Membrane cocci attach to the non-villi epithelial cells in the upper respiratory tract by the receptor, a membrane protein.
Meningococcal infection is an acute infectious disease caused by meningococcal (or meningococcal) with very diverse clinical manifestations, possibly rhinitis, meningitis, sepsis. .. The disease often causes epidemics, especially in young collectives. In severe cases the mortality rate is still very high.
Meningitis outbreaks have been known since the 2nd century BC. But the disease has only been fully described since 1805 from the meningitis outbreak that occurred in Geneva.
In 1887 Weichsel Baum found the pathogenic bacteria and described it. The serotypes of the meningococcal Dopteran is reported in 1909
In the 30s of this centuries, sulfamide was used for treatment and proved to be effective, but this antibiotic quickly became resistant in the 1940s.
Vietnam: The first outbreak in 1939-1940 came from China. Now found scattered throughout the South and the North but more common in the South.
Neisseria meningitidis is a meningococcal bacterium named Neisseria meningitidis belonging to the Neisseriaceae family, like Nesseria - is a coffee bean-shaped coccyx located in the cell.
Bacteria are 0.6-0.8 micrometres in size, have polysaccharide shell, are aerobic, are not mobile, do not form spores. Gram-negative color catches.
Bacteria grow well in the medium containing 5 - 10% CO2 at a temperature of 35 - 37 0 C (blood agar, Mueller Hinton agar ...).
Poor tolerance to physical and chemical effects (50 ° C / 5 minutes, 100 ° C / 30 seconds, ultraviolet rays kill bacteria in a moment. Disinfectants are easy to kill bacteria).
Based on the structure of the Polysaccharide shell, sera groups - denoted A, B, C, D, X, Y, Z, 29E, W13, H, I, K, L ...
Serum groups are further divided into serotypes based on the structure of the Outer Membran Protein antigen (OMP). Based on meningeal enzymes, the subtype is subdivided.
Europe: Common groups A, B, C; America: B, C; Vietnam: A, B, C.
Group A: Or cause major epidemics.
Group B: Mainly causes dissipation (10-50 patients / 10,000 people).
Group C: Causes both large, small and dispersed epidemics.
Disease season: Northern Vietnam often experiences epidemics in March-April. South Vietnam in May-June-July, but not necessarily seasonal.
The only source of the disease is the person, which can be either a patient or an asymptomatic carrier.
Inhalation, usually by direct contact with a carrier. People with rhinitis and pharyngitis are more likely to get it.
Sense of the body
Anyone can get the disease, but children without antibodies are more likely to get the disease.
After the disease, it left stable immunity to the same serotype (or cross-immunization in the same group).
Mechanism of pathogenesis and pathology
Mechanism of pathogenesis
Membrane cocci attach to the non-villi epithelial cells in the upper respiratory tract by receptor as a membrane protein (the ability of bacteria to adhere is blocked by monoclonal and polyclonal antibodies against this protein). Then penetrates through the mucosa thanks to the enzyme Hyaluronidases. If the body's resistance is good, especially the lymph ring around the mouth is not damaged by inflammation, the meninges will only cause inflammation of the nose, throat or even reside there without causing disease.
From the throat, meninges pass through the barrier of lymph into the blood and then cross the barrier of blood vessels - brain to enter the cerebrospinal cavity. The rare case of meningitis can be from the nose, throat through the sieve, especially when there is bone trauma to enter the meninges.
All 3 membranes of the meninges are inflamed. Initially secretes an inflammatory fluid, then quickly becomes pus, thick pus can block the translation holes, causing cerebrospinal fluid to block and leading to hydrocephalus, the inflammatory fluid can compress the II, III, and IV nerves. , VI, causing blindness and squint.
In the capillaries, the meninges are located in endothelial cells. Therefore, they can cause blockage and rupture of vessels, causing haemorrhage, and necrosis of the organization.
Reaction antigen - antibody - complement cytotoxicity, cell destruction, and causes blood clotting scattered intravascular and cause major bleeding.
When endotoxins are released, endotoxin shock can result.
