Neuro Infections




    IntroductionEdit section

    • Potential infections:
      • Cerebral cortex --> encephalitis
      • Meninges --> meningitis
    • Potential abscesses:
      • Crebral cortex  --> Brain abscess
      • Subdural Abscess --> (between arachnoid and dura)
      • Epidural Abscess
    • Blood brain barrier prevents entry of invading pathogens and toxic substances.  However:
      • Also prevents entry of Immunoglobulins, complement, and antibiotics.
        • Therefore, if pathogen crosses BB barrier, CNS infections progress FAST and often SERIOUS.
        • Maximal doses ("meningeal doses") of abx are often required.


    • See sub-page



    • See sub-page


    Brain AbscessEdit section

    • Symptoms:
      • MOST COMMON: Severe headache at site of abscess.
        • Sudden worsening = rupture of abscess into ventricles... high mortality rate (25-85%).
      • Many present with triad:
        • Headache
        • Fever
        • Focal Neuro Deficit
      • Other Symptoms based on location:
        • Neck stiffness only if occipital brain abscess or rupture into ventricle.
        • altered mental status, lethargy, coma.
        • Vomiting associated with incresed CSF pressure.
    • Findings:
      • Fever not present in 50%
      • Neuro findings are late.
      • Papilledema - late manifestation (25%)
      • CN VI and III palsies from high ICP.
      • Seizures if frontal brain abscess
    • Two causes:
      • 1. Direct spread from middle ear, frontal sinus, or dental infection
      • 2. Hematogenous spread from chronic pulmonary/skin/pelvic/intra-abdo infection, endocarditis, cyanotic heart disease.
      • 20-35% of patients --> do not find cause.
    • Cerebritis (infammation and edema) --> necrosis, fibrotic capsule formation.
    • Organisms:
      • Organism provides clues on site of infection.
      • Anaerobic bacteria (mouth/genital tract)
        • Bacteroides fagilis, Prevotella, Propionibacterium, fusobacterium...
      • Aerobic gram+ cocci (S. viridans, S. milleri, S. pneumo (rare), S. aureus)
      • Aerobic gram- rods  --> usually with neurosurg
      • Immunocompromised:
        • Toxoplasma, Nocardia, Aspergillus/cryptococcus/coccidioides.
      • Immigrants (parasites)
        • Cysticercosis parasite (85% of brain infections in Mexico City)
        • Entamoeba hystolytica
        • Schistosoma japonicum
        • Paragonimus
    • Diagnosis:
      • Space occupying lesion (SOL) suggested by:
        • Focal symptoms (even unilateral headache)
        • signs (neuro deficits)
        • papelledema
      • LP CONTRAINDICATED, unless SOL excluded.  (If papilledema or focal findings --> NO LP!!  CT first)
      • MRI better than CT (more sensitivity in picking up lesions) (Diffusion weighted MRI help discriminate abscess vs. neoplasms).  CT only if unable to do MRI.
        • Stages on CT:
          • Early cerebritis
            • irregular lesion of low density - no contrast enhancement.
          • Later cerebritis
            • Thick diffuse ring enhancement (enlarging) on contract injection.
          • Late cerebritis
            • Necrosis, Pre-contrast: ring of higher density surrounding edematous brain.
            • Contrast: thin ring, non-uniform in thickness.
          • Healed abscess
            • Collagen capsule becomes isodense.  No enhancement on contrast.
    • Treatment:
      • Neurosurg consult to drain abcess if >2.5cm lesion.
        • (Excision or stereotactic aspiration), culture specimens. 
      • IV abx 6-8weeks 
              +/- prolongued oral therapy if appropriate agent is available.
              (IV empiric therapy based on predisposing condition and presume pathogensis)
        • Generally:
          • Ceftriaxone (enterobacterciae) + metronidazole (anaerobic lytic due to mouth flora)
        • IF Dental Abscess: use penicillin + metronidazole to cover mouth flora
        • IF concerned of pseudomonas (neurosurg)
          • Use ceftazidime or cefepime
        • IF trauma (worry about S.aureus) add vancomycin (MRSA) or oxacillin/nafcillin (MSSA) depending on resistance patterns... aminoglycosides, erythromycin, tetracycline, 1st gen cefs also used.
        • IF hematogenous spread:
          • Typically vanco + gentamycin for empiric therapy.
      • Steroids:
        • if mass effect + mental status change.
        • IV dexamethasone (load 10mg then 4mg q6h)
        • Do not worry about immunocompromise...
        • DC as soon as possible.
          • Reduce contrast enhancement on CT (hard to monitor)
          • Decrease antibiotic penetration
          • Slow capsule formation (can rutupre into ventricles)
      • Repeat Neuroimaging
        • IMPORTANT*, every other week up to 3months after completing therapy.
        • To monitor for expansion of abscess or failure to respond.
    • Prognosis:
      • Depends on stage:
        • 0-30% generally
        • 60-100% if stupor/coma
        • 80-100% if ruptures into ventricle.


