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• Identify and define the signs and symptoms of meningitis in adults, infants and children • Describe the physical exam findings associated with meningitis (Kernig's sign, Brudzinski's sign, Papilledema, Spinal rigidity) • Formulate a work-up for CNS infections (including appropriate lab and radiographic studies) • Name the contraindications for performing a lumbar puncture • Describe the possible complications of a lumbar puncture • Differentiate bacterial, viral and tuberculosis meni…

Stiff Neck

Classic triad of Bacterial Meningitis (85%)***

Bulging Fontanelle (late sign in 1/3 neonates)

Neck stiffness is rare (15% at most)

Meningitis in Newborns


Bacterial Meningitis in Children and adolescents

Full Neurologic Exam (cranial nerves, mini mental status, tone, DTRs, strength)
Nuchal Rigidity
Spinal Rigidity
Kernig's Sign
Brudzinski's Sign

CNS Infections

Commonly an early sign of meningeal irritation

Refers to neck stiffness that prevents flexion

Nuchal Rigidity

-Also a signs of meningeal irritation
-Erector spinae muscle spasm limits spine movement
-Opisthotonos (rigid arched back) may occur (Cannot flex the patient at all)

Spinal Rigidity

Patient supine
Flex hip and knee to 90 degrees
Hold hip immobile and extend distal lower extremity

Positive Test suggests Meningeal Irritation
Resistance to knee extension
Pain in hamstrings

Kernig's Sign

Patient supine
Immobilize trunk against bed
Flex neck bringing chin to chest

Positive Test suggests Meningeal Irritation
Involuntary hip flexion

Brudzinski's Sign

Swelling of the optic disk due to increased intracranial pressure


Causes include:
Brain tumor or abscess
Cerebral trauma or hemorrhage
Arachnoidal adhesions
Cavernous or dural sinus thrombosis
Idiopathic intracranial hypertension (pseudotumor cerebri), a condition with elevated CSF pressure and no mass lesion


Rash is nonspecific for meningitis

Petechia and Purpura (both do not blanch) are commonly associated with meningococcal meningitis

Rashes associated with meningitis

Rapid onset. Usually High fever. Sometimes Altered Mental Status

Bacterial Meningitis

Usually altered mental status. Rapid onset.


Slower onset (over 3-4 days). Rarely altered mental status.

Viral Meningitis

Fever X 1 day
Headache X 2 days
Stiff neck X 1 day
Altered mental status
Nuchal rigidity

Typical Problem List of Bacterial Meningitis

Lumbar Puncture
Differentiating between viral, bacterial & other causes of meningitis

Leukocytosis, thrombocytosis, thrombocytopenia/anemia

Blood Culture
Important for identifying organism in bacterial meningitis with septicemia and when LP is contraindicated

Work-Up for CNS infections

Local infection at lumbar puncture site

Suspicion of a cerebral mass lesion/increased ICP (PAPILLEDEMA!!):
Large brain abscess
Brain Tumor (especially posterior fossa)
Subdural Hematoma
Intracranial Hemorrhage

LP Contraindications

Uncorrected Bleeding Disorder
Severe Thrombocytopenia
Focal neurological symptoms/signs, decreased level of consciousness (LOC)
Acute spinal trauma

LP Contraindications

Patient positioning
Lateral decubitus position
Sitting position

Mark midline spinous process between iliac crests
Corresponds with L3-L4 or L4-L5 interspace

LP Technique

Relatively common
Post LP headache
Post LP back pain (<1/3 of patients, due to local soft tissue trauma)

LP Complication

Infection e.g. spinal abcess, meningitis (estimated at 0.2%)
Spinal subdural / epidural hematoma (predominantly in patients with a coagulopathy)
Nerve root or spinal cord injury/irritation

Transtentorial or cerebellar herniation (risk 0-5% in patients known to have an intracranial mass and high ICP)

Complications secondary to low intracranial pressure
Hearing loss, CN VI paresis
Intracranial subdural hygroma / hematoma

