Meningococcal infection

DEPARTMENT OFDEPARTMENT OF
INFECTIOUS DISEASESINFECTIOUS DISEASES
THEME:
MENINGOCOCCAL INFECTION
Infectious diseasesInfectious diseases

Meningococcal infection is an acute infectious
disease of the human, caused by meningococcus
Neisseria Meningitigis.
The mechanism of the transmission of the
infection is air-drop.
The disease is characterized by damage of the
mucous membrane of nasopharynx (nasopharingitis),
generalization of the process in the form of specific
septicemia (meningococcemia) and inflammation of
the soft cerebral membranes (meningitis).
Meningococcal infection occurs on the all
continents. It is serious problem for public health. It is
registered in 170 countries of the world.
MENINGOCOCCAL INFECTIONMENINGOCOCCAL INFECTION

The causative agent is Neisseria meningitidis. It
is small gramm-negative diplococcus, aerobic, and
possess a polysaccharide capsule, which is the main
antigen and determines the serotype of the species.
Meningococcus may be seen inside and outside of
neutrophills. The main serogroups of the pathogenic
organisms are A, B, C, D, W135, X, Y, Z and L. The
serogroupe of a meningococcus is determined by its
lipopolysaccharide.
EtiologyEtiology

Meningococci are divisible into various serogroups:
• Group A is in most countries, the serogroup
associated with epidemic cerebrospinal meningitis.
The ability to cause epidemics seems to be as-
sociated with certain genetically defined clones;
• Group B meningococci are seen in both epidemic and
outbreak situa-tions;
• Group C strains have been associated with
epidemics, but more com-monly give rise to local
outbreaks;
Serological classificationSerological classification

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• Serogroup W135 is occasionally isolated and was
associated with a major worldwide outbreak
following the pilgrimage to Mecca in 2000 and 2001;
• A few cases due to serogroups X and Y occur;
• Serogroups Z and 29E (Z’) are killed by normal
human serum; they rarely cause disease and then
only in patients with underlying disease;
• Capsulate meningococci of serogroups H, I, J, K and
L have been described, but not appear to cause
disease.
Serological classificationSerological classification

The factors of the pathogenic action of
meningococcus are biological properties, promoting its
attachment on the mucous membrane of nasopharynx,
depression of symbiotic microflora, penetration of mucous
barriers, toxic properties and other.
Meningococci are very exacting to composition of
nutritive mediums. Its reproduction may be only in
presence of human’s protein or animal’s protein. Due to
destruction of the microbe’s cell endotoxin is delivered (of
lipopolysaccharide origin). Exotoxin is not produced. The
agent of meningococcal infection is characterized by low
resistance in the environment. Meningococci perish in the
temperature 50°C for 5 minutes, in the temperature 100°C
– for 30 seconds. Meningococci have a little resistance to
low temperature.
EtiologyEtiology

Meningococcal infections occur worldwide and
are notifiable in most countries. About two-thirds of
cases occur in the first 5 years of life. The larger part
of carriers is reveled among adults. The morbidity is
higher in the towns.
The incidence of meningococcal infection is
increasing. Acute meningitis causes about 150000
deaths per year. Epidemic meningitis due to Neisseria
meningitis (usually group A) is common in a broad belt
across sub-Saharan Africa and is also seen in parts of
Asia. In Europe and North America bacterial meningitis
is usually sporadic, with B and C strains
predominanting.
EpidemiologyEpidemiology

Areas with frequent epidemics of
meningococcal meningitis (Meningitis Belt)

Epidemic strains of group A or group B may give
rise to a high incidence of disease in susceptible
individuals who acquire such a strain. The increase in
immunity observed with increasing age is likely to be
due to asymptomatic infection with avirulent strains,
which are carried by 7-20 % of healthy population,
often for many months. Household contacts of a case
are 500-800 times more likely to develop
meningococcal infection than the general population.

