Neuro Infections Flashcards
Meningitis
● An inflammation of the meninges and subarachnoid space
● Bacterial
● Viral
● Cryptococcal
● Fungal
● Not covered today, eg. Drug rxn, etc
Bacteria reaches the meninges via ____ spread, or via _____
hematogenous ; nearby infected structures or through a defect in the skull or spine (eg. trauma, surgery)
T/F Bacterial meningitis is more severe than viral meningitis
T
Most common infective organisms in adults with bacterial meningitis
● Streptococcus pneumoniae
● Neisseria meningitidis
● Listeria monocytogenes, primarily in patients over age 50 to 60 years or
those who have deficiencies in cell-mediated immunity
Most common infective organisms in children with bacterial meningitis:
● Streptococcus pneumoniae
● Neisseria meningitidis
● Haemophilus influenzae Type B (Hib)
○ Incidence has significantly decreased since the introduction
of the Hib vaccine
● Preterm infant or < 1 month - Group B Strep, E. coli and others
Bacterial Meningitis presentation
● Classic triad: fever, stiff neck, altered mental
status
○ Nearly all pts with bacterial meningitis will
have at least two: fever, HA, stiff neck, or
AMS. (exception immunocompromised)
● Headache
● Fever
● Tachycardia
● Seizures
Bacterial Meningitis diagnosis
● Blood cultures and lumbar puncture for CSF analysis
○ Blood cultures will be positive in 50-90% of pts
○ Evaluate CSF for: cell count, glucose, protein, gram stain, culture
○ Run PCR testing
● CBC, CMP
● CT/MRI - neuroimaging
Indications for obtaining CT before LP:
● Immunocompromised pt
● Papilledema
● AMS
● New onset seizure
● Focal neuro deficits
The usual CSF findings in patients with bacterial meningitis are:
● WBC count: 1000 to 5000/microL (range of <100 to >10,000)
with a percentage of neutrophils usually greater than 80
percent,
● Protein: 100 to 500 mg/dL
● Glucose: <40 mg/dL(with a CSF:serum glucose ratio of ≤0.4).
● Turbid appearance
● Send for cultures, gram stain and appropriate PCR
● Recent or prior Abx use, can reduce culture yield
Bacterial Meningitis
Treatment:
Obtain 2 sets of Blood Cultures before starting abx.
IV Dexamethasone should also be started early to help mitigate
hearing loss and other neuro complications.
High mortality rate depending on age, severity, codependent factors
Treatment for community-acquired meningitis:
Vancomycin
PLUS
Cefotaxime OR Ceftriaxone
And Dexamethasone
FYI- Chemoprophylaxis for close contacts
Bacterial Meningitis treatment durations
H influenzae, 7 days
N meningitidis, 3-7 days
S pneumoniae, 10-14 days
L monocytogenes, 14-21 days
Gram-neg bacilli, 21 days
Viral Meningitis
Viral meningitis, also known as aseptic meningitis, although aseptic
meningitis technically includes any other causes than bacteria
(viruses, drugs, fungi etc.)
Is more benign and self-limiting than bacterial meningitis.
Most common kind of meningitis
Common infective organisms for viral meningitis:
● Enteroviruses (most common)
● Herpes simplex virus (HSV)
● Human immunodeficiency virus (HIV)
● West Nile virus (WNV)
● Varicella-zoster virus (VZV), mumps
● Lymphocytic choriomeningitis virus (LCM)
Viral Meningitis clinical presentation
● Fever
● Malaise
● Headache
● Nausea or vomiting
● Photophobia
● Nuchal rigidity
Lumbar puncture for CSF analysis findings for viral meningitis
○ Normal glucose
○ Mildly elevated protein levels
○ WBC <250
Viral meningitis diagnostics
● Lumbar puncture for CSF analysis
● PCR can detect some viruses in the CSF
○ Viral DNA or RNA- Enterovirus, herpes simplex virus, herpes zoster, West Nile viruses
Viral Meningitis treatment
● Observation without empiric Abx- usually resolves spontaneously over
weeks
● Supportive therapy
● Acyclovir and Valacyclovir for suspected herpes simplex and herpes zoster
● Empiric antibiotic treatment for the elderly, immunocompromised, or
those who have received antibiotics prior to presentation may be
considered for empiric therapy for 48 hours
What to do if the etiology of viral meningitis is unclear?