LP Complications

Elevated Lymphocytes
Protein and Glucose Normal

Viral meningits***

Elevated Neutrophils
Low Glucose
Elevated Protein

Bacterial Meningitis (eat the glucose and poop out the protein)

Gram+ cocci
Normal flora
Lancet shaped
alpha hemolytic - partial hemolysis
Polysaccharide capsule

Strep pneumoniae

Gram- diplococci
Polysaccharide capsule
A,B,C,Y and W135 serogroups

Neisseria meningitidis

Gram- coccobacilli
Capsule serovar b (Hib)
Main cause of epiglottitis

H. influenzae type-B

Virulence factors
Polysaccharide capsule - antiphagocytic --> protection

IgA protease - facilitates mucosal colonization and invasion --> protection

Pneumolysin - transmembrane pore-forming toxin --> damage
Other factors: teichoic acid, peptidoglycan fragment...--> inflammation

Strep pneumoniae

Diffuse vascular damage - endothelial damage, inflammation of vessel walls, thrombosis, disseminated intravascular coagulation - caused by action of endotoxins (LPS and LOS: lipooligosaccharides[No O antigen])

Petechial rash

Outbreaks in university dormitories, military barracks, i.e. crowded conditions

Meningococcal meningitis

Virulence factors:
Pili - binding to epithelial cells
IgA protease - mucosal colonization
Polysaccharide capsule type-b = poly-ribitol-phosphate (PRP) - anti-phagocytic
Endotoxin (LPS) - inflammation

H. influenzae type b

At risk: unvaccinated young children

Invasion into deeper tissues (invasion goes between epithelial cells)

H. influenzae type b

white blood cells + gram(+) cocci in pair or chain
alpha-hemolytic - green colonies
optochin sensitivity
bacitracin resistant

S. pneumoniae

gram(-) diplococci within polymorphonuclear cells
growth on BLOOD agar
Thayer-Martin agar: a modified (selective) chocolate agar
optimal growth with 5% CO2

N. meningitidis

white blood cells + gram(-) coccobacilli or rods
chocolate agar - provides both X & V factors needed (will not grow on blood agar)

H. influenzae type b

Latex particle agglutination test to identify capsular antigens in CSF

Neisseria meningitidis

Common virulent factor in meningitis-causing bacteria

Capsule (CLICKER)

16yo with high fever and hemorrhagic skin rash. Headache, photophobia, and neck stiffness.

Neisseria meningitidis (CLICKER)

gradual onset over a few weeks
starts with malaise, apathy and anorexia
then photophobia, neck stiffness, impairment of consciousness
serious complications and sequelae

also involved in brain abscesses

Tuberculous meningitis


Neisseria meningitidis***

Purulent exudate covers the surface of the brain and fills the sulci

Pneumococcal meningitis

Filled with neutrophils
Acute suppurative bacterial meningitis

Virchow-Robin space

Leptomeningeal vessel with necrosis of the vessel wall.


Gram+ rods that cause transplacental infection in the neonate.

Listeria monocytogenes

Antimicrobial chemoprophylaxis for close contacts of Bacterial meningitis patients


Vancomycin & 3rd generation cephalosporin (Ceftriaxone) - crosses the BBB

Bacterial Meningitis Treatment

7-valent conjugate vaccine - infants and young children
23-valent polysaccharide vaccine

Penumococcal Meningitis

Meningococcal polysaccharide vaccine (MPSV4) - adults over 55

Meningococcal conjugate vaccine (MCV4) - all children at routine preadolescent visit (11 to 12); recommended for people at increased risk

Both prevent 4 types of meningococcal disease A,C,Y,W-135 (not B because poor immunogen)

Meningococcal Meningitis

Hib conjugate vaccine

Haemophilus meningitis

GBS produce a diffusible heat-stable protein (CAMP factor) that enhances Beta-hemolysis of Staphylococcus aureus***

Streptococcus agalatiae -Identification Test


Neonate with beta hemolytic colonies - fever, respiratory distress, lethargy. Gram positive rod. Cause of the disease?