Outbreaks of meningococcal meningitis require
at least three factors:
• A population of susceptible individuals who lack
bactericidal antibodies to the current strains;
• A high transmission rate from person to person;
• A virulent, capsulate strain of meningococcus.

Meningococcal infection is typical anthroponosis.
The sourses of infection are healthy carriers of
meningococcus, the patients with meningococcal
nasopharingitis and the patients with generalized
forms of the disease.
The patients with generalized form are more
dangerous. It is proved that they are dangerous for
surrounding persons in 6 times than healthy carriers.
However, the main sources of the infection are
carriers, because 1200-1800 carriers have occasion to
one patients with generalized form of the disease.

The mechanism of transmission of the infection
is air-drop. The infection is realized in cough,
sneezing. In this the narrow contact and sufficient
exposition are necessary. It was proved that the
infection is realized on the distance less than 0,5
meter.
In meningococcal infection one of an important
characteristic of epidemic process is periodical rise and
fall of the morbidity. The duration of the period with
high morbidity is different. It may be 5-10 years and
more. Then the period of the fall of the morbidity
becomes. It is continued from 5 till 20 years.

In meningococcal infection epidemic process is
characterized by seasonal spread. It is manifested
especially in epidemics. The morbidity may compose
60-70% from year’s morbidity in seasonal rise. The
onset of the seasonal rise is in juanuary in the
countries with moderate climate. It achieves of
maximum in march – april.

PathogenesisPathogenesis
In meningococcal infection the entrance gates is
mucous membrane of nasopharynx. It is the place of
the primary localization of the agent. Meningococci
cause inflammation of the mucous membrane of the
upper respiratory tract. It leads to development of
nasopharingitis.
The stages of inculcation on the mucous
membrane of nasopharynx and penetration of
meningococcus into the blood precede to entrance of
endotoxin into the blood and cerebrospinal fluid. These
stages are realized with help of factors of permeability.
It promotes of the resistance of meningococcus to
phagocytosis and action of antibodies.

Meningococci are able to break local barriers
with help of factors of spread (hyaluronidase). Capsule
protects meningococci from phagocytosis.
Hematogenous way is the principal way of the
spread of the agent in the organism (bacteremia,
toxinemia). Only the agent with high virulence and
invasive strains may penetrate through
hematoencephalitic barrier. The strains of serogroup A
have a high invasivicity.

Meningococci penetrate into the blood after
break of protective barriers of the mucous membrane
of the upper respiratory tract. There is hematogenous
dissemination (meningococcemia). It is accompanied
by massive destruction of the agents with liberation
of endotoxin. Meningococcemia and toxinemia lead to
damage of endothelium of the vessels. Hemorrhages
are observed in the mucous membrane, skin and
parenchymatous organs. It may be septic course of
meningococcemia with formation of the secondary
metastatic focuses in the endocardium, joints, internal
mediums of the eyes.

In most of the cases penetration of
meningococci in the cerebrospinal fluid and the soft
cerebral membranes is fought about by hematogenous
ways through the hematoencephalic barrier.
Thus, the meningococci enter into subarachnoid
space, multiply and cause serous-purulent and
purulent inflammation of the soft cerebral membranes.

The inflammatory process is localized on the
surface of the large craniocerebral hemispheres, and
rarely, on the basis, but sometimes it may spread in
the covering of the spinal cord. In severe course of the
inflammatory process may lead to involvement of the
brain’s matter into inflammatory process and
development of meningoencephalitis. In some cases,
especially in increated patients the process may turn
into ependima of the ventricles.

In the pathogenesis of meningococcal infection
toxic and allergic components play an important role.
Thus, in fulminant forms of meningococcal infection
infectious-toxic shock develops due to massive
destruction of meningococcus and liberation of the
considerable quantity of endotoxin. In infectious-toxic
shock the development of thrombosis, hemorrhages,
necrosis in different organs are observed, even in
adrenal glands (Waterhause-Fridrechsen syndrome).

