accordance with a technique well known to neurologists and neurosurgeons. The first drops of it are removed (“travel” blood). Then the cerebrospinal fluid is collected into at least 2 tubes: into a regular tube (chemical, centrifuge) for general clinical and chemical analysis, and into a sterile one for bacteriological examination. On the referral form for a CSF study, the doctor must indicate not only the patient’s name, but also the clinical diagnosis and purpose of the study.
It should be remembered that cerebrospinal fluid samples delivered to the laboratory must be protected from overheating or cooling, and samples intended for the detection of bacterial polysaccharides in serological tests should be heated in a water bath for 3 minutes.
The actual laboratory study of cerebrospinal fluid (analytical stage) is carried out according to all the rules accepted in clinical laboratory diagnostics when analyzing any biological fluids and includes the following stages:
Macroscopic analysis - assessment of physical and chemical properties (volume, color, character),
- counting the number of cells,
- microscopy of the native specimen and cytological examination of the stained specimen;
- biochemical research,
- microbiological examination (if indicated).
We find it advisable and informative in some cases to supplement the study of CSF with immunological and, possibly, other tests, the significance of which is discussed in the specialized literature.
Decoding of cerebrospinal fluid indicators
Normal CSF is colorless and transparent (like distilled water, in comparison with which it is usually described). physical properties cerebrospinal fluid).
The grayish or gray-green color of the cerebrospinal fluid is usually due to the admixture of microbes and leukocytes. The red color of the CSF of varying intensity (erythrochromia) is due to the admixture of red blood cells found in recent hemorrhages or brain injury. Visually, the presence of red blood cells is detected when their content is more than 500-600 per μl.
In pathological processes, the liquid may be xanthochromic - colored yellow or yellow-brown by the breakdown products of hemoglobin. It is also necessary to remember about false xanthochromia - the color of the cerebrospinal fluid caused by medicines. Less commonly, we see a greenish color in the CSF (purulent meningitis, brain abscess). The literature also describes a crusty color of the cerebrospinal fluid - when a craniopharyngioma cyst breaks through into the cerebrospinal fluid tract.
The turbidity of the cerebrospinal fluid may be due to the admixture of blood cells or microorganisms. In the latter case, the turbidity can be removed by centrifugation. When the CSF contains an increased amount of coarse proteins, it becomes opalescent.
The relative density of cerebrospinal fluid obtained by lumbar puncture is 1.006-1.007. With inflammation of the meninges and brain injuries, the relative density of the cerebrospinal fluid increases to 1.015. It decreases with overproduction of cerebrospinal fluid (hydrocephalus).
With an increased content of fibrinogen in the cerebrospinal fluid, the formation of a fibrinous film or clot occurs, which is observed more often with tuberculous meningitis. Sometimes a test tube with liquid is left at room temperature for a day (if it is necessary to accurately determine whether a film has formed?). If a fibrinous film is present, it is transferred with a dissecting needle onto a glass slide and stained with Ziehl-Neelsen or another method to identify mycobacteria. Normal CSF is 98-99% water.
However, research on it chemical composition represents an important task. It includes determination of the level of protein, glucose and chlorides, and in some cases is supplemented by other indicators.
Protein in liquor
More than 80% of CSF protein comes from plasma by ultrafiltration. The protein content is normal in different portions: ventricular - 0.05-0.15 g/l, cisternal 0.15-0.25 g/l, lumbar 0.15-0.35 g/l. To determine the protein concentration in the cerebrospinal fluid, any of the standardized methods can be used (with sulfosalicylic acid and ammonium sulfate, and others). An increased protein content in the cerebrospinal fluid (hyperproteinarchy) can be caused by various pathogenetic factors (Table 1).
The study of cerebrospinal fluid proteins allows not only to clarify the nature of the pathological process, but also to assess the state of the blood-brain barrier. Albumin can serve as an indicator for these purposes, provided that its level in the cerebrospinal fluid is determined by immunochemical methods. The determination of albumin is carried out due to the fact that it, being a blood protein, is not synthesized locally and therefore can be a “marker” of immunoglobulins that have penetrated from the bloodstream due to impaired permeability of barriers. Simultaneous determination of albumin in blood serum (plasma) and CSF allows one to calculate the albumin index:
With an intact blood-brain barrier, this index is less than 9, with moderate damage - 9-14, with noticeable damage - 14-30, with severe damage - 30-100, and an increase of more than 100 indicates complete damage to the barrier.
In recent years, there has been increasing interest in CNS-specific cerebrospinal fluid proteins - neuron-specific enolase, protein S-100, myelin basic protein (MBP) and some others. MBP seems to be one of the most promising among them for clinical purposes. It is practically absent in normal cerebrospinal fluid (its concentration does not exceed 4 mg/l) and appears only under pathological conditions. This laboratory sign is not specific to certain nosological forms, but reflects the size of the lesion (associated mainly with the destruction of white matter). Some authors consider the determination of MBP in the cerebrospinal fluid to be promising for monitoring neurospeed. Unfortunately, today there are still problems associated with the direct determination of the concentration of this protein.
Glucose in cerebrospinal fluid
Glucose is contained in normal cerebrospinal fluid in a concentration of 2.00-4.18 mmol/l. This value is subject to significant fluctuations even in a healthy person, depending on the diet, physical activity, and other factors. To correctly assess the level of glucose in the cerebrospinal fluid, it is recommended to simultaneously determine its level in the blood, where it is normally 2 times higher. Elevated blood glucose levels (hyperglycoarchia) occur when diabetes mellitus, acute encephalitis, ischemic circulatory disorders and other diseases. Hypoglycoarchia is observed with meningitis of various etiologies or aseptic inflammation, tumor damage to the brain and membranes, less often with herpetic infection, subarachnoid hemorrhage.
Lactate (lactic acid) has some advantage over glucose as a diagnostic marker, since its concentration in the cerebrospinal fluid (1.2-2.1 mmol/l) does not depend on that in the blood. Its level increases significantly in various conditions associated with energy metabolism disorders - meningitis, especially those caused by gram-positive flora, brain hypoxia and some others.
Chlorides in cerebrospinal fluid
Chlorides - content in normal cerebrospinal fluid - 118-132 mmol/l. An increase in concentration in the CSF is observed when their elimination from the body is impaired (kidney disease, heart disease), with degenerative diseases and tumors of the central nervous system. A decrease in chloride content is observed in encephalitis and meningitis.
Enzymes in liquor
Liquor is characterized by low activity of the enzymes it contains. Changes in enzyme activity in the liquor during various diseases are mainly nonspecific in nature and parallel the described changes in the blood in specified diseases(Table 2). The interpretation of changes in creatine phosphokinase (CPK) activity deserves a different approach. This enzyme is presented in tissues in three fractions, characterized not only by molecular differences, but also by the nature of distribution in tissues: CPK-MB (myocardium), CPK-MM (muscles), CPK-BB (brain). If the total activity of CPK in the cerebrospinal fluid has no fundamental diagnostic value (it can be increased in tumors, cerebral infarction, epilepsy and other diseases), then the CPK-BB fraction is a rather specific marker of damage to brain tissue and its activity in the CSF correlates with the Glasgow scale.
Cell count and cerebrospinal fluid cytogram
When studying biological fluids, including CSF, the number of cells and the cytogram in smears stained with asureosin are usually counted (according to Romanovsky-Giemsa, Nocht, Pappenheim). Count cellular elements in the cerebrospinal fluid (determination of cytosis) is carried out using a Fuchs-Rosenthal chamber, having previously diluted it 10 times with Samson's reagent. Using this particular dye, and not any other. allows you to stain cells within 15 minutes and keep cells unchanged for up to 2 hours.
The number of cells in the entire chamber is divided by 3, so a cytosis of 1 μl is obtained. For greater accuracy, cytosis is counted in three chambers. In the absence of a Fuchs-Rosenthal chamber, you can use the Goryaev chamber by counting cells throughout the entire grid also in three chambers, the result is multiplied by 0.4. There are still discrepancies in the units of measurement of cytosis - the number of cells in the chamber, in 1 µl or 1 liter. It is probably advisable to express cytosis by the number of cells per μl. Automated systems can also be used to count the number of white blood cells and red blood cells in the CSF.
An increase in the content of cells in the CSF (pleocytosis) appears more often in inflammatory diseases, and to a lesser extent in irritation of the meninges. The most pronounced pleocytosis is observed with bacterial infection, fungal lesions of the brain and tuberculous meningitis. In epilepsy, arachnoiditis, hydrocephalus, degenerative processes and some other diseases of the central nervous system, cytosis remains normal.
Staining the cells of the native preparation with Samson's reagent makes it possible to differentiate the cells quite reliably. But their more accurate morphological characteristics are achieved after fixation and staining of prepared cytological preparations. The modern approach to the preparation of such drugs involves the use of a cytocentrifuge. However, even in the USA, only 55% of laboratories are equipped with them. Therefore, in practice, a simpler method is used - deposition of cells onto a glass slide. The preparations must be well dried in air and then painted.
Cellular elements are counted in the stained preparation. They are represented predominantly by blood cells (more often - lymphocytes and neutrophils, less often - monocytes, eosinophils, basophils), plasma cells and mast cells, macrophages, granular balls (degenerative forms) can also be found special type macrophages - lipophages in a state of fatty degeneration), arachnoendothelial cells, epindyms. The morphology of all these cellular elements is usually well known to doctors laboratory diagnostics and is described in detail in many manuals. The level of pleocytosis and the nature of the cerebrospinal fluid cytogram make it possible to clarify the nature of the pathological process (Table 3).
