Bacterial Meningitis

What is meningitis? Meningitis is an infection of the fluid of a person's spinal cord and the fluid that surrounds the brain. People sometimes refer to it as spinal meningitis. Meningitis is usually caused by a viral or bacterial infection. Knowing whether meningitis is caused by a virus or bacterium is important because the severity of illness and the treatment differ. Viral meningitis is generally less severe and resolves without specific treatment, while bacterial meningitis can be quite severe and may result in brain damage, hearing loss, or learning disability. For bacterial meningitis, it is also important to now which type of bacteria is causing the meningitis because antibiotics can prevent some types from spreading and infecting other people. !efore the "##$s, Haemophilus influenzae type b %&ib' was the leading cause of bacterial meningitis, but new vaccines being given to all children as part of their routine immuni(ations have reduced the occurrence of invasive disease due to H. influenzae. )oday, Streptococcus pneumoniae and Neisseria meningitidis are the leading causes of bacterial meningitis. What are the signs and symptoms of meningitis? &igh fever, headache, and stiff nec are common symptoms of meningitis in anyone over the age of * years. )hese symptoms can develop over several hours, or they may ta e " to * days. +ther symptoms may include nausea, vomiting, discomfort loo ing into bright lights, confusion, and sleepiness. ,n newborns and small infants, the classic symptoms of fever, headache, and nec stiffness may be absent or difficult to detect, and the infant may only appear slow or inactive, or be irritable, have vomiting, or be feeding poorly. -s the disease progresses, patients of any age may have sei(ures. How is meningitis diagnosed? .arly diagnosis and treatment are very important. ,f symptoms occur, the patient should see a doctor immediately. )he diagnosis is usually made by growing bacteria from a sample of spinal fluid. )he spinal fluid is obtained by performing a spinal tap, in which a needle is inserted into an area in the lower bac where fluid in the spinal canal is readily accessible. ,dentification of the type of bacteria responsible is important for selection of correct antibiotics.

Can meningitis be treated? !acterial meningitis can be treated with a number of effective antibiotics. ,t is important, however, that treatment be started early in the course of the disease. -ppropriate antibiotic treatment of most common types of bacterial meningitis should reduce the ris of dying from meningitis to below "/0, although the ris is higher among the elderly. Is meningitis contagious? 1es, some forms are bacterial meningitis are contagious. )he bacteria are spread through the e2change of respiratory and throat secretions %i.e., coughing, issing'. Fortunately, none of the bacteria that cause meningitis are as contagious as things li e the common cold or the flu, and they are not spread by casual contact or by simply breathing the air where a person with meningitis has been. &owever, sometimes the bacteria that cause meningitis have spread to other people who have had close or prolonged contact with a patient with meningitis caused by Neisseria meningitidis %also called meningococcal meningitis' or &ib. People in the same household or day3care center, or anyone with direct contact with a patient's oral secretions %such as a boyfriend or girlfriend' would be considered at increased ris of acquiring the infection. People who qualify as close contacts of a person with meningitis caused by N. meningitidis should receive antibiotics to prevent them from getting the disease. -ntibiotics for contacts of a person with &ib meningitis disease are no longer recommended if all contacts 4 years of age or younger are fully vaccinated against &ib disease %see below'. Are there vaccines against meningitis? 1es, there are vaccines against &ib and against some strains of N. meningitidis and many types of Streptococcus pneumoniae. )he vaccines against &ib are very safe and highly effective. !y age 5 months of age, every infant should receive at least 6 doses of an &ib vaccine. - fourth dose %7booster7' should be given to children between "* and "8 months of age. )here is also a vaccine that protects against four strains of N. meningitidis, but it is not routinely used in the 9nited :tates and is not effective in children under "8 months of age. )he vaccine against N. meningitidis is sometimes used to control outbrea s of some types of meningococcal meningitis in the 9nited :tates. Meningitis cases should be reported to state or local health departments to assure follow3up of close contacts and recogni(e

outbrea s. -lthough large epidemics of meningococcal meningitis do not occur in the 9nited :tates, some countries e2perience large, periodic epidemics. +verseas travelers should chec to see if meningococcal vaccine is recommended for their destination. )ravelers should receive the vaccine at least " wee before departure, if possible. ,nformation on areas for which meningococcal vaccine is recommended can be obtained by calling the ;enters for <isease ;ontrol and Prevention. - vaccine to prevent meningitis due to S. pneumoniae %also called pneumococcal meningitis' can also prevent other forms of infection due to S. pneumoniae. )he pneumococcal vaccine is not effective in children under * years of age but is recommended for all persons over 5/ years of age and younger persons with certain chronic medical problems.
What is meningitis? Meningitis is an illness in which there is inflammation of the tissues that cover the brain and spinal cord. Viral or 7aseptic7 meningitis, which is the most common type, is caused by an infection with one of several types of viruses. Meningitis can also be caused by infections with several types of bacteria or fungi. ,n the 9nited :tates, there are between */,$$$ and /$,$$$ hospitali(ations due to viral meningitis each year. What are the symptoms of meningitis? )he more common symptoms of meningitis are fever, severe headache, stiff nec , bright lights hurting the eyes, drowsiness or confusion, and nausea and vomiting. ,n babies, the symptoms are more difficult to identify. )hey may include fever, fretfulness or irritability, difficulty in awa ening the baby, or the baby refuses to eat. )he symptoms of meningitis may not be the same for every person. Is viral meningitis a serious disease? Viral %7aseptic7' meningitis is serious but rarely fatal in persons with normal immune systems. 9sually, the symptoms last from = to "$ days and the patient recovers completely. !acterial meningitis, on the other hand, can be very serious and result in disability or death if not treated promptly. +ften, the symptoms of viral meningitis and bacterial meningitis are the same. For this reason, if you thin you or your child has meningitis, see your doctor as soon as possible. What causes viral meningitis? Many different viruses can cause meningitis. -bout #$0 of cases of viral meningitis are caused by members of a group of viruses nown as enteroviruses, such as co2sac ieviruses and echoviruses. )hese viruses are more common during summer and fall months. &erpesviruses and the mumps virus can also cause viral meningitis.

How is viral meningitis diagnosed? Viral meningitis is usually diagnosed by laboratory tests of spinal fluid obtained with a spinal tap. )he specific cause of viral meningitis can be determined by tests that identify the virus in specimens collected from the patient, but these tests are rarely done. How is viral meningitis treated? >o specific treatment for viral meningitis e2ists at this time. Most patients completely recover on their own. <octors often will recommend bed rest, plenty of fluids, and medicine to relieve fever and headache. How is the virus spread? .nteroviruses, the most common cause of viral meningitis, are most often spread through direct contact with respiratory secretions %e.g., saliva, sputum, or nasal mucus' of an infected person. )his usually happens by sha ing hands with an infected person or touching something they have handled, and then rubbing your own nose or mouth. )he virus can also be found in the stool of persons who are infected. )he virus is spread through this route mainly among small children who are not yet toilet trained. ,t can also be spread this way to adults changing the diapers of an infected infant. )he incubation period for enteroviruses is usually between 6 and = days from the time you are infected until you develop symptoms. 1ou can usually spread the virus to someone else beginning about 6 days after you are infected until about "$ days after you develop symptoms. Can I get viral meningitis if Im around someone who has it? )he viruses that cause viral meningitis are contagious. .nteroviruses, for e2ample, are very common during the summer and early fall, and many people are e2posed to them. &owever, most infected persons either have no symptoms or develop only a cold or rash with low3grade fever. +nly a small proportion of infected persons actually develop meningitis. )herefore, if you are around someone who has viral meningitis, you have a moderate chance of becoming infected, but a very small chance of developing meningitis. How can I reduce my chances of becoming infected? !ecause most persons who are infected with enteroviruses do not become sic , it can be difficult to prevent the spread of the virus. &owever, adhering to good personal hygiene can help to reduce your chances of becoming infected. ,f you are in contact with someone who has viral meningitis, the most effective method of prevention is to wash your hands thoroughly and often %see ?&andwashing@ inA ?-n +unce of PreventionA Keeps the Berms -way@ at httpACCwww.cdc.govCncidodCopChandwashing.htm'. -lso, cleaning contaminated surfaces and soiled articles first with soap and water, and then disinfecting them with a dilute solution of chlorine3containing bleach %made by mi2ing appro2imately D cup of bleach with " gallon of water' can be a very effective way to inactivate the virus, especially in institutional settings such as child care centers. %:ee more about cleaning and disinfecting in general at

