MENINGEAL SYNDROME
http://www.nlm.nih.gov/medlineplus/meningococcalinfections.html
Definition
Meningococcal infection nis an acute infectious disease of the nhuman, caused by meningococcous Neisseria Meningitigis. nThe mechanism of the transmission of nthe infection is air-drop. The disease is ncharacterized by damage of nmucous membrane of nasopharynx (nasopharingitis), ngeneralization of the process in form of nspecific septicemia (meningococcemia) and inflammation nof the soft cerebral membranes (meningitis).
History and geographical distribution
Epidemic ncerebrospinal meningitis (one of the most nclinically expressive forms of the disease) nwas known else in profound antiquity. The ndescription of outbreaks of this infection nis contained in reports of Areteus (III ncentury of our era), Egynsky (VII century).
Meningococcal ninfection occurs on the all continents. It nis serious problem for public health. It nis registered in 170 countries of the nworld.
Etiology
The ncausative agent is Neisseria meningitidis. It is small gramm-negative ndiplococcus, aerobic, catalise and oxidase-positive, not-motile and possess a npolysaccharide capsule, which is the main antigen and determines the serotype nof the species. Meningococcus may be seen inside and outside of neutrophills. nThe main serogroups of pathogenic organisms are A, B, C, D, and W135, X, Y, Z nand L. The bacterial membrane is a lipopolysaccaride.
Meningococci nare very exacting to composition of nutritive mediums. Its nreproduction may be only in presence nof human’s protein or animal’s nprotein. Due to destruction of the nmicrobe’s cell endotoxin is delivered (of nlipopolysaccharide origin). Exotoxin is no produced. The nagent of meningococcal infection is ncharacterized by low resistance in the nenvironment. Meningococci perish during temperature n50°C through 5 minutes, during temperature
Epidemiology
Meningococcal ninfection is typical anthroponosis. The sourses nof infection are healthy carriers of nmeningococcus, the patients with meningococcal nasopharingitis nand the patients with generalized forms of nthe disease.
The npatients with generalized form are more ndangerous. It is proved that they are ndangerous for surrounding persons in 6 ntimes than healthy carriers. However, the main nsources of the infection are carriers, nbecause 1200-1800 (according other data – 50000) ncarriers have occasion to one patients nwith generalized form of the disease.
The nmechanism of transmission of the infection is air-drop. nThe infection is realized during cough, sneezing. nIn this the narrow contact and nsufficient exposition are necessary. It is nproved by A.A. Favorova (1976) that the infection nis realized on the distance less 0,5 nmeter.
In nmeningococcal infection one of an important ncharacteristic of epidemic process is nperiodical rise and fall of the morbidity. nThe duration of the period with high nmorbidity is different. It may be 5-10 nyears and more. Then the period of nthe fall of the morbidity becomes. It nis continued from 5 till 20 years.
In nmeningococcal infection epidemic process is ncharacterized by seasonal spread. It is nmanifested especially during epidemics. The morbidity nmay compose 60-70% from year’s nmorbidity during seasonal rise. The onset nof the seasonal rise is in quanuary nin the countries with temperate clinimate. It nachieves of maximum in march – april.
nThe age of carriers of meningococcal ninfection is different from the age nof the patient. The larger part of ncarriers is reveled among adults. The nportion of the children is a little. nThe morbidity is higher in the towns then nrural locality.
The nconsiderable outbreaks of the diseases were ndescribed in the educational establishments nof the closed type and especially namong military (as at peaceful time such nas during war).
Pathogenesis
In nmeningococcal infection entrance gates are nmucous membrane of nasopharynx. It is place nof primary localization of the agent. nFurther meningococci may persist in nepithelium of nasopharynx in majority of nthe cases. It is manifested by asymptomatic nhealthy carriers. In some cases meningococci nmay cause inflammation of mucous membrane nof upper respiratory tract. It leads to ndevelopment of nasopharingitis.
Meningococci n are able to break local barriers nwith help of factors of spread (hyaluronidase). nCapsule protects meningococci from phagocytosis. nHematogenous way is the principal way nof the spread of the agent in nthe organism (bacteremia, toxinemia). Only the agent nwith high virulence and invasive strains nmay penetrate through hematoencephalitic barrier. nThe strains of serogroup A high invasivicity.
