Lymphocytic choriomeningitis (LCM), or acute aseptic, serous, benign meningitis, Armstrong's disease, is one of the most pronounced forms clinical course zoonotic generalized viral infection of humans.
Diseases that occur in humans occur not only with symptoms of damage to the soft meninges and the central nervous system in the form of serous meningitis or meningoencephalitis, but also in the form of a general infectious process with clinical symptoms of influenza, pneumonia, myocarditis, mumps, otitis, orchitis, as well as in a subclinical or parasitic form .
Due to the fact that in experimental animals infected with the virus, the most pronounced pathomorphological inflammatory changes occurred in the choroid plexuses of the ventricles and pia mater of the brain with an increase in the number of lymphocytes in the CSF, this pathogen was named lymphocytic choriomeningitis virus. The etiological significance of the LCM virus in human pathology was confirmed after its isolation from the CSF of two adult patients with acute serous meningitis.
Lymphocytic choriomeningitis is widespread. The true incidence of LCM has not been studied, since sporadic cases are recorded relatively infrequently, and group cases are rare. It can be assumed that as modern virological and serological diagnostic methods are introduced into diagnostic practice, diseases will be detected in many territories of our country.
Etiology. The causative agent of LCM, isolated for the first time in 1933 by S. Armstrong and R. Lillie, belongs to the group of arenoviruses - a toxonomic association of viruses of a similar structure that are sensitive to lipid solvents. Contains RNA; the formation of mature virions occurs by budding from plasma membrane cells. The size of the virus ranges from 50 to 200 nm or more. It is preserved in a 50% glycerin solution, and in a dried state it can be viable for more than a year. Sensitive to detergents, ether, etc., quickly inactivated at a temperature of 56 °C. The LCM virus is cultivated on most cell cultures, chicken embryos, mouse macrophage cultures, as well as in cell cultures of chicken and mouse embryos. The virus causes diseases in humans and many animals (white mice, Guinea pigs, house mice, rats, monkeys). Asymptomatic forms of infection are observed in dogs, rabbits, chickens, Syrian hamsters, newborn mice.
Epidemiology. Lymphocytic choriomeningitis is a zooanthroponotic infection, in which brownies are the most common source of human infection gray mice. However, infection can also occur from other domestic and wild animals (white mice, guinea pigs, dogs, rats, hamsters, monkeys, etc.). Research by M.I. Levi (1964) showed the presence of natural foci of lymphocytic choriomeningitis, in which forest mice and voles can be the reservoir of the virus. Last years various clinical syndromes diseases in adults and children resulting from infection with the LHM virus from Syrian hamsters kept at home and carrying a latent infection. The lack of detection of diseases in humans is most likely due to polymorphism clinical symptoms illness, lack of special information from doctors and corresponding simple laboratory diagnostic methods.
The infectious process in animals occurs in a hidden, latent form, and the pathogen persists for up to 291 days or longer [Levi M.I., 1964]. From the body of animals, the virus is released into the external environment with feces, urine, nasal mucus and seminal fluid. Human infection occurs when the pathogen enters the mucous membranes of the respiratory tract and digestive tract with air and dust, or when food is contaminated. The introduction of the virus is possible through bites, scratches and other violations of the integrity of the skin. The pathogen can also be transmitted through bites from ticks, mosquitoes, mosquitoes, dung flies, bedbugs and body lice. The literature does not describe cases of human infection from patients with LCM.
Diseases occur more often in winter and in early spring, however, strict seasonality is not observed; mainly adults and older children suffer. Single sporadic cases are more often recorded in rural areas or on the outskirts of cities, but group outbreaks limited to a small number of individuals are possible. In the anamnesis of patients with LCM, as a rule, there is an indication of the presence of mice or other domestic animals in the living quarters. Infections are also possible when working with laboratory animals.