Listeria monocytogenes

Mortality rate - 20% to 30%
HIGHEST number of deaths caused by foodborne bacterial diseases

Listeria monocytogenes

Manifestations are host-dependent
Self-limited febrile gastroenteritis - immunocompetent persons
Bacteremia - during pregnancy - Listeria proliferate in placenta --> neonatal infections - stillbirth, meningitis
Sepsis and CNS infections - elderly and immunocompromised persons


-Widely distributed in nature
-Reservoir - intestine of animals and humans
-Small Gram(+) rods
-Non-spore forming, facultative anaerobes
-Growth - broad temperature range: 1C to 45C
Motile at 25C
Non-motile at 37C

Listeria monocytogenes

-ingestion of contaminated food: unpasteurized dairy products and undercooked animal products
-transplacentally in utero
-transmission during delivery

Risk groups for invasive diseases - immunocompromised individuals, pregnant women and their fetuses and neonates, and the elderly

Listeria monocytogenes

L. monocytogenes -Attachment and entry into nonphagocytic cells


L. monocytogenes- pore forming exotoxin; escape from vacuole or phagolysosome --> release into cytosol.

Listeriolysin O (LLO)

L. monocytogenes- surface protein; actin polymerization --> motile comet tails


- disease, which typically is noninvasive
-fever, myalgias, and diarrhea - last 1-3 days

Febrile gastroenteritis (Listeria infection)

-early-onset sepsis - "granulomatosis infantiseptica"
-in utero via transplacental transmission --> stillbirth or disseminated infection
-abscesses and/or granulomas in multiple organs
-late-onset meningitis - through vaginal transmission

Neonatal infections (Listeria infection)

-Listeria has a predilection for brain stem, meninges
-meningitis, encephalitis
-brain abscess in 10% of infections --> high mortality

CNS infections (Listeria infection)

occult - fever, malaise, no obvious focus during pregnancy - Listeria proliferate in placenta

Bacteremia (Listeria infection)

Nonmotile at 37C
Gram+ rods

Listeria monocytogenes

GBS, E.Coli +/- Listeria

Neonatal Bacterial Meningitis

Specific antibiotic for Listeria


Gentamicin/Cefotax + Ampicillin

Neonatal Bacterial Meningitis Treatment

screening of pregnant women for vaginal colonization
clinical factors determine risk - prolonged membrane rupture, fever...
intrapartum prophylaxis is protective (penicillin or ampicillin)

Neonatal meningitis prevention

Bacterial meningitis in a 35yo man - gram positive coccobacilli - high protein, low glucose, neutrophils in CSF

Coccobacilli = Rods = Not a cocci

Listeria monocytogenes (CLICKER)

Fibrosis of the meninges can cause this complication of meningitis


Complication of Neonatal Meningitis: Severe brain atrophy

Direct cytolytic effect of Virus

HSV, West Nile virus; poliovirus; JC virus

Inflammatory or immune mediated effects of virus

HIV, flaviviruses

Vasculitic effects of virus

VZV encephalitis


Common causes of aseptic meningitis

Majority of cases are caused by Enteroviruses (members of the Picornaviruses) esp. Coxsackie B and echoviruses.

5 types = 70% of cases; most occur in late summer and early fall.

~20,000 cases/year in the US; 90% of cases in pts <1 yr old.

Enteroviral CNS disease is generally milder than arbovirus (arthropod-borne) disease, or bacterial or fungal meningitides, and is self limiting.

Aseptic meningitis and/or encephalitis

Picornavirus family member; non-enveloped ssRNA virus. Three serotypes known.

Incidence is < 0.03/million in the US to 1/5000 in some parts of Africa.


Most infections are asymptomatic.

A minor illness presents with malaise, fever and sore throat.

The major (paralytic polio) illness has a sudden onset of symptoms: headache, fever, vomiting and neck stiffness. This lasts about a week.