    Cranial Subdural Empyema

    • Most common predisposing condition is in 40-80% of pts.
      • Organisms (in sinuses): Aerobic Streptococci, Staphylococci, Aerobic gram negatives, and Anerobic streptococci (+ other anerobes).  Polymicrobial infection is common.
    • Symptoms and signs:
      • Common: Rapidly progressive headache localized then generalized as progresses.
      • Increased ICP: nausea, vomiting etc.. 
      • Meningeal Irritation: meningitis-type symptoms.
      • Focal cortical inflammation
    • Diagnosis:
      • MRI prefered to CT.
      • Better clarity of morphologic detail.
        • MRI better because:
          • Can see empyemas not seen on CT, esp those in base of brain, falx cerebri, and those in the posterior fossa.
          • Extra-axial empyemas from sterile effusions from subdural hematomas. 
    • Treatment:
      • Surgical emergency.
        • Decompress the brain and evacuate the empyema. 
        • Often craniotomy (better than craniectomy or burr holes based on a study).
      • Empiric antimicrobial therapy with vancomycin, metronidazole and 3rd or 4rth cephalosporin. 

    Spinal Epidural AbscessEdit section

    • Spinal canal has anterior and posterior epidural space
    • Mechanism: of infection:
      • Spread from osteomyelitis or disk space
      • Spinal surgery or epidural catheter.
      • Hematogenous spread from:
        • Skin
        • UTI
        • IV drug use.
      • Organisms:
        • S. aureus (most common)
        • Can see GN's or anaerobes if GU or GI source.
    • 4 stages of clinical presentation:
    1. Back Ache and focal vertebral pain
    2. Nerve root pain (radiculopathy/parasthesias)
    3. Spinal Cord dysfunction
    4. Paraplegia
    • Symptoms:
      • Low back pain, fever, radicular pain, lower motor deficits, cord compression signs, spinous process tenderness.
      • Back pain + fever --> consider epidural abscess
      • MRI is test of choice.
    • Diagnosis:
      • MRI with Gadolinium --> procedure of choice!!!
        • Can see spinal cord + epidural space in saggital and transverse sections.
        • Can identify accompanied osteomyelitis, intra-medullary spinal cord lesions and diskitis. 
    • Treatment
      • If spinal cord compression:
        • URGENT surgery. 
        • Can return function if done in 24-36hrs following neurological change.
          • Emergency surgical drainage.
      • Empiric Abx:
        • Usually anti-staphylococcal agent (cloxacillin, nafcillin, oxacillin etc..)
          • Usually (in US and MKSAP) vancomycin for empric MRSA coverage pending susceptibility testing. 
                (HIGH MRSA rates > 50% in some cases, vanco considered first line in US and     MKSAP).
          • PLUS + antipseudomonal cephalosporin  or carbapenem (for GN bacilli, esp for IVDU or spinal procedure). 
            (I.e. MKSAP answer is vancomycin + ceftazidime)
        • Usually need prolongued (4-6weeks) tx with nafcillin, oxacillin, metronidazole, ceftriaxone.
      • Antimicrobial therapy alone can be considered in patients without long tract signs (i.e. if only pain and radicular symptoms), frequent follow-up, neuro exams, serial MRI studies to demonstrate abscess resolution are important. 
      • TB can be the cause.

    Generalized Neuropathy CausesEdit section


    • Two types of exposures:
      • Preformed Toxin:
        • home-canned foods
      • In-vivo toxin Production: (After ingestion and spore germination)
        • Honey (infants)
        • Wound contamination.
    • Symptoms (1-5 days post ingestion) --> Classic Triad:
      • Symmetric descending flaccid paralysis with prominent bulbar palsies:
        • 4 D's of bulbar palsy:
          • Diplopia
          • Dysarthria
          • Dysphonia
          • Dysphagia
      • Normal body temperature
      • Clear sensorium
    • Diagnosis:
      • Toxin in serum, stool, gastric aspirate or suspect foods.
    • Treatment:
      • Supportive
      • Passive immunization using trivalent equine antitoxin (A, B, and E).