Pathological anatomy. The LCM virus, when infecting animals, causes serous inflammation of the pia mater with lymphocytic infiltration and significant changes in the choroid plexuses of the brain. Pathomorphological studies of rare cases that resulted in the death of patients revealed the most significant changes in the pia mater and brain matter. There is perivascular, and in some cases, diffuse infiltration of lymphocytes in the pia mater and brain tissue. The substance of the brain is swollen and congested. In the dilated cavities of the ventricles - accumulation large quantity clear liquid. With a protracted and chronic course of lymphocytic choriomeningitis, ending in death, obliteration of the subarachnoid space due to proliferation was noted connective tissue, pronounced lymphocytic infiltration of the perivascular spaces, in the cerebral cortex - gliosis. Changes were also found in the white matter of the brain in the form of local and diffuse demyelination. In severe cases of the disease ending in death, sections often reveal interstitial pneumonia, as well as inflammatory changes in liver tissue.
Clinic. Clinical manifestations LCM in children and adults is extremely diverse. Acute phase The disease can occur with a clinical picture of influenza, myocarditis, pneumonia, mumps, orchitis, meningitis, meningoencephalitis, myelitis. The disease usually begins acutely, without prodromal symptoms. Initially, many patients experience chills or short-term chills, followed by an increase in body temperature to high numbers. A general infectious process develops, manifested by headache, weakness, and fatigue. In cases accompanied by selective damage to the brain substance and its membranes, meningeal syndrome is expressed from the first day of the disease and is dominant in the entire clinical picture of the disease. Patients usually complain of persistent and very intense diffuse headache, nausea, and vomiting. Occasionally, an extremely serious condition develops, manifested initially by anxiety, agitation and hallucinations, followed by loss of consciousness. Constant symptom is repeated vomiting. Body temperature rises from the first day of illness and remains at high levels from 5-7 to 8-14 days, and then decreases to normal. Subsequently, low-grade fever is often observed for 5 to 7 days, in rare cases longer. The pulse is usually increased arterial pressure slightly reduced, heart sounds muffled. There are no significant changes in the liver and spleen. The tongue is usually coated and dry; the mucous membranes of the pharynx are slightly hyperemic; tonsils are not enlarged. No pathology of the urinary system is detected.
Meningeal syndrome is manifested by rigidity of the neck muscles of varying severity, positive Brudzinsky and Kernig symptoms. Some patients exhibit general cerebral symptoms in the form of hand tremors, unstable focal lesions cranial nerves(usually the abducens and oculomotor nerves), less often - hemiparesis, and also in 20-50% of cases - blurring of the optic nerve nipples, dilatation of the veins of the fundus. Only hand tremors and some paresis persist for a longer time. Severe cases are often accompanied by blackouts, delirium and significant functional disorders of the cardiovascular system. If such a situation occurs clinical picture The disease may lead to death as a result of the development of infectious-toxic shock.
Spinal puncture reveals hypertension, reaching 30 - 40 cm of water. Art. (3-4 kPa). As a rule, after puncture there is a subjective and objective improvement in the condition of patients. CSF is usually clear, in rare cases slightly opalescent, flowing through the needle in a stream or frequent drops. At laboratory research normal or increased protein content, positive Nonne-Apelt and Pandi tests are detected; the content of sugar and chlorine ions does not change; a film in the form of a “cobweb” rarely falls out when the liquid is kept in the cold. Cytosis is often detected, reaching 0.1-0.3* 109/l and even 1.2-1.5 109/l. Microscopic examination of the CSF in the first 2-3 days of illness reveals predominantly lymphocytes and a small number of polynuclear cells, and subsequently lymphocytes predominate (up to 90-95%).
In the vast majority of cases, the disease is acute, ending with normalization of body temperature, disappearance of headache and gradual extinction of meningeal symptoms, as well as normalization of CSF. General cerebral symptoms decrease in severity, but persist for up to 2-3 weeks or longer. During the period of early convalescence, patients often experience attacks of severe headaches. In the peripheral blood, normocytosis or leukopenia, significant lymphocytosis and several increased ESR. There are no significant changes in red blood.
