Meningococcal meningitis is a form of meningococcal infection characterized by purulent inflammation of the soft and arachnoid membranes of the brain. The disease is accompanied by a typical triad of clinical signs (headache, fever and vomiting), meningeal signs, general cerebral and general toxic symptoms. Meningitis can be combined with meningococcemia, complicated by infectious and toxic shock, adrenal insufficiency, encephalitis. Methods of laboratory identification of the pathogen play a crucial role in the diagnosis. The basis of treatment is antibacterial and pathogenetic therapy.
ICD 10
A39.0 Meningococcal meningitis
General information
80% of primary bacterial meningitis is meningococcal in nature. In the form of sporadic cases or small outbreaks, pathology is registered everywhere. The greatest prevalence is observed in Africa and Asia – only in the “meningitis belt” (from Senegal to Ethiopia), about 30,000 cases are detected annually. In Western countries, residents suffer with a frequency of 0.9-1.5 cases per 100 thousand population, global statistics indicate 0.5 million affected. The peak incidence usually occurs in the winter-spring period. Meningitis can develop at any age, but most cases are diagnosed in children and adolescents (80%), young people – without significant gender differences.
Causes
The etiological factor of meningococcal meningitis is meningococcus – Neisseria meningitidis. It is a paired spherical gram-negative bacterium (diplococcus) surrounded by a capsule with cilia. The pathogen has low resistance to environmental factors, quickly dies under the influence of ultraviolet rays, high and low temperatures. Meningococci are aerobic, sensitive to pH, disinfectants.
The microbe has a complex antigenic structure. There are 13 serogroups of N. meningitidis, differing in the composition of a specific capsule polysaccharide. The most common strains of groups A, B, C, have recently registered an increase in the frequency of detection of bacteria with Y and W-135 antigens. The pathogen is characterized by high variability: it undergoes L-transformation with the loss of the capsule, shows heteromorphic growth, acquires resistance to chemotherapy drugs.
The main factor in the pathogenicity of meningococcus is considered to be endotoxin – a lipooligosaccharide complex released during the destruction of a microbial cell. The pathogen is able to produce a number of other damaging substances (hemolysin, proteases, hyaluronidase), penetrate the blood-brain barrier. Fixation to the nasopharyngeal epithelium occurs due to the cilia, and the capsule protects the bacterium from the mechanisms of phagocytosis.
The predisposition to the development of meningococcal meningitis is formed in conditions of a decrease in local and general resistance of the body. Risk factors are recognized as congenital complement deficiency, HIV infection, anatomical or functional asplenia. The mucous membrane of the nasopharynx is damaged by smoking and ARVI, which increases the risk of bacterial invasion. The spread of infection is facilitated by the large crowding of the population.
Pathogenesis
Transmission of the pathogen occurs by airborne droplets from patients with meningococcal infection or asymptomatic carriers. The entrance gate becomes the nasopharyngeal mucosa, where the primary inflammatory process develops. In 10-20% of cases, microbes, overcoming protective mechanisms, penetrate into the bloodstream, where they multiply, initiating a short-term bacteremic phase. In the subarachnoid spaces of the brain, neisseries are introduced hematogenically, less often – lymphogenously, perivascularly and perineurally through the plate of the latticed bone.
When meningococcus multiplies, serous-purulent first develops, then purulent inflammation of the soft and spider membranes. The convexital surfaces and the base of the brain are most often affected, sometimes the process spreads in the spinal direction. Macroscopically, the soft shell looks edematous, hyperemic, cloudy, the surface of the brain seems to be covered with a cap of pus. The microscopic picture is represented by pronounced infiltration by polymorphonuclear mononuclear cells. The adhesive process can cause blockage of the cerebrospinal fluid outflow pathways.
Classification
According to the clinical classification of meningococcal infection, meningitis refers to its generalized forms. Taking into account the severity of the pathological process, the infection can occur in mild, moderate, severe or extremely severe forms. Meningitis caused by N. meningitidis is purulent. Clinically , it is represented by the following options:
- Classic. The infectious process has an isolated character, only the soft and spider membranes of the brain are affected.
- Mixed. The picture of meningitis is complemented by signs of inflammation of the medulla (meningoencephalitis), bacteremia (meningococcemia).
- Complicated. It is accompanied by the development of local and systemic complications due to the influence of inflammatory changes or toxins of the pathogen.
By duration, the pathological process can be acute (up to 3 months), prolonged (up to six months), chronic (over 6 months). Depending on the localization of the affected cerebral structures, meningitis is divided into convexital (large hemispheres), basal (lower surface) and spinal. Additionally, there are limited and total forms.
Symptoms
The onset of the disease is usually preceded by nasopharyngitis, but symptoms may occur suddenly, against the background of complete well-being. With great constancy, the so–called meningeal triad is found in the clinical picture – headaches, fever, vomiting. The temperature rises sharply to 40-42 ° C, accompanied by severe chills. Excruciating headaches are diffuse, oppressive, bursting or pulsating, localized mainly in the frontal-parietal region, amplified at night, with a change in the position of the head, the action of external stimuli.
Vomiting with meningococcal meningitis occurs without prior nausea, “fountain”, does not bring relief. The clinical picture is complemented by skin hyperesthesia, increased sensitivity to sound, light and pain stimuli, odors. Sometimes, in the first hours of the disease, tonic-clonic convulsions occur. An important place in the structure of general cerebral symptoms is occupied by psychomotor agitation and increasing disorders of consciousness – from stunning to coma.
Among the objective symptoms, meningeal signs come out in the first place, which appear at the very beginning of the disease and progress rapidly. The most constant are the rigidity of the occipital muscles, the symptoms of Kernig and Brudzinsky (upper, middle, lower). In children, a sign of Lesage, swelling and pulsation of the fontanel are noted. The patient takes a forced pose – lying on his side with his head thrown back and knees pulled up to his stomach. The severity of meningeal syndrome may not correspond to the severity of the pathology.