Bacterial Meningitis

What is it? !acterial meningitis is an infection of the covering of the brain and spinal cord, called the meninges, and is caused by bacteria. !acterial meningitis is life3threatening and requires immediate medical attention. Who gets it? !acterial meningitis is more common in very young children, under the age of five. ,n adults, it affects more men than women. People at higher ris are those with chronic illnesses, such as ear and nose infections, or illnesses that impair the immune system. What causes it? )he bacteria that cause most cases of bacterial meningitis are normally present in our environment and can live in our noses and respiratory systems without causing any problems. &owever, this bacteria can infect the brain by spreading from an infection in a nearby part of the body, such as from a sinus infection, or can be carried to the brain by the blood. ,t can also enter the brain after a head inEury, such as a s ull fracture. People with bacterial meningitis are contagious anywhere from two days to two wee s, depending on the type of bacteria that causes the infection. What are the symptoms? .arly symptoms of bacterial meningitis include high fever, headache, chills, and stiff nec . )he nec is so stiff that the patient cannot lower the chin to the chest. +ther symptoms may include nausea and vomiting, confusion, irritability, and a red and purple s in rash. Very young children will be irritable and difficult to feed, e2tremely sleepy or difficult to wa e, will cry inconsolably, and may have sei(ures. ,nfants may not have stiff nec . ,n some cases, especially where treatment is delayed, bacterial meningitis can cause brain damage that results in permanent disabilities and even death. How is it diagnosed? !ecause recovery depends upon quic treatment, a fast diagnosis is e2tremely important. 1our doctor will evaluate your or your child's symptoms, loo ing for specific signs such as a s in rash and stiff nec . )o confirm the diagnosis, your doctor will need to do a lumbar puncture, also nown as a spinal tap, to withdraw some cerebrospinal fluid %;:F' and chec for a bacterial infection. !efore the fluid is withdrawn, an area in the lower bac is numbed with a

local anesthetic. )hen, a long, hollow needle is inserted into the spinal canal to withdraw the fluid. ,f the symptoms are caused by bacteria, the fluid will generally loo cloudy. )he fluid will also be e2amined under a microscope and sent to a laboratory where it will be grown %cultured' so the specific bacteria can be identified. +ther tests that may be done include blood and urine tests and a computed tomography %;)' scan of the head. What is the treatment? 1our doctor may start antibiotic treatment even before test results are in if he or she strongly suspects bacterial meningitis. -ntibiotics are given in a hospital through an intravenous %,V' line, which means it is through a needle inserted in a vein. ,V antibiotics are given for up to two wee s. 1ou or your child will also be given fluids to replace those lost through fever and vomiting. Fecovery is usually complete, especially in children, if the infection is treated within the first few hours. !ecause bacterial meningitis is contagious, patients should not resume normal activities until they have approval from their doctor. ,f you have been e2posed to bacterial meningitis, your doctor may give you antibiotics to help prevent the infection. Self-care tips Because immediate treatment is so important to recovery, seek medical treatment for yourself or your child as soon as you observe any symptoms of bacterial meningitis, especially high fever combined with headache, lethargy, and stiff neck. If you or your child has bacterial meningitis, you should wash your hands frequently to avoid passing the infection on to others. Do not share food or eating utensils, and avoid contact with bodily fluids, such as saliva. Children should routinely be immunized with the emophilus influenzae type B vaccine, which can help prevent a common type of childhood meningitis. !here is also a vaccine available that can prevent some forms of meningitis. !his is commonly given to people who live in areas where there are epidemics of bacterial meningitis.

Background ,nflammation of the leptomeninges is one of the most common manife infections of the ;>:. )he term meningitis implies lac of cerebral %encephalitis' and %myelitis' involvement, but some pathogens may cause a combination of signs and s consistent with meningoencephalitis or encephalomyelitis. ,mplicit in the term @asept nonbacterial etiology of this syndrome, although a partially treated bacterial meningi present with an @aseptic@ picture. ,n the absence of encephalitis, the clinical course o is usually self3limited, with complete recovery in =3"$ days.

For the clinician, consideration of other causes of meningitis such as bacteria, mycop crucial, since these can be associated with devastating outcomes if left untreated. Mu lymphocytic choriomeningitis viruses %G;MV' are now rare offenders in developed cou

of cases today are caused by nonpolio enteroviruses, and thus disease characteristics manifestations, and epidemiology mimic those of enteroviral infections. Polio still rem cause of debilitating myelitis in some regions of the world. )he physician should reali picture of aseptic meningitis may be caused not Eust by infectious agents but also by connective tissue disorders such as systemic lupus erythematosus. )his discussion, h on the viral agents causing the syndrome of aseptic meningitis.

!athophysiology )he viral pathogens may gain access to the ;>: by either of * m hematogenous or neural. &ematogenous is the most common route for viral penetrat nown pathogens. >eural penetration is along the nerve roots and usually is limited t %&:V3", &:V3*, and varicella (oster virus HVIVJ', ! virus, and possibly some enterov

Multiple host defenses prevent the usual viral inoculum from being effective in causin significant infection. )hese include local and systemic immune responses, s in and m and the blood3brain barrier %!!!'.

)he virus replicates in the initial organ system %ie, respiratory or gastrointestinal muc access to the bloodstream. Primary viremia introduces the virus to the reticuloendoth namely liver, spleen, and lymph nodes. ,f the replication persists despite immunologi secondary viremia occurs, which is thought to be responsible for seeding of the ;>:. viral replication probably plays a maEor role in overcoming the host defenses.

)he mechanism of viral penetration into the ;>: is not well understood. )he virus m directly at the capillary endothelial level or through natural defects %ie, area postrem that lac a !!!.' )he inflammatory response is seen in the form of pleocytosisK polym leu ocytes %PM>s' lead the differential cell count in the first *4348 hours, followed la numbers of monocytes and lymphocytes. )he cerebrospinal fluid %;:F' lymphocytes recogni(ed as ) cells, although ! cell immunity is also important in defending against

.vidence e2ists that some viruses may gain access to the ;>: by retrograde transpo roots. For e2ample, the li ely pathway for &:V3" encephalitis is via the olfactory or t roots, with the virus being transported by the olfactory fibers to the basal frontal and lobes. "re#uency

In the US: More than 10,000 cases are reported annually, but the actual incidence may be Lack of reporting is due to the uneventful clinical outcome of most cases and the inability o to grow in culture. n incidence of 11 per 100,000 population per year has been estimated

Internationally: !btaining accurate figures regarding the worldwide prevalence and incide heterogeneous and often clinically benign group of diseases is difficult. "orldwide causes include enteroviruses, mumps virus, measles virus, #$#, and %&#. 'he ma(ority )over *0+ caused by enteroviruses, followed by mumps virus. Meningitis symptoms may develop in a cases of infection by these agents. .tudies from /inland have estimated the incidence to b population in children aged 112 years. 'his is in significant contrast to 310 cases per 100,0 estimated for children younger than 1 year. 4apanese 5 encephalitis virus, the most comm

epidemic viral meningitis worldwide, accounts for over -5,000 infections annually througho estimated to cause 3001-00 times that number of subclinical infections.