Neutrophilic leukocytosis often accompanies acute infection(local and diffuse meningitis). CSF eosinophilia is observed quite rarely - with echinococcosis of the brain, eosinophilic meningitis. CSF eosinophilia does not usually correlate with the number of eosinophils in the blood. Lymphocytic pleocytosis in the cerebrospinal fluid occurs when viral meningitis, multiple sclerosis, in the chronic phase of tuberculous meningitis, after operations on the meninges. In pathological processes of the central nervous system, polymorphism of lymphocytes is observed, among which activated ones are found. They are characterized by the presence of abundant pale cytoplasm with single azurophilic granules; some cells have lacing or fragmentation of the cytoplasm (clasmatosis). Plasma cells appear in the cytogram during viral or bacterial meningitis, low-grade inflammatory processes, and during the recovery period for neurosyphilis. Monocytes, which undergo degeneration in the cerebrospinal fluid faster than lymphocytes, are observed in multiple sclerosis, progressive panencephalitis, and chronic sluggish inflammatory processes. Macrophages are the “orderlies” of the cerebrospinal fluid; they appear during hemorrhages, infections, traumatic and ischemic necrosis.
Sometimes atypical cells are found in the CSF - elements that, due to their morphological characteristics, cannot be classified as specific cellular forms. Atypical cells are found in chronic inflammatory processes (tuberculous meningitis, multiple sclerosis, etc.), and they are often tumor cells. The probability of finding tumor cells in the cerebrospinal fluid of brain tumors is low (no more than 1.5%). The detection of blast cells in the CSF in hemoblastosis suggests neuroleukemia.
When analyzing the composition of the cerebrospinal fluid, it is important to evaluate the ratio of protein and cellular elements (dissociation). With cell-protein dissociation, pronounced pleocytosis is observed with normal or slightly increased protein content. This is typical for meningitis. Protein cell dissociation is characterized by hyperproteinarchy with normal cytosis. This condition is typical for stagnant processes in the cerebrospinal fluid tract (tumor, arachnoiditis, etc.).
Clinical situations sometimes require counting the number of red blood cells in the bloody cerebrospinal fluid (to objectify the volume of hemorrhage). Red blood cells are counted in the same way as in blood. As stated above, the color of the cerebrospinal fluid changes if 1 μl contains more than 500-600 red blood cells, noticeable staining occurs when there are about 2000, and it becomes hemorrhagic when the level of red blood cells is more than 4000/μl.
Microbiological examination of cerebrospinal fluid
One of frequent illnesses CNS is purulent meningitis. In such cases, mycorobiological research becomes particularly relevant. It includes an indicative test - bacterioscopy of preparations and classical cultural techniques. CSF bacterioscopy has limited diagnostic value, especially when obtaining clear CSF. A smear prepared from the cerebrospinal fluid sediment obtained by centrifugation is stained with methylene blue or Gram stain, although some authors believe that the latter staining option “injures” the formed elements and creates artifacts. With meningitis and abscesses, a diverse flora is found, corresponding to the nature of the disease. Regardless of the results of microscopy, the diagnosis of bacterial meningitis must be confirmed by culture, which becomes decisive in the diagnosis of this group of diseases and the choice of adequate therapy. It is carried out in accordance with Order No. 375 of the Ministry of Health of the Russian Federation dated December 23, 1998 “On measures to strengthen epidemiological surveillance and prevention of meningococcal infection and purulent bacterial meningitis.” The most common cause of bacterial meningitis is the gram-negative diplococcus Neisseria meningitidis, which in 80% of cases can be detected by bacterioscopy.
CSF microscopy
Normally, only lymphocytes and monocytes are present in the cerebrospinal fluid. In various diseases and pathological conditions, other types of cells may appear in the cerebrospinal fluid.
Lymphocytes are similar in size to erythrocytes. Lymphocytes have a large nucleus and a narrow, unstained rim of cytoplasm. Normally, the cerebrospinal fluid contains 8-10 lymphocyte cells. Their number increases with tumors of the central nervous system. Lymphocytes are found in chronic inflammatory processes in the membranes (tuberculous meningitis, cysticercosis arachnoiditis).
Plasma cells in the cerebrospinal fluid. The cells are larger than lymphocytes, the nucleus is large, eccentrically located, a large amount of cytoplasm with a relatively small nucleus size (cell size - 6-12 microns). Plasma cells in the cerebrospinal fluid are found only in pathological cases with long-term inflammatory processes in the brain and membranes, with encephalitis, tuberculous meningitis, cysticercotic arachnoiditis and other diseases, in postoperative period, with sluggish wound healing.
Tissue monocytes in the cerebrospinal fluid. Cell size is from 7 to 10 microns. In normal liquids they can sometimes occur as single specimens. Monocytes are found in the cerebrospinal fluid after surgery on the central nervous system, during long-term inflammatory processes in the membranes. The presence of tissue monocytes indicates an active tissue reaction and normal wound healing.
Macrophages in the cerebrospinal fluid. They can have nuclei of various shapes; more often the nucleus is located on the periphery of the cell, the cytoplasm contains inclusions and vacuoles. Macrophages are not found in normal cerebrospinal fluid. The presence of macrophages with a normal number of cells in the cerebrospinal fluid is observed after bleeding or during inflammatory process. As a rule, they occur in the postoperative period, which has prognostic significance and indicates active cleansing of the cerebrospinal fluid.
Granular balls in the liquor. Cells with fatty infiltration are macrophages with the presence of fat droplets in the cytoplasm. In stained cerebrospinal fluid preparations, the cells have a small peripherally located nucleus and large-cellular cytoplasm. The size of the cells varies and depends on the included drops of fat. Granular balls are found in pathological fluid obtained from brain cysts in areas of decay of brain tissue, in tumors.
Neutrophils in the cerebrospinal fluid. The cells in the chamber are identical in appearance to peripheral blood neutrophils. The presence of neutrophils in the cerebrospinal fluid, even in minimal quantities, indicates either a former or existing inflammatory reaction. The presence of altered neutrophils indicates the attenuation of the inflammatory process.
Eosinophils in the cerebrospinal fluid. Determined in the cerebrospinal fluid by the existing uniform, shiny granularity. Eosinophils are found in subarachnoid hemorrhages, meningitis, tuberculous and syphilitic brain tumors.
Epithelial cells in the cerebrospinal fluid. Epithelial cells limiting the subarachnoid space are quite rare in the cerebrospinal fluid. These are large round cells with small round or oval nuclei. They are found during neoplasms, sometimes during inflammatory processes.
Tumor-like cells and complexes in the cerebrospinal fluid. They are found in the chamber and in the colored liquor preparation. Malignant cells can belong to the following types of tumors:
- meduloblastoma;
- spongioblastoma;
- astrocytoma;
Crystals in the liquor. Rarely found in the cerebrospinal fluid, in case of tumor disintegration.
Echinococcus elements in the cerebrospinal fluid—hooks, scolex, fragments of the chitinous membrane—are rarely found in the cerebrospinal fluid.
PCR diagnostics of cerebrospinal fluid
In recent years, certain prospects in the etiological diagnosis of neuroinfections have been associated with the development of molecular genetic technologies for detecting nucleic acids of pathogens infectious diseases in the cerebrospinal fluid (PCR diagnostics).
Thus, cerebrospinal fluid is a medium that clearly reacts to pathological processes in the central nervous system. The depth and nature of its changes are related to the depth of pathophysiological disorders. Correct assessment of laboratory liquorological symptoms allows you to clarify the diagnosis and evaluate the effectiveness of treatment.
V.V. Bazarny Professor of USMA, Deputy Chief Physician of OKB No. 1
Please enable JavaScript to view the1. It is advisable to prescribe to bacteria carriers of toxigenic corynebacteria diphtheria:
1) antitoxic anti-diphtheria serum
2) ADS toxoid
3) antibiotic wide range actions *
2. When calculating the dose of antitoxic serum administered to a patient with diphtheria, take into account:
1) body weight
2) clinical form of the disease *
3. If diphtheria is suspected, the clinic doctor is obliged to:
1) administer anti-diphtheria serum to the patient
2) carry out emergency hospitalization *
3) administer an antibiotic to the patient
4. For localized form of oropharyngeal diphtheria:
1) temperature over 40 degrees C
2) sharp pain when swallowing
3) bright hyperemia of the tonsils
4) plaques that do not extend beyond the tonsils *
5) swelling of the neck tissue
5. Specific complications of diphtheria include all of the following, except:
1) myocarditis
2) meningoencephalitis *
3) polyneuritis
4) jade
6. Vaccination against diphtheria is carried out in the absence of contraindications in young children:
3) AD-M toxoid
7. What rash is characteristic of scarlet fever:
1) petechial
2) small spotted *
3) maculopapular
4) vesicular
8. What microorganism causes scarlet fever:
1) Staphylococcus aureus
2) pneumococcus
3) beta hemolytic streptococcus *
9. Specify the incubation period for scarlet fever:
1) 2-7 days *
2) 11-21 days
3) 5-35 days
1) cephalosporins
2) semisynthetic penicillins
3) fluoroquinolones *
4) natural penicillins
5) macrolides
11. Indicate the ways of transmission of scarlet fever:
1) airborne
2) contact-household
3) food
4) all of the above *
12. With scarlet fever, the rash is located on:
1) unchanged skin background:
2) hyperemic skin background *
13. What complications are typical for scarlet fever:
1) toxic
2) septic
3) allergic
4) all of the above *
14. To which line of pathogenesis in scarlet fever do early complications belong:
1) toxic
2) toxic and septic *
3) allergic
4) all of the above
15. With scarlet fever, the patient’s face:
1) puffy, pasty
2) swelling of the eyelids, scleritis, conjunctivitis, serous discharge from the nasal cavity