Divide the clinical form
Infection from 1-10 days (average 5-7 days). Clinical manifestations of meningococcal infections are very diverse, there are many diseases: rhinitis, septicaemia, meningitis ..., there are diseases combined in many organs. The following common diseases are:
Symptoms study by individual
Sudden fever of 38-39 ° C, headache - a burning pain in the throat, runny or purulent runny nose. Fever lasts 1-3 days, sometimes up to 5-7 days.
Throat and Amidala congestion, enema, may be coated with pus; red and pus-filled nasal mucosa. Rhinopharyngitis lasts 5-7 days; Lymph nodes return to normal after 14-16 days.
Laboratory tests: Peripheral blood leukocytes increased, polymorphonuclear leukocytes (N) increased. About 30-50% of rhinitis is associated with meningitis or septicaemia.
The disease happened suddenly and frantically. A fever that is suddenly high 40-41 ° C, is constant or fluctuating, and is accompanied by shivering chills. Headache, aching muscles, joints all over the body.
Necrotic purpura or "necrosis" is a valuable diagnostic sign. The rash may appear very soon after 5-15 hours or later after a few days. Features of the rash: At first, the measles-like maculopapular nodules turn into petechiae-necrotic spots after a few hours with 5 characteristics:
The rash is on the whole body (especially children), but usually appears at the ends of blood vessels such as: the tips of the fingers or hands-feet, the ear, the nose ...
Uneven size (from 1-2 mm to 1-2 cm).
The banks are rough, not round, the shape is not certain, the star-shaped or map-shaped shape.
Tends to spread out, join together. Necrosis is usually black necrosis, in the middle, a blister is raised and then the pus becomes bloody.
Not growing at the same time. The more serious the disease, the more necrotic nodules and stick together into haemorrhagic plaque.
Liver, spleen, soft.
The test showed that peripheral blood leukocytes increased and turned left. Blood sedimentation rate increases.
Paroxysmal sepsis (also known as shock or septicaemia):
The patient presents with septicaemia accompanied by endotoxin shock, which progresses very quickly (extreme) with the following main features:
Endotoxin shock from the beginning: Drop in blood pressure, small tachycardia, pale skin, cold (temperature below 36 ° C) sweating, oliguria or anuria.
Severe early and early development of haemorrhagic syndrome: Large, fast-progressing necrotic purpura. Accompanied by bleeding of mucosa and viscera.
Progression: Usually critical and fatal within the first 1-2 days of cardiovascular failure and acute renal failure.
Endotoxin shock due to microcirculatory disorders associated with the development of scattered intravascular coagulation syndrome (DIC).
Simple, typical meningitis:
Meningitis usually occurs after nasopharyngitis or septicaemia, but the first symptoms can also be symptoms of meningitis.
Toxic Infection Syndrome: Sudden fever 39-40 °C constant or fluctuating. Fatigue, headache
Meningeal syndrome: Early, typical and complete symptoms: Severe headache, vomiting, constipation. Examination: lying in the trigger position (common in children due to hypertonia of the folded muscles - analgesic posture), signs of stiff neck (+), Kernig (+), Brudzinski (+), meninges (+).
Typically: High pressure, pus; Protein increases, Glucose and Sodium chloride decrease; cells are elevated and are predominantly polymorphonuclear leukocytes.
Atypical: Clear water due to: mild or treated form (also known as "head loss" meningitis). If lemon yellow or bloody: meningeal haemorrhage.
Meningitis - encephalitis (paroxysmal meningitis with encephalitis):
In addition to the symptoms of meningitis alone, paroxysmal cerebral edema stands out: coma, irritability, accompanied by symptoms of severe intracranial hypertension syndrome: bradycardia in increased blood pressure. , severe respiratory disorder, fundoscopy showed swelling of both sides of the papillae in which varicose veins, constricted arteries, Sometimes retinal haemorrhage Patients die from respiratory failure in the early hours, rarely on day 2-3 or even day 5-7 of illness.
Meningitis + septicemia
Account for 25-50% of all meningococcal infections.