Neurological examination often reveals asymmetry of tendon and skin reflexes, weakening as intoxication increases, pathological stop signs. Basal meningitis is accompanied by damage to cranial nerves, especially III, IV, VII, VIII pairs. The presence of persistent red dermographism indicates concomitant vegetative disorders. Signs of intoxication are first tachycardia, and then relative bradycardia, hypotension, muffled heart tones. Patients are breathing faster, the tongue is covered with a dirty brown coating, dry.
Complications
An extremely unfavorable option is a lightning-fast course of the disease with edema-swelling of the brain. The situation threatens the insertion of stem structures into the large occipital foramen of the skull, which leads to a violation of vital functions. Slow resolution of purulent inflammation is dangerous with the development of hydrocephalus, cerebral hypotension and subdural effusion may occur in young children.
The result of severe or combined forms of meningococcal meningitis are infectious and toxic shock, acute adrenal insufficiency. With delayed or inadequate treatment, the purulent process passes to the ventricular ependyma and medulla, complicated by ventriculitis (ependymatitis), encephalitis. At a later date, there is a risk of deafness, epilepsy, and delayed psychomotor development in children.
Diagnostics
It is possible to establish the origin of meningococcal meningitis on the basis of clinical data when it is combined with bacteremia. The probable etiology of isolated forms of the disease is indirectly indicated by epidemiological and anamnestic information (the presence of nasopharyngitis, contact with the patient). Accurate verification of pathology is provided by laboratory and instrumental methods:
- Clinical tests. The hemogram shows pronounced leukocytosis with a shift of the formula to the left, aneosinophilia, acceleration of ESR. Polymorphonuclear pleocytosis, a decrease in glucose concentration, and an increase in protein are noted in the cerebrospinal fluid. Changes in the urine analysis are nonspecific, indicate toxic phenomena.
- Bacterioscopy and seeding. Meningococci are detected in neutrophils by direct bacterioscopy of Gram-stained smears. Sowing liquor on serum agar or other nutrient media makes it possible to clarify the cultural, enzymatic, antigenic properties of the pathogen, to determine its sensitivity to antibiotics.
- Serological tests. After the meningococcus is isolated, it can be identified by serogroups when an agglutination reaction is set up. To detect antibodies in the blood, RNGA is used, express diagnostics is carried out using ELISA, methods of counter immunoelectrophoresis.
- Molecular genetic analysis. In addition to standard procedures, PCR is used to detect bacterial DNA. This is a fast and sensitive diagnostic test. It acquires special value when it is impossible to isolate the pathogen from the cerebrospinal fluid or blood.
- Neuroimaging. Indications for cerebral tomography may be impaired consciousness, focal neurological symptoms. CT scan of the brain confirms cerebrospinal hypertension, intracerebral hemorrhages, cerebral edema. MRI with contrast is preferable, since it better visualizes the meningeal membrane, the subarachnoid space.
As an additional study in convulsions, an EEG is prescribed to record the bioelectric activity of the brain. Assistance in the diagnostic search is provided by an ophthalmologist (examination of the fundus), an infectious disease specialist. The disease must be differentiated with meningitis of a different etiology, epidural abscess, subdural empyema. Encephalitis, acute disseminated encephalomyelitis, subarachnoid hematoma should be excluded.
Treatment
Any form of generalized infection is associated with a high risk of death and severe complications. Therefore, meningococcal meningitis should be considered as an urgent condition requiring urgent hospitalization in a specialized hospital. Usually, patients immediately enter the intensive care unit under the round-the-clock supervision of specialists. They are shown strict bed rest. The basis of treatment is pharmacotherapy:
- Etiotropic. The central place is given to antibiotic therapy with penicillin (benzylpenicillin, ampicillin) or cephalosporin drugs (ceftriaxone, cefotaxime). Alternative medications are carbapenems, chloramphenicol. First, empirical therapy is prescribed, which is then adjusted taking into account antibiotic sensitivity data.
- Pathogenetic. Glucocorticoids, osmotic and loop diuretics (mannitol, furosemide) are used to relieve cerebral edema. Hemodynamic instability and toxicosis require infusion support (crystalloids, colloids, plasma), the introduction of vasopressors, oxygen therapy. In severe cases, extracorporeal detoxification is performed.
- Symptomatic. In the complex treatment of meningococcal meningitis, symptomatic drugs are used. Anticonvulsants (diazepam, sodium oxybutyrate) are indicated for convulsive activity. High fever is stopped with antipyretics.
Discharge from the hospital is carried out with full clinical recovery. All patients who have suffered meningococcal meningitis should be under the medical supervision of a neurologist with regular examination. The consequences and residual effects are eliminated by complex rehabilitation, which includes physiotherapy, therapeutic gymnastics, cognitive correction.
Prognosis and prevention
With timely specific therapy of meningococcal meningitis, the prognosis is relatively favorable, combined and complicated forms significantly worsen the outcome. Generalized infection is always associated with the risk of life–threatening conditions – even against the background of treatment, the mortality rate is 10-15%. Focal neurological symptoms, impaired consciousness, laboratory shifts (anemia, thrombocytopenia, leukopenia) are considered poor prognostic factors.
Prevention implies an impact on all links of the epidemic process. In relation to the source of infection, early detection, isolation and treatment of patients, rehabilitation of carriers are carried out. Sanitary and hygienic measures, disinfection in the hearth help to break the transmission mechanisms. To create specific immunity in susceptible individuals, vaccination against meningococcal infection is recommended. Hardening, timely therapy of respiratory diseases contributes to the increase of nonspecific resistance.