3) bright blush of the cheeks, crimson lips, pale nasolabial triangle *
16. The incubation period for measles in unvaccinated children who have not received immunoglobulin is:
1) from 9 to 17 days *
2) from 9 to 21 days
3) from 11 to 21 days
17. Active immunization against measles is carried out:
1) DTP - vaccine
2) gamma globulin
3) toxoid
4) live viral vaccine *
5) inactivated viral vaccine
18. For measles, antibacterial therapy is prescribed:
1) in the prodromal period
2) in the midst of illness
3) in the presence of complications *
19. Measles rash is characterized by all symptoms except:
1) phasing
2) maculopapular, prone to fusion
3) against a constant skin background
4) without thickening in the natural folds of the skin
5) on hyperemic skin *
20. In case of measles, early ocular manifestations of the disease may be:
1) ptosis and strabismus
2) eye redness and photophobia *
21. The following appear on the oral mucosa during measles:
1) blistering rashes
2) filmy overlays
3) Filatov-Koplik spots*
22. Specific complications of measles are listed, except:
1) pneumonia, laryngitis, laryngotracheitis, bronchitis
2) stomatitis, enteritis, colitis
3) encephalitis, meningoencephalitis, meningitis
4) blepharitis, keratitis, keratoconjunctivitis
5) endocarditis *
23. Characteristic symptoms of the catarrhal period of measles are all except:
1) nasal congestion and mucous discharge
2) obsessive cough
3) conjunctivitis
4) increase in temperature
5) photophobia
6) joint pain *
24. How long should a patient with measles be isolated?
1) before the 3rd day of the catarrhal period
2) up to the 2nd day of the rash period
3) until pigmentation disappears
4) up to and including the 5th day of rash *
25. Causative agent of whooping cough:
1) Bordetella pertussis *
2) Haemophylus influenzae
3) Bordetella parapertussis
26. Mechanisms of transmission of whooping cough:
1) airborne *
2) fecal-oral
3) transplacental
4) parenteral
27. Cough with repeated episodes is typical for:
2) croup syndrome
3) whooping cough *
4) pneumonia
28. During a relapse with whooping cough it is difficult to:
29. The separation of children who have been in contact with a patient with whooping cough is expected to:
2) 7 days *
30. For whooping cough, the most appropriate prescription is:
1) oxacillin
2) penicillin
3) erythromycin *
4) lincomycin
31. The severity of whooping cough is assessed according to the following criteria, except:
1) frequency and nature of attacks
2) severity of symptoms of oxygen deficiency
3) the presence of vomiting after a convulsive cough
4) degree of impairment of the cardiovascular system
5) lethargy, malaise, loss of appetite *
6) presence of complications
32. A patient with whooping cough is isolated from his peers for the following period:
1) 25-30 days from the onset of the disease
2) for 14 days from the onset of the disease *
33. Chickenpox is primarily transmitted:
1) fecal-oral route
2) by airborne droplets *
3) parenterally
34. Chickenpox rashes occur:
1) for several days in spurts *
2) step by step: on the 1st day of illness - on the face, on the 2nd day of illness - on the torso, on the 3rd day of illness - on the limbs
3) simultaneously
35. Herpes zoster occurs in a person who has had:
1) herpes simplex
2) chickenpox *
3) infectious mononucleosis
36. Antibacterial therapy for chickenpox is carried out:
1) when vesicles appear on the mucous membranes of the oral cavity
2) upon manifestation purulent complications *
3) with encephalitis
4) to prevent complications
37. For chickenpox, the administration of corticosteroid hormones is indicated:
1) in severe form
2) when purulent complications appear
3) with encephalitis *
38. The incubation period for chickenpox is:
1) from 8 to 17 days
2) from 11 to 21 days *
3) from 8 to 21 days
39. A patient with chickenpox is contagious:
1) one day before the appearance of the rash and 5 days after the onset of the rash
2) one day before the appearance, the entire period of the rash and 5 days after the last rash *
3) one day before the appearance of the rash and 7 days from the onset of the rash
40. Chickenpox is characterized by the following nonspecific complications, except:
1) impetigo
2) phlegmon
3) stomatitis
4) encephalitis *
41. When treating congenital cytomegalovirus infection, the following is used:
1) acyclovir
2) cytotect*
42. With congenital herpetic infection, the development of meningoencephalitis:
1) typical *
2) not typical
43. Specify the typical nature of the rash in meningococcemia:
1) petechial
2) roseola
3) hemorrhagic stellate *
44. Prevention of meningococcal infection is carried out:
1) live vaccine
2) killed by vaccine
3) polysaccharide vaccine *
45. The hypertoxic form of meningococcal infection occurs more often in children:
1) early age *
2) older
46. With meningococcal infection in the peripheral blood the following is determined:
1) leukocytosis + lymphocytosis
2) leukocytosis + neutrophilia *
47. The main route of transmission of meningococcal infection:
1) fecal-oral
2) airborne *
3) vertical
4) contact-household
48. When contacting a patient with meningococcal infection in the family, the following is carried out:
1) hospitalization of the children of this family
2) double bacteriological examination of family members
3) one-time bacteriological examination of family members and chemoprophylaxis *
49. In case of meningococcal meningitis, it is possible to discontinue the antibiotic if cytosis in the cerebrospinal fluid is no more than:
1) 1000 cells in 1 µl, neutrophilic in nature
2) 100 cells in 1 µl, lymphocytic in nature *
3) 300 cells in 1 µl, mixed
50. With meningococcemia, cytosis is detected in the cerebrospinal fluid:
1) neutrophilic
2) lymphocytic
3) normal *
51. Specify the dose of benzylpenicillin for the treatment of meningococcal meningitis of varying severity:
1) 50 mg/kg per day
2) 100 mg/kg per day
3) 200-300-500 mg/kg per day *
4) all of the above
52. Name the method of transporting a patient with suspected meningococcal infection to an infectious diseases hospital:
1) independently on public transport
2) independently using personal transport
3) in an ambulance with the obligatory accompaniment of a doctor *
4) all of the above
53. Most common reason death of young children due to meningococcal infection:
1) acute adrenal insufficiency *
2) acute respiratory failure
3) all of the above
54. Which of the following symptoms indicate possible damage to the meninges:
2) headache
3) positive meningeal symptoms
4) all of the above *
55. Skin over the affected parotid salivary gland during epidemic mumps:
1) not changed *
2) hyperemic
56. It is not typical for meningitis of mumps etiology:
1) fever
2) repeated vomiting
3) headache
4) meningeal signs
5) hemorrhagic rash *
57. It is not typical for orchitis with mumps:
1) increase in testicle size
2) testicular pain
3) swelling of the scrotum
4) irradiation of pain to the groin area
5) difficulty urinating *
58. At what age is vaccination against mumps carried out:
1) at 3 months
2) at 6 months
3) at 12 months *
4) at 6-7 years old
59. Pathogens infectious mononucleosis are viruses of the Herpesviridae family:
1) true *
2) incorrect
60. In the peripheral blood during infectious mononucleosis the following are possible:
1) leukocytosis, neutrophilia, atypical mononuclear cells
2) lymphopenia, atypical mononuclear cells
3) lymphocytosis, atypical mononuclear cells *
61. For infectious mononucleosis, ampicillin is used to treat tonsillitis:
1) do not use *
2) use
62. Initial symptoms of infectious mononucleosis:
1) fever, cough, conjunctivitis, swollen lymph nodes
2) fever, tonsillitis, swollen lymph nodes, rash
3) fever, tonsillitis, swollen lymph nodes, nasal congestion *
63. Infectious mononucleosis of EBV etiology in the acute period is characterized by the presence of the following markers in the blood, except:
1) Ig M to capsid antigen
2) Ig G to early antigens
3) Ig G to nuclear antigen *
64. Human immunodeficiency virus belongs to the family:
1) retroviruses *
2) picornaviruses
3) myxoviruses
4) reoviruses
65. In stage V of HIV infection in the peripheral blood the following are detected:
1) leukocytosis + lymphocytosis
2) lymphocytosis + leukopenia
3) leukopenia + lymphopenia *
66. In case of HIV infection, serum immunoglobulin levels:
1) low
2) normal
3) elevated *
67. Determination of specific antibodies in HIV-infected people is possible through:
1) 10-14 days
2) 15-30 days
3) 3 or more months *
68. In HIV infection, the number of helper T-lymphocytes:
1) rises
2) decreases *
3) remains unchanged
69. To identify the influenza virus, you can use:
1) virological method
4) study of paired sera (antibody titer)
5) all of the above *
70. The degree of laryngeal stenosis is determined by:
1) presence of moist rales in the lungs
2) degree of respiratory failure *
3) noisy breathing
71. Specify the leading syndrome of respiratory tract damage during influenza:
2) bronchitis
3) tracheitis *
4) laryngitis
72. Stage 1 laryngeal stenosis is characterized by:
1) acrocyanosis, marbling of the skin
3) inspiratory dyspnea with anxiety, physical activity *
4) all of the above
73. For adenovirus infection characterized by the presence of:
1) catarrh of the upper respiratory tract
2) conjunctivitis
3) hepatosplenomegaly
4) lymphadenopathy
5) all of the above *
74. What complications are typical for influenza:
1) pneumonia
2) encephalitis
3) Guillain-Barré syndrome
4) meningitis
5) all of the above *
75. Stage 3 laryngeal stenosis is characterized by:
1) marbling of the skin, diffuse cyanosis
2) participation in the act of breathing of auxiliary muscles
3) inspiratory dyspnea at rest
4) all of the above *
76. Pharyngoconjunctival fever is observed with:
1) rhinovirus infection
2) flu
3) adenoviral infection *
4) parainfluenza
77. Changes in the oropharynx during rubella are characterized by all symptoms except:
1) moderate hyperemia of the tonsils
2) spotted enanthema on the soft palate
3) diffuse hyperemia, swelling of the mucous membrane, arches *
78. The following vaccine is used to prevent rubella:
1) live *
2) chemical
3) recombinant
79. The classic syndrome of congenital rubella (Greg's triad) is:
1) cataracts, heart defects, deafness *
2) glaucoma, heart defects, deafness
3) hydrocephalus, heart defects, cataracts
4) cataracts, meningitis, hepatitis
80. Hematological data for rubella are characterized by symptoms, except:
1) leukopenia
2) lymphocytosis
3) neutropenia
4) presence of plasma cells
5) eosinophilia *
81. Postrubella encephalitis should be diagnosed if:
1) on the 4-5th day of illness with rubella
2) a new rise in temperature to 39-40 degrees Celsius
3) headache, vomiting, loss of consciousness, convulsions, focal symptoms
4) all listed symptoms *