Meningitis with decreased intracranial pressure syndrome
Common in young children, the pressure of cerebrospinal fluid is very low. The disease progresses often very seriously with complications: Subdural hematoma, brain drain ... and death. It is common in cases of severe dehydration and electrolyte disturbances.
Lung type, arthritis, eyelid inflammation ...
Nerve paralysis: II, III, IV, VII, VIII lead to blindness, blindness, deafness.
Meningeal thickening (due to late antibiotic use).
If sticky thickening causes high obstruction (Monro hole, Luschka hole or Sylvius drain) leads to protein dissociation (elevated) and cell (normal) and eventually hydrocephalus.
In the bloodstream
Clogging causes necrosis.
Hemorrhage (especially when there is scattered intravascular coagulation).
Complications that cause premature death
Respiratory failure due to severe brain edema.
Massive bleeding due to intravascular scattered clotting.
Implementing the quadrants
Sudden high fever, chills, pharyngitis (sore throat in 50% of cases may be accompanied by).
Meningeal syndrome or a drop in blood pressure.
Necrotic hemorrhagic rash.
Peripheral blood: Leukocytes increased (polymorphonuclear leukocytes increased), blood sedimentation rate increased.
Microorganisms: Cultured to find meningitis in blood, cerebrospinal fluid, blister fluid (in necrotic purpura), pharyngeal mucus. Gram staining and bright smear can also be used, but of little value.
Many people suffer (into translation).
Differential diagnosis (depending on the individual)
Note the distinction between purulent meningitis from fluid meningitis.
The principles of treatment
Treat the cause
Bacteria are also susceptible to many antibiotics. Sulfamid alone since 1943 has reported resistance of group A, later on both B, C. Penicillin is still the top antibiotics of choice, recently, meningococcal hypersensitivity to this antibiotic has been reported in the UK. Spain and parts of America.
Penicillin dosage depends on the type of disease
Rhinitis: 500,000 - 1 million / day ´ 7 days.
Sepsis: 100-200 mg / kg / day.
Meningitis: 200-400mg / kg / day.
Meningitis - encephalitis: ³ 400 mg / kg / day.
May be combined with chlorocid: 30-40mg / kg / day or sulfadizine 200mg / kg / day.
If resistant to penicillin can be used
Methicilin, lincocin, carbenicilin, oxacilin.
Ampicilin: 200 mg / kg / day.
3rd generation cephalosporin: 100-150 mg / kg / day.
Treatment according to the pathogenetic mechanism
Cardiovascular aids, infusion detoxification and correction of electrolyte disorders.
High dose corticosteroids in paroxysmal sepsis (Hydrocortison 30mg / kg).
Heparin in the presence of phase 1 scattered intravascular coagulation (hypercoagulation): Heparin 5 mg / kg.
If there are seizures, use anticonvulsants, sedatives (seduxen - meprobamat).
Treatment of patient isolation.
Find people who carry bacteria: Swipe throat culture, scan. Temporarily isolate people with fever and sore throat during an epidemic.
Sanitation: light, ventilation.
Prophylactic antibiotics are only used for people in the outbreaks on business trips to other places and people from other places to the outbreak (sulfamides; tetracycline, chlorocides. Penicillin is not used).
Vaccination: Currently, the strategy of mass vaccination has been discontinued nationwide, but only in areas where the epidemic is at risk (where there is the first case or where there is a high risk).
With group A
Vacxin PS (Polysaccarit).
Over 4 years of age the effect is longer.
First year: 100%.
Under 4 years old:
PS vaccines of groups A, C, Y, W135 have been prepared intramuscularly with 0.5 ml containing 50 micrograms / each. A and C vaccines are being attached to the tetanus toxoid to cause higher antibody production.
With group B
Use of polysaccharide (PS) antigen for vaccine production is not effective because it is thought that the polysaccharide of group B meningitis is similar to the PS of the human brain, so the body does not respond to immunity. Currently, research is using the membrane protein (OMP) of Serotyp 2a group B to produce vaccines.