DISEASEICD-10 CODE
VIRAL MENINGITISICD-10 A87
NONPYOGENIC MENINGITISICD-10 G03.0
BACTERIAL MENINGITISICD-10 G00
MENINGOCOCCAL MENINGITISICD-10 A39.0
HEMOPHILUS MENINGITISICD-10 G00.0
PNEUMOCOCCAL MENINGITISICD-10 G00.1
NEONATAL MENINGITISICD-10 P37.8, P35-P37, G00, G03

Meningitis is caused by inflammation of the meninges that covers the brain and spinal cord, and it can be caused by a variety of organisms that include bacteria, fungi, or viruses. It is a serious condition that can be life-threatening.

Viral Meningitis (aseptic meningitis, nonbacterial meningitis)

Clinical features

A relatively common but rarely serious clinical syndrome with multiple viral etiologies, characterized by sudden onset of febrile illness with signs and symptoms of headache with meningeal involvement. Cerebrospinal fluid (CSF) findings are pleocytosis (usually mononuclear, occasionally polymorphonuclear in early stages), increased protein, normal sugar, and absence of bacteria. A rubella-like rash characterizes certain types caused by enteroviruses, including coxsackieviruses, echoviruses, and the more recently identified numbered enteroviruses (e.g., EV68-EV115), and excluding the rhinoviruses. Vesicular and petechial rashes may also occur. Active illness seldom exceeds 10 days. Transient paresis and encephalitic manifestations may occur; paralysis is unusual. Residual signs lasting a year or more may include weakness, muscle spasm, insomnia, and personality changes. Recovery is usually complete. Gastrointestinal and respiratory symptoms may be associated with enterovirus infection.

Various diseases caused by nonviral infectious agents may mimic viral meningitis. These include inadequately treated pyogenic meningitis; tuberculous and cryptococcal meningitis; meningitis caused by other fungi; cerebrovascular syphilis; and lymphogranuloma venereum. Post-infectious and postvaccinal reactions require differentiation from sequelae to measles, mumps, varicella, and immunization against rabies and smallpox; these syndromes are usually encephalitic in type. Leptospirosis, listeriosis, syphilis, lymphocytic choriomeningitis, viral hepatitis, infectious mononucleosis, influenza, and other diseases may produce the same clinical syndrome.

Infection by enteroviruses (excluding rhinoviruses) transmitted from the mother is a frequent cause of neonatal fever with neurological signs. In polio-free countries, the most prevalent infectious agent causing flaccid paralysis is enterovirus 71, responsible for outbreaks of meningitis and paralysis in many countries. Children and adults with B cell deficiencies are subject to chronic relapsing meningitis, usually caused by enteroviruses.

Causative agents

A wide variety of causative agents exist, many associated with other specific diseases. Predominant causative agents can vary by geographic location and season. Several viruses can produce meningeal features. The causative agent may not be identified in a large proportion of viral meningitis cases (e.g., 50%). In epidemic periods, mumps may be responsible for more than 25% of cases of established etiology in nonimmunized populations. In developed countries, enteroviruses (coxsackieviruses, echoviruses, and the numbered enteroviruses) cause many epidemics/outbreaks of known etiology. Arboviruses, measles, herpes simplex and varicella viruses, lymphocytic choriomeningitis virus, adenovirus, enterovirus, and others may cause sporadic cases. Incidence of specific types varies with geographic location and time. Leptospira may cause up to 20% of cases of aseptic meningitis in various areas (see Leptospirosis), and this bacterial infection should be included in the differential diagnosis of viral meningitis.

Diagnosis

Epidemiologic patterns, patient characteristics (e.g., age, clinical findings, vaccination history) and laboratory information should be used to make a diagnosis and identify the causative agent. Under optimal conditions, specific identification is possible in about half of all viral meningitis cases, through molecular diagnostic, serological, and isolation techniques. Molecular diagnostic methods often yield a more rapid diagnosis and are available for the detection and characterization of most viruses. Viral agents may be detected in early stages from nasopharyngeal and oropharyngeal swabs and stool, CSF, and blood/serum. Other specimens, such as pathologic specimens may also be useful in some instances.

Occurrence

Worldwide, as epidemics and sporadic cases; true incidence is unknown. Seasonal increases in late summer and early autumn are due mainly to arboviruses and enteroviruses, while late winter outbreaks may be due primarily to mumps.

Reservoir

Varies according to the causative agent (see specific disease chapters).

