| disease | Epidemic Cerebrospinal Meningitis |
| alias | Epidemic Cerebrospinal Meningitis |
Epidemic cerebrospinal meningitis is a purulent meningitis caused by meningococcus. The pathogenic bacteria invade the bloodstream from the nasopharynx, leading to septicemia, and eventually localize in the meninges and spinal meninges, forming purulent cerebrospinal meningeal lesions. The main clinical manifestations include fever, headache, vomiting, skin petechiae, and neck stiffness, among other meningeal irritation signs. The cerebrospinal fluid shows purulent changes.
bubble_chart Epidemiology
The disease is prevalent or sporadic in countries around the world, with an average annual incidence of 2.5 per 100,000, highest in the central African epidemic zone.
(1) Source of pestilence Humans are the only source of pestilence for this disease, with the pathogen residing in the nasopharynx of carriers or patients. During epidemics, the carrier rate in the population can reach as high as 50%, and a carrier rate exceeding 20% suggests the possibility of an outbreak. In non-epidemic periods, group B is the predominant carrier strain, while during epidemics, group A accounts for a higher percentage. About 10–20% of post-infection individuals become carriers, shedding the bacteria for several weeks to up to 2 years. Those who carry the bacteria for more than 3 months are termed chronic carriers, often harboring drug-resistant strains deep within the nasopharyngeal lymphoid tissue. Carriers pose a greater risk to those around them than patients do.
(2) Route of pestilence The pathogen is transmitted directly through airborne droplets. Since the bacteria have very weak viability outside the host, indirect transmission via everyday objects is rare. Close contact is particularly significant for the incidence of the disease in infants under 2 years of age.
Whether sporadic or epidemic, the incidence rate increases with the arrival of winter, generally rising from November, peaking between February and April, and declining from May onward. Respiratory viral infections during this period also facilitate disease transmission. Indirect transmission through everyday objects is less common.(3) Population susceptibility The disease is rare in newborns, but cases can occur in infants as young as 2–3 months, with the highest incidence in infants aged 6 months to 2 years, after which it gradually declines. Newborns have bactericidal antibodies from their mothers, so they rarely contract the disease. Antibody levels drop to their lowest between 6 and 24 months, then gradually rise again, reaching adult levels around the age of 20. The susceptibility of the population is closely related to antibody levels. Variations in immunity among different age groups lead to differences in incidence rates across regions. In large cities, cases are scattered, with the highest incidence in children under 2 years old. In small and medium-sized cities, the peak incidence occurs in children aged 2–4 or 5–9 years. In remote mountainous areas, the introduction of a pestilence source often leads to outbreaks, with individuals aged 15 and older accounting for over half of the total cases. The incidence rates are roughly equal between males and females. On average, there is an epidemic peak every 10 years, due to declining population immunity and the gradual accumulation of new susceptible individuals over time. In recent years, two major epidemiological issues have been the shift in bacterial strains and the increase in sulfonamide-resistant strains.
bubble_chart PathogenMeningococcus belongs to the genus Neisseria and is a Gram-negative coccus, oval in shape, often arranged in pairs. This bacterium is found only in humans and can be detected in the nasopharynx of carriers, as well as in the blood, cerebrospinal fluid (CSF), and skin petechiae of patients. In CSF, the bacteria are mostly found within neutrophils, with only a few located extracellularly. It does not grow easily on ordinary culture media but thrives on media containing blood, serum, exudate, or egg yolk fluid, typically growing better in an environment with 5–10% carbon dioxide. This bacterium is highly sensitive to cold, dryness, and disinfectants. It dies very easily outside the body and can produce autolytic enzymes, so collected specimens must be immediately sent for examination and inoculation.
Meningococcus can be grouped using serum agglutination tests and is classified into nine serogroups: A, B, C, D, X, Y, Z, 29E, and W135. Domestically, besides the same A, B, C, and D groups as abroad, seven new serogroups have been identified: 1889, 1890, 1892, 319, 1916, 1486, and 1811. However, over 90% of cases are caused by serogroups A, B, and C, with large-scale epidemics exclusively caused by serogroup A, while B and C groups only cause sporadic cases or small outbreaks. According to data from China, serogroup A remains the primary cause of disease and outbreaks, accounting for 97.3% of isolated pathogenic strains, followed by B (1.93%) and C (0.39%). This differs from other countries, where serogroup B accounts for 50–55%, C for 20–25%, W135 for 15%, Y for 10%, and A for only 1–2%.