Diseases caused by the LCM virus also occur with the development of the clinical symptom complex of influenza, acute respiratory infection, pneumonia, myocarditis, mumps, orchitis or in erased and latent forms. Clinical manifestations of catarrh of the mucous membranes of the nose, pharynx and upper section respiratory tract are expressed very slightly or completely absent. In some cases, a cough with serous sputum is associated, and unstable, scanty fine rales are heard over the lungs.
The disease can manifest itself as fever, tachycardia, muffled heart sounds, arterial hypotension and other symptoms of myocardial damage. It is also possible to develop focal inflammatory phenomena in the salivary glands or testes. Such variants of the course of the disease are manifested not only by swelling and increase in size salivary glands or testes, pain and tenderness when palpated, but also a general reaction in the form of increased body temperature, headache, decreased appetite and other symptoms. The latent form occurs without disruption of general well-being or the appearance of any symptoms and is detected on the basis of epidemiological data and the increase in specific antibodies in blood serum. The mentioned clinical forms of the disease end in recovery, but in some cases they lead to the development of meningitis or encephalitis with all clinical manifestations.
Group diseases that arose as a result of infection from hamsters were characterized by diversity clinical forms- from asymptomatic and influenza-like infections to classic manifestations of meningitis and encephalitis.
Prevention. To prevent infection of people, it is necessary to take measures to protect residential premises, food warehouses and other storage places food products from the penetration of mice, rats and other mouse-like rodents. You should also keep food and food products out of reach of mice. After feeding and caring for domestic and laboratory animals (cats, dogs, rabbits, guinea pigs, hamsters, etc.), you must wash your hands thoroughly hot water with soap. It is necessary to avoid bites and scratches by domestic and laboratory animals (if the skin is damaged, it must be treated with 5% alcohol solution iodine), contact with skin insects, as well as bites from ticks, mosquitoes and other arthropods.
Lymphocytic choriomeningitis I
Lymphocytic choriomeningitis (choriomeningitis lymphocytica; synonym: acute lymphocytic, acute lymphocytic benign, acute serous Armstrong meningitis)
In the meningeal form, the onset of the disease is sudden with a sharp rise in body temperature, repeated vomiting, and an intense headache of a bursting nature. Patients often complain of eyeballs Oh. From the very first day of the disease, pronounced rigidity of the nuchal muscles, Kernig, upper and lower symptoms Brudzinsky, general is possible. In some cases, in the first days of the disease, pyramidal signs, mild, and paresis of the cranial nerves, most often the oculomotor ones, are noted. Sometimes observed in children. Almost half of the patients have mild congestion in the fundus. Possible lethargy, stupefaction, rarely deeper. Arterial, muffled heart sounds are detected. coated, dry, pharynx slightly hyperemic. Diagnosis. The influenza-like form of the disease is usually diagnosed as an acute respiratory viral infection or influenza. The meningeal form is recognized on the basis of clinical and epidemiological data: the presence of mice, less contact with other animals, a pronounced picture of meningitis, high lymphocytic pleocytosis in the cerebrospinal fluid, leukopenia. H. l. can be confirmed by the results of complement fixation and neutralization reactions. Complement-fixing ones appear in the 2-4th week of the disease, and virus-neutralizing ones - in the 3rd-4th and later. Diagnostic value has an increase in antibody titer of at least 4 times when studying paired sera taken at an interval of 7-10 days. Differential diagnosis is carried out with other viral serous meningitis (Meningitis) ,
meningeal form of tick-borne and mosquito-borne encephalitis, Poliomyelitis a ,
tuberculous meningitis, less often with purulent meningitis. Treatment meningeal form of the disease is carried out in a hospital. The basis of treatment is the use of saluretics (furosemide, diacarb) or osmotic diuretics (mannitol, concentrated plasma, 10-20% albumin solution,). Sedatives are also used. In severe cases, they are prescribed (prednisolone, dexamethasone), as well as ribonuclease 10-150 mg per day. After discharge from the hospital, you must be released from work (study) for at least 2-4 weeks. and from physical work (physical education) for 6-12 months. Those who have had H. l. are under the supervision of a neurologist (children's psychoneurologist) for 2 years. Forecast, as a rule, favorable. Fatalities in the acute course of the disease are extremely rare. An unfavorable outcome is also possible with a chronic course of the disease. Prevention. Specific has not been developed. Highest value has protection of residential premises, food warehouses, food storage areas from the penetration of house mice and other rodents, and contamination of food products by them. Bibliography: Acute neuroinfections in children, ed. A.P. Zinchenko, s. 82, L., 1986; Guide to Zoonoses, ed. IN AND. Pokrovsky, s. 73, L., 1983; Timakov V.D. and Zuev V.A. Slow infections, p. 94, M., 1977; Zucker M.B. Clinical childhood, With. 24, M., 1986. infectious disease, caused by the virus of the same name of the adenovirus genus, characterized by the development of choriomeningitis with a benign course and an increased content of lymphocytes in the cerebrospinal fluid.