● Observe, with repeat LP in 6 to 24 hours
● If patient appears seriously ill, obtain blood
and CSF cultures and begin empiric
treatment with antibiotics immediately until
bacterial etiology can be ruled out
Fungal Meningitis
● Maybe insidious or chronic in nature
● Coccidioides, Histoplasma, etc
● Cryptococcal in immunocompromised
● Possible after epidural steroid injection w/ occasional outbreaks
● Diagnosis- CSF culture, pleocytosis (↑cell count), serologic tests
● Treatment is directed at the source
Most common cause of fungal
meningitis
Cryptococcal Meningitis
Risk factors for Cryptococcal Meningitis
● Immunodeficiency
○ HIV infection
○ Transplant recipients
○ Corticosteroid therapy
○ Hematologic malignancy eg. Hodgkin’s lymphoma
Cryptococcal Meningitis
Clinical presentation
● HA - usually first symptom
● Then fever and malaise
● Confusion and other mental status changes
● Cranial nerve abnormalities
● Nausea and vomiting
● Nuchal rigidity and meningeal signs
Diagnostic consideration of cryptococcal meningitis
● CSF analysis
○ Presence of cryptococcal antigen = diagnostic
● MRI more sensitive than CT for CNS abnormalities
Cryptococcal Meningitis treatment
● Amphotericin B PLUS Flucytosine
● Followed by Fluconazole 10 wks
Encephalitis
Inflammation of the brain
Most common infective organisms:
● Generally viral
○ HSV 1 and 2 (most common in US)
■ Important to r/o because it can be fatal
○ Arboviruses (eg. West Nile virus)
○ Enteroviruses
Encephalitis etiology
● A common cause: HSV type 1
● Other viral pathogens may be suggested by geographic location (eg, St. Louis
encephalitis in North America and Japanese encephalitis in Asia)
● Exposure history (eg, bat exposure or dog bite and rabies)
● Regional outbreaks (eg, enterovirus type 71 in Denver, Colorado)
● Clinical clues, such as profound weakness and rash with West Nile.
● Uncommon causes include varicella zoster virus, Epstein-Barr virus, HIV,
human herpes virus-6, Zika virus, and COVID-19
Encephalitis
Clinical presentation:
● AMS (Always!)- helps distinguish from meningitis
● Fever
● Headache
● Seizures
● Change in behavior (confusion, agitation)
● Focal neurologic abnormalities (hemiparesis, cranial nerve palsies,
exaggerated DTRs)
● Meningeal signs maybe less prominent
Encephalitis
Diagnostic consideration:
● CSF analysis (crucial for diagnosis!)
○ Polymerase chain reaction testing for viruses
■ HSV 1 and 2, enteroviruses
■ PCR available for many viruses
○ Can also do viral cultures- although are not routine
● Obtain neuroimaging - CT or MRI (characteristic brain edema)
● Electroencephalography is often abnormal in acute encephalitis.
Encephalitis
Treatment:
● Begin empiric treatment for HSV1 with Acyclovir (10mg/kg
tid IV) ASAP if the pt appears to have encephalitis without
apparent explanation, while waiting for test results.
○ Early therapy is associated with a significant decrease in
mortality and morbidity
● Otherwise- Supportive care
Meningitis vs Encephalitis differentiation
The presence or absence of normal brain function is the important
distinguishing feature between encephalitis and meningitis.
Patients with meningitis may be uncomfortable, lethargic, or distracted
by headache, but will have normal cerebral function.
In encephalitis, however, abnormalities in brain function are a
differentiating feature, including altered mental status, motor or
sensory deficits, altered behavior and personality changes, and speech
or movement disorders
Cerebral Abscess
● Presents as an intracranial space-occupying lesion
○ A collection of infected pus
● Arises as a sequela of disease of the ear or nose
○ Otitis media, mastoiditis, sinusitis, dental infections
● May be a complication of infection elsewhere in the body
● May result from infection introduced intracranially by trauma or surgical procedures
Most common infective organisms in a cerebral abscess
● Streptococci
● Staphylococci
● Bacteroides
● Gram-neg bacilli
● Mouth anaerobes
Cerebral Abscess clinical presentation
● HA- most common symptom
○ Occuring in 69%
● Vomiting, fever, change in mental status, neck stiffness
● Focal neuro manifestations
● Drowsiness, inattention, confusion, seizures
● May or may not show signs of infection
● May be preceded by an infection in distant site
Cerebral Abscess diagnosis
● MRI (imaging study of choice) or CT with contrast
○ If positive for abscess, NO lumbar puncture should be
performed (d/t risk of herniation)
● Specimen from stereotactic CT- guided needle aspiration of pus
should be sent for testing to identify specific organisms
○ Gram stain, cultures, histopathology, etc.
● Lumbar puncture is contraindicated in patients with focal
symptoms (eg, unilateral HA, hemiparesis, etc.)