Pathogenic bacteria invade the human body through the nasopharynx. If the body's immunity is strong, the pathogens can be quickly eliminated or a carrier state may develop. If the body lacks specific bactericidal antibodies or the bacteria are highly virulent, the pathogens can penetrate the nasopharyngeal mucosa into the bloodstream, leading to septicemia, which may subsequently affect the meninges, resulting in purulent meningoencephalitis.
The bacteria can produce an enzyme that cleaves the heavy chain of local IgA. Additionally, the adhesion of pili to nasopharyngeal epithelial cells plays a significant role in pathogenesis.During the septicemic phase, the bacteria often invade the inner walls of skin blood vessels, causing embolism, necrosis, hemorrhage, and cellular infiltration, leading to petechiae or ecchymoses. Due to thrombosis, thrombocytopenia, or the effects of endotoxin, varying degrees of hemorrhage occur in internal organs.
Fulminant septicemia is a special type, formerly known as Waterhouse-Friderichsen syndrome. It was once thought to result from acute adrenal cortical failure due to bilateral adrenal cortical hemorrhage and necrosis. However, it has now been demonstrated that adrenal cortical function is mostly not impaired and does not play a major role in the pathogenesis. Instead, the lipopolysaccharide endotoxin of meningococci can cause microcirculatory disturbances and endotoxic shock, subsequently leading to disseminated intravascular coagulation (DIC), which is the primary pathological basis.
The occurrence and progression of fulminant meningoencephalitis are also related to endotoxin. Type III hypersensitivity may also play a role in the pathogenesis, as evidenced by the deposition of immunoglobulins, complement, and meningococcal antigens in the damaged vascular walls.
bubble_chart Pathological Changes
The main pathological changes during the septicemia stage are damage to the vascular endothelium, with inflammation, necrosis, and thrombosis in the vessel walls, accompanied by perivascular hemorrhage. Focal hemorrhages may also occur in the subcutaneous tissue, mucous membranes, and serous membranes.
In fulminant septicemia, the skin and visceral blood vessels exhibit endothelial cell destruction and detachment, with thrombosis in the vascular lumen. Widespread hemorrhages are present in the skin, heart, lungs, gastrointestinal tract, and adrenal glands. Myocarditis and pulmonary edema are also quite common. The pathological changes in the meningeal inflammation stage primarily involve the pia mater. In the early stage, there is congestion, minor serous exudation, and focal small hemorrhages, while in the late stage [third stage], large amounts of fibrin, neutrophils, and bacteria appear. The lesions affect the surface of the cerebral hemispheres and the base of the skull. At the skull base, purulent adhesions, compression, and direct invasion by suppurative changes can lead to cranial nerve damage, including the optic, abducens, oculomotor, facial, and auditory nerves, which may even become permanent. The superficial layer of brain tissue undergoes degenerative changes due to toxin effects. Additionally, inflammation can spread along blood vessels into the brain tissue, causing congestion, edema, focal neutrophil infiltration, and hemorrhage.
In fulminant meningoencephalitis, the brain tissue exhibits severe pathological changes, with marked congestion and edema, significantly increased intracranial pressure, and a high likelihood of unconsciousness and convulsions due to encephalitis. Some patients may develop tentorial herniation and foramen magnum herniation, manifesting as pupillary changes, hemiplegia, decerebrate rigidity, respiratory failure, and other severe symptoms. A small number of chronic patients may develop hydrocephalus due to obstruction of the ventricular foramina and impaired cerebrospinal fluid circulation.
bubble_chart Clinical Manifestations
The condition of epidemic cerebrospinal meningitis is complex and variable, with severity ranging from mild to severe. Generally, it can manifest in three clinical forms: the ordinary type, the fulminant type, and the chronic septicemia type. The incubation period ranges from 1 to 7 days, usually 2 to 3 days.
(1) Ordinary Type: Accounts for about 90% of all cases. It can be divided into three stages based on its progression: the upper respiratory tract infection stage, the septicemia stage, and the meningitis stage. However, the clinical stages are not clearly demarcated.
