What Is the Difference Between Viral and Bacterial Meningitis?

Bacterial meningitis is a serious infectious disease of the central nervous system. It is common in adults, especially in children. Many bacteria can cause this disease. Among them, meningococcus is the most common, followed by influenza bacillus, pneumococcus, Escherichia coli, and other gram-positive bacilli, staphylococci, listeria, and anaerobic bacteria.

Bacterial meningitis is a serious infectious disease with a high mortality and sequelae. Prompt and effective antibacterial treatment on the basis of full consideration of the pathogenic characteristics and antibacterial drugs and pharmacological characteristics is a guarantee to improve the cure rate, reduce the mortality rate and reduce the sequelae.

Overview of bacterial meningitis diseases

Definition of bacterial meningitis

Bacterial meningitis meningitis

Meningococcal meningitis is a purulent meningitis caused by meningococcus. Pathogenic bacteria invade the blood circulation from the nasopharynx to form sepsis, and are finally confined to the meninges and spinal membranes, forming purulent cerebrospinal membrane lesions. The main symptoms are meningeal irritation such as fever, headache, vomiting, skin petechiae and neck stiffness. Cerebrospinal fluid showed purulent changes.

The condition of meningococcus is complex and changeable, with different severity. Generally, there are three clinical manifestations, namely common type, fulminant type and chronic sepsis type. The common type accounts for about 90% of all patients, and can be divided into three classes according to the development process of the upper respiratory tract infection, sepsis and meningitis. Meningitis patients have high fever and persistent toxemia. There are still petechiae and ecchymosis throughout the body, but the symptoms of central nervous system disease are worse. Due to increased intracranial pressure, patients have frequent headaches and vomiting, blood pressure can increase and pulse slows, and often have skin allergies, photophobia, mania and convulsions. After 1-2 days, the patient enters a delirium coma and may experience respiratory or circulatory failure. Late-onset meningitis is more common in children.

Bacterial meningitis disease symptoms

Bacterial meningitis--bacteria The so-called bacterial meningitis can be caused by bacterial or viral infection. The symptoms of viral meningitis are very mild, but the symptoms of bacterial meningitis can be life-threatening. Children under 5 are most likely to develop this condition. It usually occurs as sporadic cases.

Symptoms of bacterial meningitis

Symptoms in early infancy include: lethargy, fever, vomiting, refusal to eat, increased crying, and restless sleep.

Larger children may also experience severe headaches, hate glare and loud sounds, stiff muscles, especially the neck.

In patients of all ages, progressive drowsiness usually occurs after the initial symptoms, and occasionally coma or convulsions may occur. Some children with meningitis may also have a special rash (pink or purplish red, flat, non-fading fingertips).

Bacterial meningitis precautions

Bacterial meningitis 1. Newborns should always pay attention to sepsis or congenital defects of the nervous system. Ask the mother and child if they have a severe infection, choritis, early water breakage, long labor, or a history of birth canal infection. Pay attention to the child's body temperature, whether there is difficulty in sucking, vomiting, diarrhea, reduced activity, crying or not crying, irritability, irregular breathing or dyspnea, paroxysmal asphyxia, convulsions, jaundice, cyanosis, etc.

2. Infants and children should pay attention to whether there is a history of respiratory or digestive tract infections in the past few days, often acute onset, irritability, sudden screaming, blindness, fever, headache, vomiting, loss of appetite, debilitating, convulsions, Lethargy, delirium, and coma. Carefully check for external ear canal purulence and mastoiditis, skin stasis, pustules, fast heartbeat, weak pulse, low blood pressure, irregular breathing rhythms, varying pupil sizes, hepatosplenomegaly, positive skin scratch test, knee Hyperreflexia, full anterior condyle, angulated arch, meningeal irritation, increased intracranial pressure; fundus examination for neglect of papillary edema, arterial spasm, bleeding points, etc.

3. Those who have the following conditions should consider the presence of subdural effusion with meningitis showing a chronic process; acute purulent meningitis, the temperature does not drop after active and reasonable treatment; and after the condition improves, high fever, vomiting, lethargy, coma, and convulsions Other symptoms; increased head circumference, continuous or repeated uplift of the anterior condyle; focal neurological signs. Transcranial radiography or subdural puncture should be performed (such as fluid on one side> 2ml, protein> 40mg, red blood cells 2ml, protein> 40mg, red blood cells <1.0 × 1012 / L for diagnosis). Or CT or magnetic resonance examination.