The severe complication may develop as a result
of expressive toxicosis. It is cerebral hypertension,
leading frequently to lethal outcome, cerebral coma.
This state develops due to syndrome of edema,
swelling of the brain with simultaneous violation of
outflow of cerebrospinal fluid and its hyperproduction.
The increased volume of the brain leads to pressure of
brain’s matter, its removement and wedging of
medulla oblongata into the large occipital foramen,
pressure of oblong brain, paralysis of the breath and
cessation of the cardio-vascular activity.

Clinical formsClinical forms
I. Primarily localized forms:
a) meningococcal carrier state (clinical manifestations
are absent)
b) acute nasopharyngitis;
c) pneumonia.
II. Gematogenously generalized forms:
a) meningococcemia: typical, acute meningococcal
sepsis; chronic;
b) meningitis; meningoencephalitis;
c) mixed forms (meningococcemia + meningitis,
meningoencephalitis).
d) rare forms (endocarditis, arthritis, iridocyclitis).

Clinical manifestationClinical manifestation
Meningococcal nasopharingitis.
The most common complains of the a patients
are headache, mainly in the frontal-parietal region,
sore throat, dry cough, blocked nose, fatigue,
weakness, loss of the appetite, violation of the
sleep. In the most of the patients body temperature
rises up to subfebrile and lasts for not more than 3-7
days. The skin is pale, conjunctival vessels and sclera
are injected. There are hyperemia and edema of the
mucous membrane of the nose. In many patients the
posterior wall of the pharynx is covered by mucous or
mucous – purulent exudation.

Inflammatory changes in the nasopharynx can
be noticed after 5-7 days, hyperplasion of lymphoid
follicles lasts longer. In the peripheral blood moder-
ate leukocytosis with neutrophylosis and a shift of
leukocytaric formula to the left. Nasopharyngitis often
precedes the development of generalized forms of the
disease.

Meningococcal meningitis.
It may start after meningococcal
nasopharyngitis, but sometimes primary symptoms of
the disease arise suddenly. In meningitis three
symptoms are constantly revealed: fever, headache
and vomiting. Temperature increases quickly with chill
and may reach 40-41°C for few hours. The patients
suffer from severe headache, having diffuse or
pulsatory character. Headache is very intensive at the
night. It increases due to change of the body position,
sharp sounds, bright light.

Vomiting arises without precedent nausea.
There is no connection with food and relief after
vomiting. It is, as rule, plentiful, by “fountain”,
repeated. Sometimes, vomiting arises on the peak of
headache.
The disorders of consciousness occupy the
great place in the clinical picture (from sopor till
coma). The loss of consciousness develops after
psychomotoric excitement. The loss of consciousness
at the first hours of the disease is unfavorable sign.

On objective examination meningeal symptoms
stand at the first place. It is described near 30
meningeal signs. A few meningeal signs are used in
practice: rigidity of occipital muscles, Kernig’s
symptom, Brudzinsky’s symptom (upper, middle and
lower).
The multiple symptoms of the lesion of the
other organs and systems are connected with
intoxication. There is tachycardia at the first hours of
the disease. Then it may be bradycardia. Arrhythmia,
tachypnoea (30-40 times in minute) are possible.
In hemogram high leukocytosis,
neuthrophylosis with shift of the formula to the left.

Position of patient with meningitis

The examination of cerebrospinal fluid (CSF)
has the great meaning in diagnostics of meningitis.
On lumbar punction cerebrospinal fluid flows out
under high pressure and with frequent drops.
Cerebrospinal fluid is opalescent in initial stages of
the disease. Then it is turbid, purulent, sometimes
with greenish shade. Pleocytosis is high. Pleocytosis
achieves till 10-30*103
in 1 mcl. Neutrophils
leukocytes predominate in cytogram. Neutrophilous
compose 60-100 % of the all cells. On microscopy
neuthrophils cover inrarely all fields of the vision.
Quantity of protein of cerebrospinal fluid increases.