1. Upper Respiratory Tract Infection Stage: Lasts about 1 to 2 days. Most patients are asymptomatic, while some experience sore throat, congestion of the nasopharyngeal mucosa, and increased secretions. Pathogens may be detected via nasopharyngeal swab culture, but diagnosis is often difficult at this stage.
2. Septicemia Stage: Patients suddenly develop high fever, fear of cold, shivering, accompanied by headache, loss of appetite, and mental dullness. In young children, symptoms may include crying, restlessness, skin hypersensitivity, and convulsions. A few patients may experience arthralgia or arthritis. About 70% of patients develop petechiae (or ecchymoses) on the skin and mucous membranes, ranging in size from 1–2 mm to 1 cm. In severe cases, petechiae and ecchymoses may rapidly expand, with central skin necrosis due to thrombosis. About 10% of patients develop herpes simplex around the lips, usually around the second day of illness. A few patients may have splenomegaly. Most patients progress to meningitis within 1 to 2 days.
3. Meningitis Stage: Patients continue to have high fever and toxemia, with persistent petechiae and ecchymoses, but symptoms of central nervous system involvement worsen. Due to increased intracranial pressure, patients experience severe headache, frequent vomiting, elevated blood pressure, and slowed pulse. Skin hypersensitivity, photophobia, agitation, and convulsions are common. Within 1 to 2 days, patients may enter a state of delirium or unconsciousness, with possible respiratory or circulatory failure.
Infants often present atypically. In addition to high fever, refusal to eat, restlessness, and crying, convulsions, diarrhea, and cough are more common than in adults. Signs of meningeal irritation may be absent, but bulging of the anterior fontanelle (if not yet closed) is highly diagnostic. However, frequent vomiting and dehydration may cause the fontanelle to appear sunken.
(2) Fulminant Type: A few patients experience a sudden and severe onset. Without timely treatment, death may occur within 24 hours.
1. Fulminant Septicemia: More common in children but not rare in adults. Symptoms begin with high fever, headache, and vomiting, accompanied by severe toxicity, extreme lethargy, and varying degrees of impaired consciousness, sometimes with convulsions. Within 12 hours, widespread petechiae and ecchymoses appear all over the body, rapidly expanding and merging into large ecchymotic patches with subcutaneous necrosis. Circulatory collapse is the hallmark of this type, manifesting as pallor, cold extremities, cyanosis of the lips and fingertips, rapid and thready pulse, significantly decreased blood pressure, and narrowed pulse pressure. Many patients may have blood pressure dropping to zero, with reduced or no urine output. Signs of meningeal irritation are mostly absent, and cerebrospinal fluid is usually clear with only mild cell count elevation. Blood and petechial cultures are often positive, and laboratory tests may confirm disseminated intravascular coagulation (DIC). Thrombocytopenia and a white blood cell count below 10,000/mm3 often indicate a poor prognosis.
2. Fulminant encephalitis This type is also commonly seen in children. The clinical symptoms of brain parenchyma damage are obvious. Patients rapidly progress into unconsciousness, with frequent convulsions, often positive pyramidal tract signs, unequal reflexes on both sides, persistently elevated blood pressure, and optic disc edema visible in the fundus. Some patients develop cerebral herniation. Tentorial herniation is caused by the uncus or hippocampus herniating into the tentorial notch, which can compress the diencephalon and oculomotor nerve, leading to ipsilateral pupil dilation, loss of light reflex, fixed or abducted eyeball, contralateral limb paresis, followed by respiratory failure. In cases of occipital bone foramen magnum herniation, the cerebellar tonsils herniate into the foramen magnum, compressing the medulla oblongata. In this seasonal disease, the patient's unconsciousness deepens, the pupils become markedly constricted or dilated, or fluctuate in size, with irregular edges. Bilateral limb muscle tone increases or becomes rigid, with the upper limbs often internally rotated and the lower limbs exhibiting extensor rigidity. Breathing becomes irregular, varying in speed, depth, or pauses, or manifests as sobbing or nodding respirations, progressing to Cheyne-Stokes breathing, often indicating imminent respiratory arrest. Before respiratory failure occurs, patients may show the following warning signs: ① pale complexion, frequent vomiting, severe headache, and dysphoria; ② sudden unconsciousness, persistent convulsions, and continuously elevated muscle tone; ③ unequal pupil size, marked constriction or dilation, irregular edges, sluggish or absent light reflex, and fixed eyeballs; ④ altered respiratory rhythm; ⑤ elevated blood pressure.