82. Respiratory syncytial virus often causes the formation of:
1) tracheitis
2) laryngitis
3) bronchiolitis *
4) all of the above
83. Rubella rash:
1) maculopapular, pink on an unchanged skin background *
2) urticaria, irregular shape
3) papular-vesicular
4) hemorrhagic
84. The incidence of intestinal infections in children in the first half of life is most often caused by infection:
1) salmonella enteritidis
2) Yersinia enterocolitica
3) opportunistic microflora *
4) Boyd's Shigella
5) leptospira
85. Newborns and children under 6 months of age. rarely suffer from rotavirus infection, which can be explained by:
1) anatomical and physiological characteristics of the child’s gastrointestinal tract
this age
2) the presence of passive immunity *
3) the nutritional characteristics of children of this age
4) compliance with strict epidemiological regime in neonatal departments
86. A high incidence of enteropathogenic escherichiosis occurs in children aged:
1) up to 3 years *
2) older
87. Enteroinvasive escherichiosis mainly affects children:
1) early age and newborns
2) older *
88. The main cause of death in enterohemorrhagic escherichiosis is the development of:
1) intestinal bleeding
2) intestinal perforation
3) hemolytic-uremic syndrome (Gasser) *
4) DIC syndrome
89. Pseudomembranous colitis of newborns is most often the result of infection:
1) antibiotic-resistant strains of Clostridium perfringens
2) antibiotic-induced strains of Clostridium deficille *
3) Escherichia coli 0157:H7
90. The rise in incidence in the summer-autumn period of the year has:
1) rotavirus infection
2) shigellosis Sonne and Flexner *
3) intestinal yersiniosis
91. Intestinal yersiniosis has an increase in incidence in the winter-spring period of the year, since:
1) the main route of infection is vegetables and fruits stored in places accessible to rodents (cellar, vegetable warehouses, etc.) *
2) infection occurs by airborne droplets
3) during this period of the year, the susceptibility of children to yersinia increases sharply
infections due to inhibition of T-helper immunity
92. Infection of breastfed children most often occurs during acute intestinal infections of bacterial etiology:
1) by food
2) by water
3) contact-household *
4) airborne
93. With foodborne infection and massive infestation, shigellosis begins with:
1) high fever, headache, repeated vomiting, then colic appears
syndrome *
2) severe cramping pain in the abdomen, loose stools, then increased
body temperature and vomiting
94. In the pathogenesis of the development of neurotoxicosis syndrome in shigellosis in children, the leading one is:
1) a massive breakthrough of toxic substances into the blood (exo- or endotoxins) with
overcoming the blood-brain barrier *
2) hyperergic response of the body to the introduction of the pathogen
3) accumulation of toxic metabolic products in the blood and their direct
effects on the central nervous system
95. Diarrheal syndrome in Sonne shigellosis is the result of:
1) development of disaccharidase deficiency, increased osmotic activity and impaired absorption of water and electrolytes by enterocytes
2) inflammatory process throughout the gastrointestinal tract
3) invasion of Shigella into colonocytes and development of the inflammatory process *
4) disturbances in the system of cyclic nucleotides and prostaglandins
96. Abdominal pain with Flexner’s shigellosis:
1) cramping, not associated with the act of defecation
2) cramping, appear before defecation *
3) constant, without clear localization, aching in nature
97. A characteristic feature of diarrhea syndrome in shigellosis is the presence of:
1) liquid, foamy, undigested stool with pathological impurities
2) abundant, loose stool with a lot of cloudy mucus, greenery and blood
3) scanty, foul-smelling stool mixed with mucus, greens and blood
4) scanty stool without fecal odor mixed with cloudy mucus and streaks of blood.*
98. A feature of cholera is:
1) the onset of the disease with loose stools, then vomiting *
2) the onset of the disease with vomiting, then loose stools appear
3) acute onset with repeated vomiting, hyperthermic syndrome, severe abdominal pain, at the same time or several hours later, loose stools appear.
99. Zooanthroponosis is:
1) salmonellosis *
2) rotavirus infection
100. The water route of infection is the leading one for the following intestinal infection:
1) cholera *
2) rotavirus infection
3) salmonellosis
4) botulism
101. A feature of shigellosis in children of the first year of life is not:
1) mild or absent distal colitis
2) distal colitis expressed from the first hours of the disease *
3) enterocolitis character of the stool
4) the presence of tenesmus equivalents
102. Salmonellosis in older children through the food route of infection occurs as:
1) gastroenteritis *
2) enterocolitis
4) gastroenterocolitis
103. Stool with a typical form of shigellosis:
1) thin, copious, watery
2) scanty with a lot of mucus and streaks of blood *
104. A feature of typhoid fever in young children is not:
1) acute, violent onset of the disease with high fever and convulsions
2) liquid stool with pathological impurities from the first days of illness
3) absence or appearance of a scanty roseola rash
4) typhoid status with maximum severity by the end of the first week from the onset of the disease *
105. For how long should children who have suffered acute intestinal infections be observed in the clinic:
1) 3 months
2) 6 months
3) 2 weeks
4) 1 month *
106. Is active immunization against escherichiosis carried out in the Russian Federation:
1) not carried out *
2) only for epidemiological indications
3) only for enterotoxigenic escherichiosis
107. The clinical criterion for diagnosing botulism in children is:
1) uncontrollable vomiting and profuse diarrhea
2) sharp constriction of the pupils
3) visual impairment (double vision, “fog” before the eyes, etc.) *
4) blackout, up to coma
108. A clinical symptom that allows one to suspect the Proteus etiology of intestinal infection is:
1) constant pain in the right iliac region
2) liquid, foamy with an admixture of mucus, blood with a sharp putrid odor of stool *
3) loose stools with a lot of mucus, green stuff like “swamp mud”
4) compliance and gaping of the anus
109. Changes in the color of urine during viral hepatitis are caused by the appearance in the urine of:
1) urobilin
2) conjugated bilirubin *
3) biliverdin
110. A serological marker confirming the etiology of hepatitis A in the acute period of the disease is:
1) anti-HAV IgG
2) anti-HBc IgM
3) anti-HBe
4) anti-HAV IgM *
111. Hepatitis B always ends in recovery:
2) incorrect *
112. When viral hepatitis And the patient’s well-being from the moment of the appearance of jaundice:
1) gets worse
2) improves *
113. In the first year of life, children are more likely to get sick:
1) hepatitis A
2) hepatitis B *
114. The most common outcome of hepatitis A is:
1) chronic hepatitis
2) chronic cholangitis
3) cholecystitis
4) complete recovery *
115. The morphological basis of the fulminant form of hepatitis B and D is:
1) balloon dystrophy
2) massive necrosis *
3) cirrhosis
116. For the treatment of chronic viral hepatitis the following is currently used:
1) recombinant interferon *
2) normal human immunoglobulin
3) vaccine against hepatitis B
117. Tactics for managing a newborn born from a mother with HBV infection:
1) there are no management features
2) carrying out specific vaccination *
3) prescription of glucocorticoid therapy
118. In response to the administration of the hepatitis B vaccine, the body produces:
1) Anti-HAV IgG
3) Anti-HBcore (total)
119. The anicteric form of acute viral hepatitis is characterized by:
1) increased level serum transaminases *
2) normal level serum transaminases
120. Hepatitis E occurs most unfavorably in:
1) young children
2) pregnant women *
3) school-age children and teenagers
121. The vaccine currently used to prevent hepatitis A is:
2) plasma
3) recombinant
4) inactivated *
122. With viral hepatitis C, the following is often noted:
1) fulminant form
2) chronization of the process *
3) recovery
123. With viral hepatitis A, the source of infection poses the greatest epidemiological danger in:
1) pre-icteric period *
2) icteric period
124. In chronic hepatitis C, the level of serum transaminases is always elevated:
125. Contraindications to vaccination against hepatitis B are:
1) chronic hepatitis C
2) hyperthermic reaction to the DTP vaccine
3) acute phase of an infectious disease *
126. The main route of transmission of hepatitis B to children of the first year of life:
1) breast milk
2) airborne droplet
3) intrapartum *
127. For active immunization against hepatitis B, the following is used:
1) live vaccine
2) toxoid
3) recombinant yeast vaccine *
128. A serum marker indicating complete recovery from hepatitis B is:
1) anti-HBc IgG
2) anti-HBs*
3) anti-HBe
129. The effectiveness of antiviral therapy for chronic viral hepatitis is judged by:
1) normalization of sublimate test parameters
2) normalization of serum transaminase levels *
3) reducing the level of hyperbilirubinemia
130. Superinfection with the delta virus poses a danger to patients:
1) hepatitis B *
2) hepatitis A
3) hepatitis C
131. The most common form of chronic hepatitis in children is:
1) autoimmune
2) viral *
3) biliary
4) medicinal
5) alcoholic
132. Vaccine prevention of hepatitis B protects the patient from hepatitis D:
1) true *
2) incorrect
133. For congenital immunodeficiency, the following vaccines are allowed:
1) measles
2) polio
3) mumps
4) recombinant against hepatitis B *
134. Routes of transmission of pseudotuberculosis:
1) contact-household
2) nutritional *
3) transplacental
4) airborne
5) parenteral
135. What syndrome is leading in pseudotuberculosis:
1) arthralgia
2) exanthema *
4) meningitis
136. Who is the main source of infection in pseudotuberculosis:
2) mouse-like rodents *
137. In case of damage caused by wild animals, the following is used to prevent rabies:
1) anti-rabies gamma globulin
2) rabies culture vaccine
3) anti-rabies gamma globulin + anti-rabies vaccine *
138. The most common symptom of leptospirosis:
1) jaundice
2) pain in the calf muscles *
3) exanthema
4) hepatosplenomegaly
139. Etiotropic therapy for leptospirosis is mainly carried out:
1) carbopenems
2) penicillin *
3) fluoroquinolones
140. The main route of transmission of acquired toxoplasmosis:
1) airborne droplet
2) nutritional *
3) transmission
141. Lyme disease is caused by:
1) rickettsia
2) spirochetes *
3) viruses
4) the simplest
142. Post-exposure prevention of Lyme disease is carried out:
1) vaccination
2) introduction of specific immunoglobulin
3) antibiotics *
143. Dispensary observation of convalescents of disseminated Lyme disease with damage to the nervous system in the form of meningoencephalitis is carried out:
1) within 1 year
2) within 2 years
3) at least 5 years *
144. Kozhevnikov epilepsy can develop in all forms tick-borne encephalitis, except:
1) poliomyelitis *
2) encephalitic
3) meningoencephalitic
145. For the treatment of progressive forms of tick-borne encephalitis the following are used:
1) specific immunoglobulin
2) recombinant interferons *
3) specific vaccine
146. For specific active prevention of tick-borne encephalitis the following is used:
1) live vaccine
2) non-live vaccine *
3) combination vaccine
147. Flaccid paralysis develops in all forms of tick-borne encephalitis, except:
1) polyencephalitic
2) polioencephalomyelitis
3) polio
4) meningoencephalitic *
148. The HFRS syndrome complex includes all syndromes, except:
1) intoxication
2) acute renal failure
3) hemorrhagic
4) diarrhea *
149. What serum urea value is an indication for hemodialysis:
1) 15 mmol/l and above
2) 30 mmol/l and above *
3) 45 mmol and above
150. What serum creatinine value is an indication for hemodialysis:
1) more than 100 µmol/l
2) more than 200 µmol/l
3) more than 300 µmol/l
4) more than 350 µmol/l *
151. Dispensary observation of HFRS convalescents is carried out during:
1) 3 months
2) 6 months
4) for life
152. Infection with leptospirosis occurs through:
4) objects
153. For the treatment of leptospirosis it is necessary:
1) infusion therapy
2) antibiotic therapy in combination with the use of a specific polyvalent
immunoglobulin *
3) desensitizing therapy
154. Outcome of herpetic encephalitis:
1) recovery with severe focal neurological symptoms
2) vegetative state
3) lethal
4) all of the above *
155. When enterovirus infection noted:
1) joint pain
2) necrotizing tonsillitis
3) encephalitis and myocarditis of newborns *
156. In paralytic poliomyelitis the following is not detected:
1) sensitivity disorder *
2) lymphocytic cytosis in the cerebrospinal fluid
3) motor dysfunction
157. For visceral leishmaniasis all symptoms are characteristic, except:
1) acute onset of the disease *
2) gradual onset of the disease
3) undulating fever
5) hepatosplenomegaly
158. The main symptom of tetanus:
1) loss of consciousness
4) convulsions *
159. Tetanus cannot be transmitted through:
1) damaged skin
2) intact skin *
3) damaged mucous membranes
4) umbilical cord remnant
160. In the treatment of tetanus the following is used:
1) Zovirax
2) enterosorbents
3) specific immunoglobulin + toxoid *
161. The main source of malaria is:
1) sick person *
2) rodents
Section 8. Principles of treatment, anti-epidemic measures and vaccine prevention, dispensary observation of convalescents of infectious diseases. Allergic conditions.
1. IN THE FORMATION OF LOCAL IMMUNITY THE MAIN ROLE PLAYS:
2. INFECTIOUS PROCESS IS:
A) the spread of infectious diseases among animals
B) the presence of pathogens in the environment
B) interaction of micro- and macroorganisms *
D) infection by infectious agents of vectors
D) the spread of diseases among people
3. INDICATE AN INCORRECT STATEMENT. INFECTIOUS DISEASES ARE CHARACTERIZED BY THE FOLLOWING FEATURES:
A) the ability of the pathogen to overcome the protective barriers of the macroorganism
B) polyetiological *
B) cyclical flow
D) infectiousness
D) formation of immunity
4. INDICATE THE INCORRECT STATEMENT. INFECTIOUS DISEASES ARE CHARACTERIZED BY:
A) specificity of the pathogen
B) the presence of an incubation period
B) contagiousness
D) formation of immunity
D) acyclic flow *
5. EMERGENCY NOTIFICATION OF AN INFECTIOUS PATIENT SHOULD BE SENT TO:
A) to the local health department
B) to the city bacteriological laboratory
B) to the local center of the State Sanitary and Epidemiological Supervision *
D) to the disinfection station
D) to the Ministry of Health
6. A 46-year-old man suffered deep wounds when he fell from a tractor. PSS SHOULD NOT BE ENTERED IN THE FOLLOWING CASE:
A) the last administration of tetanus toxoid was 12 years ago
B) he did not receive tetanus toxoid
B) he has received 2 injections of tetanus toxoid during his life
D) he received a full course of immunization and a revaccination 2 years ago *
D) antitetanus serum was administered five years ago
7. ARTIFICIAL ACTIVE IMMUNITY IS ACQUIRED AS A RESULT OF:
A) infectious disease
B) asymptomatic infection
B) administration of the vaccine *
D) administration of immunoglobulin
D) administration of immune serum
8. NATURAL ACTIVE IMMUNITY IS ACQUIRED AS A RESULT OF:
A) asymptomatic infection *
B) vaccinations
B) seroprophylaxis
D) administration of normal human immunoglobulin
D) administration of specific immunoglobulin
9. A HOMOLOGIC DRUG IS:
A) anti-diphtheria serum
B) antitetanus serum
B) anti-botulinum serum
D) anti-influenza immunoglobulin *
D) brucellin
10. TO CREATE PASSIVE IMMUNITY THEY USE:
A) live vaccine
B) inactivated vaccine
B) bacteriophage
D) immunoglobulin *
D) interferon
11. TO CREATE ACTIVE IMMUNITY THEY USE:
A) bacteriophage
B) homologous serum
B) heterologous serum
D) toxoid *
D) immunoglobulin
12. IN SEPSIS:
A) the most common pathogens are pathogenic microorganisms
B) hospital strains of opportunistic microorganisms pose the greatest danger *
C) the disease is characterized by a cyclical course
D) clinical manifestations of the disease primarily depend on the etiological factor
D) the disease develops more often in individuals with uncomplicated premorbid background
13. WILLING TYPE OF FEVER (HECTIC) IS CHARACTERIZED BY:
A) for sepsis *
B) for hemorrhagic fevers
B) for leptospirosis
D) for infectious mononucleosis
D) for tetanus
14. THE TEMPERATURE CURVE OF THE HECTIC TYPE IS MOST CHARACTERISTIC:
A) for typhus
B) for typhoid fever
B) for sepsis *
D) for brucellosis
D) for scarlet fever
15. INDICATE AN INCORRECT STATEMENT. THE MOST CHARACTERISTIC CLINICAL MANIFESTATIONS OF SEPSIS ARE:
A) fever of the wrong type
B) chills, sweats
B) hepato-lienal syndrome
D) severe intoxication
D) polyadenopathy *
16. INDICATE AN INCORRECT STATEMENT. WHEN SEPSIS IS MOST OFTEN OBSERVED:
A) damage to the digestive organs *
B) skin rashes
B) destructive pneumonia
D) kidney damage
D) progressive anemia
17 INDICATE THE INCORRECT STATEMENT. TO CONFIRM THE DIAGNOSIS OF SEPSIS THE FOLLOWING METHODS ARE USED:
A) bacteriological blood test
B) detection of antibodies against the pathogen *
C) detection of pathogen antigens by enzyme immunoassay
D) bacteriological examination of discharge from purulent-inflammatory foci
E) bacteriological examination of sputum, pleural exudate, urine, cerebrospinal fluid and other biosubstrates, depending on the location of septic foci
18. INDICATE AN INCORRECT STATEMENT. SEPSIS:
A) usually caused by opportunistic bacterial flora
B) is usually an autoinfection
B) usually develops as a result of exogenous infection *
D) develops in individuals with impaired defense mechanisms
D) characterized by persistent bacteremia
19. IN SEPSIS:
A) etiotropic drugs should be prescribed after establishing the etiology of the disease
B) when establishing the etiology of the disease, broad-spectrum antimicrobial drugs should be used
C) antimicrobial therapy should be carried out taking into account the sensitivity of the pathogen *
D) sanitation of the primary lesion is not significant for the outcome of the disease
D) if there is no noticeable clinical effect within 2 days, you need to change antibiotics
20. INDICATE AN INCORRECT STATEMENT. SEPSIS IS CHARACTERISTIC:
A) the presence of an entry gate of infection or a primary focus
B) persistent bacteremia
C) the formation of multiple secondary foci of infection
D) cyclical course of the disease *
D) severe intoxication syndrome
21. INDICATE AN INCORRECT STATEMENT. WHEN TREATING SEPSIS:
A) antimicrobial therapy plays a leading role
B) surgical sanitation of the primary purulent-inflammatory focus is important
C) specific and nonspecific replacement immunotherapy is effective
D) after determining the sensitivity of the pathogen, broad-spectrum antimicrobial drugs should be prescribed *
D) measures are necessary aimed at preventing dysbiosis
22. FIRST LINK OF THE EPIDEMIC PROCESS
susceptible organism
transmission mechanism
source of infection *
transmission route
transmission factors
23. THE EPIDEMIC PROCESS CONSISTS OF
three different pathogens
three interconnected links *
transmission of diseases from one to another
host change phases
transmission routes
24. FACTOR IMPLEMENTING THE FECAL-ORAL TRANSMISSION MECHANISM
cerebrospinal fluid
25. TRANSMISSION MECHANISM DEPENDS ON
forms of the disease
type of pathogen
pathogen localization *
characteristics of the body
forms of the disease
26.. THE HOUSEHOLD CONTACT WAY OF TRANSMISSION OF AGENTS IS CHARACTERIZED
the occurrence of diseases along the chain *
minimum incubation period
predominant disease of adults
connection with a water source
presence of rodents
27.. THE POSSIBILITY OF AIR DUST TRANSMISSION IS DETERMINED
climatic conditions
resistance of the pathogen in the external environment *
features of the pathological secretion secreted by the patient
the rate of decrease in the virulence of the pathogen in the external environment
aerosol dispersion
28. TRANSMISSION MECHANISM IS IMPLEMENTED
non-sterile medical instruments
cockroaches
blood-sucking insects*
29. VERTICAL MECHANISM MEANS THAT THE PATIENT IS TRANSMITTED
through the air
contaminated soil
contaminated vegetables
through dust into the home
from mother to fetus *
30. ANTI-EPIDEMIC MEASURES DIRECTED AT THE SECOND LINK OF THE EPIDEMIC PROCESS
identification of patients
identification of bacteria carriers
final disinfection *
hospitalization of patients
31. MEASURES PERFORMED AT THE OUTCOME IN REGARD TO THE SOURCE OF INFECTION
deratization
hospitalization of the patient *
vaccine prevention
extermination of arthropods
disinfection
32. PREVENTIVE ACTION DIRECTED AT THE THIRD LINK OF THE EPIDEMIC PROCESS
disinfection
deratization
vaccination of the population *
identification of patients
carrier identification
33. A DISTRICT DOCTOR WHO SUSPECTS AN INFECTIOUS DISEASE IS OBLIGATED TO DETERMINE THE BOUNDARY OF THE FOCUS
fill out the “emergency notice” *
carry out final disinfection
organize measures to eliminate the outbreak
carry out disinfection measures
Meningococcal infection is a contagious disease that is transmitted by airborne droplets, affects the central nervous system, joints, heart muscle and often causes infectious-toxic shock. The causative agent of the disease, Neisseria meningitides, is a close relative of gonococcus, but unlike it, it uses the epithelium of the upper respiratory tract as an entrance gate. The contagiousness of meningococcus is low, so outbreaks of the disease occur in crowded conditions and close contact: in kindergartens, schools, barracks, and boarding homes.
