Disclosures I have no disclosures. NEUROINFECTIOUS DISEASES 201: - - PowerPoint PPT Presentation

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Felicia Chow, MD, MAS Assistant Professor University of California, San Francisco Department of Neurology and Division of Infectious Diseases February 13, 2020

NEUROINFECTIOUS DISEASES 201: BEYOND THE BASICS

Disclosures

• I have no disclosures.

Title slide photo credit, Teresa Zgoda, 4th place in Nikon’s small world contest: https://www.nikonsmallworld.com/galleries/2017- photomicrography-competition/taenia-solium-everted-scolex

Learning objectives

• Discuss atypical presentations of common neuroinfectious

diseases and typical presentations of less common neuroinfectious diseases

• Identify pitfalls of diagnostic testing in the evaluation and

management of neuroinfectious diseases

• Be familiar with updates in treatment strategies for several

neuroinfectious diseases

Case One

• 40-year-old man with no PMH presents with confusion, found to have

”idiopathic communicating hydrocephalus” requiring VP shunt

• Developed persistent headaches a few weeks post-operatively;

presented several times to the ED and diagnosed with migraines

• Six months after the shunt surgery, the headaches became acutely

worse, often accompanied by neck stiffness, N/V, and fever

• Brought into ED from work after a possible seizure  LP w/ 2,000

WBC (98% neutrophils), 1392 RBC, glucose <5, protein 778; CSF gram stain and bacterial culture negative

• Started empirically on vancomycin and ceftriaxone  broadened to

vancomycin and cefepime

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Case One Case One Case One

• VP shunt removed  improved but then encephalopathy

and ventriculomegaly worsen, requiring EVD

• Serial CSF evaluations, most of which were from

ventricular fluid, demonstrated marked improvement in pleocytosis and other parameters over 1 week  WBC 3, glucose 60, protein 23

• Transferred to UCSF for further evaluation and

management

Case One

• EXAM: Afebrile. Eyes open, abulic; briefly regards, does

not track, intermittently follows simple commands. No verbal output. Pupils equal and reactive to light. No blink to threat bilaterally. Sustains arms antigravity, withdraws legs to tickle.

• Broad spectrum antibiotics continued  clinically

improved at first…but then worsens again

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Case One Case One

• Ventricular CSF with 0 WBC, 180 RBC, glucose 57, protein

<10

• Lumbar CSF with 8 WBC (36% neutrophils), glucose 22,

protein 240

• Negative studies from CSF
• Gram stain and bacterial culture
• Bacterial antigen testing for H influenzae, group B strep, Strep

pneumo, N meningitidis, E. coli

• Coccidioidomycosis complement fixation and immunodiffusion
• M. tuberculosis PCR
• Negative blood cultures, HIV and Quantiferon-TB Gold

Case One

• Social history/exposures
• Married, no children
• Lives in Monterrey with his wife
• Works in construction, mostly on roads
• Infrequent alcohol use; never smoker, no other substance use.
• Born in rural part of Jalisco, Mexico
• Moved to Monterrey, CA in early 1990s
• Has a dog at home, no other animal exposures
• Does not consume unpasteurized dairy
• No history of incarceration or homelessness
• No known TB contacts

Case One

40-year-old man with a history of “idiopathic communicating hydrocephalus” s/p right VP shunt who presents with meningitis with improvement in CSF pleocytosis on broad- spectrum antibiotics but persistent, progressive radiological changes concerning for ventriculitis

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What do you think is the most likely diagnosis?

• A. Incompletely treated nosocomial bacterial ventriculitis
• B. Neurocysticercosis
• C. Neurobrucellosis
• D. TB meningitis
• E. CNS Coccidioidomycosis

I n c

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p l e t e l y t r e a t e d n . . . N e u r

• c

y s t i c e r c

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i s N e u r

• b

r u c e l l

• s

i s T B m e n i n g i t i s C N S C

• c

c i d i

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d

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y c

• s

i s

16% 20% 31% 22% 11%

Case One: Back to the beginning Case One

• 4th ventricle lesion concerning for intraventricular cysticercosis
• Serum cysticercus ELISA positive 2.49
• CSF cysticercus ELISA from ventricular fluid negative, but

positive from lumbar fluid

• MRI brain with FIESTA sequences negative for visualized

intraventricular cysts

• Started on dexamethasone with albendazole

Intraventricular neurocysticercosis

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Neurocysticercosis (NCC)

• Infection of the nervous system

with larval stage of the tapeworm, Taenia solium

• 50+ million people affected

worldwide

• >2000 cases diagnosed annually

in US

• One of the most common causes
• f acquired epilepsy in endemic

countries (Latin America, sub- Saharan Africa, parts of Asia)

Ndimubanzi et al. PLOS Negl Trop Dis 2010

Natural history, clinical presentation, diagnostic testing, and management of NCC

Location

• f cysts

Stage of cysts Number

• f cysts

Location, location, location

• Intraparenchymal (70%)
• Cortical (>90%), deep gray matter

(5%), brainstem/infratentorial (uncommon)