3. Mixed type Combines the clinical manifestations of the above two types, often appearing simultaneously or sequentially, and is the most severe form of the disease.
（三）Chronic meningococcal septicemia Relatively rare, more common in adult patients. The course of the disease often lasts for several months. Patients frequently experience intermittent episodes of chills, shivering, and fever, each lasting about 12 hours before subsiding, with recurrences every 1 to 4 days. During episodes, symptoms such as petechiae, macules and papules, and pain in the knee and wrist joints may appear. Diagnosis primarily relies on blood cultures during febrile periods, often requiring multiple tests to yield positive results. Smear tests have a low positive rate. During the course of the illness, it may sometimes progress to purulent meningitis or endocarditis, leading to a rapid deterioration of the condition.
bubble_chart Auxiliary Examination
(1) Blood Picture The total white blood cell count is significantly increased, generally around 20,000/mm3, with higher counts reaching 40,000/mm3 or more, and neutrophils accounting for 80–90%.
(2) Cerebrospinal Fluid Examination In the initial stage [first stage] of the disease, only the pressure is increased, and the appearance is normal. During the typical meningitis stage, the pressure can rise above 1.96 kPa, and the appearance becomes turbid or purulent. The white blood cell count ranges from several thousand to tens of thousands per cubic millimeter, predominantly neutrophils. The protein content is significantly elevated, while the sugar content is markedly reduced, sometimes undetectable, and chloride levels are lowered. If clinical symptoms and signs of meningitis are present but the early cerebrospinal fluid examination is normal, a repeat test should be performed within 12–24 hours. After antibiotic treatment for meningococcal meningitis, the cerebrospinal fluid changes may not be typical.
(3) Bacteriological Examination
1. Smear Examination A needle is used to puncture a skin petechia, and a small amount of blood and tissue fluid is squeezed out for smear staining and microscopic examination, with a positive rate exceeding 80%. The positive rate for cerebrospinal fluid sediment smears is 60–70%. The cerebrospinal fluid should not be left standing for too long, as the pathogens may autolyze and affect detection.
2. Bacterial Culture Blood cultures have a relatively low positive rate in meningococcal meningitis. However, blood cultures are crucial for diagnosing the bacteremic phase of ordinary meningococcal meningitis, fulminant bacteremia, and chronic meningococcal bacteremia. Therefore, blood must be collected for bacterial culture before administering antibiotics, and multiple blood samples should be sent for testing. Cerebrospinal fluid should be centrifuged in a sterile tube, and the sediment should be directly inoculated onto chocolate agar and also injected into glucose broth, then cultured in a 5–10% carbon dioxide environment.
(4) Immunological Tests These are rapid diagnostic methods for meningococcal meningitis developed in recent years. Detection of antigens in cerebrospinal fluid aids in early diagnosis, offering high sensitivity and strong specificity. Currently, commonly used clinical antigen detection methods include counterimmunoelectrophoresis, latex agglutination, reverse indirect hemagglutination, coagglutination, radioimmunoassay, and enzyme-linked immunosorbent assay (ELISA). The positive rate for counterimmunoelectrophoresis exceeds 80%, while latex agglutination has a positive rate of 85–93%. Coagglutination also shows high positive rates for groups A and C. Reverse indirect hemagglutination has a positive rate of 94.2% (cerebrospinal fluid) and 78.8% (blood). ELISA is more sensitive than reverse indirect hemagglutination for detecting group A antigens. Antibody detection is not suitable for early diagnosis due to its lower sensitivity and specificity, leading to declining clinical use. Counterimmunoelectrophoresis, radioimmunoassay, and indirect hemagglutination tests have diagnostic value if the convalescent-stage serum titer is at least four times higher than the acute-stage titer.