    Guillain-Barre Syndrome

    • Symptoms:

      • Typically: Antecedent infection (gastroenteritis from Campylobacter)

      • Ascending paralysis and parasthesias

      • Can have oculomotor findings (like botulism).


    Paralytic Shellfish Poisoning

    • Ingestion of any type of filter-feeding molluscan shellfish (i.e. clams, oysters, scallops, muscles)

      • Specific neurotoxin (saxitoxin) produced by algae accumulated.

    • Symptoms hours to days post-ingestion

      • Tinging of lips + tongue. ---> progresses to parasthesias of hand digits and feet.

        • Eventually can lose control of hands and feet.

      • If lots of toxin ingested:  thorax and abdo muscles can paralyze causing respiratory difficulty.


    Tick Paralysis

    • Associated with Dermacentor ticks (U.S. Pacific Northwest)

    • Symptoms:

      • Ascending paralysis (proximal large muscles).

    Prion Diseases of CNS

    • Prions are novel, composed of transmissable proteins that lack genetic material.
    • Cause 5 syndromes in humans.
      • Kuru
      • Gerstmann-Straussler-Scheinker Syndrome
      • Fatal Familial Insomnia
      • Sporadic Creutzfeldt Jakob Disease  (two most common)
      • Variant Creutzfeldt-Jakob Disease
    • Diagnosis:

      • Progressive neurologic impairment
      • Absence of inflammatory CSF findings
      • Presence of spongeform changes on neuropathologic exam (biopsy). [often post-mortem :( ]


    • No treatments available... fatal. 


    Creutzfeldt-Jakob Disease

    • Classified as:
      • Sporatic (most common) 85%
      • Familial
      • Iatrogenic  (~1%)
      • Variant  (~1%)
    • Probable Sporatic CJD criteria
      • WHO Probable CJD: (must meet all criteria)

        1. 1. Progressive dementia
        2. 2. Clinial Signs
        3. 3. Lab or EEG findings
        4. 4. NO alternative diagnosis found on routine investigations. 
    • Clinically:
      • Psych symptoms, cognitive decline, motor dysfunction.
      • Extrapyramidal signs in >65%.
      • Myoclonus, rapidly progressive dementia are hallmarks on disease.
    • Median survival after onset is 5 months.
    • Labs:
      • Unrevealing.
      • CSF usually acellular (normal), maybe slight protein elevation.
      • 14-3-3 protein - specific neuronal protein in CSF fluid is elevated = indirect marker of sporatic CJD.
        • Low Sn + Sp, only available in one lab. 
      • EEG - some findings.
      • MRI - focal cortical hyperintensity on DWI or FLAIR = predictive of infection. 
      • Neural biopsy - spongiform changes - histopathologic staining for PRCSC prion protein (usually made post-mortem)
    • Surgical procedures discouraged - can contaminate surgical instruments... exposes healthcare workers.
      • Normal autoclaves do not remove prions!
      • Need special procedures. 

    Variant Creutzfeldt-Jakob Disease

    • In 1990's cluster of cases in UK --> had variant CJD.
      • They were younger, psychiatric presentations, less rapid disease progression.
      • Found that this outbreak is unique.
    • ON biopsy: heavy concentrations of amyloid plaque in cerebrum + cerebellum
      • Stain for a type of prion protein - PRPSC Type 4 pattern in tonsillar tissue...unique.  Allows premortem dx.
      • Consumption of beef during an epidemic of bovine spongiform encephalopathy supports animal to human transmission.
    • Diagnosis:
      • Radiographic + neuropathologic exam.
        • MRI - pulvinar sign.
        • Identification of prion protein (on stains) in tonsillar tissue allowing for pre-mortem histopathologic diagnosis.
    • Changes of animal feeding and buchering practices lead to decline in variant CJD.
    Tag page (Edit tags)
    • No tags
    Pages that link here
    Page statistics
    20763 view(s), 11 edit(s) and 18486 character(s)


    You must login to post a comment.

    Attach file