Meningococci npenetrate into the blood after break nof protective barriers of mucous membrane nof upper respiratory tract. There is hematogenous ndissemination (meningococcemia). It is accompanied by nmassive destruction of the agents with nliberation of endotoxin. Meningococcemia and ntoxinemia lead to damage of endothelium nof the vessels. Hemorrhages are observed in nmucous membrane, skin and parenchymatous organs. nIt may be septic course of nmeningococcemia with formation of the secondary metastatic focuses in the nendocardium, joints, internal mediums of the eyes.
Thus the nmeningococci enter into subarachnoid space, multiply and course nserous-purulent and purulent inflammation of the soft cerebral coverings. The ninflammatory process is localized on the surface of the large craniocerebral nhemispheres, and rarely, on the basis, but sometimes it may spread nin the covering of the spinal cord. During severe duration of the ninflammatory process the cranium is covered by purulent mather (so-cold n“purulent cap”). It may lead to ninvolvement of the brain’s matter ninto inflammatory process and meningoencephalitis.
The nprocess may engulf the rootlets of – VII, VIII, V, VI, III and XII pairs nof cranial nerves.
Pathogenic nproperties of the agent, state of macroorganism, nstate of immune system, functional state of nhematoencephalitic barrier have the meaning in nthe appearance of meningitis of any netiology.
The nnext stages may single out in npathogenesis of purulent meningitis:
1. nPenetration of the agent through hematoencephalic nbarrier, irritation of receptors of soft ncerebral membrane of the brain and systems, nforming cerebrospinal fluid.
2. nHypersecretion of cerebrospinal fluid.
3. nDisorder of circulation of the blood nin the vessels of the brain and nbrain’s membranes, delay of resorbtion of ncerebrospinal fluid.
4. nSwelling-edema of the brain hyperirritation nof the brain’s membranes and radices nof cerebrospinal nerves.
In the npathogenesis of meningococcal infection toxic and allergic components play aimportant role. Thus, in fulminate forms of nmeningococcal infection infectious-toxic shock ndevelops due to massive destruction of nmeningococcus and liberaton of considerable quantity nof endotoxin. In infectious-toxic shock the ndevelopment of thrombosis, hemorrhages, necrosis in ndifferent organs are observed even in nthe adrenal glands (Waterhause – Fridrechsen syndrome).
Meningococcous nmeningitis is characterized by serous or purulent inflammation of pia mater.
Clinical manifestation
The nincubation period is 1-10 days, more frequently 5-7 days.
Classificatioof the clinical forms of meningococcal infection:
I. nPrimarily localized forms:
a) nmeningococcal carrier state
b) acute nnasopharyngitis;
c) npneumonia.
II. nGematogenously generalized forms:
a) meningococcemia: ntypical acute meningococcal sepsis; chronic;
b) nmeningitis; meningoencephalitis;
c) mixed nforms (meningococcemia + meningitis, meningoencephalitis).
d) rare nforms (endocarditis, arthritis, iridocyclitis).
Imeningococcal carriers the clinical manifestations are absent.
Meningococcal nasopharingitis
The most ncommon complains of the a patients are headache, mainly in the frontal-parietal nregion, sore throat, dry cough, blocked nose, fatigue, weakness, loss of nappetite, violation of the sleep. In most of the patients nbody temperature rises upto subfebrile and lasts for not more than 3-7 days, nsometimes 5-7 days. The skin is pale, conjunctival vessels and sclera are ninjected. There are hyperemia and edema of the mucous membrane of nthe nose. In many patients the posterior wall of the pharynx seem to be covered nby mucous or mucous – purulent exudation.
Inflammatory nchanges in the nasopharynx can be noticed after 5-7 days, hyperplasion of lymphoid nfollicles lasts longer (till 14-16 days). In the peripheral blood temperate nleukocytosis with neutrophylosis and a shift of leukocytaric formula to the nleft, increase in ERS may be revealed. Nasopharyngitis nprecedes to development of generalized nforms of the disease.
Meningitis
It nmay start after meningococcal nasopharyngitis, nbut sometimes primary symptoms of the ndisease arise suddenly. In meningitis three symptoms nare revealed constantly: fever, headache and vomiting. Temperature nis increases quickly with chill and nmay reach 40-41°C during few hours. nIntermittent, remittent, constant, double waved types nof the temperature occur in meningitis. The npatients suffer from severe headache, having ndiffuse or pulsatory character. Headache is nvery intensive at the night. It increases ndue to change of body position, sharp nsounds, bright light. Vomiting arises without nprecedent nausea. There is no connection nwith food and relief after vomiting. It nis rule abundant, by “fountain”, repeated. Sometimes, nvomiting arises on the peak of headache.