1. Small medical encyclopedia. - M.: Medical encyclopedia. 1991-96 2. First health care. - M.: Great Russian Encyclopedia. 1994 3. encyclopedic Dictionary medical terms. - M.: Soviet Encyclopedia. - 1982-1984.
See what “lymphocytic choriomeningitis” is in other dictionaries:
- (choriomeningitis lymphocytica; synonym: Armstrong acute serous meningitis, benign meningitis, acute lymphocytic meningitis) an infectious disease caused by the virus of the same name of the genus adenovirus, characterized by the development... ... Big medical dictionary
Armstrong's serous lymphocytic choriomeningitis. Acute lymphocytic meningitis- Acute serous meningitis caused by adenovirus. Infection occurs from rodents or by airborne droplets, as well as through nutrition. The incubation period is 6–13 days, the course is acute or subacute. General infectious and meningeal manifestations,... ...
Acute lymphocytic choriomeningitis- Syn.: Armstrong's meningitis. Primary serous meningitis caused by a ubiquitous adenovirus isolated in 1934 from the cerebrospinal fluid of patients Armstrong and Lily. The main natural reservoir of the virus is home and laboratory... ... Encyclopedic Dictionary of Psychology and Pedagogy
Lymphocytic choriomeningitis- Lymphocytic choriomeningitis, and other rodents, characterized by damage to the central nervous system. The virus is also dangerous for humans: outbreaks of L. x. in the USA, related to the sale to the public of hamsters that were infected with this... ... Encyclopedia "Animals in the House"
Large medical dictionary
- (arenavirus. singular lat. arena sand + Viruses) a group of infectious diseases caused by arenoviruses, occurring with fever, often with severe hemorrhagic syndrome. Includes Argentine and Bolivian hemorrhagic... ... Medical encyclopedia
- (Ch. J. Armstrong, 1886 1958, American bacteriologist) see Lymphocytic choriomeningitis ... Large medical dictionary
- (meningitis benigna) see Lymphocytic choriomeningitis... Large medical dictionary
- (Ch.J. Armstrong, 1886 1958, American bacteriologist) see Lymphocytic choriomeningitis ... Medical encyclopedia
- (meningitis lymphocytica acuta) see Lymphocytic choriomeningitis... Medical encyclopedia
The causative agent is a filterable virus isolated by Armstrong and Lilly in 1934. The main reservoir of the virus is gray house mice, which excrete the pathogen in nasal mucus, urine and feces. Human infection occurs due to consumption of food products contaminated with mice, as well as through airborne droplets when inhaling dust. The disease is often sporadic, but epidemic outbreaks are also possible.
Clinical picture
The incubation period ranges from 6 to 13 days. A prodromal period is possible (weakness, weakness, catarrhal inflammation of the upper respiratory tract), after which the body temperature suddenly rises to 39-40 °C and within a few hours a pronounced meningeal syndrome develops with severe headache, repeated vomiting and (often) confusion.
A visceral or influenza-like phase of infection is characteristic, preceding the development of meningitis. The temperature curve has two waves, the beginning of the second wave coincides with the appearance of meningeal symptoms.