In a minority of these pts, paralysis occurs. Any or all muscles can be affected.


Paralysis is of the motor neuron type with flaccidity of affected muscles.

Bulbar polio shows involvement of the cranial nerves, resulting in
paralysis of the pharynx, requiring mechanical support for respiration.


Transmitted via the fecal-oral route.

Virus replicates in the oral cavity and gut, then infects neurons via the blood.

Poliovirus has an affinity for motor neurons. Causes paralysis by infecting and killing cells in the anterior horn of the spinal cord (LMN= flaccid paralysis).

Polio Pathogenesis

Killed virus vaccine - SALK - protection in the gut - less risk in immunocompromised children (avoid developing encephalitis)

Live virus vaccine - SABIN - get 2 layers of protection - in the gut and serum

Polio vaccines

Member of the Rhabdoviridae. Bullet-shaped morphology; enveloped ssRNA virus.

100% (only 8 known survivors!) lethal encephalitis.

A zoonotic disease, spread mostly via bites from infected animals, aerosol contagion is known to occur.


About 50,000 deaths/year worldwide; only 1-3 deaths/year in the US. However, 20-40,000 post-exposure vaccinations are required each year in the US.

In the US, exposure to bats is the most common cause of rabies. Dog bites are the most common means of transmission worldwide. Always inquire as to pt's travel and animal exposure history when suspecting rabies.


the most common wild animal reservoirs of rabies in the US

Skunks, foxes, racoons

Despite the severity of the disease, pathology in the CNS is minimal, and pathogenesis is poorly understood. Immunopathogenesis doesn't appear to contribute to the disease.

Virus travels up axons via retrograde movement and has a particular affinity for hippocampal neurons.

Rabies pathogenesis

Diagnostic of rabies infection

Negri bodies***

Incubation period: 4-12 weeks. Appearance of symptoms dependent upon proximity of bite to CNS.

Symptoms: initially non-specific. Pain around bite area, muscle spasms, tremors, agitation.

Rabies-clinical course

Encephalitic (furious) = more common. Symptoms include excitement, tremors, muscular contractions and convulsions, phobic spasms (esp. muscles of swallowing), increased sensitivity of the nervous system, and hypersalivation.

Paralytic (dumb): symptoms include lack of aggression, paralysis of muscles, speech and respiration.

Two forms of Rabies

Virus is present in saliva, tears, skin, and brain**


Treatment: none, once symptoms appear.

Antivirals, IFNg, steroids and other immunosuppressants have been tried but are not effective.

Coma induction has been tried and only successful in 3/12 cases.

Rabies: response

Wounds should be washed thoroughly AND pt given:

Passive immunization: Human anti-rabies immune globulin should be administered promptly AND:

Vaccine: Inactivated viral vaccine should be used within 8 days of suspected contact. Vaccine is given i.m. in 3-5 doses at 0, 3, 7, 14 and 28 days.

Rabies: response

Animals free of symptoms for 10 days after biting can be considered rabies-free. Brains of killed animals should be examined for Negri bodies, and by PCR.

With animal bites, regard ANY wild animal (bat, raccoon, fox, etc) as rabid unless the area is known to be rabies free, or until the animal can be tested.

Rabies: response

Results from the reactivation of latent varicella zoster virus (VZV) infection.
It presents as the painful, often debilitating eruption of a rash, usually unilateral, along a dermatome.

Herpes zoster (shingles)

Operationally defined as pain that persists for more than 3 months after the resolution of the skin lesions of Herpes Zoster.

Post-herpetic neuralgia (PHN)

Affects 106 people/year, (50-70% >50 yrs of age). At least 10-20% of patients with HZ will progress to PNH (50% of these will be >60). Reactivation results from a decline in VZV-specific T cell immunity.

Changes in sensation in the dermatome, resulting in either hypo- or hyperesthesia, are common.

HZ and PHN

Treatment: First-line treatments include anti-convulsants (gabapentin or pregabalin), and lidocaine patches.