In nmeningitis hyperthermia, hyperkynesia, photophobia, hyperalgesia, nhyperosmia are noticed. These symptoms are nrevealed more frequently in children. The nsevere convulsions arise in the many npatients at the first hours of the ndisease (clonic, tonic or mixed types). In small nchildren meningococcal meningitis may start nwith convulsions.
The ndisorders of consciousness occupy the ngreat place in clinical picture (from sopor ntill coma). The loss of consciousness develops nafter psychomotoric excitement. The loss of nconsciousness at the first hours of nthe disease is unfavorable sign.
During nobjective examination meningeal symptoms stand nat the first place. It is described nnear 30 meningeal signs. A few meningeal nsigns are used in practice: rigidity of noccipital muscles, Kernig’s symptom, Brudzinsky’s nsymptom (upper, middle and lower). The estimate nof state of fontanelle is very nimportant in infants. There are three nsymptoms of meningitis in infant: swelling, tensio and absence of fontanelles pulsation.
There nis no accordance between expression of nmeningeal syndrome and severity of the disease. nThe expression of different symptoms is no nsimilar at the same patient. The patient nhas compulsory pose during serious cases. nHe lays on side with deflection of nthe head backwards. The legs are curved nin knee-joint and pelvic-femoral joint. The nlegs are pulled to abdomen. Asymmetry and nincreased tendinous, periostal and dermal nreflexes are observed in the patients. nThese reflexes may be decreased during nexpressive intoxication. Pathological reflexes may be nrevealed (such as Babinski’s, Hordon’s, nRossolimo’s reflexes, foot’s clones), and also nsymptoms of damage cranial nervous (more nfrequently III, VI, VII, VIII pairs).
Fulminate course of meningitis
With nsyndrome of brain’s swelling and nedema is the most unfavorable variant. nThere is hypertoxicosis during this form nand high percentage of mortality. The main nsymptoms are consequence of inclination of nthe brain in to foramen magnum and nstrangulation of medulla oblongata by ntonsils of cerebellum. Immitant symptoms from ncardiovascular and respiratory systems develop nquickly. Bradycardia appears. Then it is changed nby tachycardia. Arterial pressure may fall ncatastrophically, but it increases more nfrequently till high level. Tachypnoea arises n(till 40-60 times/min) with help of naxillary muscles. The disorders of breath nlead to its sudden interruption. These symptoms ndevelop in hyperthermia, clonic cramps and loss nof consciousness. Cyanosis of the skin, hyperemia nof the face are marked. Pyramidal signs, nsometimes symptoms of damage of cranial nnerves, decreased corneal reflexes contraction of npupils and its decreased reaction on nlight are determined. Death occurs due nto respiratory failure at the first nhours of the disease, rarely on 2-3 nday or on 5-7 day.
Meningitis nwith syndrome of cerebral hypotension
It nis rare variant of the course of nmeningococcal meningitis. It is observed nprincipally in children.
Meningitis nwith syndrome of ependimatitis (ventriculitis)
Now nit is rare form of meningitis. This nform develops during late or insufficient ntreatment of the patients. Especial severity nof the disease is connected with nspread of inflammation on ventricles membranes n(ependime) and involvement of brain’s nsubstance in to pathological process.
Meningoencephalitis
It nis rare form of meningococcal infection. In nthis case the symptoms of encephalitis npredominate, but meningeal syndrome is weakly nexpressed. Meningococcal encephalitis is characterized nby rapid onset and impetuous cramps, nparesises and paralyses. Prognosis is unfavorable. nThe mortality is high and recovery is nincomplete even in modern conditions.
Meningococcemia (meningococcal sepsis)
The ndisease is more impetuous, with symptoms of toxicosis and development of nsecondary metastatic foci. The onset of the disease is an acute. nBody temperature may increase upto 39-41
The nother symptoms of intoxication arise nsimultaneously with fever: headache, decreased appetite nor its absence, general weakness, pains in nthe muscles of the back and limbs. nThirst, gryness in the mouth, pale skin or cyanosis, ntachycardia and sometimes dysphnoea are nmarked. The arterial pressure increases in the nbeginning of the disease. Then it decreases. It nmay be decreased quantity of urine. nDiarrhea may be in some patients. It nis more typical for children.