)he distribution and attac characteristics of some agents, such as arboviruses transmitted by arthropod vectors, show strong geographic variability. Gac of e vaccination policies in some )hird Lorld countries is another factor causing this discrepancy in the distribution of these infections worldwide. $ortality%$orbidity

67cluding the neonatal period, the mortality rate associated with viral meningitis is less tha rate is also low.

.ome controversy e7ists as to the long1term effects on children, with some studies attribut disabilities, neuromuscular impairments, and deafness to viral meningitis. .ome investigat of these cases must involve the 9:. parenchyma, causing encephalitis or encephalomyel complain of irritability, incoordination, and inability to concentrate for several weeks or long enteroviral meningitis during the first few months of life may have an increased risk of alter development.

;hysicians must reali<e that viruses capable of causing meningitis also can cause more se the 9:. as well as other organs. 'he "orld %ealth !rgani<ation )"%!, statistical reports enteroviral meningitis with sepsis as the fifth most fre=uent cause of neonatal mortality. 9o brain edema, hydrocephalus, and sei<ures can occur in the acute period and are discusse

&ace >o specific racial predilection has been identified.

'e( <epending on the type of viral pathogen, the ratio of affected males to females .nteroviruses are thought to affect males ".63"./ times more often than females. Mu nown to affect males 6 times more frequently than females. Most arboviruses have characteristics, affecting both se2es but at different ages. Age

'he incidence of viral meningitis drops with age. s a general rule, the younger the patient of viral meningitis.

:eonates are at greatest risk and are the group with the most significant risk of morbidity a this type of infection.

&n neonates older than 7 days, enteroviruses are the most common cause of aseptic menin presumably due to the na>ve immune profile of the young in confronting new viral antigens greatly reduced the incidence of viral meningitis from mumps, polio, and measles viruses. 'he incidence during the first year of life is 30 times higher than in older children and adult .ome of the arboviruses strike at the e7tremes of age, with the elderly at greater risk of inf and measles peak in the later teenage years.

CLINIC L
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Section ! of

History

@pon presentation, most patients report fever, headache, irritability, nausea, vomiting, stiff weakness within the past 1*1-A hours.
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%eadache is almost always present and often is reported as severe. 'he classic ab headache of my life,C which usually is attributed to aneurysmal subarachnoid hemor uncommon, however.

9onstitutional symptoms of vomiting, diarrhea, cough, and myalgias appear in more patients.

%istory of temperature elevation occurs in 7A1100+ of patients who come to medica common pattern is low1grade fever in the prodromal stage and higher temperature e onset of neurological signs.

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Dounger children may not report a headache or photophobia and may simply be irri :ewborn infants may present with poor feeding and lethargy.

.ome viruses cause rapid onset of symptoms, while others may involve prodromal nonspe symptoms, such as malaise, myalgia, and upper respiratory symptoms. &n many cases, sy biphasic pattern8 the nonspecific flu1like symptoms and low1grade fever preceding neurolog appro7imately 2* hours. "ith the onset of neck stiffness and headache, the fever usually r

Meticulous history taking is essential and must include evaluation of e7posure to ill contact and outdoor activities in areas of endemic Lyme disease, travel history with possible e7pos as well as history of medication use, intravenous drug use, and se7ually transmitted diseas nother important part of history is prior antibiotic use, which may alter the clinical picture meningitis.

!hysical Beneral physical findings in aseptic meningitis are common to all causative some viruses cause unique clinical manifestations that may help clinicians focus their approach. )he classic tetrad of meningitis is fever, meningismus, irritability, and pho e2amination reveals no focal neurological deficits in the maEority of cases.

/ever is common )*01100+ of cases, and usually ranges between -* and 20 degrees 9el

;hotophobia is a relatively common finding but may be mild. :oise also may irritate the pa

:uchal rigidity or signs of meningeal irritation may be seen in over half of patients, but thes severe than in bacterial meningitis.

&rritability, disorientation, and altered mentation may be seen. .evere lethargy or bulging fo are signs of increased intracranial pressure but may be absent in over half of cases. 'he n hypotonia, irritability, and poor feeding. 'he clinical picture may mimic neonatal bacterial s be accompanied by multiple organ system involvement.

.ei<ures occur occasionally and are usually from the fever, although the involvement of br )encephalitis, should be considered. Elobal encephalopathy and focal neurological deficits present. ?eep tendon refle7es are usually normal but may be brisk.

!ther signs of infection characteristic to certain viral agents can aid in the diagnosis. 'hese and pleurodynia in enteroviral infections, characteristic skin manifestations such as the <os #$#, maculopapular rash in measles and enteroviral infections, vesicular eruption in herpe and herpangina in co7sackievirus infections. 6pstein15arr virus )65#, infections are sug presence of pharyngitis, lymphadenopathy, and splenomegaly. &mmunodeficiency and pne suggest an adenovirus, cytomegalovirus )9M#,, or %&# as the causative agent. ;arotitis an with mumps, while most enteroviral infections have associated gastroenteritis and rash.

Causes Multiple viruses are capable of causing meningitis. :ome have unique ris fa manifestations. )his discussion will attempt to simplify the microbiological characteris family with emphasis on disease manifestations and ris factors unique to that group that in as many as one third of cases no causative agents are identified. )his number new testing methodologies.

6nteroviruses include echoviruses, co7sackieviruses and 5 with their subgroups, poliovi numbered enteroviruses. :onpolio enteroviruses account for over *5+ of all cases of viral overwhelming ma(ority of cases caused by multiple serotypes of co7sackie and echoviruse belong to the viral family ;icornaviridae )BpicoC for small, BrnaC for ribonucleic acid,. 6nterov and 71, which e7hibit strong neurotropism, are associated with meningoencephalitis, polio1 syndromes, and Euillain15arrF syndromes as well as aseptic meningitis. 9o7sackievirus 5 for over A0+ of meningitis cases in children younger than - months.
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6nteroviruses can enter the human host by oral1fecal or respiratory routes and have attack rate in the warm months. .pread of these enteroviruses in the summer and early fall is ubi=uitous, and enteroviruses to cause infection during the warmer months is the ma(or facto high incidence of aseptic meningitis during that time. 'he associated clinical findings in enteroviral infections include pharyngitis, p and pericarditis.

&nfants of mothers infected with co7sackievirus 5 are also at great risk for this poten the neonatal period.

rboviruses account for about 5+ percent of cases of aseptic meningitis in :orth merica encephalitis ).L6, virus being the most common. 4apanese 5 virus is the most common o throughout the world. More than 500 viruses from different viral families are included here multiply in both vertebrates and arthropods as vectors of transmission.
o

'he most common clinical manifestation is one of meningoencephalitis rather than p

meningitis.
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.ome of the important viruses include the eastern and western e=uine encephalitis the 'ogavirus family8 .L6, 4apanese 5, and Murray #alley viruses of the /lavivirus group and 4amestown 9anyon viruses from the 5unyaviridae family. 9olorado tick f coltivirus in the western regions of the @nited .tates.

9hildren with .t. Louis or 9alifornia group encephalitis viruses may not e7hibit any n altered mental status.

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.ei<ures are more common with arboviral meningitis than any other group of viruse

67posure to mos=uito or tick vectors is a risk factor for transmission8 thus the numb is also highest in the summer and early fall owing to the high mos=uito population.

.ome agents preferentially infect certain age groups, such as the .L6, which affect age, and 9alifornia virus, which infects young children.