The incidence of meningococcal infection varies in waves. The indicator periodically creeps up for several years, after which a stable decline is observed for 8-10 years. In the Russian Federation, the incidence on average remains at the level of 5 cases per 100 thousand population, in European countries - up to 3 per 100 thousand, in the countries of Central Africa - 20-25, reaching 800 cases per 100 thousand population in unfavorable years. African countries form the “meningitis belt” of the planet due to the high prevalence of the disease.
Mostly children and young people under 30 years of age suffer from meningococcal infection, but the disease is most severe in infants under one year of age and in persons over 60 years of age. Sometimes events develop so quickly that a fulminant form of the disease is separately identified. The consequences of meningococcal infection depend on the severity of its course and the prevalence of the pathogen; it can lead to severe disability and death.
Pathogen
Meningococcus is a round, gram-negative bacterium, nonmotile, and does not form spores. In human cells, it is located in pairs, forming structures similar in appearance to coffee beans. A similar organization of bacteria is called diplococcus. Young meningococci have thin and delicate filaments on the surface of the cell wall, with which they attach to epithelial cells.
Bacteria secrete a large number of aggressive substances that facilitate their penetration into the blood and various tissues of the body. For example, hyaluronidase breaks down the main component of connective tissue - hyaluronic acid, due to which collagen bundles are loosened and a passage for meningococcus is formed. Cell wall bacteria is a powerful toxin for the human body. It negatively affects the central nervous system, kidneys, heart muscle and causes powerful activation of the immune system.
The pathogen is unstable in the external environment. It quickly dies when heated, under the influence of ultraviolet radiation, or when treated with disinfectants. The most favorable conditions for its life are high humidity (70-80%) and air temperature in the range of 5-15 degrees C, in which it remains active for up to 5 days. For this reason, the incidence increases significantly in the cool season - from February to April, subject to a warm and snowy winter.
The source of infection is a sick person or carrier. Carriage of meningococcus does not manifest itself in any way subjectively, so a person does not know that he is dangerous to others. The pathogen is localized in the nasopharynx and is released with droplets of saliva when talking, coughing, or sneezing. It has been noted that when carriers accumulate to about 20% in the population, massive outbreaks of meningococcal infection occur. People with meningitis or the common form of the infection are more contagious, but they are usually isolated from society and pose a danger only to the people caring for them.
Mechanism of disease development
Meningococcus enters the mucous membrane of the nasopharynx of a susceptible person and firmly attaches to it. Further interaction between the macroorganism and the microorganism depends on the activity of the immune system and the aggressiveness of the pathogen’s toxins. If local immunity is well expressed, then carriage of meningococcal infection develops: bacteria multiply moderately in the nasopharynx and are released into the external environment in small quantities. After some time they leave the body.
If the virulence of meningococcus is sufficient to penetrate deep into the mucous membrane, meningococcal disease develops. Bacteria destroy body cells and release aggressive substances into tissues, which entails a reaction of blood vessels and the immune system. Blood intensely flows to the site of inflammation, its liquid part enters the mucous membrane - hyperemia and edema are formed. They are designed to limit the pathological focus and prevent further spread of the pathogen.
Sensitive nerve endings in the area of inflammation react biologically active substances, which release destroyed cells and send a pain impulse to the brain as a distress signal. It is further enhanced by bacterial toxins and the pressure of edematous tissue on the receptor. As a result, a person feels pain and sore throat.
If the inflammatory reaction does not stop meningococcus in the nasopharynx, it penetrates into the bloodstream and lymphatic vessels. In the blood, the pathogen attacks immune cells and protective proteins, which is why most of microorganisms die with the release of a dangerous toxin. In situations where the forces are approximately equal, the disease ends at this stage, manifesting itself as a rash and intoxication.
diseases caused by meningococcus
If immune cells waste their potential before they destroy all bacteria, then incomplete phagocytosis occurs. The leukocyte captures the meningococcus, but cannot digest it, so the pathogen remains viable and travels throughout the body in this form. Further developments depend on where the bacteria penetrate. Having penetrated the meninges, they cause purulent arthritis through the joint capsule, and iridocyclitis into the iris of the eyeball.
Meningococci settle in peripheral blood vessels and damage their vascular wall, causing blood to rush into the tissue. Thus, a hemorrhagic rash forms on the skin, which is local hemorrhages.
A large amount of meningococcal toxin in the blood leads to paralytic vasodilation in the periphery and sharp fall blood pressure. A redistribution of blood flow occurs: blood is deposited in small vessels and does not flow in sufficient quantities to the vital important bodies– brain, heart, liver. Infectious-toxic shock develops - a fatal condition.
Classification of the disease
The interaction of meningococcus with the human body occurs according to various scenarios, each of which requires special approach and treatment. In this regard, in 1976, Academician Pokrovsky developed a classification of meningococcal infection, which doctors use to this day. According to it, there are:
Localized forms:
- Carriage of meningococcus is asymptomatic;
- Acute nasopharyngitis – manifested by symptoms of acute respiratory infections;
- Pneumonia is clinically no different from other bacterial infections.
Generalized forms:
Clinical manifestations
From the moment of infection until the appearance of symptoms of meningococcal infection, it takes from 1 to 10 days, on average the incubation period lasts 2-4 days.
Nasopharyngitis
The disease begins acutely with scanty mucous discharge. The temperature rises only in half of the patients and does not exceed 38.5 degrees C. It is accompanied by signs of intoxication: aching muscles and joints, headache, lack of appetite, lethargy. The fever lasts no more than 4 days, after which the patient quickly recovers.
When examining the pharynx, hyperemia is visible back wall pharynx, from the 2-3rd day of illness it becomes granular due to the reaction of small lymphoid follicles. The tonsils, their arches, and the uvula remain unchanged, although in children under 3 years of age the inflammation also spreads to them.
Meningococcemia
The presence of meningococcus in the blood causes a quick and powerful immune response, which immediately affects the patient’s condition. The disease begins acutely with a sharp increase in temperature to 39 degrees C and above. Signs of severe intoxication appear: chills, pain in the lower back, muscles, joints, headache, severe weakness. The patient may vomit without abdominal pain and have no appetite.
hemorrhagic rash due to meningococcemia
6-24 hours after the temperature rises, the most characteristic sign of meningococcemia appears - hemorrhagic rash. Initially, it may look like pink spots, pinpoint hemorrhages, which quickly transform into large irregular bruises. Elements of the rash have different shape and size, bulge somewhat above the surface of the skin, sensitive when touched. Most often they are located on the thighs, buttocks, legs and feet and have a star-shaped outline.
The rash develops over the course of 1-2 days, after which the reverse development of its elements begins. Small ones become pigmented and completely disappear after a while; large ones can leave behind retracted scars. The early appearance of the rash (up to 6 hours after the rise in temperature) and the location of its elements on the face and upper half of the body are signs of an extremely severe course of meningococcemia. Sometimes it ends with necrosis of the tip of the nose, fingers and toes.
The presence of meningococcus in the blood is fraught with the development of a serious complication - infectious-toxic shock. It usually begins in the first hours after the onset of the disease and without emergency help inevitably leads to the death of the patient. The first signs of incipient shock are marble pallor of the skin, a drop in body temperature and blood pressure. The patient gradually loses consciousness and falls into a coma; death occurs from insufficient blood supply to the brain, heart and liver.
Another dangerous complication meningococcemia is Friederichsen-Waterhouse syndrome. It develops when the adrenal cortex dies under the influence of massive hemorrhage into it. The patient stops producing adrenal hormones, which are responsible for water-salt metabolism and maintaining blood pressure. As a result, he dies from dehydration or heart failure.