In the epidemic season, the sudden onset of high fever, headache, vomiting, accompanied by altered consciousness, and physical examination revealing petechiae or ecchymoses on the skin and mucous membranes, along with positive meningeal irritation signs, can preliminarily establish a clinical diagnosis. Confirmation relies on cerebrospinal fluid examination and the detection of pathogenic bacteria, while immunological tests facilitate early definitive diagnosis.
bubble_chart Treatment Measures
(1) Treatment of Common Meningococcal Meningitis
1. Antibacterial Therapy
(1) Sulfonamides: Given that most A-group strains prevalent in China are sensitive to sulfonamides, they remain the first-line treatment. Sulfadiazine is absorbed and excreted slowly, with cerebrospinal fluid concentrations reaching about 40-80% of blood levels. The initial dose is 40-80mg/kg, administered orally or intravenously in four divided doses. The parent drug tends to crystallize in acidic urine, potentially injuring renal tubules and leading to crystalluria, hematuria, lumbago, oliguria, anuria, or even uremia. Concurrent administration of an equal amount of sodium bicarbonate and adequate fluids (maintaining a daily urine output of at least 1200ml in adults) is recommended. Significant improvement is usually observed within 24-48 hours after sulfadiazine administration, with fever subsiding, consciousness clearing, and meningeal irritation signs diminishing or disappearing within 2-3 days. If symptoms persist or fever remains after 48 hours of treatment, the possibility of drug-resistant strains should be considered, and alternative medications should be promptly initiated.
(2) Penicillin and Chloramphenicol: Penicillin G should be used in the following scenarios: ① Significant hematuria occurs after sulfonamide monotherapy, or in cases of pre-existing renal insufficiency, severe dehydration, oliguria, or anuria; ② No improvement in seasonal disease is observed after 24-48 hours of sulfonamide monotherapy; ③ Drug sensitivity tests indicate sulfonamide-resistant strains. The adult dosage of penicillin G is 8-12 million units daily, while children should receive 200,000 units/kg daily; intrathecal administration is unnecessary. For patients allergic to penicillin, chloramphenicol can be used instead. Chloramphenicol readily crosses the blood-brain barrier, achieving cerebrospinal fluid concentrations of 30-50% of serum levels. The initial dose is 50mg/kg, followed by 50-100mg/kg daily, with a maximum adult daily dose of 4g, administered intravenously or orally in divided doses. Close monitoring for chloramphenicol-induced bone marrow suppression is essential.
(3) Other Antibiotics: Ampicillin can also be used at a dose of 150mg/kg daily, administered intravenously in divided doses. Both ampicillin and chloramphenicol exhibit antibacterial activity against meningococci, pneumococci, and Haemophilus influenzae, making them suitable for infant cases with unclear pathogens.
2. Symptomatic Treatment For high fever, alcohol sponging, nasal drops of metamizole, or small-dose intramuscular injections of metamizole can be used. Headache may be managed with codeine, aspirin, or intravenous hypertonic glucose as appropriate. For convulsions, intramuscular paraldehyde at 0.2ml/kg or 10% chloral hydrate enema (20ml per dose for adults) can be administered. Sedatives should not be overdosed to avoid interfering with clinical observation.
(2) Treatment of Fulminant Meningococcal Septicemia
1. Antibacterial Therapy Penicillin G is the mainstay, with a daily dose of 200,000-400,000 units/kg for adults, totaling 20 million units daily, administered intravenously in divided doses.
2. Anti-Shock Therapy
(1) Volume Expansion and Acidosis Correction Refer to Section 51 "Septic Shock" for details.
⑵ Application of Vasoactive Drugs If shock persists after volume expansion and correction of acidosis, vasoactive drugs may be administered. For patients with a pale-gray complexion, mottled skin, and retinal arteriolar spasm, vasodilators should be selected. The preferred choice is tangut anisodus alkaloid (654-2), which has minimal side effects, as it exhibits anti-sympathomimetic and direct vasodilatory effects. Additionally, it stabilizes neuronal membranes, relieves bronchospasm, and reduces bronchial secretions, with minimal central nervous system stimulation. The dose of tangut anisodus alkaloid is 0.3–0.5 mg/kg per administration, which can be increased to 1–2 mg/kg for critically ill children, administered intravenously every 10–20 minutes. If tangut anisodus alkaloid is unavailable, atropine may be used as an alternative (dose: 0.03–0.05 mg/kg per administration). Typically, after several injections, if the complexion becomes rosy, microcirculation improves, urine output increases, and blood pressure rises, the dosing interval can be extended, the dose reduced, and the drug gradually discontinued. If no improvement is observed after 5–10 administrations of tangut anisodus alkaloid or atropine, a combination of isoproterenol, metaraminol, and dopamine, or phentolamine and norepinephrine, may be used instead.
