Meningococcus

N. Meningitidis - the causative agent of purulent cerebrospinal meningitis - was first discovered in 1884 by E. Markeiafova and E. Chelly, and was isolated in 1887 by A. Weixelbaum.

Meningococcus is gram-negative globular cells with a diameter of 0.6-0.8 microns. In smears prepared from the material taken from the patient, they are in the form of coffee beans, often located in pairs or tetrads, or randomly, often inside the leukocytes - incomplete phagocytosis. In smears from cultures, meningococci have a regular round shape, but different sizes, are arranged randomly or tetrads, along with gram-negative can be Gram-positive cocci. There is no dispute, they do not have flagella. All meningococci, except group B, form a capsule. The content of G + C in DNA is 50.5 - 51.3 mol%. Meningococcus - strict aerobes, on normal media do not grow. For their growth, it is necessary to add serum, which is optimal for pH growth of 7.2-7.4, and a temperature of 37 ° C, do not grow below 22 ° C. Colonies on dense media are tender, transparent, 2-3 mm in size. Broth is formed by cloudiness and a small precipitate on the bottom.On the surface after 2-3 days a film appears.When sown from patients, meningococci are more often secreted in the S-form, but when cultured on nutrient media they often become R-forms and lose a number of biological properties, including some antigens, which must be taken into account s.

The biochemical activity of meningococci is small. They ferment glucose and maltose to form acid without gas, do not liquefy gelatin, oxidase-positive.

[1], [2], [3], [4], [5], [6], [7], [8],

Antigenic structure of meningococci

In meningococci, four antigenic systems are considered.

Capsular polysaccharide antigens; Depending on their specificity, meningococci are divided into the following groups: A, B, C, Y, X, Z, D, N, 29E, W135, H, I, K, L. Most of the known serogroups determine the chemical composition of specific polysaccharides, for example in serogroup A - N-acetyl-3-O-acetyl-mannose-aminophosphate.

• Protein antigens of the outer membrane. They are divided into 5 classes. Proteins of classes 2 and 3 define 20 serotypes, and class 1 proteins are subtypes.
• Protein antigen, common to the whole species N. Meningitidis.
• Lipopolysaccharide antigens - 8 serotypes.

Accordingly, the antigenic formula of meningococcus has the following form: serogroup: serotype for protein: subtype for protein: serotype for LPS. For example, B: 15: P1: 16 - serogroup B, serotype 15, subtype 16. The study of the antigenic structure is important not only for the differentiation of meningococci, but also for clarifying those antigens that have the greatest immunogenicity.

[9], [10], [11], [12], [13], [14], [15], [16],

Resistance of meningococci

Meningococci is extremely unstable to the action of environmental factors. Quickly die under the influence of direct sunlight, from drying die after several hours, when heated to 80 ° C - after 2 minutes. Conventional chemical disinfectants kill them in a few minutes. Unlike many other bacteria, they quickly die at low temperatures, which should be taken into account when delivering material from patients in the winter.

Factors of pathogenicity of meningococci

Meningococci have pathogenicity factors that determine their ability to adhere and colonize cells, infect and protect against phagocytosis. In addition, they have toxicity and allergenicity. Factors of adhesion and colonization are saws and proteins of the outer membrane. Invasiveness factors - hyaluronidase and other enzymes, depolymerizing substrates of the host tissue. The main factor of pathogenicity of meningococci are capsular polysaccharide antigens, which protect them from phagocytosis. In beskapsulnyh meningococci serogroup In protection from phagocytosis also provides polysaccharide antigen B. The suppression of phagocyte activity promotes the unhindered spread of meningococci in the body and the generalization of the infectious process.

The toxicity of meningococci is due to the presence of lipopolysaccharide, which, in addition to toxicity, has pyrogenic, necrotic and lethal effects. As factors of pathogenicity, one can also consider the presence of such enzymes as neuraminidase, some proteases, plasmocoagulase, fibrinolysin, as well as the manifestation of hemolytic and antilizymic activity, although they are detected and manifested in different degrees in different serogroups.

[17], [18], [19], [20], [21], [22], [23], [24], [25], [26]

Postinfectious immunity

After the transferred illness, including in a mild form, a strong long-term antimicrobial immunity is formed against all serogroups of meningococci. It is caused by bactericidal antibodies and immune memory cells.

Epidemiology of meningococcal infection

The source of infection is only a person. A special feature of the epidemiology of meningococcal infections is the rather wide spread of the so-called "healthy" carrier, i.e., the carriage of meningococci by practically healthy people. This carrier is the main factor that supports the circulation of meningococci among the population and therefore creates a constant threat of outbreaks. The ratio of patients with meningococcal infection and "healthy" carriers can vary from 1: 1000 to 1: 20 000. The cause of "healthy" meningococcal carriage requires clarification.

All major outbreaks of meningococcal infections were associated with meningococcus serogroups A and, less frequently C. After the creation of effective vaccines against these serogroups, the main role in the epidemiology of meningitis was played by the meningococci of serogroup B. Meningococci of other serogroups cause sporadic diseases.

[27], [28], [29], [30]

Symptoms of meningococcal infection

Infection occurs by airborne droplets. The entrance gate of the infection is the nasopharynx, wherece the meningococci penetrate into the lymphatic vessels and into the blood. Meningococci can cause the following clinical forms of the disease: nasopharyngitis (the easiest form of the disease); meningococcemia (meningococcal sepsis); as a result of overcoming the blood-brain barrier, meningococci can penetrate into the cerebrospinal fluid and cause the most severe form of the disease-epidemic cerebrospinal meningitis-a purulent inflammation of the cerebral membranes of the spinal cord and brain. In these patients, the liquor is turbid, contains many leukocytes, and when punctured, it flows out due to high blood pressure. In some cases, meningococcal endocarditis develops. When meningococcemia affects the adrenal glands and blood coagulation system. The variety of clinical manifestations of the disease is determined, apparently, by the state of specific immunity, on the one hand, and the degree of virulence of meningococcus, on the other. Lethality in severe forms of meningitis before the use of sulfonamide drugs and antibiotics reached 60-70%. It remains high enough so far, to a large extent it depends on the appearance of resistance to sulfanilamide preparations and antibiotics in meningococci.

Laboratory diagnosis of meningococcal infection

The following methods are used.

Bacteriological - isolate the pure culture of the pathogen and test its sensitivity to sulfanilamide preparations and antibiotics. The material for the study is the cerebrospinal fluid, blood, exudate, mucus from the throat and nasopharynx.

It is not always possible to isolate the causative agent from a sick person, so serological reactions are very important, with the help of which either specific meningococcal antigens or antibodies to them are detected in patients.

To detect antigens, the following serological reactions can be used: coagglutination, latexagglutination, reverse immuno-electrophoresis, enzyme immunoassay, and erythroimmunoadsorption micromethod.

To detect antibodies in the blood of patients and those who have recovered, RPGA and IFM are used, in which group-specific polysaccharides are used as antigens.

Treatment of meningococcal infection

Treatment of meningococcal infection is the use of sulfonamide drugs and antibiotics (penicillin, rifampicin, etc.).

Specific prophylaxis of meningococcal infection

To create artificial immunity against meningitis, vaccines obtained from highly purified polysaccharides of serogroups A, C, Y and W135 are proposed, but each of them forms only group-specific immunity. The serogroup B polysaccharide was non-immunogenic. Since after the transferred disease immunity arises against all serogroups of meningococci, the search for such antigens (including serogroup B), which would create reliable immunity against all serogroups, including serogroup B.