4. Check the white blood cell count and alkaline phosphatase staining points, and smear on the skin to find bacteria. Cerebrospinal fluid examination, including stress, routine, biochemical, bacterial culture and smear staining to check for germs, convection immunoelectrophoresis and immunofluorescence tests of common bacteria when conditions permit. Determination of lactate, LDH and immunoglobulin. Determination of serum sodium, chloride, urine sodium and osmotic pressure, etc., and review as appropriate.

5. Differential diagnosis The disease should be differentiated from tuberculous meningitis, Japanese encephalitis, meningoencephalitis, and toxic encephalopathy.

Treatment options for bacterial meningitis

General management of bacterial meningitis

Bacterial meningitis--image Bacterial meningitis requires emergency management, and any delay in diagnosis and treatment will result in permanent disability and death. The treatment includes general supportive treatments such as keeping the airway open, cooling, and controlling seizures. Special attention is paid to maintaining electrolyte balance. Low sodium can aggravate cerebral edema; actively anti-intracranial pressure increase and anti-shock; if intravascular condensation occurs Heparinization treatment was given in time. Blood tests and cultures should be taken immediately, and the infusion channel should be retained afterwards; an emergency skull CT examination should be performed to exclude intracranial space occupying lesions; and then a lumbar puncture diagnosis should be performed immediately. Appropriate antibiotics should be given immediately from the beginning (after blood culture); it is not appropriate to start antibiotic therapy after waiting for imaging and cerebrospinal fluid test results.

General treatment is quiet in bed, pay attention to disinfection and isolation, keep the airway open, give oxygen, and sputum. Anticonvulsants can be given by intravenous injection of diazepam 0.1-0.2mg / kg (up to 10mg each time); intramuscular injection of phenobarbital sodium 5-7mg / kg, intravenous injection of each half; phenytoin sodium 6mg / kg intravenous injection, repeat if necessary, Change to oral as soon as possible; 0.3ml / kg enema.

Antibacterial treatment for bacterial meningitis

(1) Influenza B strain: Use ampicillin 400mg / (kg.d), divided into 6 intravenous injections, and discontinue the treatment after 5 days of heat withdrawal, the course of treatment is 10-14 days; or the lymphocytes in the cerebrospinal fluid after the course of foot treatment <50 × 106 / L, protein <500mg / L, the drug can be discontinued. Chloramphenicol 50-100mg / (kg.d), divided into two intravenous injections, the course of treatment is 7d.

(2) Pneumococcus pneumoniae: Penicillin 800,000-1 million U / (kg.d), intravenous drip, ampicillin 150-400mg / (kg.d), or erythromycin 50-60mg / (kg? D), Intravenous infusion, if allergic to penicillin, can be changed to 80mg / kg cefpirin, 4 intravenous injections, plus 5-25mg / d intraspinal injection.

(3) Staphylococcus: cefpirin. Penicillin is used for sensitive strains and cefpirin is injected intraspinally.

(4) The pathogen is unknown: ampicillin. If you are allergic to penicillin, you can change to chloramphenicol.

(5) For the treatment of cerebral hyponatremia, such as serum sodium <120mmol / L, symptoms of hyponatremia, 3% sodium chloride 12ml / kg can be intravenously dripped within 2-3 hours, which can increase blood sodium by about 10mmol / L, if necessary, can be repeated after several hours.

Mannitol

(6). Treatment of subdural effusion Early transcranial radiography or CT examination found effusion, but no symptoms of increased intracranial pressure, no need for puncture treatment. If there is a lot of effusion and symptoms of increased intracranial pressure, puncture can be performed. The puncture should be performed daily, and the fluid should not be more than 30mi each time, and the puncture should be performed every other day until the fluid is discharged. Reduction, or excessive fluid volume, puncture pumping fluid can not reduce the symptoms of intracranial hypertension, continuous drainage, if still not effective, consider surgical removal of the capsule.

(7). Treatment of increased intracranial pressure 20% mannitol or 25% sorbitol 1-2g / kg, rapid hydrostatic in 20-30min, supplemented with 50% glucose solution for 1 / 8-12h, available 2-3 Second, the course of treatment is generally 2d. Or use a 30% urea solution (diluted with 10% sorbitol). Maintenance therapy can be 1-2g / kg of glycerol for 1 / 4-6h, orally or nasally.