MumpsG member of the ;aramy7ovirus family, mumps virus was one of the first known c meningitis and meningoencephalitis.
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'he incidence of mumps in the vaccination era has decreased significantly, to 1 per in the @nited .tates. :onetheless, mumps continues to be the cause in 10130+ of c of the world.

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Males aged 1A131 are at highest risk of developing this infection, with a -G1 maleHfem 9lusters of cases occur in schools and colleges in the winter months. 9oncomitant parotitis is a helpful clinical tool but may be absent in as many as half involvement.

cohort study of 13,000 unvaccinated children from northern /inland revealed mum meningoencephalitis accounting for 20.0+ of all viral 9:. infections. &t also remain of aseptic meningitis in 6ngland and 4apan.

%erpes family virusesG %.#11, %.#13, #$#, 65#, 9M#, and human herpesvirus A collectiv appro7imately 2+ of cases of aseptic meningitis, with %.#13 being the most common offe
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'hey may attack any time of the year. 'he disease often is self1limited and does not re=uire specific antiviral therapy, unle encephalitis. %.#11 remains the most common cause of sporadic encephalitis, while %.#13 infec are restricted to aseptic meningitis. %.#13 genital infection often precedes meningitis8 se7ual contact with actively infec of the known risk factors. Maternal1fetal transmission can occur, leading to significa including infantile septicemia and death. %.#11 and 13 and 65# have been associated with recurrent cases of aseptic menin 9M# and 65# infections occur mostly in immunocompromised hosts. 9M# may cau

encephalitis in patients with &?.. 9ongenital 9M#, which is a much more serious f significant associated morbidity and mortality. 9hildhood or adult chickenpo7 infections by #$# only rarely are complicated by men involving any dermatome may lead to meningitis or meningoencephalitis.

Lymphocytic choriomeningitis virusG L9M# belongs to the family of arenaviruses. :ow a ra meningitis, the virus is transmitted to humans by contact with rodents )eg, hamster, rats, m 'hose at highest risk are laboratory workers, pet owners, or persons living in nonhygienic a investigation suggested that congenital L9M# infections may be underdiagnosed. denovirusG denovirus is a rare cause of aseptic meningitis in immunocompetent individu cause of meningitis in patients with &?.. 'he infection may occur simultaneously with an infection. MeaslesG 'his Morbillivirus is another now rare cause of aseptic meningitis. 'he characteri rash aids in the diagnosis. 'he ma(ority of cases occur in younger people in schools and c remains a worldwide health threat with the highest attack rate of any infection. 'he eradica important public health goal of the "%!. %&#G %&# may be a cause of atypical aseptic meningitis characteri<ed by chronicity and rec time of seroconversion, patients may present with 9./ pleocytosis, elevated protein level high intracranial pressure. Ieports have suggested that as many as 5110+ of %&# infection by aseptic meningitis. !ther than the usual meningeal signs of nuchal rigidity, photophobia infections may cause global encephalopathy, sei<ures, and focal neurological deficits. .om chronically abnormal 9./ findings with mild or no symptoms. %&# often can be isolated fro 'uberculous, fungal, mycoplasmal, and other causes of nonbacterial meningitis are not inc discussion because these agents are not viruses. %owever, they are important causes of a and should be suspected in the appropriate clinical setting. /or e7ample, Lyme borreliosis number of cases of aseptic meningitis in areas of endemic disease in the :ortheast and M 'he diagnosis is suggested by the history of tick bite or outdoor activity in areas of endemi presence of erythema chronicum migrans at the site of the tick bite is pathognomonic for L meningitis has a predilection to cause focal cranial nerve palsies, with the seventh nerve b affected. 9linicians must consider partially treated bacterial meningitis as a possible etiolog nature of their patientJs disease. ;atients with bacterial otitis and sinusitis who have been taking antibiotics may present wit 9./ findings identical to those of viral meningitis.

Iecurrence of aseptic meningitis )Mollaret meningitis, usually is due to %.#11 and 13 infec herpesvirus A, 65#, and %&# also have been implicated. 'hese viruses are known to stay nervous system, such as the dorsal root ganglia in the case of %.#. #I$$%&%N'I LS

Section ( of

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-bnormal >eonatal ..B -cute <isseminated .ncephalomyelitis -septic Meningitis !rucellosis ..B in :tatus .pilepticus &,V3" -ssociated ;>: ;onditionsA Meningitis &,V3" -ssociated +pportunistic ,nfectionsA ;>: ;ryptococcosis &,V3" -ssociated +pportunistic ,nfectionsA ;>: )o2oplasmosis

&,V3" -ssociated +pportunistic ,nfectionsA ;ytomegalovirus .ncephalitis &aemophilus Meningitis &erpes :imple2 .ncephalitis &ydrocephalus Geptomeningeal ;arcinomatosis Gow3Brade -strocytoma Gumbar Puncture %;:F .2amination' Gyme <isease Migraine Variants >eonatal Meningitis >eurocysticercosis >eurosarcoidosis >eurosyphilis :taphylococcal Meningitis :ubdural .mpyema :ystemic Gupus .rythematosus )uberculous Meningitis Varicella Ioster )ther !roblems to be Considered Partially treated bacterial meningitis Parameningeal infection Coccidioides immitis infection Cryptococcus neoformans infection Histoplasma capsulatum infection Candida species infection Blastomyces dermatitidis infection Mycoplasma infection Gisteria infection Geptospira infection <rugs &eavy metals :urgically implanted materials :EMgren syndrome !ehNet disease ..B in neurological infections W)&*U+
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*ab 'tudies

Ioutine chemistry and hematology tests, including serum sodium and serum "59 count, neonatal and other severe cases, arterial blood gases analysis, coagulation studies, and li

serum "59 count may be elevated or normal and is not a sensitive indicator of the severit abnormal because of dehydration or the rare occurrence of syndrome of inappropriate anti amylase level may be elevated in cases caused by mumps virus, even in the absence of p reactive protein )9I;, levels in the serum of children with bacterial meningitis whose 9./ bacteria8 a comparable group of children with viral meningitis did not have similar elevation meningitis group vs K30 in viral meningitis group,.

9./ e7amination is the most important test in differentiating the cause of meningitis. 9' sc with any abnormal neurological sign to help e7clude an intracranial lesion or obstructive hy 9./ culture remains the criterion standard in discerning bacterial or pyogenic from aseptic meningitis may present with a negative Eram stain result and thus appear aseptic. 'he fol support the diagnosis of viral meningitisG
o

9ellsG ;leocytosis with "59 counts in the range of 50 to L1000 7 10 0HL of blood has Mononuclear cell predominance is the rule, but ;M:s may comprise the ma(ority of usually is then dominated by lymphocytes in the classic 9./ pattern of viral mening bacterial meningitis, which has a much higher cell count and a predominance of ;M an absolute rule, however.

;roteinG 9./ protein level usually is only slightly elevated, but it may be as high as 3 Elucose level is normal in most cases, but severe hypoglycorrhachia has been repo #ery low glucose levels with a lymphocytic pleocytosis may be seen in tuberculous

9ulture, Eram stain, and acid1fast stainG 'hese tests should be performed, as well a the likely viral pathogens in selected cases. %igh "59 count in the 9./ )especially glucose level should suggest the diagnosis of a bacterial meningitis, though some v profiles. ddition of a drop of 9./ sediment to an &ndia ink preparation may aid in th although antigen assay testing for 9ryptococcus is the preferred test.

ntigensG 9./ late7 antigen testing helps to rule out bacterial causes such as Haem ;9I tests of 9./ for enterovirus, %.#, 9M#, and %&# may aid in rapid and reliable

&nitiating the work1up with routine Eram stain and cultures for bacterial and common saving 9./ for less common tests )ie, ;9I for %&# and 9M#, if the cause of menin

'he e7act se=uence of testing for these agents depends on the clinical condition an of the patient. /or e7ample, most cases of viral meningitis do not re=uire ;9I testin

Imaging 'tudies

&maging for suspected viral meningitis and encephalitis may include 9' scan of the head w with gadolinium.