Dermal nrashes appear through 5-15 hours, sometimes on nthe second day from the onset of nthe disease. In meningococcal infection rash nmay be different over character, size nof rash’s elements and localization. Hemorrhagic nrash is more typical (petechias, ecchymosis and npurpura).
The nelements of the rash have incorrect n(“star-like”) form, dense, coming out over nthe level of the skin. Hemorrhagic nrash is combined inrarely with roseolous nand papulous rash.
The nsevere development of the rash depends nfrom the character, size and depth of nthe its elements. The deep and nextensive hemorrhages may be necrosed. Then nit may be formation of deep ulcers. nSometimes deep necrosis is observed on nthe limbs and also, necrosis of the ear, nnose and fingers of the hands nand legs.
During nbiopsy meningococci are revealed. Exanthema is nleucocytaric-fibrinous thrombosis, contained the agent nof meningococcal infection. Thus, in meningococcal ninfection rash is the secondary metastatic nfoci of the infection.
In nthe peripheral blood high leukocytosis, nneuthrophillosis with shift of the formula n to the left aneosinophyllia, nincreased ESR are observed. Thrombocytopenia ndevelops inrarely.
There nare alterations in urine as during nsyndrome of “infectious-toxic kidneys”. nProteinuria, microhematuria, cylinderuria are marked.
Meningococcal nsepsis is combined with meningitis in majority cases. In 4-10 % nof the patients meningococcemia may be nwithout damage of the soft cerebral ncovering. Frequency of meningococcal sepsis is nusually higher in the period of epidemic.
Fulminate nmeningococcemia ( acutest meningococcal sepsis, Waterhause-Friedrichesyndrome)
It is nthe more severe, unfavorable form of meningococcal infection. nIts base is infectious-toxic shock. Fulminate sepsis is ncharacterized by acute sudden beginning and impetuous course. nTemperature of body rises up to 40-41 oC. It is accompanied by chill. nHowever, hypothermia may be observed through some nhours. Hemorrhagic plentiful rash appears at nthe first hours of the disease with ntendency to confluence and formation large nhemorrhages, necroses. A purple-cyanotic spots arise on the skin (“livors nmortalis”). The skin is pale, but with a total cyanosis. Patients nare anxious and excited. The cramps are observed nfrequently, especially in children. The recurrent blood vomiting narise inrarely. Also, a bloody diarrhea may be too. nGradually, a prostration becomes more excessive and it results is a loss of the nconsciousness.
Heat’s nactivity decreases catastrophically. Anuria develops n(shock’s kidney). Hepatolienalic syndrome is nrevealed frequently. Meningeal syndrome is ninconstant.
In nthe peripheral blood hyperleukocytosis (till 60*109/l), nneutrophylosis, sharp shift leukocytaric formula to nthe left, thrombocytopenia, increased ESR (50-70 mm/h) nare reveled. The sharp disorders of nhemostasis are marked – metabolic acidosis, ncoagulopathy of consumption, decrease of nfibrinolitic activity of the blood and nother.
Mixed forms (meningococcemia + meningitis)
These nforms occur in 25-50 % cases of generalized meningococcal infection. In nthe last years there is tendency of increase frequency of mixed forms igeneral structure of the disease, especially in periods of epidemic outbreaks. nIt is characterized by combination of symptoms of meningococcal sepsis and ndamage of cerebral membranes.
Rare nforms of meningococcal infections
These nforms (arthritis, polyarthritis, pneumonia, iridocyclitis) are consequence of nmeningococcemia. Prognosis is favorable in opportune nand sufficient therapy.
Diagnostics
The ndiagnosis of all forms of meningococcal infection is based on the complex of nepidemiological and clinical data. The final diagnosis nis established with help of the nlaboratory examination. Separate methods have different ndiagnostical significance in various clinical forms of meningococcal infections.
The ndiagnosis of meningococcal carrier is possible only by use of bacteriological nmethod. The material for analysis is the mucus from proximal portions of nupper respiratory tract. In diagnostics of meningococcal nasopharyngitis nepidemiological and bacteriological methods occupy the main nplace. Clinical differention of meningococcal nasopharyngitis from nnasopharyngitis of the other genesis is no possible or very difficult.
Irecognition of generalized forms, anamnestical and clinical methods of ndiagnostics have real diagnostic significance, mainly in combination of nmeningococcemia and meningitis.