(8). To prevent cerebrospinal fluid obstruction and late treatment of cerebrospinal fluid, hydrocortisone or dexamethasone can be given intravenously; or 1-2mg of dexamethasone can be injected intrathecally, which can improve the efficacy.

(9). Anti-shock patients with septic shock should be treated as septic shock. If there is DIC, treat it as DIC.

Bacterial meningitis care

(1).

Mannitol General pediatric nursing routine, coma nursing routine.

(2). Children with coma, persistent convulsions or shock should be guarded specially. Monitor changes in breathing, pulse, body temperature, blood pressure, and condition, the number of bowel movements and the amount of in and out.

(3). Prepare for emergency treatment and report any convulsions, coma, or sudden changes to the doctor in time.

(4). Eat a small number of meals and eat less after eating to avoid vomiting. If the disease permits, you can lift or raise the bedside for about 20 minutes. Nasal feeding can be used for dysphagia. Those who use sulfa or nephrotoxic antibiotics should be given adequate fluids.

(5). Keep the airway unobstructed, and turn your head to one side when vomiting, and remove nasopharyngeal secretions and vomitus in time to prevent inhalation suffocation. Pay attention to oral care.

Bacterial meningitis disease review

Changes in bacterial meningitis

Bacterial meningitis--bacteria Because of the widespread use of new vaccines, the pathogens of bacterial meningitis are quietly changing, which has led to changes in the epidemiology of bacterial meningitis. Dr. Swartz, Department of Internal Medicine, Massachusetts General Hospital, Boston, USA, introduced the progress in the treatment of bacterial meningitis over the past 90 years.

The history of community-acquired bacterial meningitis is undoubtedly the best example of the outstanding effects of antibiotics. Before the clinical use of specific antisera, the prognosis of patients with various bacterial meningitis was extremely poor. Boston Children's Hospital in the United States reported that in the 1920s, 78 deaths of 78 cases of Haemophilus influenzae meningitis in the hospital; similarly, the prognosis of untreated pneumococcal meningitis patients was very poor, 300 patients All died; within the first 10 years of the 20th century, those with untreated meningococcal meningitis had a mortality rate of 75% -80%. Treatment of bacterial meningitis with antiserum

In 1913, Flexner first used intrathecal injection of anti-meningococcal horse serum to treat bacterial meningitis and achieved a certain effect: they reduced the mortality of 1300 meningococcal meningitis patients to 31%. Between 1928 and 1936, Bellevuee Hospital in New York treated 169 meningococcal meningitis children with intrathecal injection of antisera. The effect was better: the mortality rate was about 20%.

Bacterial meningitis treatment enters antibiotic era

In the 1930s, the advent of sulfa drugs reduced the mortality of meningococcal meningitis to 5% -15%. By 1944, 87 children with Haemophilus influenzae meningitis type b had been treated with sulfa and intravenous rabbit antisera, reducing the mortality rate to 22%. In the early 1960s, chloramphenicol (plus sulfadiazine) further reduced the mortality of Haemophilus influenzae meningitis to 5% -10%, and the use of antisera therapy has since become a history. However, the effect of sulfonamide on pneumococcal meningitis is poor, and the mortality rate fluctuates between 45% and 95%.

Penicillin for pneumococcal meningitis began in the mid 1940s. The fatality rate of penicillin for systemic and intrathecal applications was 49%. In 1949, Dowling treated 21 patients with pneumococcal meningitis with high-dose penicillin (1 million intramuscular injections every 2 hours), reducing the mortality rate to 38%, and pioneered the achievement of "brain spine" without intrathecal administration Membrane Dose "A New Era of Modern Therapy.

In the past 15 years, community-acquired bacterial meningitis has been treated with intravenous penicillin (or ampicillin) and / or a third-generation cephalosporin. At this time, the case fatality rate of meningococcal meningitis hovered around 10%, the case fatality rate of Haemophilus influenzae meningitis had fallen below 5%, and the case fatality rate of pneumococcal meningitis remained at about 20%. Beek et al. (See related link) confirmed this result through a large number of Dutch cases: the mortality rate of meningococcal meningitis was 7%, and the mortality rate of pneumococcal meningitis was 30%.