The fulminant course of meningitis with syndrome
of brain swelling and edema is the most unfavorable
variant. There is hypertoxicosis in this form and high
percentage of the mortality. The main symptoms are
consequence of inclination of the brain into foramen
magnum and strangulation of medulla oblongata by
tonsils of cerebellum. The immitant symptoms from
cardiovascular and respiratory systems develop.
Bradycardia appears. Then it is changed by tachycardia.
Arterial pressure may fall catastrophically, but it increases
more frequently till high level. Tachypnoea arises (till 40-
60 times/min) with help of axillary muscles. Death
occurs due to respiratory failure at the first hours of the
disease, rarely on 2-3 day or on 5-7 day.

Meningococcemia (meningococcal sepsis).
The disease is more impetuous, with symptoms
of toxicosis and development of the secondary
metastatic foci. The onset of the disease is an acute.
Body temperature may increase up to 39-410
C and lasts
for 2-3 days. There is no accordance between degree of
increase of the temperature and severity of the course
of the disease.
The other symptoms of intoxication arise
simultaneously with fever: headache, decreased
appetite or its absence, general weakness, pains in the
muscles of the back and limbs.

Exanthema is more clear, constant and
diagnostically valuable sign of meningococcemia.
Dermal rashes appear in 5-15 hours, sometimes on the
second day from the onset of the disease.
Hemorrhagic rash is more typical (petechias,
ecchymosis and purpura). The elements of the rash
have incorrect (“star-like”) form, dense, coming out
over the level of the skin.
The deep and extensive hemorrhages may be
necrosed. Then it may be formation of deep ulcers.
Sometimes deep necrosis is observed on the limbs and
also, necrosis of the ear, nose and fingers of the hands
and legs. On biopsy meningococci are revealed.

Angular and irregular meningococcal skin lesions
in a 5-year-old girl.

Meningococcemia showing striking involvement of the
extremities with relative sparing of the skin of the child’s body
surface.

Meningococcemia in adolescent female with disseminated
intravascular coagulation.

Exanthema is leucocytaric-fibrinous thrombosis,
contained the agent of meningococcal infection. Thus,
in meningococcal infection rash is the secondary
metastatic foci of the infection.
Meningococcal sepsis is combined with meningitis
in the majority cases. In 4-10 % of the patients
meningococcemia may be without injury of the soft
cerebral membranes.

Fulminate meningococcemia (Waterhause-
Friedrichen syndrome).
It is the most severe, unfavorable form of
meningococcal infection. Its base is infectious-toxic
shock. The fulminant sepsis is characterized by acute
sudden beginning and impetuous course. The body
temperature rises up to 40-41o
C. It is accompanied by
chill. However, hypothermia may be observed in some
hours. Hemorrhagic plentiful rash appears at the first
hours of the disease with tendency to confluence and
formation of the large hemorrhages, necroses. A
purple-cyanotic spots arise on the skin (“livors
mortalis”). The skin is pale, but with a total cyanosis.

Patients are anxious and excited. The cramps are
observed frequently, especially in children. The
recurrent blood vomiting arise inrarely. Also, a bloody
diarrhea may be too. Gradually, a prostration becomes
more excessive and it results is a loss of the
consciousness.
In the peripheral blood hyperleukocytosis (till 60
109
/l), neutrophylosis, sharp shift leukocytaric formula
to the left, thrombocytopenia, increased ESR (50-70
mm/h) are reveled. The disorders of hemostasis are
marked - metabolic acidosis, coagulopathy of
consumption, decrease of fibrinolitic activity of the
blood and other.

Laboratory diagnosticLaboratory diagnostic
The final diagnosis is confirmed, as a rule, with
bacteriological method. In any suspected
meningococcal infection, blood culture must be
undertaken; if meningitis is suspected, a lumbar
puncture should be performed as soon as possible
unless there are signs of raised intracranial pressure.
Non-cultural methods are increasingly used
because the rapid institution of chemotherapy
reduces the chance of successful culture.
Meningococcal capsular polysaccharide may be
demonstrated in CSF by countercurrent electro-
phoresis, by latex agglutination and by PCR.