• Most commonly present with

seizures

• Extraparenchymal (30%)
• Sylvian fissure, basal cisterns,

intraventricular, spinal (usually extramedullary)

• Most commonly present with

hydrocephalus and increased intracranial pressure

• Associated with more protracted

course and worse prognosis

• Mixed (10-30% of cases)

Intraventricular NCC

• Presenting form of NCC in 10-20% of

cases

• Acute hydrocephalus is the most

common complication of ventricular NCC

• Viable/vesicular cysts: Transient

mechanical obstruction of CSF outflow through “ball-valve” movement, including with change in head position (Bruns syndrome)

• Degenerating cysts: Can adhere to

ependymal lining and surrounding tissue, leading to ventriculitis, periventricular edema, and hydrocephalus

Nash et al. Am J Trop Med Hyg 2018, Sierra et al. PLOS Neg Trop Dis 2017

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Neyaz et al. Neurol India 2012

a: T1 b: T2 c: SWI d: FIESTA

FIESTA/CISS and SWI to detect IV cysts

Surgical intervention for intraventricular NCC

• Extraction of cysts is mainstay
• f treatment for viable, non-

inflamed intraventricular cysts

• Cyst rupture during surgical

removal has NOT been associated with adverse

• utcomes
• Pre-treat with steroids but not

antiparasitic therapy

Nash Am J Trop Med Hyg 2018, Campbell J Rare Dis Res Treat 2017, Khade World Neurosurg 2013, Ho Cureus 2015, Li World Neurosurg 2017

Intraoperative video of endoscopic extraction of intraventricular cyst

Rangel-Castilla et al. Am J Trop Med Hyg 2009

Medical therapy for ventricular cysts

As an alternative to surgery

• High risk of complications (e.g., hemorrhage,

neurologic deficits) associated with surgical removal

• f inflamed, adherent cysts  treat with albendazole

+/- praziquantel + steroids

As an adjunct to surgery?

• Consider albendazole + steroids for up to 4 weeks after

surgical removal of viable, non-inflamed cysts, although many experts suggest this may be unnecessary if residual cysts are not seen on imaging

Khade World Neurosurg 2013, Husain Acta Neurochir 2007, Goel J Clin Neurosci 2008, White Clin Infect Dis 2018

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Ventricular versus lumbar CSF: does it matter?

• Discordant profiles of CSF sampled from

different compartments is a common phenomenon in CNS infections, especially those that cause a basal meningitis (e.g., TB, coccidioidomycosis, cryptococcosis, neurocysticercosis)

• Typically ventricular CSF profile more

‘normal’ compared with lumbar fluid

• In addition to discrepant CSF parameters,

microbiological testing can be positive from one compartment but not the other

• May not be able to compare CSF results

from different compartments

Khan OFID 2019

Neuro-Infectious Diseases 201: Beyond the Basics

Key learning points

• Obtain serologies for neurocysticercosis in patients with epidemiological

risk factors presenting with unexplained ventriculomegaly/hydrocephalus

• r culture-negative neutrophil or lymphocyte-predominant pleocytosis
• FIESTA sequences can help to identify difficult-to-visualize subarachnoid

and intraventricular cysts in neurocysticercosis

• Surgical removal of viable intraventricular cysts is first-line therapy; cysts

that have begun to degenerate, however, are typically not amenable to surgery

• Remember that ventricular and lumbar CSF profiles can look vastly

different in patients with certain CNS infections (e.g., basal meningitis), and the diagnostic yield of microbiologic testing may depend on the CSF compartment tested

Case Two

• 60-year-old man with essential thrombocytosis,

polycythemia vera, and nephrotic syndrome 2/2 minimal change disease on prednisone who presented with several days of double vision, gait imbalance, and right facial droop

• Endorsed fever, chills, drenching night sweats, and

malaise for 1 month

Case Two

• EXAM: T 39.5. Awake, alert, conversant. Neck supple, no
• meningismus. Binocular horizontal diplopia with impaired

abduction of right eye and right INO. Dense right facial weakness involving upper and lower face. Moderate

• dysarthria. Normal tone. Strength in upper and lower

extremities intact. Wide-based ataxic gait.

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Case Two Case Two

• Lumbar CSF with 1525 WBC (83% neutrophils), 2 RBC, protein 120, glucose

40

• Empiric coverage for a brain abscess with meningitis initiated with

vancomycin, ceftriaxone, metronidazole, and voriconazole  ceftriaxone and metronidazole changed to meropenem due to intolerance

• Negative testing from CSF:
• Gram stain and bacterial culture
• Fungal and AFB cultures
• Cryptococcal antigen
• Coccidioidomycosis immunodiffusion and complement fixation
• Universal bacterial, fungal, and mycobacterial PCR
• Blood cultures negative
• Chest CT scan and PET scan negative

Case Two

• Repeat MRI of the brain one week into empiric therapy

demonstrated decrease in enhancement and edema surrounding the pontine lesions

• Lumbar CSF with WBC 300 (95% neutrophils), RBC 1

cell/mm3, protein 72 mg/dL and glucose 40 mg/dL; gram stain and bacterial culture negative