Sometimes stagnant changes in the fundus are detected. In the first days of the disease, transient paresis of the eye and facial muscles is possible. The cerebrospinal fluid is transparent, the pressure is significantly increased, pleocytosis is within several hundred cells in 1 μl, usually mixed (lymphocytes predominate), later lymphocytic. The content of protein, glucose and chlorides in the liquor is within normal limits.
Diagnostics
Etiological diagnosis is carried out by isolating the virus, as well as using the neutralization reaction and the complement fixation reaction. Differential diagnosis is carried out with tuberculous meningitis, as well as with other acute meningitis caused by influenza viruses, mumps, tick-borne encephalitis, polio, Coxsackie, ECHO, herpes (Table 31-4).
Table 31-4. Differential diagnostic criteria for serous meningitis in children
Treatment
Specific therapy for viral serous meningitis is aimed directly at the virion, which is in the stage of active reproduction and lacks a protective shell.
The principles of therapy for serous meningitis, aimed at preventing or limiting the formation of irreversible cerebral disorders, are as follows: protective regime, use of etiotropic drugs, reduction intracranial pressure, improving blood supply to the brain, normalizing brain metabolism.
Patients with meningitis should be on bed rest until complete recovery (until the cerebrospinal fluid is completely normalized), despite normal body temperature and the disappearance of pathological symptoms. Tiloron (a drug that has a direct antiviral effect on DNA and RNA viruses, 0.06-0.125 g once a day for 5 days, then every other day for up to 14 days), and recombinant interferons are used as etiotropic therapy. In severe cases, when vital functions are threatened, immunoglobulins are prescribed intravenously.
It is advisable to use antibiotics for serous viral meningitis only if bacterial complications develop. in the treatment complex viral meningitis A protective regime for 3-5 weeks is required. If necessary, detoxification and symptomatic therapy. For intracranial hypertension (increased cerebrospinal fluid pressure >15 mm Hg), dehydration (furosemide, glycerol, acetazolamide) is used.
A unloading lumbar puncture is performed with slow removal of 5-8 ml of cerebrospinal fluid. In severe cases (complications of meningitis or encephalitis with cerebral edema), mannitol is used. The use of sodium polydihydroxyphenylene thiosulfonate (0.25 g 3 times a day for 2-4 weeks), an antioxidant and antihypoxant of the third generation, is highly effective. Due to the fact that sodium polydihydroxyphenylene thiosulfonate also stimulates the antiviral activity of monocytes and inhibits the process of primary fixation of the virus on the cell membrane, its early and combined use with antiviral drugs(tilorone) contributes not only to the rapid relief of inflammatory changes in the cerebrospinal fluid, but also prevents the formation of residual manifestations. It is mandatory for serous meningitis to use drugs that improve neurometabolism: nootropics [pyritinol, gamma-hydroxybutyric acid (calcium salt), choline alfoscerate, hopantenic acid, etc.] in combination with vitamins. In the acute period, intravenous administration of ethylmethylhydroxypyridine succinate 0.2 ml/kg per day for children and 4-6 ml/day for adults is possible.
In the presence of focal symptoms, among neurometabolic drugs, preference should be given to the central cholinomimetic choline alfoscerate (prescribed at a dose of 1 ml/5 kg of body weight intravenously, 5-7 infusions, then orally at a dose of 50 mg/kg per day for up to 1 month).
After acute period serous meningitis or in the presence of residual manifestations, a course of treatment with polypeptides of the cerebral cortex of cattle is carried out at a dose of 10 mg/day intramuscularly, 10-20 injections 2 times a year, etc.
Prevention
Anti-epidemic measures are carried out in accordance with the characteristics of the etiology and epidemiology of meningitis. In the event of acute lymphocytic choriomeningitis, the main attention is paid to the control of rodents in residential and office premises; in case of meningitis of other etiologies - increasing the nonspecific resistance of the body, as well as specific prevention.