Incubation period

Varies according to the causative agent (see specific disease chapters).

Transmission

Varies according to the causative agent (see specific disease chapters).

Risk groups

Varies according to the causative agent (see specific disease chapters).

Prevention

Varies according to the causative agent (see specific disease chapters).

Management of patient

  1. 1) Diagnosis depends on laboratory data not usually available until after recovery. Therefore, enteric precautions are indicated for 7 days after onset of illness, unless a nonenteroviral diagnosis is established.
  2. 2) Treatment: treatment is often supportive. Specific treatment is available depending on the causative agent (e.g., acyclovir may be given for herpes simplex meningitis). No antiviral therapy is presently available for enterovirus infections.

Management of contacts and the immediate environment

  1. 1) Immunization of contacts: depends on causative agent.
  2. 2) Investigation of contacts and source of infection are not usually indicated.
  3. 3) Risk of acquiring infection can be lowered if good personal hygiene (e.g., handwashing), disinfection of environmental surfaces/items, enteric precautions, and avoiding close contact with an infected person are maintained.

Special considerations

  1. 1) Reporting: depends on causative agent.
  2. 2) Epidemic measures: refer to the chapter relevant to the causative agent.

Bacterial Meningitis

Neisseria meningitidis, Streptococcus pneumoniae and Haemophilus influenzae type b (Hib) are thought to cause more than 75% of all bacterial meningitis, and 90% of bacterial meningitis in children. Meningitis due to Hib, previously the most common cause of bacterial meningitis, has largely been eliminated in many industrialized countries through immunization programs. Meningococcal disease is unique among the major causes of bacterial meningitis in that it causes both endemic disease and large epidemics. The less common bacterial causes of meningitis, such as staphylococci, enteric bacteria, group B streptococci and Listeria, occur in susceptible persons (such as neonates and patients with impaired immunity) or as the consequence of head trauma.

Meningococcal Meningitis (cerebrospinal fever)

Clinical features

An acute bacterial meningitis, characterized by sudden onset of fever, intense headache, nausea and often vomiting, stiff neck, and photophobia. A petechial rash with pink macules or occasionally vesicles may be observed in Europe and North America, but rarely in Africa. Even with antibiotics, case-fatality remains high at 8%–15%. In addition, 10%–20% of survivors will suffer long-term sequelae, including neurologic deficits, hearing loss, and limb loss. Invasive disease is characterized by one or more clinical syndromes including meningitis (the most common presentation), bacteremia, and sepsis. Meningococcemia, or meningococcal sepsis, is the most severe form of infection, with petechial rash, hypotension, disseminated intravascular coagulation, and multiorgan failure. Other forms of meningococcal disease, such as pneumonia, purulent arthritis, and pericarditis, are less common.

Causative agents

N. meningitidis, also called meningococcus, is a Gram-negative, aerobic diplococcus. Neisseria are divided into serogroups according to the immunological reactivity of their capsular polysaccharide. Groups A, B, and C account for at least 90% of cases worldwide, although the proportion of groups W, X, and Y is increasing. In most European and many Latin American countries, serogroups B and C cause the majority of disease, while A is the main cause in Africa and Asia. Serogroup Y causes about one-third of disease in the USA, but less in other countries. As countries introduce meningococcal conjugate vaccine programs against the most common circulating serogroups (serogroup C in Europe, serogroup A in Africa), the proportion of disease caused by serogroup B is increasing.

Diagnosis

The gold standard for diagnosis is recovery of meningococci from a sterile site, primarily CSF or blood. However, the sensitivity of culture, especially in patients who have received antibiotics, may be low. In culture-negative cases, identification of group-specific meningococcal polysaccharides in CSF by latex agglutination can help but false-negative results are common, especially for serogroup B. Polymerase chain reaction (PCR) offers the advantage of detecting meningococcal deoxyribonucleic acid (DNA) in CSF or plasma and does not require live organisms, but it is not yet widely available in many countries. Microscopic examination of gram-stained smears from petechiae may show Neisseria.

Occurrence

In Europe and North America the incidence of meningococcal disease is higher during winter and spring; in sub-Saharan Africa the disease classically peaks during the dry season.