9' scan with contrast helps in ruling out intracranial pathology. 9ontrasted scans should b along the meninges and to e7clude cerebritis, intracranial abscess, subdural empyema, or available, an MI& of the brain with gadolinium may be performed.

MI& with contrast is the criterion standard in visuali<ing intracranial pathology in viral ence affects basal frontal and temporal lobes with a typical picture of diffusely enhancing bilatera

)ther +ests

ll patients whose condition is not improving clinically within 3212* hours should have mor meningitis.
o o o o

5lood, feces, and throat swabs may be sent for viral serology and cultures.

cid1fast staining of 9./ should be performed and the remaining fluid should be se .erum titers of antibodies against %&# and to7oplasma should be obtained.

dditional serum collection 10131 days later may aid in discerning rising titers in the 21fold increase in viral antibodies confirms the diagnosis. 'his is particularly useful f helpful in ruling out to7oplasmosis, leptospirosis, borreliosis, and rickettsial infection an immediate result for clinical decision making, they may be useful for prognostica

&n case of suspected encephalitis, MI& with contrast enhancement and ade=uate visuali<a necessary.

66E may be performed if encephalitis is suspected or when sei<ures are atypical. ;eriodic 66E often occur with herpetic encephalitis.

!rocedures

L; is the most important and the most common procedure used in diagnosis of viral menin on the severity of the disease and individual indications, include intracranial pressure moni or shunting.

9' scan usually is performed prior to L; to rule out intracranial hematoma, mass effect, or provide significant symptomatic relief, presumably due to the decrease in intracranial press sterile fashion, and the opening pressure of 9./ should be measured. 9oagulopathy due relative contraindication to L;. 'he clinician should e7ercise caution and, as for all medica associated with each individual case.

&ntracranial pressure monitoring rarely is needed in patients with meningoencephalitis com of intracranial hemorrhage in cases with coagulopathy often outweigh the diagnostic benef under strictly sterile conditions by a neurosurgeon or neuro1intensivist.

!perative brain biopsy for confirmation of herpetic encephalitis largely has been replaced b encephalomalacia due to an unknown viral infection may be confused with vascular infarct "ith the use of stereotactic locali<ation and a needle biopsy, morbidity is minimal.

Histologic $indings: 5ecause of the low mortality rate associated with acute viral meningitis, pa response within the 9./ are generally not in evidence. 'he leptomeninges undergo acute inflamm in the acute phase of the disease. ;erivascular cuffing, neuronophagia, and increased number of from patients who died of viral encephalitis. '&% ',%N'
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$edical Care )reatment for viral meningitis is mostly supportive. Fest, hydration, a inflammatory medications may be given as needed. )he most important decision in il antimicrobial therapy for bacterial meningitis pending clear identification of the cause antibiotics should be administered in severe cases as soon as bacterial meningitis is s symptoms of meningoencephalitis should receive empiric acyclovir early to possibly c modified further as the results of Bram stain, cultures, and P;F testing become avail condition need critical care unit admission for airway protection, neurologic chec s, a complications.

.nteroviruses and &:V are both capable of causing viral septic shoc in newborns an soon as the diagnosis is suspected, broad3spectrum antibacterial coverage and acyclo attention should be paid to fluid and electrolyte balance %especially sodium', since :, diuretics, and rarely hypertonic saline infusion may be used to correct the hyponatre of urinary tract and pulmonary systems is of paramount importance.

"aiting for L; results should not significantly delay administration of antibiotics when warr coverage is attained by administration of ampicillin and a third1generation cephalosporin )c cefta<idime can also be used,. minoglycosides are given in severe infections in neonates antiretroviral medications are reserved for cases that are strongly suggested clinically or th article on bacterial meningitis for specific recommendations.

.ei<ures should be treated immediately with &# anticonvulsants such as phenytoin, lora<ep patients with viral encephalitis may be in nonconvulsive status epilepticus, and 66E may b 9erebral edema does occur in cases of severe encephalitis, and may re=uire intracranial p initial dose followed by 0.3510.5 gHkg every A hours,, &# de7amethasone, or intubation and around 3*1-0 mm %g. ;lacement of an intracranial pressure monitor with transduced intrap these cases.

Multiple antiviral medications currently are being tested in the general population8 their imp of viral meningitis have not yet been established.
o o o

&n herpetic viral infections, use of acyclovir still is reserved for severe cases or those to be significantly beneficial only if given very early in the course of the infection. nti1%&# therapy is initiated when the history or associated risk factors suggest the e Eanciclovir for 9M#1related infections is reserved for severe cases with positive 9M &?.1related infection is strongly suspected.

;leconaril is a drug currently undergoing phase &&& trials for enteroviral meningitis wi available soon. &t also is being studied in a :ational &nstitutes of %ealthMsponsored sepsis.

dministration of &#&g to neonates with overwhelming enteroviral meningitis has met with o cases lacking other therapeutic options.

'urgical Care >o surgical therapy is usually indicated. ,n rare patients in whom vir hydrocephalus, a ;:F diversion procedure, such as ventriculoperitoneal %VP' or GP sh Ventriculostomy with an e2ternal collection system is indicated in the rare cases of a meningeal or parenchymal biopsy for definitive diagnosis of rare viral infections is req

required for some cases of encephalitis, usually can be performed at bedside. Consultations

:eurology 1 .ei<ure control, 66E, management of brain edema in refractory cases, neuro1

:eurosurgery 1 ;lacement of intracranial pressure monitor, 9./ shunting or temporary dra intensive care

&nfectious disease 1 9ontrol of epidemics, isolation of patient and contacts, choice of antibi :eonatology 1 ny newborn or infant with severe viral meningitis re=uiring intensive care

,iet >o special diet is required.

Activity )he activity limitations should be individuali(ed on the basis of each patien recommended for the acute phase of infection.

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:ymptomatic control with antipyretics, analgesics, and antiemetics is usually all that uncomplicated viral meningitis.

)he decision to start antibacterial therapy for treatment of possible bacterial meningi antibacterial therapy for li ely pathogens should be considered in the conte2t of the c meningitis for details'.

,n herpetic viral infections, the use of acyclovir usually is reserved for severe cases o -nti3&,V therapy is initiated when the history is strongly suggestive andCor confirmat )hese medications are covered in other articles. Banciclovir for ;MV3related infection positive ;MV culture, congenital infection, or immunocompromised patients. Pleconar ,,, trials for enteroviral meningitis. ,t has shown some promising results so far and m considered e2perimental and will be included in this te2t after F<- approval. -dminis overwhelming enteroviral meningitis has met with only occasional success and is not anticonvulsant therapy, refer to articles covering status epilepticus and pediatric sei(

<rug ;ategoryA Antiemetic agents 33 )hese agents are used mostly to prevent ch
vomiting.

#rug Name dult #ose +ediatric #ose Contraindications Interactions +regnancy +recautions

!ndansetron )$ofran, 11 .elective 51%'-1receptor antagonist tha serotonin both peripherally and centrally. %as efficacy in patients not respond well to other antiemetics. 21* mg &# =*hH=13h 0.1 mgHkg slow &# ma7imum of 2 mgHdose8 may repeat =13h ?ocumented hypersensitivity

.timulators of cytochrome ;1250 system, including barbiturates, phenytoin, and phenylbuta<one, change clearance8 inhibitors of h ;1250 system, such as cimetidine, allopurinol, and disulfiram, inc to7icity 5 1 @sually safe but benefits must outweigh the risks.