3. Application of cardiac stimulants and adrenocortical hormones. For details, refer to Section 51 "Septic Shock."
4. Treatment of DIC. If shock does not improve after comprehensive treatment, and even if petechiae do not increase, DIC should be considered. Relevant coagulation and fibrinolysis tests should be performed, and heparin therapy should be initiated. If skin petechiae continue to increase and show a tendency to merge into ecchymoses, heparin can be administered regardless of the presence of shock. The initial dose is 1.5 mg/kg, administered intravenously by bolus or slowly infused in 100 ml of solution. Subsequently, 1 mg/kg is infused every 4–6 hours. The course of treatment should not be too long and can be discontinued once the condition improves, usually lasting 1–2 days. During heparin therapy, the clotting time should be monitored using the test tube method, aiming for approximately twice the normal value (15–30 minutes). If severe bleeding occurs during treatment, protamine sulfate should be administered intravenously immediately, with 1 mg of protamine neutralizing 1 mg (125 units) of heparin.
In severe shock, increased plasmin activity leads to intravascular fibrinolysis, exacerbating bleeding. Therefore, for patients with extensive bleeding, epsilon-aminocaproic acid (6-aminocaproic acid) can be administered after heparinization at a dose of 4–6 g, infused in 100 ml of glucose solution over 30 minutes.
(III) Treatment of Fulminant Meningococcal Meningitis
1. Antibiotic selection is the same as for fulminant septicemia.
2. Use of dehydrating agents. Mannitol is the primary agent, administered at 1–2 g/kg (20%) per dose. Depending on the condition, rapid intravenous infusion or bolus injection is given every 4–6 or 8 hours until respiration, blood pressure, pupil size, and other symptoms of intracranial hypertension normalize. During dehydration, fluids and potassium salts should be appropriately supplemented to maintain a grade I dehydration state. Mannitol can be combined with furosemide (40–100 mg) or alternated with 50% glucose (40–60 ml per dose).
3. Management of respiratory failure. Dehydration therapy should be intensified, along with oxygen administration, sputum suction, and head cooling to prevent cerebral edema, brain herniation, and respiratory failure. If respiratory failure has already occurred, respiratory stimulants such as lobeline, nikethamide, dimefline, or methylphenidate can be administered. A large dose of anisodine (2–3 mg/kg per dose) given intravenously can improve microcirculation and reduce cerebral edema. Hormones also help lower intracranial pressure, but the treatment course should not exceed 3 days. For patients with high fever and frequent convulsions, sub-hibernation therapy may be used. If breathing stops, endotracheal intubation or tracheostomy should be performed immediately, followed by intermittent positive-pressure ventilation.
Since the introduction of sulfonamides and penicillin for the treatment of meningococcal meningitis, the mortality rate has dropped to below 5%. However, the prognosis remains poor for fulminant cases and infants under 1 year of age.
Since the use of antibacterial drugs such as sulfonamides and penicillin G, the mortality rate has dropped to 5-15%, or even below 5%. The following factors are related to prognosis: ① The course of fulminant cases is severe, with a poorer prognosis. ② Patients aged under 2 years or elderly individuals have a worse prognosis. ③ Cases occurring during the peak of an epidemic have a poorer prognosis, while those in the late stages fare better. ④ Patients with recurrent convulsions or persistent unconsciousness have a poorer prognosis. ⑤ Delayed or incomplete treatment leads to a worse prognosis and increases the likelihood of complications and sequelae.
(1) Early detection of patients and local isolation for treatment.
(2) During epidemics, conduct health education campaigns, avoid large gatherings and group activities as much as possible, refrain from taking children to public places, and wear masks when going out.