PHN intervention

Second-line treatments include opioids, topical capsaicin, and tri-cyclic anti-depressants such as amitriptyline or nortriptyline.

NSAIDS are ineffective.

PHN intervention

There is no evidence that use of anti-virals prevents PNH.

Prevention: Live, attenuated vaccine (Zostavax) is approved for the prevention of HZ in persons > 60 years of age. (the same one given to children)

PHN intervention

Infections manifest as either Herpes simplex encephalitis (HSE), which is mainly due to HSV-1.

Neonatal HSE is usually due to HSV-2, but Adult HSE is due to HSV-1. HSV encephalitis accounts for 10-20% of cases of acute encephalitis

HSV infection

Herpes simplex meningitis (HSM), which is mainly due to HSV-2.

HSV-2 now ranks second among the causes of viral meningitis in adolescents and adults.

HSE/HSM may result from primary infection, or from reactivation infection, with spread into the CNS. How HSV enters the CNS is unknown.

HSV infection

HSE is a medical emergency!!!

Untreated, the mortality rate is 70%.

Even when treated, survivors of HSE can be left with a permanent memory impairment, abnormalities in personality and behavior, epilepsy or dementia.

HSV infection

HSE is usually accompanied by headache, confusion, lethargy, seizures and progressively deteriorating mental aberrations.

HSE characteristically produces focal hemorrhagic*** necrosis of the temporal or frontal lobes (which contrasts with other viral encephalitides).

HSV infection

manifests similarly to other meningitides, typical as a complication of primary genital herpes.

Herpes simplex meningitis (HSM)

More common in Mollaret's syndrome (a syndrome of benign recurrent episodes of aseptic meningitis).


IV Acyclovir reduces HSE mortality to 20-30%. Steroids are sometimes given as well, but are not considered standard treatment.

HSV treatment

PCR analysis of the CSF for the presence of HSV DNA is the procedure of choice.

Cranial CT or MRI as soon as possible after presentation.

CSF lymphocytosis is observed in >90% of pts. RBCs in CSF are typical for HSV encephalitis, but NOT diagnostic.

Diagnosis of HSV infections

Member of the Flavivirus family.

Now established in the US since 1999. The strain circulating in North America has >99.8% nucleotide homology with viruses isolated in Israel.

West Nile Virus

Main carrier in the USA is the mosquito Culex pipiens.

Predominant hosts are birds.

Epidemics are associated with massive mortality in local bird and horse populations.

West Nile Virus

About 80% of WNV infections are asymptomatic, and only 1/150 infections yield symptomatic illness from neuroinvasive disease (NID, see next slide).

About 20% of infections yield West Nile fever: an acute, self-limited flu-like illness with sudden onset: fever, headache, myalgia, headache, nausea and vomiting. 50% of pts will have a rash on face and trunk.

West Nile Virus Infection

Advanced age (>55) is the greatest risk factor for Neuroinvasive Disease

West Nile Virus infection

Neuroinvasive disease appears as either aseptic meningitis, encephalitis, poliomyelitis, or in many cases, a combination of these syndromes.

Multifocal chorioretinitis appears to be a specific marker of WNV infection.

West Nile Virus infection

Pts most at risk are >70 yrs old. Highest mortality rates for these is ~8-10%. The overall mortality rate for WNV infection is ~4%.

Younger affected pts may have polio-like symptoms, with motor neuron infection leading to flaccid paralysis.

West Nile Virus pathogenesis

Tremor is seen in up to 80% of pts, unlike other viral meningitides. Neck pain, pleocytosis, myalgia, vomiting, chills are also very common.

WNV meningitis

Consists of fever, headache and altered mental status, and majority of pts have postural or kinetic tremor, unlike other viral encephalitides (except StLE or JBE).

WNV encephalitis

Pts have a rapid onset of asymmetric flaccid limb paralysis.