.hould be scheduled rather than given prn8 data support prevent chemotherapy1induced nausea and vomiting rather than delayed treatment8 administer for prevention of nausea and vomiting, not rescue of nausea and vomiting

#rug Name dult #ose +ediatric #ose Contraindications Interactions +regnancy +recautions

?roperidol )&napsine, 11 :euroleptic agent that may reduce emes blocking dopamine stimulation of chemoreceptor trigger <one. ls antipsychotic and sedative properties. 3.515 mg &#H&M =21A prn KA monthsG :ot established LA monthsG 0.0510.0A mgHkgHdose &#H&M =21A prn ?ocumented hypersensitivity

tropine and lithium increase to7icity8 fentanyl and other analges cause increased 5; )administration with epinephrine may decrea 9 1 .afety for use during pregnancy has not been established.

.afety in children KA mo not established8 caution in patients with sei<ures, bone marrow suppression, or severe liver disease8 sign

hypotension can occur8 tardive dyskinesia, e7trapyramidal reactio ;arkinson1like state, and akathisia have been reported, especiall elderly8 orthostatic hypotension and altered state of mind can occ especially in elderly May cause N' prolongation )delayed recharging of heart betwee within minutes following in(ection at doses at or below recommen levels8 prolonged N' can cause potentially fatal heart arrhythmia as torsades de pointes )'d;,8 all patients should undergo a 131le prior to administration of drug to determine if N' interval is prolon N'c L220 msec for males or 250 msec for females,8 if N' interva prolonged, droperidol should not be administered8 for patients in potential benefit of droperidol treatment is felt to outweigh risks o potentially serious arrhythmias, 69E monitoring should be perfor prior to treatment and continued for 31- h after completing treatm monitor for arrhythmias

<rug ;ategoryA Antiviral agents 33 -nti3enteroviral therapy is under investigation

become available. -nti3&,V and anti3tuberculosis regimens are not covered here, but are strongly suggested clinically or confirmed by testing. .mpiric therapy can be disc meningitis has been established and bacterial meningitis e2cluded.

#rug Name dult #ose +ediatric #ose Contraindications Interactions +regnancy +recautions $)LL)W-U+

cyclovir )$ovira7, 11 'o be started as soon as diagnosis of herpe meningoencephalitis suspected. &nhibits activity of both %.#11 an 3. -0 mgHkgHd divided =*h for 10112 d -0 mgHkgHd divided =*h for 10 d ?ocumented hypersensitivity 9 1 .afety for use during pregnancy has not been established. 9aution in renal failure or when using nephroto7ic drugs

;robenecid or <idovudine prolongs half1life and increases 9:. to

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"urther Inpatient Care

&f the 9./ Eram stain result is negative but moderate to severe pleocytosis is noted )"59 considered in 1311* hours. ll patients with suspected bacterial meningitis should be treate the bacterial Eram stain, late7 antigen tests, and cultures return negative, antibacterial the testing of 9./ and viral culture for herpes simple7 are negative, acyclovir can be discontin recommended. &f no clinical improvement is noted and all the common bacterial and viral p tests should be performed and the therapy modified depending on their resultsG
o o

9./ 1 #enereal ?isease Iesearch Laboratories test )#?IL,, ;9I for 9M#, acid1fa .kin 1 ;urified protein derivative );;?, to help e7clude tuberculosis

5lood 1 %&# antibody and ;9I, rapid plasma reagent )I;I,, Lyme antibody )in area to7oplasmosis antibody )especially in infants and newborns,

;revention of secondary infections, control of sei<ures, management of electrolyte abnorm nutritional support are paramount for successful management of these patients.

"urther )utpatient Care

lthough most patients with signs of meningitis are hospitali<ed, a subgroup with aseptic m ambulatory setting. bsolute criteria for discharge of these patients from the emergency de recent investigations in children suggest that age L1 year, nonto7ic clinical appearance, no negative 9./ Eram stain, ade=uate control of symptoms, and a reliable family setting may to discharge. ;rospective studies would aid in further delineating guidelines for patient disc &# hydration, empiric antibiotics, and observation, or if a diagnosis other than viral meningi

rrange follow1up with the primary care physician in 11- days with e7plicit instructions to re worsening. follow1up call in a day to report on the status of the patient seems like a comm

&n selected patients, additional serum specimens 10131 days later may reveal a specific vir arboviral, L9M#, and some nonviral causes of aseptic meningitis.

&n cases complicated by sei<ures, outpatient anticonvulsants should be continued and clos week after discharge.

In%)ut !atient $eds

!utpatient supplies of antipyretics such as acetaminophen and antiemetics such as prome who do not appear clinically to7ic. :o strict criteria e7ist for discharging patients with viral m include anticonvulsants in cases complicated by sei<ures. &npatient medications include em discussed.

+ransfer

;atients with focal signs, severe lethargy, or headache should be transferred to the closes younger than 1 year and neonates should be transferred to a hospital e=uipped with pedia

Medications should be instituted prior to transfer in select cases, particularly empiric therap

,eterrence%!revention

;regnant women should avoid e7posure to rodents, rats, and house mice, which carry L9M avoidance of public pools by pregnant women in the third trimester to decrease the risk of fetus. :eonates should be kept away from e7posure to mos=uitos for prevention of arbovir

Complications

9ommunicating hydrocephalus is a rare complication of viral meningitis, and it is due to the inflammatory debris. 'he usual time of onset is within weeks of the original symptoms. #; setting. Less common is acute hydrocephalus, which has its onset within hours to a few da

ventriculostomy with an e7ternal collection system.

Long1term neurological se=uelae from uncomplicated viral meningitis are rare. .e=uelae in sensorineural hearing loss, weakness, paralysis, cranial nerve palsy, learning disabilities, b delay in children have been reported in the literature, especially for infants and young child

!rognosis

'he prognosis is usually e7cellent, with the ma(ority of cases resolving in 7110 days. &mplic this disease. 'his is not the case during the neonatal period, when viral meningitis can be 9hildren with viral meningitis may suffer from neuromuscular impairment )ie, mild paresis o disabilities. 9oncomitant encephalitis adds significant potential for adverse outcomes. .ys hepatitis, which may occur concurrent to the 9:. disease, may be other indicators of poor

!atient -ducation

#accination remains the most effective means of combating infections by polio, measles, m general hygiene remains a problem in some developing countries, and strict handwashing the spread of enterovirus1related infections. lthough enteroviruses are ubi=uitous, some r third trimester should avoid public swimming pools to decrease the risk of enteroviral colon

'he education of se7 partners about the use of barrier devices can significantly decrease t

;rotection of infants from mos=uito e7posure in areas of endemic western e=uine encepha these agents from attacking that vulnerable group of patients. 9ontrol of insect vectors by breeding sites is important in preventing arbovirus infections.

voidance of e7posure to rodents can decrease the incidence of L9M# meningoencephali risk to pregnant women.