(3) Drug prophylaxis: Sulfonamides are still used domestically. Close contacts may take sulfadiazine (SD), with adults taking 2g/day divided into two doses along with an equal amount of sodium bicarbonate for 3 consecutive days; children should take 100mg/kg daily. During a meningococcal meningitis epidemic, individuals exhibiting any two of the following four symptoms—① fever accompanied by headache; ② lethargy; ③ acute pharyngitis; ④ skin or oral mucosal bleeding—should be given a full course of sulfonamide treatment, which can effectively reduce the incidence and prevent outbreaks. Internationally, rifampin or minocycline is used for prophylaxis. Rifampin is taken at 600mg daily for 5 days, while children aged 1–12 should take 10mg/kg daily.
(4) Vaccine prophylaxis: Currently, capsular polysaccharide vaccines for groups A and C are widely used domestically and internationally. The ultracentrifuge-purified group A polysaccharide vaccine has a protection rate of 94.9%, with the average antibody titer increasing by 14.1 times after immunization. Domestically, polysaccharide vaccines are also used for "emergency" prophylaxis. If the incidence of meningococcal meningitis in January or February exceeds 10 per 100,000 or is higher than the same period in the previous year, preventive vaccination can be administered to the population.
Complications include secondary infections, suppurative changes caused by the spread of sepsis to other organs, damage to the brain and surrounding tissues due to meningitis itself, and allergic diseases.
Secondary infections are most commonly pneumonia, especially in the elderly and infants. Others include bedsores, corneal ulcers, and urinary tract infections.
Suppurative metastatic changes include panophthalmitis, otitis media, suppurative arthritis (often monoarthritis), pneumonia, empyema, endocarditis, myocarditis, orchitis, and epididymitis.
Damage to the brain and surrounding tissues due to inflammation or adhesions includes oculomotor palsy, optic neuritis, damage to the auditory and facial nerves, limb movement disorders, aphasia, cerebral insufficiency, epilepsy, and brain abscesses. In chronic cases, especially in infants, hydrocephalus or subdural effusion may occur due to adhesions in the interventricular foramen or subarachnoid space, or thrombophlebitis of the bridging veins between the meninges.
Allergic diseases—In the late stage [third stage] of the disease, vasculitis, arthritis, and pericarditis may occur.
Sequelae can result from any complication, with common ones being deafness (which may develop into deaf-mutism in children), blindness, oculomotor nerve palsy, paralysis, intellectual or personality changes, mental abnormalities, and hydrocephalus.
1. Other purulent meningitis can be preliminarily distinguished based on the route of invasion. Pneumococcal meningitis mostly occurs secondary to pneumonia or otitis media, staphylococcal meningitis often develops during the course of staphylococcal sepsis, Gram-negative bacillary meningitis is prone to occur after craniocerebral surgery, Haemophilus influenzae meningitis is more common in infants and young children, and Pseudomonas aeruginosa meningitis often follows lumbar puncture, anesthesia, contrast imaging, or surgery.
2. Epidemic encephalitis B (Japanese encephalitis) mostly occurs in the months of July to September, with severe damage to the brain parenchyma. Unconsciousness and convulsions are common, but skin petechiae are generally absent. The cerebrospinal fluid is relatively clear, with cell counts mostly below 500/mm³ 3. Sugar and protein levels are normal or slightly elevated, and chloride levels are normal. Immunological tests such as specific IgM and complement fixation tests can aid in differentiation.
3. False meningitis (meningism) may present with meningeal irritation signs in patients with acute infections such as sepsis, cold-damage disease, or lobar pneumonia when severe toxemia is present. However, except for slightly increased pressure, the cerebrospinal fluid is otherwise normal.
4. Toxic bacterial dysentery is mainly seen in children and occurs in summer and autumn. Symptoms include high fever, convulsions, unconsciousness, shock, and respiratory failure within a short period, but petechiae are absent, and cerebrospinal fluid examination is normal. Diagnosis relies on stool bacterial culture.
5. Subarachnoid hemorrhage is more common in adults, with sudden onset and severe headache as the main symptom, followed by unconsciousness in severe cases. Body temperature usually does not rise. Meningeal irritation signs are obvious, but there are no skin or mucosal petechiae, ecchymoses, or significant toxic symptoms. The cerebrospinal fluid is bloody. Cerebral angiography may reveal aneurysms, vascular malformations, or other abnormalities.