WNV poliomyelitis

CSF findings show granulocytic
pleocytosis, in ~50% of pts, elevated
protein and normal glucose

ELISA for IgM anti-viral antibodies is the mainstay of diagnosis.

WNV lab diagnosis

Mosquito-borne. About 20-200 cases annually in the US; tends to occur in episodic outbreaks. Most infections are subclinical, but has an 8% mortality rate (higher in elderly pts) in those who become clinically ill. Neurologic sequelae are common.

St. Louis encephalitis (StLE) (flavivirus encephalitides)

World-wide, the largest cause of epidemic encephalitis. Common throughout southern, eastern, and southeast Asia; ~30-50,000 cases/year and 10-15,000 deaths occur annually (mortality rate of 20-30%) and neurologic sequelae are common. Mosquito-borne.

Most cases occur in children <10 yrs.

Vaccine: Inactivated virus vaccine available for travelers to endemic regions.

Japanese B encephalitis (JBE) (flavivirus encephalitides)

Most medically important pathogen is Eastern equine encephalitis. Mosquito-borne.

Mostly occurs in the eastern US. Infections are very rare, but tend to occur in local outbreaks. A 2006 outbreak of seven cases occurred in New Hampshire, with two fatalities.

Most infections are asymptomatic, but EEE has a mortality rate of ~33%.

Acute symptoms are typical of encephalitis.

Those who recover from encephalitis have permanent neurologic sequelae.

Togavirus encephalitides

One sign of primary HIV infection can be aseptic meningitis, manifested by headache, confusion, seizures or cranial nerve palsies. Seen in up to 17% of cases of primary HIV infection and may be associated with faster disease progression.

In most patients, the clinical findings resolve without treatment.

Neuropathogenesis of HIV

HIV-infected cells (in particular monocytes) appear to infiltrate the CNS very soon after peripheral infection and provoke a neuropathological response involving all cell types in the brain.

Despite overt neuronal pathology, HIV does not directly infect neurons.

Neuropathogenesis of HIV

Neuronal dysfunction or death is largely an indirect consequence of disrupted function of macrophages, microglia, and astrocytes, and the cellular toxins released by infected cells.

This can induce severe and debilitating neurological problems that include behavioral abnormalities, motor dysfunction, and frank dementia.

Neuropathogenesis of HIV

HAD-HIV-associated dementia is a neurodegenerative syndrome that is clinically characterized by progressive cognitive, motor and behavioral abnormalities, and is associated with high viral loads. Seen in 20-40% of pts with advanced AIDS, and 7% of HIV- 1-infected patients treated with HAART.

HAD is an AIDS-defining disorder.

Neuropathogenesis of HIV

MND- Mild neurocognitive disorder is seen in ~30% of HIV+ pts. Diagnosed by having at least two of the following: impaired attention or coordination, mental slowing, impaired memory, slowed movements, or impaired coordination. MND does NOT progress to HAD.

Mental deficits are much less pronounced in MND than in HAD.

Neuropathogenesis of HIV

Standard treatment for HAD is HAART, combined with aggressive treatment of associated psychiatric problems (such as mood, anxiety, or substance use disorders).

HIV intervention

Nonenveloped DNA virus.

Member of the Polyoma virus subfamily of the Papovaviridae).

JC virus is an opportunistic pathogen. Infection is widespread (60-90% of the population is antibody-positive) and nearly all infections are asymptomatic.

JC polyoma virus infection

Causes progressive multifocal leukoencephalopathy (PML), a degenerative demyelinating disease, in immunosuppressed pts. 80% of PML pts have HIV/AIDS.

After toxoplasmosis, PML is the most common opportunistic infection to affect the CNS (~10-14% of pts, even in the age of HAART).

JC polyoma virus infection

JC virus is cytolytic for glial cells and oligodendrocytes.

PML frequently presents as hemiparesis, ataxia,
visual disturbances (hemianopia) or higher cortical
dysfunction [ex. dysphasia or agnosia rather than global
impairment], with rapid progression to death.