/or e7cellent patient education resources, visit eMedicineJs 5rain and :ervous .ystem 9e .tings 9enter. lso, see eMedicineJs patient education articles Meningitis in dults, Menin ,ISC%LL N%)US

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$edical%*egal !itfalls

,eningitis- .acterial
Last Updated: :ovember A, 3002

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Eet 9M6

Synonyms and related /eywords: pyogenic meningitis

U'H)& IN$)&, 'I)N

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uthorG shir *umar- ,#, ;rofessor, ?epartments of ;ediatrics and %uman ?evelopment, Mich 9ollege of Medicine and 6" .parrow %ospital shir Oumar, M?, is a member of the following medical societiesG &nfectious ?iseases .ociety of 6ditor)s,G #a1id 2aimo1ich- ,#, .ection 9hief, ?ivision of 9ritical 9are, %ope 9hildrenJs %ospita ;ediatrics, ssistant ;rofessor, ?epartment of ;ediatrics, @niversity of &llinois at 9hicago8 &o3er ?irector, 9linical ccount Management, ncillary 9are Management8 2oseph #omachows/e- , ?epartment of ;ediatrics, ?ivision of &nfectious ?iseases, .tate @niversity of :ew Dork1@pstate M &o3ert W 'olan- 2r- ,#, 9hief of llergy, &mmunology and &nfectious ?iseases, 'he 9hildrenJs % @niversity %ospital, 9linical ssociate ;rofessor of ;ediatrics, ?re7el @niversity 9ollege of Medic ,#, ;rofessor and #ice 9hairman, ?epartment of ;ediatrics, %ead, ?ivision of &nfectious ?iseas @niversity %ealth .ciences 9enter <isclosure

IN'&)#UC'I)N
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Secti

Background !acterial meningitis is a life3threatening illness resulting from bacteria meninges. :ince the routine use of Haemophilus influenzae type b vaccine in the 9ni has fallen. Most patients are children younger than / years, and =$0 of cases occur than * years.

Predisposing factors include respiratory infection, otitis media, mastoiditis, head trau human immunodeficiency virus %&,V' infection, and other immune deficiency states. penicillin3resistant Streptococcus pneumoniae has resulted in new challenges to treat !acterial meningitis during the neonatal period is considered separately because it ha and etiologic features.

!athophysiology !acteria reach the subarachnoid space by a hematogenous route locali(es to other organs. !acteria may reach the meninges directly in patients with a of infection.

,nterleu in3" %,G3"', tumor necrosis factor3alpha %)>F3 ', and enhanced nitric o2ide roles in triggering inflammatory response and ensuing neurologic damage. ,nfection response later affect penetrating cortical vessels, resulting in swelling and proliferatio cells of arterioles. - similar process can involve the veins, causing mural thrombi and )he result is an increase in intracellular sodium and intracellular water.

!rain edema further compromises cerebral circulation, resulting in increased intracra herniation. ,ncreased secretion of antidiuretic hormone results in the syndrome of ina

hormone secretion %:,-<&', which occurs in most patients with meningitis and cause free water. )hese factors contribute to the development of focal or generali(ed sei(ur edema also results in a caudal shift of midline structures with their entrapment in the foramen magnum. ;audal shifts produce herniation of the parahippocampal gyri andC intracranial changes appear clinically as an alteration of consciousness and postural r displacement of the brainstem causes palsy of the third and si2th cranial nerves. ,f u result in decortication or decerebration and can progress rapidly to respiratory and ca !athogenesis of neonatal meningitis

!acteria from the maternal genital tract easily infect the infant after membrane ruptu streptococci, enteric gram3negative rods, and Listeria monocytogenes can reach the and cause infection. >ewborns also acquire bacterial pathogens from their surroundin factors predispose newborns to bacterial sepsis and meningitis. !acteria reach the m bloodstream and cause inflammation. -fter reaching the ;>:, bacteria spread from t lateral sinuses to the meninges, the choroid ple2us, and the ventricles.

,G3" and )>F3 also mediate local inflammatory reactions by inducing phospholipase the production of platelet3activating factor and arachidonic acid pathway. )his proces of prostaglandins, thrombo2anes, and leu otrienes. !y activating adhesion3promotin endothelial cells, these cyto ines result in attraction of leu ocytes, and then release from the leu ocytes causing alteration of blood brain permeability, activation of coag edema, and tissue damage.

,nflammation of the meninges and ventricles produces a polymorphonuclear respons cerebrospinal fluid %;:F' protein content, and utili(ation of glucose in ;:F. ,nflamma destruction in the form of empyema and abscesses are more pronounced in gram3ne inflammatory e2udate causes bloc age of the aqueduct of :ylvius and other ;:F path obstructive and communicating hydrocephalus. "re#uency

In the US: 5efore the widespread use of con(ugate H influenzae type b vaccine, incidence annually. .ince the marked reduction in H influenzae type b disease, Neisseria meningitidi per 100,000 children )aged 113- mo,. 'he risk of secondary cases is 1+ for family contact contacts. 'he S pneumoniae meningitis rate is A.5 cases per 100,000 children )aged 113-

,ncidence of neonatal bacterial meningitis is $.*/3" case per "$$$ live births. , $."/ case per "$$$ full3term births and *./ cases per "$$$ premature births. newborns with clinical sepsis have associated bacterial meningitis. $ortality%$orbidity

Mortality rates vary with age. ?espite effective antimicrobial and supportive therapy, morta remain high, with significant long1term se=uelae in survivors. 5acterial meningitis also caus results in significant mortality beyond the neonatal period. Mortality rates are highest durin decreasing in midlife and increasing again in the elderly.

&ace

&ncidence rates are higher in frican merican and :ative merican populations.

'e(

Male infants have a higher incidence of gram1negative neonatal meningitis. /emale infants are more susceptible to L monocytogenes infection. Streptococcus agalactiae )group 5 streptococci, affects both se7es e=ually.

Age

Most patients are children younger than 5 years, and 70+ of cases occur in children young

CLINIC L
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Secti

History

:eonatal 1 .ymptoms are nonspecific and include the followingG

o o o o o o o o o o

;oor feeding Lethargy &rritability pnea Listlessness pathy /ever %ypothermia .ei<ures 4aundice

o o o o o o o

5ulging fontanelle ;allor .hock %ypotonia .hrill cry %ypoglycemia &ntractable metabolic acidosis

&nfants and children 1 'he following symptoms are readily recogni<ed as associated with m
o o o o o o o o o o o o o o

:uchal rigidity !pisthotonos 5ulging fontanelle 9onvulsions ;hotophobia %eadache lterations of the sensorium &rritability Lethargy nore7ia :ausea #omiting 9oma

/ever )generally present, although some severely ill children present with hypotherm

!hysical

:eonatal
o

high inde7 of suspicion and awareness of risk factors usually results in early diagn treatment.

9ardinal signs of meningitis )eg, fever, vomiting, stiff neck, are rarely present. /or n signs are the e7ception, rather than the rule.

&nfants and children

o

Oernig and 5rud<inski signs are helpful indicators when present, but they may be ab rigidity, in very young, debilitated, or malnourished infants.

.kin findings range from a nonspecific blanching, erythematous, maculopapular ras or purpuric rash.

;atients also may have other foci of infection. ;resenting symptoms may point towa unnecessary delay in diagnosis of bacterial meningitis.

ppro7imately 15+ of patients have focal neurologic signs upon diagnosis. 'he pre signs predicts a complicated hospital course and significant long1term se=uelae.

Eenerali<ed or focal sei<ures are observed in as many as --+ of patients. .ei<ures - days of illness usually have little prognostic significance. %owever, prolonged or d especially when observed beyond the fourth hospital day, are predictors of a compl serious se=uelae.

&n later stages of the disease, a few patients develop focal 9:. symptoms and othe indicating a significant collection of fluid in the subdural space. &ncidence of subdura the bacterial organism causing meningitis.

ppro7imately A+ of affected infants and children show signs of disseminated intra endoto7ic shock. 'hese signs are indicative of a poor prognosis.

Causes

6tiology of neonatal meningitis

o

5acteria often are ac=uired from the maternal vaginal flora. Eram1negative enteric f streptococci are predominant pathogens. &n premature newborns who receive multi hyperalimentation, and who undergo various surgical procedures, Staphylococcus e species also are reported in greater fre=uency. L monocytogenes is another well kn etiologic pathogen.

6arly onset group 5 streptococcal meningitis occurs during the first 7 days of life an obstetric complications. 'he disease is seen most often in premature or low birth we ac=uired before or during the birth process.