Serous meningitis caused by neurotropic viruses. To date, solid data have been accumulated on the viral origin of most serous meningitis. Among the pathogens include enteroviruses (Coxsackie and ECHO), Armstrong virus - the causative agent of acute lymphocytic choriomeningitis, polio virus, etc. With the last two, meningeal forms occur. A certain proportion of serous meningitis is made up of arboviral diseases, endemic to certain regions of the world. Many of these diseases were periodically epidemic in nature, which made it possible to describe their clinical picture in detail.
Enteroviral meningitis Coxsackie and ECHO. Clinically, they are similar in many manifestations. It is not possible to differentiate them in each individual case outside of an epidemic outbreak. The disease begins suddenly after a 2-10-day incubation period with a high rise (up to 38.5-40.5 ° C) temperature, severe headache and vomiting. The duration of fever is 4-7 days, often it has a two-wave, and sometimes three-wave character. The main symptoms of enteroviral meningitis are headache and vomiting, which become more pronounced during the second rise in temperature. During normal temperature patients feel relatively well.
Usually during the second wave fever patients feel worse and MS is more pronounced (S.G. Cheshik). Headache is diffuse in nature, in some patients it is localized in the forehead and temples. Vomiting is repeated and more intense during fever. At the beginning of the disease it may be absent. In addition to MS, there is hyperemia of the face, eyelids, conjunctiva, and injected sclera. Often on the 2-6th day of illness, especially with ECHO infection, a rash appears from polymorphic to maculopapular with uncertain localization. The rashes do not last long - from several hours to 2-3 days, they disappear without a trace. Severe muscle pain is possible, especially in the abdominal muscles, mainly in the epigastric region.
Marked muffling of heart sounds, bradycardia, hypotension. Sometimes the liver and spleen are enlarged. At the beginning of the disease, before the development of MS, patients note loose stools and even diarrhea for several days. In serous meningitis caused by Coxsackie viruses, MS may precede myalgia. Later myocarditis may occur. In general, MS with enteroviral meningitis is unstable and has varying degrees of severity. Sometimes only the rigidity of the neck muscles is determined in the absence or mild severity of the Kernig sign and other meningeal symptoms. CSF is clear and colorless and flows out under pressure. Lymphocytic pleocytosis is determined, the protein level is slightly elevated or normal, the sugar and chloride content is within normal limits.
Serous meningitis due to Coxsackie infection can be combined with herpangina, epidemic myalgia (Bornholm disease), and with ECHO infection is often accompanied by exanthema.
Serous lymphocytic choriomeningitis(Armstrong's disease), like enteroviral meningitis, occurs with damage to the meninges and choroid plexuses of the brain, characterized morphologically by lymphocytic infiltration. The disease is associated with an increase in the number and migration of rodents. Approximate incubation periods range from 5-7 to 12 days. The disease with the development of meningitis begins suddenly in the midst of full health, or MS appears with the onset of the second wave of fever.
U sick severe headache, repeated vomiting and general weakness are noted. The headache is diffuse, painful or localized in the forehead and temples, accompanied by dizziness, pain when moving the eyeballs, and photophobia. MS tends to worsen over several days. Patients are lethargic, sleep poorly, and have decreased appetite. The pulse often lags behind the temperature. Dry wheezing in the lungs. The liver and spleen may be enlarged, and constipation may occur. CSF is clear or opalescent. Lymphocytic pleocytosis (in 90%) from several to 2 thousand cells; protein content is increased or normal. In the blood, leukopenia is more common, ROE is normal or slightly accelerated. The disease lasts from several days to 2 months. CSF returns to normal after clinical recovery, and pleocytosis persists for several days and even months. The course of the disease is accompanied by periods of exacerbation.
Lymphocytic choriomeningitis(LHM) - viral infection, transmitted to humans from rodents and accompanied by predominant damage to the meninges and choroid plexuses of the central nervous system.
It was identified as an independent nosological unit by Armstrong (S. Armstrong) and Lillie (R. D. Lillie) in 1933. In the structure of pathogens of neuroinfections, it accounts for about 10% [E. P. Dekonenko et al., 1986].