The nexamination of cerebrospinal fluid (CSF) has ngreat meaning in diagnostics of meningitis. nIn lumbar punction cerebrospinal fluid flows out nunder high pressure and by frequent drops. nThe cerebrospinal fluid may flow out by nrare drops only due to increased nviscosity of purulent exudation or partial nblockade of liquor’s ways. Cerebrospinal fluid nis opalescent in initial stages of nthe disease. Then it is turbid, purulent, nsometimes with greenish shade.
Pleocytosis nachieves till 10-30 103 in 1 mcl. Neuthrophils nleukocytes predominate in cytogram. Neuthrophilous ncompose 60-100% of all cells. In microscopy nneuthrophils cover intirely all fields of nvision, inrarely. Quantity of protein of ncerebrospinal fluid increases (till 0,66-3,0 g/l). nThere is positive Nonne-Appelt’s reaction. The nreaction of Pandy composed (+++). Concentration nof glucose and chlorides are usually ndecreased.
In ngeneralized forms the final diagnosis is nconfirmed by bacteriological method. In ndiagnostics immunological methods are used too. nReactions of hemagglutination, latex agglutination are nmore sensitive.
Differential diagnosis
In nmeningococcemia the presence of rash nrequires of differential diagnostics with nmeasles, scarlet fever, rubella, diseases of the blood n(thrombocytopenic purpura Werlgoff’s disease; nhemorrhagic vasculitis – Sheinlein-Henoch’s ndisease). Sometimes it is necessary nto exclude epidemic typhus, grippe, hemorrhagic fevers.
It nis necessary to differentiate meningococcal nmeningitis with extensive group of the ndiseases:
1. nInfectious and noninfectious diseases with nmeningeal syndrome but without organic ndamage of central nervous system (meningismus). nMeningismus may be in grippe, acute shigellosis, nuremia, lobar pneumonia, toxical food-borne infectious, ntyphoid fever, epidemic typhus, infectious mononucleosis, npielitis, middle otitis.
2. nDiseases with organic damage of central nnervous system, but without meningitis (brain abscess, ntetanus, subarachnoid hemorrhage).
3. nMeningitis of other etiology. In purulent meningitises netiological factors may be pneumococci, staphylococci, nstreptococci, bacterium coli, salmonella, fungi, Haemophilus ninfluenzae. In purulent meningitis nonmeningococcal netiology it is necessary to reveal nprimary purulent focus(pneumonia, purulent processes non the skin, otitis, sinusitis, osteomyelitis).
Treatment
The ntherapeutic tactics depends from the nclinical forms, severity of the course of nthe disease, presence of complications, premordal nstate. In serious and middle serious course nof nasopharyngitis antibacterial remedies are nused. Peroral antibiotics oxacillin, ampyox, chloramphenicol, nerythromycin are used.
The nduration of the therapy is 3-5 days nand more. Sulfonamides of prolonged action nare used in usual dosages. In light nduration of nasopharyngitis the prescription nof antibiotics and sulfonamides is no nobligatory.
In ntherapy of generalized forms of nmeningococcal infection the central place nis occuped by antibiotics, in which salt nbenzil penicillin stands at the first place. Benzyl npenicillin is used in dosage of n200,000-300,000 IU/kg/day. In serious form of meningococcal ninfection daily dosage may be increased nto 500,000 IU/kg/day. Such doses are recommended nparticularly in meningococcal meningoencephalitis. In npresence of ependimatitis or in signs nof consolidation of the puss the dose nof penicillin increases to 800 000 IU/kg/day.
In nsimilar circumstances it is necessary to ninject sodium salt of penicillin by nintravenously in dose 2 000 000-12 000 000 units nin day. Potassium salt of penicillin is no ninjected by intravenously, because it is npossible the development of hyperkalemia. Intramuscular ndose of penicillin is preserved.
Endolumbar ninjection of penicillin is no used npractically last years. Daily dose is injected to nthe patient every 3 hours. In some ncases interval between injections may be nincreased up to 4 hours. The duration nof the therapy by penicillin is ndecided individually depending on clinical and nlaboratory data. The duration of penicicllin therapy nusually 5-8 days.