Mortality rate is 30-50%; survivors have devastating neurologic deficits.

Progressive multifocal leukoencephalopathy (PML)

Neuroimaging, particularly brain MRI, is crucial for early diagnosis of PML.

Detection of JC DNA in CSF via PCR is required for a definite diagnosis of PML.

HAART and immune reconstitution are the only effective treatments for PML.

PML intervention

Most likely virus in meningitis in 2year-old patient?

Enteroviruses (CLICKER)

Definitive Diagnostic Test for Herpes Virus Encephalitis?


Symptoms of Meningitis

Temperature Instability (Hypothermia or Fever)
High pitched crying
Refusal to eat
Weak sucking response
Respiratory distress
Bulging Fontanelle (late sign in 1/3 neonates)

Newborns and Infants

Attempt to passively flex the patient's neck and touch his chin to his chest
If nuchal rigidity is present, this maneuver triggers pain and muscle spasms
The patient may also notice nuchal rigidity when he attempts to flex his neck during daily activities
May herald life-threatening subarachnoid hemorrhage or meningitis
It may also be a late sign of cervical arthritis

Nuchal Rigidity

Kernig's Sign

Brudzinski's Sign

Gram(-) large rods with thick mucoid capsule cause meningitis in the aged

Klebsiella pneumoniae

Gram(+) cocci in normal vaginal flora

Streptococcus agalactiae

When would you worry about HSV and start acyclovir?

high RBC in CSF without a "traumatic tap", focal neurologic deficits, simple partial seizure, etc

General sequelae in 10-20% of the cases of bacterial meningitis: mental retardation, learning disabilities, hearing loss


Suppurative Meningoencephalitis
-complication of bacterial CNS infections

Cerebral abscess: liquefactive center with yellow pus surrounded by a thin wall.

Abscesses usually result from hematogenous spread of bacterial infection, but may also occur from direct penetrating trauma or extension from adjacent infection in sinuses.

-transmission during delivery
-infected amniotic fluid
-ruptured amniotic membranes and prematurity increase risk

-GBS - polysaccharide capsule
-E. Coli - K1 polysaccharide capsule

Neonatal Meningitis pathogenesis from colonized mother

Polysaccharide capsule - antiphagocytic

Peptidase - inactivates C5a (major chemo-attractant of PMNs)

Hydrolytic enzymes - tissue destruction and systemic spread

Streptococcus agalactiae (GBS)

Strains containing the K1 polysaccharide capsule

Pili involved in adherence to brain microvascular endothelial cells


E. coli

sensitive and specific
identification of GBS antigen in urine or in CSF

Latex particle agglutination (LGA) test of urine -rapid screening for GBS, E coli, and S. pneumoniae

CSF and blood cultures

Diagnosis of Neonatal Meningitis

Microscopy - blood or CSF
Gram stain

Culture of blood or CSF
Blood agar - Beta-hemolytic
Motility test

CSF analysis
pleocytosis, elevated CSF protein levels, low CSF glucose levels

Listeria monocytogenes Diagnosis

Pregnant women should avoid eating uncooked food thought to be of particular risk (coleslaw, soft cheese, unpasteurized milk, hotdogs...)

Improve the safety of processed meats through meticulous in-plant sanitation and post-packaging pasteurization

Education for high-risk consumers to reduce their risk of listeriosis

Listeriosis Prevention

Complication of Neonatal GBS Meningitis: Multiple Abscesses

Complication of Meningitis: Hydrocephalus

Exits of the fourth ventricle become obstructed by fibrosis

Viral (aseptic) encephalitis/meningitis
JC virus
Prion disease

Viral infections of the CNS

-Direct cytolytic effects
-Inflammatory or immune mediated effects
-Vasculitic effects

Viruses enter the brain by crossing the blood-brain barrier directly (polio), by being transported by infected lymphocytes or macrophages (flaviviruses, HIV), or by retrograde axonal transport (polio, rabies).

Pathology of viral infections of the CNS

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