Cerebral Abscess treatment
● Drainage (aspiration preferred to surgical excision)
● Antibiotics (targeting isolated organisms, per culture and sensitivity)
● Steroids (to use when substantial mass effect is seen on imaging and mental status is significantly depressed)
○ Dexamethasone
Example of an empiric regimen:
Metronidazole IV, + Ceftriaxone IV, +/- Vancomycin if traumatic or
hematogenous spread
Treatment Duration for a cerebral abscess
● Fine tune antibiotic based on culture and susceptibility
● Generally IV antibiotics for 6-8 weeks
○ The pt should be monitored by serial CT scans or MRI (every 2
weeks and when worsening)
If the abscess is small, or cannot be drained, or if there are multiple,
treatment includes antibiotics for 6-8 weeks, without drainage
Epidural Abscess
● An accumulation of pus in the epidural
space that can mechanically compress
the spinal cord or brain
● Spinal epidural abscess (SEA)
○ More common than IEA by 9x
○ Usually occur in the thoracic or lumbar
regions
● Intracranial epidural abscess (IEA)
○ Can result from direct extension of sinusitis and hematogenous
osteomyelitis
Epidural Abscess pathogenesis
● Can occur from direct extension
from nearby infected tissue
● Or via direct inoculation into the
spinal canal (spinal procedures
or surgery)
● Hematogenously
Epidural Abscess
Risk factors for SEA:
● Epidural catheters
● Diabetes mellitus
● Alcoholism
● HIV infection
● Bacteremia
● IV drug use
Epidural Abscess
Most common infective organisms:
● S. aureus
● Gram-negative bacilli
● Streptococci
● Coagulase-negative staphylococci
● Anaerobes
● Others (eg, fungi, parasites)
● Unknown
Epidural Abscess
Clinical presentation: SEA vs IEA
● SEA: fever, spinal pain, and neurologic deficits
○ Rare to have all three symptoms
○ Other nonspecific symptoms- malaise, back pain, fever
● IEA : fever, headache, lethargy, nausea, and vomiting are common
○ Increased suspicion in patients with severe HA and fever and recent
history of an intracrancial neurosurgical procedure, or a known or
suspected nearby source of infection (sinusitis, otitis media, etc.)
If left untreated, a spinal epidural abscess can causes symptoms
that progress in a typical sequence:
● Back pain, which is often focal and severe, then
● Nerve root pain, described as “shooting” or “electric shocks” in
the distribution of the affected nerve root, then
● Motor weakness, sensory changes, and bladder or bowel
dysfunction, and then
● Paralysis
Epidural Abscess Diagnosis:
● MRI with contrast (Gold Standard)
The two principles of therapy of a SEA are:
● Reduction in size and ultimate elimination of the inflammatory mass
● Eradication of the causative organism
Treatment for both SEA and IEA:
● Surgical decompression and drainage
● Antibiotic therapy
Start antibiotic therapy asap, but first, obtains two sets of blood
cultures
Example for SEA: Vancomycin PLUS ceftriaxone or cefotaxime or meropenem
Example for IEA: Vanc PLUS metronidazole PLUS a 3rd/4th gen cephalosporin
Prion Diseases
● Misfolding a normal brain cell- surface protein
○ Cellular prion protein PrPᶜ- normal (function is not clear)
○ Misfolded proteins are referred to as PrPˢᶜ
● PrPˢᶜ is pathogenic and can self replicate
○ Chain reaction when PrPˢᶜ induces conformational change
to the PrPᶜ protein.
● Induces neuronal cell death
● Is considered transmissible
● Symptoms could occur months to years after exposure
Prion Diseases
Examples, but other types exist
● Sporadic Creutzfeldt- Jakob Disease (sCJD)
● Variant CJD- inherited and acquired by consuming contaminated beef
● Gerstmann-Straussler-Scheinker- inherited
● Kuru- ritual cannibalism
Prion Diseases etiology
● Transmission source for sporadic cases often remains unknown
● Inherited disease are from defects in PrP gene- there are many 50+
● Infections transmission- organ/tissue transplant, surgical equip, animal source
Prion Diseases
Symptoms
● Memory loss, confusion
○ Prion could be considered in a dementia diagnosis
specifically if rapidly progressive
● Incoordination and ataxia
● Myoclonus due to noise or startle myoclonus- later stage
● Anxiety and depression
● Ocular disturbance, hallucinations and seizures can occur
Prion Diseases
Diagnosis
● MRI
● CSF Fluid analysis- detect specific proteins
● EEG
● Rule Out mimics
Prion Diseases
Treatment
● Supportive Care
● No specific treatment is available
● Set up a DNR- death in 6-12 months
Prion Diseases prevention
● Disinfection concerns exist with standard techniques
○ Prevention with autoclave 132℃ for 1 hour
○ Immersion sodium hydroxide or sodium hypochlorite x 1 hr