The highest burden of the disease lies in the African meningitis belt, a large area that stretches from Senegal to Ethiopia and affects all or part of 21 countries. In this region, high rates of sporadic infections (1–20 cases/100,000 population) occur in annual cycles, with periodical superimposition of large-scale epidemics (usually caused by serogroup A, occasionally C, and more recently W-135). In the countries of the African meningitis belt, epidemics with incidence rates as high as 1,000 cases per 100,000 population have occurred every 8–12 years over the course of at least the past 50 years. In addition, major epidemics have occurred in adjacent countries not usually considered part of the African meningitis belt (such as Kenya and the United Republic of Tanzania).

Reservoir

Humans.

Incubation period

2–10 days, commonly 3–4 days.

Transmission

Through direct contact, including respiratory droplets from the nose and throat, although this usually causes only a subclinical mucosal infection. Up to 5%–10% of people may be asymptomatic carriers with nasopharyngeal colonization by N. meningitidis. Carrier rates of up to 25% have been documented in some populations in the absence of any cases of meningococcal disease. Less than 1% of those colonized will progress to invasive disease. In contrast, during some meningococcal outbreaks in industrialized countries, no carriers of the “outbreak stain” have been identified. Fomite transmission is insignificant.

Communicability continues until live meningococci are no longer present in discharges from nose and mouth. Meningococci usually disappear from the nasopharynx within 24 hours after institution of antimicrobial treatment to which the organisms are sensitive, and with substantial concentrations, in oronasopharyngeal secretions. Penicillin will temporarily suppress the organisms but does not usually eradicate them from the oronasopharynx.

Risk groups

Travelers to countries where disease is epidemic, Hajj pilgrims, military groups, and individuals with underlying immune dysfunctions, such as asplenia, properdin deficiency, and a deficiency of terminal complement components. Crowding, low socioeconomic status, active or passive exposure to tobacco smoke, and concurrent upper respiratory tract infections also increase the risk of meningococcal disease. Infants are at highest risk but rates decrease after infancy and then increase in adolescence and young adulthood. Group-specific immunity of unknown duration follows even subclinical infections.

Prevention

  1. 1) Several meningococcal polysaccharide conjugate vaccines are available. Different serogroup compositions are licensed in different countries, usually determined by the epidemiology of disease in those countries. In many European countries, Serogroup C and and quadrivalent (serogroups A, C, Y, and W) conjugate vaccines are licensed. In the USA, 2 quadrivalent vaccines, and one bivalent meningococcal conjugate vaccine, are licensed. In Africa, a serogroup A conjugate vaccine is licensed. Routine recommendations for targeted age groups have been implemented in many countries. In the meningitis belt in Africa, countries have implemented mass vaccination campaigns with conjugate meningitis A vaccine of persons aged 1–29 years being a strategy to eliminate serogroup A epidemic meningitis.
  2. 2) Vaccines are licensed against serogroup B meningococcal disease in certain countries where they are used against specific epidemic clones (i.e., New Zealand, Cuba). In serogroup B outbreaks, increasing public awareness and reducing overcrowding may prevent spread of disease.

Management of patient

  1. 1) Respiratory isolation for 24 hours after start of chemotreatment.
  2. 2) Concurrent disinfection of discharges from the nose and throat and articles soiled therewith. Terminal cleaning.
  3. 3) Treatment: Ceftriaxone or penicillin given parenterally in adequate doses is the drug of choice for proven meningococcal disease; ampicillin and chloramphenicol are also effective. Penicillin-resistant strains have been reported in many countries, including Spain, the UK, and the USA; strains resistant to chloramphenicol have been reported in France and Viet Nam. Treatment should start as soon as the presumptive clinical diagnosis is made, even before meningococci have been identified. In children, until the specific agent has been identified, the drug chosen must be effective against Hib as well as S. pneumoniae. While ampicillin is the drug of choice for both as long as the organisms are ampicillin-sensitive, it should be combined with a third-generation cephalosporin, or chloramphenicol or vancomycin should be substituted in the many places where ampicillin-resistant H. influenzae or penicillin-resistant S. pneumoniae strains are known to occur. Patients with meningococcal or Hib disease should receive rifampicin or ciprofloxacin prior to discharge if neither a third-generation cephalosporin nor ciprofloxacin was given as treatment, to ensure elimination of the organism from the nasopharynx.

Management of contacts and the immediate environment

  1. 1) Close surveillance of household, day care and other intimate contacts for early signs of illness, especially fever. Initiate appropriate therapy without delay.
  2. 2) Prophylaxis of close contacts: throat or nasopharyngeal cultures are of no value in deciding who should receive prophylaxis, since nasal carriage is variable and there is no consistent relationship between that found in the normal population and that found in an epidemic.