Late1onset meningitis is defined as disease occurring after 7 days of life. 6tiologic a ac=uired and nosocomial pathogens. S agalactiae )group 5 streptococci, are classi serotypesG &a, &b, &c, &&, and &&&. lthough these serotypes occur with almost e=ual fre of disease, serotype &&& causes 00+ of late1onset disease.

@se of respiratory e=uipment in the nursery increases the risk of infection caused b Pseudomonas aeruginosa, and Proteus species. &nvasive devices predispose infan by Staphylococcus epidermidis, Pseudomonas, Citrobacter, and Bacteroides specie

&nfection with Citrobacter diversus and Salmonella species, though uncommon, carr these patients often develop brain abscesses.

6tiology of meningitis in infants and childrenG &n children older than 2 weeks, S pneumonia the most common etiologic agents. H influenzae type b, once the most common pathogen disappeared in countries where the con(ugate vaccine is routinely used. S pneumoniae meningitis

S pneumoniae are lancet1shaped, gram1positive diplococci and are the leading cau serotypes, numbers 1, -, A, 7, 12, 10, and 3- are the ones most often associated w meningitis.

9hildren of any age may be affected, but incidence and severity are highest in the v elderly.

o o o o

ppro7imately one half of patients have an associated parameningeal focus of infec &n patients with recurrent meningitis, typical history includes recent or remote head suspected dural defect. 'his organism also has a predilection for causing meningitis in patients with sickle c hemoglobinopathies, and functional or anatomical asplenia. &mmunity is type specif S pneumoniae coloni<es the upper respiratory tract of healthy individuals8 however, a recently ac=uired isolate. 'ransmission is person1to1person, usually by direct cont are rare. 'he incubation period varies from 117 days, and infections are more preva viral respiratory disease is prevalent. 'he disease often results in sensorineural hea and other 9:. se=uelae. 6ffective antimicrobial therapy can eradicate the organism from nasopharyngeal se !ver the past decade, pneumococci have developed resistance to a variety of antib development is seen worldwide, resistance rates to penicillin vary from 101A0+. ;en pneumococci is due to alterations in en<ymes necessary for growth and repair of th proteins8 thus, beta1lactamase inhibitors offer no advantage. ;enicillin1resistant pne demonstrate resistance to sulfametho7a<oleHtrimethoprim, tetracyclines, chloramph %owever, selected third1generation cephalosporins )eg, cefota7ime, ceftria7one, do some resistant isolates. 'o date, all isolates remain susceptible to vancomycin and various o7a<olidinones. fluoro=uinolones )eg, levoflo7acin, trovaflo7acin,, although contraindicated in childre against most pneumococci and achieve ade=uate 9:. penetration.

N meningitidis meningitis
o

N meningitidis are gram1negative, kidney bean1shaped organisms and fre=uently ar !rganisms are grouped serologically on the basis of capsular polysaccharide8 , 5, 1-5 are the prevalent serotypes. #arious serotypes of meningococci, especially 5, 9 for appro7imately 15135+ of childhood cases. Eroup strains also have resulted in meningococcal meningitis throughout the world and in outbreaks in military barracks tract fre=uently is coloni<ed with meningococci, and transmission is person1to1perso through infected droplets of respiratory secretions, often from asymptomatic carriers generally is fewer than 2 days, with a range of 117 days. Most cases occur in infants aged A113 months8 a second lower peak occurs among purpuric rash fre=uently is seen. Mortality rates are significant in patients who have fulminant form of the disease. :ormocellular 9./ also has been reported in patients meningitis. Most deaths occur within 32 hours of hospital admission in patients who with poor prognosis )eg, hypotension, shock, neutropenia, e7tremes of ages, petech hours duration, disseminated intravascular coagulopathy, acidosis, presence of org peripheral smear, low erythrocyte sedimentation rate Q6.IR or 91reactive protein Q9 %igher rates of fatality and physical se=uelae such as scarring and amputation are r serogroup 9 disease. Long1term se=uelae are rare in patients who have an uneven

H influenzae type b meningitis

o o o

H influenzae type b is a pleomorphic gram1negative rod whose shape varies from a long curved rod. H influenzae meningitis occurs primarily in children who have not b influenzae type b vaccine, with *0100+ of the cases occurring in children aged 1 mo years, a significant number of nonimmuni<ed children ac=uire antibodies against the polyribophosphate of H influenzae type b, which are protective. Mode of transmission is person1to1person, by direct contact, through infected drople 'he incubation period generally is fewer than 10 days. 9urrent mortality rates are less than 5+. Most fatalities occur during the first few da ;lasmid1mediated resistance to ampicillin due to the production of beta1lactamase e being reported increasingly, and now -01-5+ of the isolates are ampicillin resistant may have subtle long1term se=uelae. dministration of de7amethasone early in trea morbidity and se=uelae.

L monocytogenes meningitisG L monocytogenes causes meningitis in newborns and immu 'he disease also has been associated with the consumption of contaminated foods )eg, m are caused by serotypes &a, &b, and &#b. .igns and symptoms in patients with listerial men and diagnosis often is delayed. &n the laboratory, this pathogen can be misidentified as a d streptococci. !ther causes
o o o

S epidermidis and other coagulase1negative staphylococci fre=uently cause mening infection in patients with hydrocephalus or following neurosurgical procedures. &mmunocompromised children can develop meningitis caused by species of Pseudo and diphtheroids. ;atients with lymphoreticular malignancies following ra19 treatment can develop s predisposes them to Streptococcus mitis bacteremia and meningitis. Mortality rates patients are treated with vancomycin.

#I$$%&%N'I LS
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-crodermatitis .nteropathica .ndocarditis, !acterial )ther !roblems to be Considered !rain abscess !rain tumors ;>: leu emia Gead encephalopathy Meningitis, fungal Meningitis, tuberculous )uberculoma

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Eeneral guidelines
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Meningitis is a medical emergency. firm diagnosis usually is made when bacteria demonstrated by increased pleocytosis, elevated protein, and low glucose in the 9.

lumbar puncture )L;, may be contraindicated in some of the following conditionsG meningitis, tuberculous meningitis, and tuberculoma. .pecific hematologic, roentge

Eroup 5 streptococcal antigen test in urine also can have positive results due to con not help to confirm the diagnosis of sepsis or meningitis.

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;resence of bacterial antigens in urine, 9./, or blood in the presence of 9./ inflam

9./ chemistries and cytology vary depending upon the maturity and age of the new of antibiotics.

&nfants and children

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?efinitive diagnosis is based upon 9./ findings. 'he opening pressure of 9./ shou be recorded.

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&f the spinal fluid is not crystal clear, administer treatment immediately without waitin

&f the patient shows signs of pending herniation, consider treatment without perform intracranial pressure is controlled and the patient is clinically stable. 9' scan or M herniation.

;erform chemistries )ie, glucose, protein,, total and differential cell count, Eram stai testing may be considered. Eenerally, 9./ glucose is less than 50+ of simultaneou %owever, these values may be within the reference range in patients with very early not show cytological or chemical changes in 9./.

Most untreated patients have an increased "59 count with a predominance of poly cytocentrifuged 9./ may reveal bacterial morphology. 'he 9./ should be plated im obtained. .mears of petechial lesions may reveal microorganisms on Eram stain. . microorganisms.

.everal tests based upon the principle of agglutination for the detection of bacterial out in samples of 9./, blood, and urine. ntigen detection tests are most helpful in 9./ but antigens persist in body fluids. ntigen detection in the urine is particularly the laboratory. .everal gram1negative bacteria and higher serotypes of S pneumon polyribophosphate. 9apsular antigens of group 5 meningococcus cross1react with O rapid diagnostic tests for the detection of N meningitidis.

;artially treated meningitis