Meningitis
Meningococcal meningitis begins with a rise in temperature to 38.5-39.5 degrees C and headache, which increases significantly by the end of the first day of illness.
meningitis symptoms
Pain in the head is bursting in nature, most often localized in the frontotemporal or occipital regions, but can cover the entire skull. Painful sensations intensified by bright light, loud sounds, when changing body position. It is often accompanied by fountain vomiting, which does not bring relief and occurs without previous nausea.
first sign of meningitis in a baby
By the end of the first day, symptoms of irritation of the meningeal membrane (meningeal signs) appear. These include soreness of the posterior cervical muscles, the inability to fully straighten the leg in knee joint with the hip bent. In infants, the first signs of meningitis are a complete refusal to eat, a constant monotonous cry, and a bulging fontanel on the head. If you take a sick baby by the armpits, he will bend his legs towards his body - this is a symptom of suspension.
On the 3rd-4th day of illness, in the absence of antibacterial treatment, the patient takes the characteristic “coping dog” pose. He lies on his side with his legs bent and his head thrown back, while his back is strongly arched and tense. In children, this position is more common and more pronounced than in adults. By this time, consciousness becomes cloudy, the patient is inhibited, does not respond to questions or answers in monosyllables. In some cases, hearing is turned off, and paralysis of the eyeballs, limbs, and swallowing muscles develops. Often, meningococcal meningitis is combined with meningococcemia, which is manifested by a hemorrhagic rash on the skin.
Video: meningococcal meningitis
Diagnostics
Diagnosis of meningococcal infection is carried out by doctors of various specialties, which depends on the form of the disease and its manifestation. Patients with acute nasopharyngitis usually turn to a local physician or ENT doctor; with a rash - to an infectious disease specialist or dermatovenerologist; with headaches and paralysis - to a neurologist. Cases of severe meningococcal infection are diagnosed in emergency departments. However, like any infectious disease, it relates primarily to the competence of an infectious disease specialist.
The doctor examines the patient, collects anamnesis, and studies complaints. Epidemiological data play an important role: if over the last 10 days the patient has had prolonged contact with a person with nasopharyngitis or a case of meningococcal infection has been identified in his team, then it is highly likely that meningococcal infection has occurred. The diagnosis is also supported by the acute onset of the disease, a rise in temperature, the presence of a hemorrhagic rash on the skin, meningeal signs, and impaired consciousness.
All patients with signs of meningitis undergo a lumbar puncture to obtain cerebrospinal fluid (CSF) for analysis. With meningococcal infection, cerebrospinal fluid leaks under pressure, higher than normal, and has a yellow or yellow-green color. It's muddy because high content protein and cellular elements.
The following methods are used to confirm the diagnosis:
General blood analysis– in patients with meningococcemia and meningitis, a pronounced increase in neutrophils in the blood, acceleration of ESR, and anemia are observed;
- General urine analysis- at acute inflammation a small amount of protein is determined; in case of shock, there is a sharp decrease in the amount of urine and its density;
- Biochemical analysis of blood, cerebrospinal fluid– infection causes an increase in serum levels C-reactive protein, gammaglobulins, seromucoid. The glucose content in the liquor decreases and the protein concentration increases.
- Bacteriological culture of blood, cerebrospinal fluid– the material is taken into a sterile tube and sown on nutrient media; if meningococcus is present in the blood, characteristic colonies grow in 3-5 days. The method allows you to assess the sensitivity of bacteria to antibiotics;
- Microscopy of blood, cerebrospinal fluid– makes it possible to visually determine the presence of a pathogen in the received material. Meningococci are located in pairs inside neutrophils; in the blood plasma, during severe infection, they can lie freely. A large number of living and dead neutrophils are determined in the cerebrospinal fluid, which indicates the purulent nature of the inflammation;
- PCR of blood, cerebrospinal fluid– the method allows you to quickly and accurately determine the presence of meningococcus in the material under study.
- Normal body temperature for more than 5 days;
- Absence of inflammatory changes in the nasopharynx;
- Disappearance of the rash;
- No headaches or meningeal signs;
- Normalization of blood counts;
- Negative culture and PCR study of cerebrospinal fluid.
If necessary, instrumental research methods are used. An ECG is performed if there is a suspicion of toxic damage to the heart, CT or MRI of the brain if signs of focal damage to the central nervous system (paralysis, hearing loss) appear.
Treatment
Patients with meningococcal infection are hospitalized in an infectious diseases hospital or in intensive care (for infectious-toxic shock). The period of hospitalization is up to 30 days in severe cases of the disease. During treatment, the patient is prescribed a diet with a predominance of easily digestible protein, some fluid restriction and table salt. Elements of the skin rash are treated with local antiseptics - fucorcin, brilliant green, potassium permanganate solution.
Drug treatment includes:
Recovery criteria include:
Follow-up after recovery
After discharge from the hospital, the patient must be monitored by a local physician for a year. During this period, a person who has recovered from the disease must take 4 tests. general analysis blood (once every 3 months), if necessary, he is shown an ECG, CT and MRI of the brain. 5 days after discharge, a bacteriological examination is repeated, for which a swab is taken from the nasopharynx. At negative result a person is allowed into the team and to work.
Any vaccine is contraindicated for a person who has been ill for 3 months after recovery. For one year, he should not sunbathe in the sun, suddenly change the climate zone, or overheat in a bathhouse or sauna.
Prevention of meningococcal infection
If a patient with meningococcal infection is identified in a team, a quarantine is imposed for 10 days, during which all its participants are examined for carriage of meningococcus, and thermometry and throat examination are carried out daily. Besides, all contacts are advised to take antibiotics for prophylactic purposes: rifampicin 600 mg 2 times a day for 2 days, ciprofloxacin 500 mg intramuscularly once.
Specific prevention is the introduction of a special meningococcal vaccine. Since 2013, she entered national calendar Russian Federation vaccinations. It is administered intramuscularly to healthy children over 2 months of age twice with an interval of 2 months. Emergency vaccination is carried out in the first 5 days after contact with a patient with meningococcal infection. The planned introduction is shown to first-year students living in a dormitory and conscript soldiers.
Vaccination against meningococcal infection is carried out using the following vaccines:
- Dry vaccine meningococcal polysaccharide A (“Menugate”);
- Meningococcal polysaccharide vaccine A+C;
- Meningococcal tetravalent vaccine (against serotypes A, C, U, W-135) – “Mencevax”.
In addition, a combined vaccine is produced for intramuscular administration against hemococcus and pneumococcus. Persistent immunity is formed within 1 month after vaccination.
Meningococcal infection is an infectious disease with airborne transmission caused by N.meningitidis, the generalized forms of which occur with the development of inflammation of the meninges - meningitis, meningococcal sepsis - meningococcemia or a combined form (meningitis + meningococcemia).
Etiology. Neisseria meningitidis are gram-negative, nonmotile, aerobic diplococci.
Pathogenesis and pathological anatomy. The incubation period of the disease is 2-10 days. During this time, the microorganism adheres to the receptor structures of the nasopharyngeal mucosa (CD46, CD66, etc.), local protective factors are suppressed and the microorganism multiplies (accumulates).
The pathoanatomical characteristics of the process are acute dystrophic changes in internal organs, a detailed picture of disseminated intravascular coagulation with numerous hemorrhages in various organs and tissues, including the adrenal glands (Waterhouse-Friderichsen syndrome).
Meningococci are capable of adhesion to the endothelium of brain capillaries. Breakdown of the blood-brain barrier leads to the penetration of the microorganism into the subarachnoid space, which has limited bactericidal properties, and the development of purulent meningitis. Morphologically, meningitis is manifested by perivascular infiltration with the formation of edema-swelling of the brain, purulent exudate, especially pronounced in the area of the trunk, parietal and frontal lobes, and in some cases hydrocephalus.
Epidemiology. The incidence of meningococcal infection in the European Union is 1-2 per 100,000. In the Republic of Belarus, over the past 5 years, this figure is 1.9-2.8 per 100,000.
The age most susceptible to the occurrence of generalized forms of infection is 4–24 months, i.e. after the expiration of protective maternal immunity until the appearance of own antibodies. Children in the first two years of life account for more than half of all cases of generalized meningococcal infection. An increase in incidence is also observed at the age of 15-19 years.
Clinical picture. Currently, the clinical classification of V.I. is generally accepted. Pokrovsky.
I. Localized forms
carriage of meningococcus
acute nasopharyngitis
II. Generalized forms
meningococcemia
meningitis
meningoencephalitis mixed form (meningococcemia + meningitis)
III. Rare forms
endocarditis
polyarthritis
pneumonia
iridocyclitis
chronic meningococcemia.
Localized forms of meningococcal infection predominate significantly. It is believed that for one case of generalized meningococcal infection there are 2000-50000 localized ones.
During the inter-outbreak period, bacteria carriers make up 1-3% of the population, and this number increases significantly during outbreaks and epidemics. The period of healthy bacterial carriage varies greatly. It lasts from several days to several weeks, less often months. Numerous cases of resumption of bacterial carriage after a course of antibiotic therapy have been described. It is this contingent that plays the main role not only in the formation of collective immunity, but also in the spread of meningococcal infection.
Meningococcal nasopharyngitis is a disease that is often detected during directed bacteriological examination, more often in foci of infection. The epidemiological role of these patients is significant due to the presence of catarrhal symptoms (sneezing, coughing). Nasopharyngitis is characterized by a “dry” runny nose (difficulty in nasal breathing with scanty mucous rhinorrhea), dryness and sore throat, headache, and low-grade fever. For an objective diagnosis of the disease, examination of the posterior wall of the pharynx is most important, allowing to identify nested hyperplasia of lymphoid follicles.