    Effective prophylactic treatment should be given to intimate contacts, such as household contacts; military personnel sharing the same sleeping space; and people socially close enough to have shared eating utensils (e.g., close friends at school but not the whole class). Younger children in day care centers, even if not close friends, should all be given prophylaxis after an index case is identified.

    Rifampicin, ceftriaxone, and ciprofloxacin are equally effective prophylactic agents. Rifampicin should not be given to pregnant women and may reduce the effectiveness of oral contraceptives. Health care personnel are rarely at risk even when caring for infected patients; only intimate exposure to nasopharyngeal secretions (e.g., as in mouth-to-mouth resuscitation) warrants prophylaxis.

    Persons who have been vaccinated with meningococcal conjugate vaccine should also receive chemoprophylaxis, and it should be given immediately, even before the result of the serogroup testing is available.

Special considerations

  1. 1) Reporting: case report is obligatory in most countries.
  2. 2) Epidemic measures: outbreaks may develop in situations of forced crowding. When an outbreak occurs, major emphasis must be placed on surveillance, early diagnosis and identification of serogroup, vaccination if caused by a vaccine-preventable serogroup and immediate treatment of suspected cases. A high index of suspicion is necessary. A threshold approach tailored to the epidemiology of the country is used in many countries to differentiate endemic disease from outbreaks. When thresholds are passed and the serogroup causing the outbreak is vaccine-preventable, immunization campaigns should be considered.

    • Thresholds for a country with high rates of endemic disease (African meningitis belt):
      • Alert threshold: 5 cases per 100,000 population or increase in relation to previous nonepidemic years. Once alert threshold is reached: mandatory investigation, confirmation of agent, reinforcing of surveillance, enhancing of preparedness, and treatment of patients.
      • Epidemic threshold: 10 cases per 100,000 population and alert threshold crossed early in meningitis season or weekly doubling of cases each week during a 3-week period or 15 cases per 100,000 population or 2 cases at a mass gathering or among refugees or displaced persons. Once epidemic threshold is reached: mass vaccination, provision of drugs to health units, treatment of cases, and public education.
    • Steps used in some industrialized countries:
      • Determine whether the outbreak is organization-based (e.g., school, university, prison) or community-based (town, city, county).
      • Investigate links between cases, because secondary or coprimary cases are excluded from calculations.
      • Calculate attack rates with the outbreak strain among the population at risk.
      • Subtype N. meningitidis isolates, if available, from cases of disease, using molecular typing methods.

        If at least 3 cases have occurred during a 3-month period, the attack rate exceeds 10 cases per 100,000 in the population at risk, and the strain is vaccine-preventable (serogroup A, C, Y, or W), immunization of those in the group at risk should be considered.

    Reduce overcrowding and ventilate living and sleeping quarters for all people exposed to infection because of living conditions (e.g., soldiers, miners, and prisoners).
    Mass chemoprophylaxis is not usually effective in controlling outbreaks. In outbreaks involving small populations (e.g., a single school), consider chemoprophylaxis to all members of the community, especially if the outbreak is caused by a serogroup not included in the available vaccine. If undertaken, chemoprophylaxis should be administered to all members at the same time. Intimate contacts should all be considered for prophylaxis, regardless of whether the entire small population is treated.

    Vaccination in all age groups affected is strongly recommended if an outbreak occurs in a large institutional or community setting in which the cases are due to groups A, C, W-135, or Y. Meningococcal vaccine has been very effective in halting epidemics due to A and C serogroups.

    In countries where large-scale epidemics occur, mass vaccination of the entire population in affected areas should be considered when vaccine supply and administrative facilities allow. Geographical distribution of cases, age-specific attack rates, and available resources all must be considered in estimating the target population. Decisions about vaccination should consider where the intervention is likely to have the largest impact in preventing disease and death.

  3. 3) Although the disease is not covered by the International Health Regulations, some countries may require a valid certificate of immunization against meningococcal meningitis as a condition of entry (e.g., Saudi Arabia for Hajj pilgrims). Further information can be found at: http://www.who.int/topics/meningitis/en.

Hemophilus Meningitis (meningitis due to Haemophilus influenzae)

Clinical features

In industrialized countries, before widespread use of Hib conjugate vaccines, Hib most commonly presented as meningitis. Epiglottitis and bacteremia without focus were the next most common presentations. In developing countries, the primary manifestation of Hib is lower respiratory tract infection. It may account for 5%–8% of all pneumonia in children in these areas, and causes an estimated 480,000 pneumonia deaths each year among children younger than 5 years.