After the phenomenon that the bacterial components in the cerebrospinal fluid (CSF) can cause the release of inflammatory cytokines was revealed, people began to study the adjuvant treatment of dexamethasone. Four studies conducted in the early 1990s proved that dexamethasone did not change the mortality rate of children with Haemophilus influenzae meningitis, but reduced the incidence of neurological sequelae, mainly sensorineural deafness. Dutch scientists in 2002 demonstrated that adjuvant dexamethasone can reduce the incidence of sequelae in adult patients from 25% to 15%. Among them, pneumococcal meningitis has the best prognosis.

Another major advance in the past 20 years is a CT scan of the skull. It can identify other intracranial suppurative infections and find cerebral edema and space-occupying lesions. However, clinicians often delay the use of CT tests because they wait for the results of CT and lumbar puncture tests to delay antibacterial treatment. Beek et al. Studied 696 patients and found that out of 337 patients who underwent CT examinations before lumbar puncture, two-thirds of them did not receive antibacterial treatment before the CT examination results were available. Yale University in the United States studied 301 adult patients suspected of meningitis in an emergency room of a city hospital. It was found that certain clinical characteristics (such as previously suffered from central nervous system disease, sensory central abnormality, limb paresis, aphasia, and visual field abnormalities) can lead to abnormal CT examination results, and 96 patients without the above problems, at least 97 The CT test results were normal in 1% (only 1 patient had mild placeholder performance). Therefore, researchers believe that it is possible to determine which patients do not need CT examination before lumbar puncture based on clinical characteristics.

Changes in bacterial meningitis pathogens

In the last few decades

Sulfa drugs Within, the population of pathogens that cause community-acquired bacterial meningitis is often changing. If all cases of bacterial meningitis after the neonatal period are taken into account, the main pathogens before 20-30 years are Haemophilus influenzae (45%), and then Streptococcus pneumoniae (18%) and Neisseria meningitis Bacteria (14%). As infants were vaccinated against Haemophilus influenzae protein-polysaccharide conjugate vaccine, the incidence of bacterial meningitis changed significantly 10 years ago. The annual incidence of Haemophilus influenzae type B illness in the United States has decreased by 55%, and the annual incidence of Haemophilus influenzae meningitis has decreased by 94%. Results Streptococcus pneumoniae became the main pathogen of bacterial meningitis (47%), followed by Neisseria meningitidis (25%) and Listeria monocytogenes (8%), which is very different from the results reported in the Netherlands. similar. Another change is that the proportion of adult patients with bacterial meningitis in urban hospitals caused by nosocomial infections has increased. For example, the Massachusetts General Hospital in Boston, USA, has a value of about 40%.

Finally, due to the era of antibiotics, the problem of resistance to antibiotics caused by community-acquired bacterial meningitis will persist for a long time. For example, resistance to sulfa was found in Neisseria meningitidis in the 1960s, and resistance to ampicillin by Haemophilus influenzae in the 1970s; pneumonia chains isolated from meningitis patients in the United States in the 1990s Coccus strains are resistant to penicillin (moderately resistant to 21% and highly resistant to 14%), so a third-generation cephalosporin and vancomycin had to be treated in combination. The majority of patients reported by Beek et al. In the Netherlands started using amoxicillin (or penicillin) and / or third-generation cephalosporins; of the 351 Streptococcus pneumoniae isolates, only 2 were resistant to penicillin (moderate) Therefore, it is not necessary to use vancomycin at the beginning of treatment as in the United States.

21 21st Century Outlook for Bacterial Meningitis

According to Swarte, today

Sulfa drugs Progress in post-prevention is greater than progress in treatment. For example, the 7-valent pneumococcal protein-polysaccharide conjugate vaccine, which was introduced in early 2000, appears to prevent invasive infections in children and may unexpectedly reduce invasive infections in the elderly. The development of a quadrivalent meningococcal conjugate vaccine (A / C / Q / W-135) may have greater immunity than polysaccharide vaccines currently in use and provide longer protection. In addition, the incidence of Listeria monocytogenes meningitis is increasing, and it is common in (but not limited to) those with decreased immunity. Increasing the safety measures of food processing can reduce its incidence.

Prevention of bacterial meningitis disease

Routine immunization can prevent infection with Haemophilus influenzae. Immunization can also prevent some types of meningitis of the coccus type in the short term, and this vaccine can be used when the encephalitis is epidemic. Taking antibiotics in close contact with children is another way to prevent the spread of bacterial meningitis.