Meningococcemia is the most severe clinical form of generalized meningococcal infection, which has a high mortality rate. The disease begins acutely, suddenly, although in some cases it is preceded by catarrhal symptoms (meningococcal nasopharyngitis). The first manifestation is an increase in temperature. Quite often, especially in severe clinical forms of the disease, the temperature reaction is pronounced, reaches 39.7-40°C and is not controlled by antipyretics. Such severe hyperthermia should always alert the doctor. Against the background of increasing intoxication, a rash appears after 4-8 hours - the main clinical sign of meningococcemia. Exanthema has a known polymorphism, especially at the beginning of the disease. In some cases, these are maculopapular, less often roseolous elements without a specific localization, within which point hemorrhages appear (at first, not in all). As the disease progresses, the hemorrhagic component of the rash becomes more and more prevalent. Dense, stellate primary hemorrhagic elements that do not disappear with pressure and tend to spread and merge are considered typical. The rash is located on any part of the body, most often on the legs (feet!), buttocks, scrotum, and shoulders.
The so-called “bright period” is described for meningococcemia, when at 6-8 hours of the disease some stabilization of the patient’s condition occurs. However, this period is short-lived (1-2 hours) and should not be misleading. The most important complications of meningococcemia are infectious-toxic shock and multiple organ failure, the development of which determines the clinical picture of the later stages of the disease and is the main cause of death.
Clinical and laboratory criteria for ITS are hypotension, manifested by a decrease in arterial systolic pressure below 90 mmHg. or more than 40 mm Hg. in hypertensive patients compared to normal figures (main criterion); microcirculation disorders (presence of a long-lasting - more than 3 seconds - white spot that appears when a finger is pressed on the patient’s skin); signs of decompensated metabolic acidosis and tissue hypoxia; severe tachycardia, absence of pulse in the periphery or decrease in its properties; laboratory and clinical signs of DIC stages 2 and 3.
Waterhouse-Friderichsen syndrome (hemorrhage into the adrenal glands with acute adrenal insufficiency) is manifested primarily by persistent, increasing hypotension.
The fulminant form of meningococcemia begins with severe symptoms of intoxication and severe hyperthermia. The rash appears at once, as if “manifesting”, covering large areas of the torso and limbs. In the early stages of the disease, it is characterized as “cloud-shaped”, since its contours are not clear enough. The hemorrhagic and necrotic components grow very quickly. As with the fulminant forms of some infectious diseases, the symptom of “jumps” is characteristic - in the early stages of the disease, extensive symptoms of intoxication and skin hemorrhagic manifestations predominate with a temporary lag in other typical symptoms of severe bacterial damage: disorders of consciousness, adynamia, anuria, tachypnea, etc. However, these symptoms appear as ITS and multiple organ failure develop, which in the fulminant form of meningococcemia occur already on the first day of the disease.
When diagnosing meningococcal meningitis, it is necessary to strictly take into account the age of the patient, on which the underlying clinical symptoms of the disease directly depend. In adults and older children, this is a headache of increasing intensity, usually diffuse or predominantly localized in the frontal and parietal regions, not relieved by taking analgesics; sudden, non-relief, “cerebral” vomiting that occurs without nausea; temperature rise, usually to high numbers (meningeal triad). In young children who cannot complain about headache, the main manifestations are hyperthermia and symptoms of increasing intoxication, vomiting without severe diarrhea (!), convulsions, as well as lethargy of the child and rapidly developing stupor. As the disease develops (from about 8-12 hours of illness), meningeal symptoms appear in both children and adults, which are based on the phenomenon of a decrease in the sensitivity threshold of nervous tissue with an increase in intracranial pressure.
Depending on the age of the patient and the characteristics of his reactivity, the severity of meningeal symptoms varies greatly. Therefore, if there is a suspicion of meningitis, only a lumbar puncture will confirm or exclude the diagnosis. CSF in meningococcal meningitis usually flows out under high pressure (in frequent drops or streams), often opalescent (cytosis up to 1000 cells in 1 μl), cloudy (cytosis up to 3000-5000 cells in 1 μl) or greenish (cytosis over 5000 in 1 μl) . CSF protein is increased, glucose is decreased. A purulent process is characteristic (predominance of neutrophils), however, this typical feature still cannot be absolute. At the very beginning of the disease, the cerebrospinal fluid may be serous in nature (predominance of lymphocytes). The rapid increase in clinical symptoms, the severity of the patient, changes in blood tests typical of a bacterial disease (leukocytosis, band shift) are characteristic of meningococcal (or other bacterial) meningitis.
The combined form is meningococcemia + meningitis. In 2/3 of cases, the generalization of meningococcal infection is manifested by a combined course of meningococcemia and meningitis. With this form of the disease, the patient has both signs of meningitis (headache, vomiting, meningeal symptoms) and signs of meningococcemia (high intoxication, hemorrhagic rash, hemodynamic disorders).
Diagnosis of meningococcal infection. To confirm the diagnosis for localized forms of meningococcal infection, bacteriological examination of mucus from the nasopharynx is used. Nasopharyngeal mucus is collected with a sterile swab before starting antibacterial therapy. The taken material should be stored at 37°C for no more than 1 hour and transported at 37°C (heating pad, portable thermostat), because The pathogen is extremely unstable in the external environment.
In case of meningococcemia, blood culture is also done, as well as its bacterioscopic examination.
For meningitis, in addition to studies of nasopharyngeal mucus and blood, cultures and bacterioscopy of the cerebrospinal fluid are performed. If a bacterioscopic examination of blood has very limited information content, then bacterioscopy of the cerebrospinal fluid in the case of detection of Gram-negative diplococci serves as a reliable criterion for early laboratory confirmation of meningococcal infection.
Differential diagnosis. Most often in adults, meningitis must be differentiated from an acute respiratory viral infection (influenza). Influenza has a clear seasonality, pronounced catarrhal syndrome, usually of moderate severity. Meningeal symptoms are not typical. If they are present, then with influenza they are associated with the development of meningism (increased intracranial pressure without changing the cellular composition of the cerebrospinal fluid). The presence of meningeal symptoms always requires immediate, urgent hospitalization of the patient and a lumbar puncture, without which it is impossible to determine the nature of the disease.
With subarachnoid hemorrhage, the disease begins suddenly with a sharp headache. The temperature appears later and usually does not reach high values. The cerebrospinal fluid is bloody or xanthochromic. Xanthochromia persists after centrifugation; the sediment consists of leached red blood cells.
With serous meningitis, the clinical picture is usually less severe, fever and symptoms of general intoxication are less pronounced. In clinical blood tests there is no pronounced leukocytosis and a shift of the leukocyte formula to the left. Lymphocytes predominate in the cerebrospinal fluid, protein is slightly increased, and cerebrospinal fluid glucose is within normal limits.
In children under 2 years of age, the presence of vomiting and hyperthermia requires differential diagnosis with acute gastroenteritis. Meningococcal meningitis does not cause diarrhea, which is typical for gastroenteritis. General cerebral symptoms, stupor, and convulsive syndrome appear quickly.
The greatest difficulties in diagnosing meningococcemia arise during an inattentive examination, when the doctor does not find a rash in the patient. If it is present, especially on the first day of the disease, when the rash can be extremely polymorphic, there is a need to differentiate it from allergic exanthema. With meningococcemia, the rash occurs against the background of severe intoxication, as a rule, is hemorrhagic in nature, and is not accompanied by itching. A general blood test reveals leukocytosis and band shift. Any rash in a child, regardless of its nature, that appears against the background of fever and severe intoxication, should be regarded as possible meningococcemia.
Treatment. Antibiotic therapy for meningococcal infection is not a problem. The pathogen retains good sensitivity to penicillin, which is used at a dose of 300 thousand units per kg of body weight per day, divided into 6 doses. The alternative use of 3rd generation cephalosporins (ceftriaxone, cefatoxime) in maximum dosages is justified. Ceftriaxone is prescribed for children at 50-80 mg/kg/day in 2 doses (the maximum dose should not exceed 4 g/day), for adults 2 g. 2 times a day. Cefatoxime is prescribed in a daily dose of 150-200 mg/kg/day, divided into 3-4 doses. The highest daily dose for adults is 12 grams. In case of intolerance to b-lactam antibiotics, an alternative drug may be chloramphenicol succinate 80–100 mg/kg per day for 3 doses (no more than 4 g per day for adults). Reserve drug for treatment purulent meningitis is meropenem (for meningitis/meningoencephalitis, 40 mg/kg is prescribed every 8 hours). Maximum daily dose adults – 6 g, divided into 3 doses.
The principles of pathogenetic therapy of purulent meningitis consist of:
Ensuring adequate breathing - timely transfer to mechanical ventilation;
Dehydration - the effect is achieved by using osmodiuretics, primarily mannitol at a dose of 0.5-1.0 g/kg dry matter weight per day and saluretics (furosemide);
Moderate detoxification under the control of central venous pressure, diuresis, physiological needs and pathological losses. The introduction of excessive volumes leads to worsening cerebral edema;
Administration of glucocorticosteroids (preferably dexamethasone 0.5 mg/kg per day or prednisolone 2-3 mg/kg per day). Drugs in this group can be administered only in the first two days of treatment.
Symptomatic therapy – combating convulsions, hyperthermia, headaches.
For pathogenetic therapy of meningococcemia the following are used:
Detoxification measures (starting solutions are crystalloid. Fresh frozen plasma is not administered as a starting solution);
Glucocorticosteroids in average therapeutic dosages in the first days of treatment;
Correction of acid-base status;
Correction of electrolyte balance.
Prevention. In case of close contact with a patient with a generalized form of meningococcal infection, prophylaxis is recommended - for adults, ciprofloxacin 500 mg orally once or rifampicin 600 mg orally every 12 hours for 2 days. For children under 1 month, rifampicin 5 mg/kg orally, and over 1 month, 10 mg/kg body weight orally (but not more than 600 mg) every 12 hours for 2 days. For prophylactic purposes, a single administration of ceftriaxone can also be used for adults at a dose of 250 mg, for children under 15 years of age 125 mg.
There are monovalent vaccines A and C, bivalent A-C and quadrivalent A-C-Y-W135. They are used for preventive purposes, usually among limited groups of people in the presence or threat of an outbreak.