At nthe last years increased resistant strains nof meningococcus are marked (till 5-35%). Besides nthat, in some cases the injection of nmassive doses of penicillin leads to nunfavorable consequences and complications (endotoxic nshock, hyperkalemia due to using of potassium nsalt of penicillin, necroses in the places nof injections and other). Also, the npatients occur with allergy to penicillin nand severe reactions in anamnesis. In nsuch cases it is necessary to nperform etiotropic therapy with use other nantibiotics. In meningococcal infection semisynthetic npenicillins are very effective. These remedies nare more dependable and preferable for n“start-therapy” of the patients with npurulent meningitis till establishment etiological diagnosis. nIn meningococcal infection ampicillin is nthe best medicine, which is prescribed in ndosage 200-300 mg/kg/day intramuscularly every 4 nhours.
In nthe most serious cases the part of nampicillin is given intravenously. Daily dose nis increased to 400 mg/kg/day. Oxacillin is nused in dose not less than 300 nmg/kg/day every 3 hours. Metycyllin is nprescribed in dose – 200-300 mg/kg every n4 hours. In meningococcal infection nchloramphenicol is highly effective. It is the nmedicine of the choice in fulminate nmeningococcemia. It is shown, that endotoxic nreactions arise more rarely during treatment of nthe patients by chloramphenicol than during ntherapy by penicillin. In cases of meningoencephalitis nchloramphenicol is not prescribed due to nits toxic effects on neurons of brain. nChloramphenicol is used in dose 50-100 nmg/kg 3-4 ties a day. In fulminate nmeningococcemia it is given intravenously nevery 4 hours till stabilization of narterial pressure. Then chloramphenicol is injected nintramuscularly. The duration of the treatment nof the patients by this antibiotic is n6-10 days.
There nare satisfactory results of the treatment nof meningococcal infection by remedies from nthe group of tetracycline. Tetracycline is ninjected in dose 25 mg/kg intramuscularly and nintravenously in the cases of resistant nagents to the other antibiotics.
Pathogenetic ntherapy has exceptional significance in ntherapeutic measures. It is performed nsimultaneously with etiotropic therapy. The basis nof pathogenetic therapy is the struggle nwith toxicosis. Salt solutions, macromolecular colloid nsolutions, plasma, albumin are used. Generally 50-40 ml of fluid is ninjected on
The ntherapy of fulminate meningococcemia includs nthe struggle with shock. Adrenaline and nadrenomimetics are not used due to npossibility of capillary spasm, increased hypoxia of n the brain and kidneys and development nof acute renal failure. The early nhemodialysis is recommended in the case nof acute renal failure due to toxicosis.
The nbasis of the therapy of infectious-toxic shock is complex of measures, nincluding application of antibiotics, improvement of blood circulation. The ncourse of infectious-toxic shock is very serious, with high mortality (50% of nthe patient die during the first 48 hours of the disease). Because, it is nnecessary to prescribe intensive therapy immediately. Antibiotics of wide nspectrum of action are prescribed. Steroid hormones have important meaning ithe treatment of infectious-toxic shock. Hormones decrease general reaction of nthe organism on toxin, positively act on hemodynamics. Treatment by nglucocorticoids is conducted during 3-4 days.
Prophylaxis
Prophylactic nmeasures, directional on the sources of nmeningococcal infection include early revelation nof the patients, sanation of meningococcal ncarriers, isolation and treatment of the npatients. Medical observation is established in nthe focuses of the infection about ncontact persons during 10 days.
The nmeasures against of the transmissive mechanism, nare concluded in performance of sanitary n and hygienic measures and disinfection. It nis necessary to liquidate the congestion, nespecially in the closed establishments n(children’s establishments, barracks’s and nother). The humid cleaning with using of nchlorcontaining disinfectants, frequent ventilation, nultra-violet radiation are performed at the nlodgings.
The nmeasures, directional on receptive contingents, include nincrease nonspecific resistance of the people n(tempering, timely treatment of the diseases of nrespiratory tract, tonsils) and formation of nspecific protection from meningococcal infection. nActive immunization is more perspective nwith help of meningococcal vaccines. There are nseveral vaccines, for example, polysaccharide vaccines nA and C.
Vaccine nfrom meningococcus of the group B was nalso obtained. However, the group B capsular polysaccharide is not nsufficiency immunogenic to produce a reliable antibody response in humans to be neffective, several solutions to this problem are being studied, including the nchemical alterations of the capsular B antigen to make it more immunogenic and nthe search for other cell wall antigens that are capable of neliciting bactericidal antibodies against B meningococci with a minimum of nserious side effects. New vaccines against meningococcus are under development.