Etiology. The causative agent of LCM belongs to the arenavirus family (Arenaviridae). The spherical virions have a diameter from 110 to 130 nm, and are surrounded on the outside by closely adjacent villi 10 nm long. Inside the virions there are ribosome-like formations with a diameter of 20-25 nm, numbering from 10 to 16. The virus is sensitive to the action of detergents, ether, merthiolate, low values pH and divalent cations. Virions contain single-stranded RNA consisting of two components. Virions contain three major proteins. The virus reproduces in most cell cultures tested, in chicken embryos, and macrophage cultures. Has a cytopathic effect.
Epidemiology. The main reservoir of the virus is gray house mice, which excrete the pathogen in nasal mucus, urine and feces. Human infection usually occurs due to consumption of food contaminated by mice. Infection through the respiratory tract and also transplacentally is possible. The disease is often sporadic, but epidemic outbreaks have also been described. The highest incidence occurs in the cold season, although individual cases are also registered in the summer. The FCM virus is distributed almost everywhere.
Pathogenesis. Once a virus enters the human body, it spreads hematogenously, penetrating the blood-brain barrier. The virus causes inflammatory process in membranes with exudation of lymphoid elements, as a result of which mainly lymphocytes appear in the cerebrospinal fluid. The inflammatory reaction of the membranes leads to increased production of cerebrospinal fluid, which, in turn, causes an increase in intracranial pressure and a number of symptoms associated with it. In some fatal cases, inflammatory phenomena were observed in the membrane, in the ependyma and choroid plexuses of the brain, characterized by lymphocytic infiltration. The changes are especially pronounced at the base of the brain. Vessels of the medulla, cortex and brainstem, especially bulbar department, hyperemic to stasis, perivascular spaces are dilated; cellular elements are in a state of tirolysis. Inflammatory phenomena are also detected in the lungs, liver and kidneys.
It has been proven that reassortants of various strains of the virus, as a result of infection of newborn mice with them, cause the development of a slowly progressive disease characterized by growth retardation and death of animals, while parental strains and reciprocal reassortants do not cause such diseases. It is possible that the features of the pathogenesis of this disease are associated with the induction of interferon with a simultaneous pronounced increase in virus titers and subsequent liver necrosis.
In case of intrauterine infection of the fetus with the LCM virus, the pathogenesis of the slow form of the infectious process has not yet been sufficiently studied. It is only known that in this case the disease is characterized by meningoencephalitis, ependymatitis, plexitis, fusion of the meninges, fusion of the liquor ducts (hydrocephalus), pronounced lymphocellular infiltration and exceptionally high titers of antiviral antibodies in the cerebrospinal fluid, which may indicate the possibility of antibody synthesis in the central nervous system. Sometimes there is a picture of a slowly progressing proliferative process in the area of the choroid plexus, subependyma, along the Sylvian aqueduct. In all cases, phenomena of encephalovasculitis and perivascular round cell infiltrates, as well as degenerative changes, are detected.
Symptoms and course. The disease can occur with different degree of severity, ranging from an asymptomatic form to rare cases of systemic disease resulting in death.
In the acute form of LCM incubation period ranges from 6 to 13 days. A prodromal period is possible (weakness, weakness, catarrh of the upper respiratory tract), after which the body temperature suddenly rises to 39-40°C, and within a few hours a pronounced meningeal syndrome develops with severe headaches, repeated vomiting and often confusion. Pulse and breathing are increased, but as development progresses neurological symptoms tachycardia gives way to bradycardia. Among the neurological disorders, the most common are meningeal signs in the form of Kernig and Brudzinski symptoms, as well as stiff neck. The duration of existence of meningeal signs is on average 14 days. Objectively, mild disturbances of cranial innervation, mainly oculomotor, are also noted: sluggish reaction of the pupils to light, horizontal nystagmus, insufficiency of the abducens nerves, exophthalmos, weakness of convergence. Possible mild paresis facial nerve according to the central type, mild cerebellar disorders in the form of unsteadiness of gait, instability in the Romberg position, intention tremor. These deviations are temporary and usually smooth out after 3-4 weeks. Pathological reflexes (Babinsky, Rossolimo, Gordon, Oppenheim, etc.) can be expressed with varying intensity; they sometimes appear together, sometimes in isolation. Changes in the fundus (congestive atrophic pale nipple) are very characteristic. Swelling of the nipples optic nerves appears already in the first days of the disease, but as recovery progresses, there is a tendency for congestion in the fundus to reverse.