Infection is usually associated with bacteremia. Onset can be subacute but is usually sudden, including fever, vomiting, lethargy, and meningeal irritation, with bulging fontanelle in infants or stiff neck and back in older children. Progressive stupor or coma is common. Occasionally, there is a low-grade fever for several days, with subtler central nervous system symptoms. Overall mortality rate for Hib meningitis is 5%; 6% of the survivors have permanent sensorineural hearing loss; 25% have significant disability of some type.

Causative agent

H. influenzae are Gram-negative coccobacilli that are divided into unencapsulated (nontypeable) and encapsulated strains. The encapsulated strains are further classified into serotypes a through f, based on the antigenic characteristics of their polysaccharide capsules. Hib is the most pathogenic.

Diagnosis

May be made through isolation of organisms from blood or cerebrospinal fluid. Specific capsular polysaccharide may be identified by slide agglutination or latex agglutination techniques. Polymerase chain reaction offers the advantage of detecting meningococcal DNA in CSF or plasma and does not require live organisms, but it is not yet widely available in many countries.

Occurrence

Worldwide. Most prevalent among children aged 2 months to 3 years; unusual in those older than 5 years. In developing countries, peak incidence is in children younger than 6 months; in industrialized countries, it is generally in children aged 6–12 months. As of the late 2000s, with widespread vaccination in early childhood, Hib meningitis has virtually disappeared in industrialized countries and in developing countries that have introduced Hib vaccine. Secondary cases in families and day care centers are rare.

Reservoir

Humans.

Incubation period

Unknown; probably 2–4 days.

Transmission

Through droplet infection and discharges from nose and throat during the infectious period. The portal of entry is most commonly the nasopharynx. The period of communicability lasts as long as organisms are present, which may be for a prolonged period even without nasal discharge. Transmission stops within 24–48 hours of starting effective antimicrobial therapy.

Risk groups

Susceptibility is assumed to be universal. Immunity is associated with the presence of circulating bactericidal and/or anticapsular antibodies, acquired transplacentally, from prior infection, or through immunization.

Prevention

Routine childhood immunization. Several protein polysaccharide conjugate vaccines have been shown to prevent Hib meningitis in children older than 2 months and are licensed in many countries, both individually and combined with other vaccines. Immunization is recommended, starting at 2 months of age, followed by additional doses after an interval of 2 months; dosages vary with the vaccine in use. All vaccines require boosters at 12–15 months of age. Immunization is not routinely recommended for children older than 5 years.

Hib conjugate vaccines have been available since the 1980s and efforts to introduce them are increasing worldwide.

Management of patient

  1. 1) Respiratory isolation for 24 hours after start of chemotherapy.
  2. 2) Treatment: ampicillin has been the drug of choice. However, about 30% of strains are now resistant due to beta-lactamase production. Ceftriaxone, cefotaxime, or chloramphenicol is thus recommended concurrently or singly until antimicrobial susceptibility has been ascertained. The patient should be given rifampicin prior to discharge from hospital to ensure elimination of the organism from the nasopharynx.

Management of contacts and the immediate environment

  1. 1) Prophylaxis is recommended for Hib but not other serotypes of H. influenzae. Rifampicin should be given to all household contacts (including adults) in households with any children younger than 1 year (other than the index case) or with a child aged 1–3 years who is inadequately immunized. When 2 or more cases of invasive disease have occurred within 60 days and unimmunized or incompletely immunized children attend the child care facility, all attenders and supervisory personnel should receive rifampicin. When a single case has occurred, the use of rifampicin prophylaxis is controversial.
  2. 2) Observe contacts younger than 6 years, especially infants, for signs of illness, such as fever.
  3. 3) Educate parents about the risk of secondary cases in siblings younger than 4 years and the need for prompt evaluation and treatment if fever or stiff neck develops.

Special considerations

  1. 1) Reporting: case report may be required in some endemic areas.
  2. 2) Monitor for cases occurring in susceptible population settings, such as day care centers and large foster homes.

Pneumococcal Meningitis

Clinical features

Onset is usually sudden with high fever, lethargy or coma, and signs of meningeal irritation. It can be fulminant and occurs with bacteremia but not necessarily with any other focus, although there may be otitis media or mastoiditis. Pneumococcal meningitis has a high case-fatality rate.