TreatmentTreatment
The therapeutic tactics depends on the clinical
forms, severity of the course of the disease, presence
of complications, premorbid state. In the serious and
middle serious course of nasopharyngitis antibacterial
remedies are used.
Peroral antibiotics oxacillin, ampyox,
chloramphenicol, erythromycin are admistered. The
duration of the therapy is 5-7 days and more.
In the therapy of generalized forms of
meningococcal infection the central place is occuped
by antibiotics, in which salt benzil penicillin stands at
the first place.

TreatmentTreatment
Benzyl penicillin is used in dosage of 300 000
U/kg/day. In the serious form of meningococcal
infection daily dosage may be increased up to 500
000 U/kg/day. Such doses are recommended
particularly in meningococcal meningoencephalitis. In
the presence of ependimatitis or in the signs of the
consolidation of the puss the dose of penicillin
increases up to 800 000 U/kg/day.
Daily dose is injected to the patient every 3
hours. In some cases interval between injections may
be increased up to 4 hours. The duration of the
antibi-otic therapy is decided individually depending
on clinical and laboratory data.

TreatmentTreatment
It is necessary to research of a spinal liquid for
an estimation of efficiency of antibacterial therapy. If
at control research (in 7-10 days of antibacterial
therapy) pleocytosis has decreased less than 100
cells in 1 mcl and prevail lymphocytes, antibacterial
therapy can be cancelled.
If pleocytosis more than 100 cells in 1 mcl or
prevail neutrophyles antibacterial therapy is
necessary for continuing. In 3-5 days of therapy it is
necessary to investigate a spinal liquid again.

TreatmentTreatment
In meningococcal infection chloramphenicol is
highly effective. It is the medicine of the choice in the
fulminant meningococcemia. It is shown, that
endotoxic reactions arise more rarely in the treatment
of the patients with chloramphenicol than in the
therapy with penicillin. In cases the of menin-
goencephalitis chloramphenicol is not prescribed due
to its toxic effects on neurons of brain.
Chloramphenicol is used in dose 50-100 mg/kg
4 times per day. The duration of the treatment of the
patients with this antibiotic is 6-10 days.

TreatmentTreatment
Pathogenetic therapy has exceptional
significance in the therapeutic measures. It is
performed simultaneously with etiotropic therapy.
The basis of pathogenetic therapy is the
struggle with toxicosis. Salt solutions,
macromolecular colloid solutions, plasma, albumin
are used. Usually 50-40 ml of fluid is injected on 1 kg
of body mass per day in adults under the control of
diuresis.
Prophylaxis of hyperhydratation of the brain is
performed simultaneously.

TreatmentTreatment
Diuretics (lasix, mannitol) are injected. In the
serious cases glucocorticosteroids are prescribed.
Dose depends on dynamics of the main symptoms
and presence of complications.
Oxygen therapy has great significance in the
treatment of the patients.
The therapy of fulminant meningococcemia is
concluded in the struggle with shock.

ProphylaxisProphylaxis
Prophylactic measures, directing on the sources
of meningococcal infection include early revelation of
the patients, sanation of meningococcal carriers,
isolation and treatment of the patients. The
measures, directing on the rupture of the mechanism
of the transmission of the infection, is concluded in
disinfection.
Resistance to meningococcal infection is closely
associated with the possession of bactericidal
antibodies that may be maternal in origin or actively
produced in response to carriage.

ProphylaxisProphylaxis
Vaccines containing the pure group-specific
capsular polysaccharidae of meningococci of groups
A, C, Y and W135 are available and are good
immunogens.
However:
• The protection provided is group-specific;
• It lasts at most 3 years;
• It does not prevent meningococcal carriage;
• They are poorly immunogenic in children aged
under 2 years.
These shortcomings have limited their use
largely for travel to parts of the world in which
epidemics due to group A or C meningococci are in
progress or are to be expected.

Meningococcal infection

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