Stagnant changes in the fundus indicate acute hypersecretory dropsy of the brain. In the first days of the disease, transient paresis of the eye and facial muscles is often observed.
Leukopenia is usually detected in the blood, although we cannot exclude slight leukocytosis and an increase in ESR. The cerebrospinal fluid is clear, the pressure is significantly increased. In the first days of the disease, pleocytosis is often observed within several hundred cells in 1 μl, usually mixed (70% lymphocytes, 30% neutrophils), later lymphocytic. The protein, sugar, and chloride content of the cerebrospinal fluid usually remains normal, although a slight increase in protein content and a decrease in sugar levels may occur.
Electrophysiological studies (electro-, echoencephalography) indicate mildly expressed diffuse changes bioelectrical activity involving the midline formations of the brain and hypertensive-hydrocephalic phenomena. In some cases, “finger impressions” may be noted on radiographs of the skull.
The course of meningitis is usually favorable. Improvement in the condition and sanitization of the cerebrospinal fluid is observed in the 3-4th week. The average duration of inpatient treatment is 30-35 days. By discharge, residual asthenovegetative effects may persist.
Detailed clinical and virological studies of patients with LCM conducted by A. G. Panov, A. I. Shvarev and P. I. Remezov showed that influenza-like forms, syndromes of encephalitis, encephalomyelitis, polyradiculoneuritis and visceral manifestations of infection are not uncommon. The visceral and influenza-like phase of infection preceding the development of meningitis is very characteristic. The temperature curve has a two-wave character; the onset of the second wave coincides with the appearance of meningeal symptoms.
The slow form of LCM is also characterized by an acute onset, high temperature, development of meningeal syndrome. Following the development acute stage The disease may experience a visible improvement with increasingly pronounced weakness, dizziness, development of ataxia, and fatigue. This is accompanied by headaches, weakening of memory, mental depression, and changes in character. Signs of damage to the cranial nerves appear. Sometimes such a disease lasts several (up to 10) years, is accompanied by the development of paresis and paralysis of the limbs and ends in death.
In congenital LCM, the slowly progressive process is characterized by hydrocephalus, which can be detected already at birth, although in about half of cases hydrocephalus develops in the 1st to 9th week after birth. At the height of the development of the disease, children react little to the environment, almost do not come into contact, lie in a forced position with their arms brought to the body with clenched fists, legs extended and crossed. Sometimes, in the absence of obvious signs of hydrocephalus, signs of chorioretinitis or infantile cerebral palsy However, in such cases latent internal hydrocephalus may be observed. In rare cases, microcephaly occurs. In approximately 80%, hydrocephalus syndrome is combined with chorioretinitis. Death can occur in the 2-3rd year of life.
Complications at acute forms LCM, as a rule, are not observed.
Diagnosis and differential diagnosis. Clinically, the diagnosis of LCM is established based on the following: characteristic features: acute onset of the disease with increased body temperature (more than 1/3 of patients have a two-wave fever), headache, vomiting, as well as moderate inflammation in the upper respiratory tract, meningeal signs, lymphocytic nature of pleocytosis in the cerebrospinal fluid, a slight increase in protein content and a decrease in sugar levels (with meningeal forms), often congestion in the fundus, a benign course of the disease and, as a rule, the absence of residual effects. Etiological diagnosis is carried out by isolating the virus, as well as detecting antibodies to it in neutralization reactions and complement fixation.