Causative agent

S. pneumoniae, a Gram-positive diplococcus. Nearly all strains causing meningitis and other severe forms of pneumococcal disease are encapsulated. There are 90 known capsular serotypes. The distribution of serotypes varies regionally and with age. In North America the 13 serotypes in pneumococcal conjugate vaccine are those that cause a substantial proportion of pneumococcal meningitis in children and adults.

Diagnosis

May be by isolation of organisms from blood or cerebrospinal fluid. Pneumococcal capsular polysaccharide may be identified by the Quellung reaction or polymerase chain reaction.

Occurrence

Worldwide. Most prevalent among children aged 2 months to 3 years. In developing countries infants are at highest risk; in North America, risk peaks at 6–18 months old.

Reservoir

Humans. Pneumococci are often found in the upper respiratory tract of healthy persons. Carriage is more common in children than in adults.

Incubation period

Unknown; probably 1–4 days.

Transmission

Through droplet spread and contact with respiratory secretions; direct contact with a person with pneumococcal disease generally results in nasopharyngeal carriage of the organism rather than in disease. The period of communicability lasts as long as organisms are present, which may be for a prolonged period, especially in immunocompromised hosts.

Risk groups

A sporadic disease in young infants, the elderly, and other high-risk groups, including asplenic and hypogammaglobulinemic patients. Predisposing factors are cochlear implantation and basilar fracture causing persistent communication with the nasopharynx (see Pneumococcal Pneumonia section in "Pneumonia"). Immunity is associated with the presence of circulating bactericidal and/or anticapsular antibody, acquired transplacentally, from prior infection, or from immunization.

Prevention

Vaccination is the mainstay of prevention. In many industrialized countries, pneumococcal conjugate vaccines are recommended for children younger than 2 years and those aged 2–4 years with certain high-risk conditions, such as immunocompromising conditions, sickle cell disease, asplenia, heart or lung disease, or cochlear implantation. The vaccines cover either the 10 or 13 serotypes that often cause pneumococcal meningitis in industrialized countries. Developing countries are introducing pneumococcal conjugate vaccines into their routine infant vaccine schedules. A polysaccharide vaccine containing 23 of the most common serotypes has been available since 1983. This is recommended in several countries for use in persons aged 65 years and older and those aged 2–64 years with immunocompromising conditions or certain chronic illnesses.

Management of patient

  1. 1) Concurrent disinfection of nasal and throat secretions.
  2. 2) Treatment: penicillin, ceftriaxone, or cefotaxime are the drugs of choice. Because resistance is common in many areas, blood and cerebrospinal fluid culture should be performed for all patients with suspected bacterial meningitis, and susceptibility testing performed on pneumococci. Where resistance is widespread, ceftriaxone or cefotaxime given along with vancomycin are recommended for empirical therapy until susceptibility results are known. Intravenous dexamethasone early in the course of the illness along with antibiotics has been shown to reduce the long-term complications of pneumococcal meningitis.

Management of contacts and the immediate environment

Protection of contacts is not necessary except during an outbreak (see Special Considerations discussed next).

Special considerations

  1. 1) Reporting: case report to local health authority may be required in some areas.
  2. 2) Epidemic measures: pneumococcal meningitis can occur as part of a cluster of pneumococcal disease in institutional settings. Immunization using either the 23-valent polysaccharide vaccine or a conjugate vaccine, depending on the setting and the serotype, should be used to control outbreaks. Targeted antimicrobial prophylaxis (e.g., penicillin) may be useful in some outbreaks, especially those caused by nonvaccine type strains and when the outbreak strain is not resistant to antimicrobial agents. Widespread antimicrobial prophylaxis is not always effective and can induce resistance.

Neonatal Meningitis

Infants with neonatal meningitis develop lethargy, seizures, apneic episodes, poor feeding, hypo- or hyperthermia, and sometimes respiratory distress, usually in their first week of life. The white blood cell count may be elevated or depressed. CSF culture yields group B streptococci, L. monocytogenes (see Listeriosis), Escherichia coli K-1, or other organisms acquired from the birth canal. Infants aged 2 weeks to 2 months may develop similar symptoms, with recovery from the CSF of group B streptococci or organisms of the Klebsiella-Enterobacter-Serratia group, acquired from the nursery environment. Meningitis in both groups is associated with septicemia. Treatment is with ampicillin, plus a third-generation cephalosporin or aminoglycoside until the causal organism has been identified and its antimicrobial susceptibilities determined.

Author

[A. Cohn]

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