• Empiric therapy continued for 8 weeks with clinical

improvement in symptoms

• Six days after discontinuation of antibiotics, he developed a

severe headache with light-headedness…

Case Two

• Repeat CSF
• WBC 3126 (88% neutrophils)
• RBC 11 cell/mm3
• Protein 102 mg/dL
• Glucose 21 mg/dL
• Gram stain with moderate

polys, no organisms

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Case Two

• 60-year-old man with myeloproliferative

disease and nephrotic syndrome on prednisone with fever, chills, night sweats for 1 month, found to have multiloculated pontine brain lesion, persistent neutrophilic meningitis and ventriculitis despite 8-week course of broad-spectrum antimicrobial therapy

What is the most likely diagnosis?

• A. CNS Nocardia
• B. CNS Listeria
• C. CNS Tuberculosis
• D. CNS Toxoplasmosis
• E. CNS Lymphoma, EBV-associated

CNS Nocardia CNS Listeria CNS Tuberculosis CNS Toxoplasmosis CNS Lymphoma, EBV-asso...

14% 26% 17% 17% 25%

Infectious causes of brain mass lesions

Bacteria

• Pyogenic (Strep and Staph

species, Enterobacteriaceae, anaerobes)

• Nocardia
• Listeria
• Actinomyces
• Mycobacteria, including

tuberculosis Parasites

• Cysticercosis
• Echinococcus
• Toxoplasma
• Balamuthia
• Acanthameba

Fungi

• Coccidioidomycosis
• Histoplasmosis
• Blastomycosis
• Candida
• Mucormycosis
• Fusarium
• Aspergillosis
• Cryptococcus

Lesions caused by these pathogens will typically enhance on post-contrast imaging BUT not all are commonly associated with intense, homogeneous restricted diffusion

CNS Nocardiosis

Courtesy of Steve Miller, UCSF Microbiology Image Archive

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CNS Nocardiosis

• After pulmonary infection, CNS is second most

common site of nocardiosis (up to 33% of cases)

• Primarily an opportunistic infection affecting

immunocompromised individuals (e.g., transplant patients, hematologic malignancy, steroid use, HIV)

• Typically causes a localized or systemic

suppurative (i.e., pus-forming) infection  brain abscess +/- meningitis, often with insidious, subacute to chronic presentation

• Abscesses can form anywhere (e.g., cortex, white

matter, basal ganglia, cerebellum), although brainstem is relatively uncommon site

Chow BMJ Cas Rep 2013, Lerner CID 1996, Durmaz Clin Neurol Neurosurg 2001, Kilincer J Clin Neurosci 2006, Marnet Rev Neurol 2009

Laboratory investigation for Nocardia

• CSF profile in CNS Nocardia is consistent with

an acute bacterial meningitis

• Neutrophil-predominant pleocytosis (83% >500

cells/mm3)

• Elevated protein (61% >100 mg/dL)
• Low glucose (64% <40 mg/dL)
• BUT CSF may be bland if abscess present without

concomitant meningitis

• Pathogen can be difficult to recover 

multiple, large volume CSF specimens may increase the yield, although direct pus may be needed for positive culture

• Direct sampling of abscess may be needed to

establish diagnosis

Patil Histopathology Reviews and Recent Advances 2012

Lerner CID 1996, Bross Rev Infect Dis 1991

Treatment of CNS nocardiosis

• Trimethoprim/sulfamethoxazole (TMP/SMX) is considered first-

line therapy for Nocardia and is often the backbone of treatment regimens

• For CNS disease, empiric coverage with 2 (or more) agents

while awaiting susceptibility testing: combination of TMP-SMX, meropenem, ceftriaxone, linezolid, and amikacin often used

• Duration of therapy depends on immune status, and clinical

response; CNS infections usually treated for minimum of 1 year

• Consider surgical intervention for brain abscesses >2.5 cm,

those that do not decrease in size after 4 weeks of therapy, or for any clinical deterioration

Mamelak Neurosurgery 1994, Mcneil Infect Dis Clin Practice 1995, Moylett CID 2003, Brown-Elliott J Clin Microbiol 2012, Uhde CID 2010, Chow BMJ Cas Rep 2013

Neuro-Infectious Diseases 201: Beyond the Basics

Key learning points

• Consider CNS Nocardia inpatients, especially if

immunocompromised, presenting with brain abscesses and/or a persistent neutrophilic meningitis with poor or incomplete response on empiric antimicrobial therapy

• Diagnostic yield of CSF culture may be limited in cases of brain

abscess, even if a concomitant meningitis is present

• CNS Nocardia infections require a longer course of

antimicrobial therapy than standard causes of CNS bacterial infections  consider nocardiosis in patients with recurrent or worsening symptoms after cessation of antimicrobial therapy

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Case Three

• 51-year-old man with hypertension and

hypercholesterolemia who developed URI symptoms followed by vertigo and nausea/vomiting. No fever, chills, headache, neck stiffness.

• Seen by PMD who diagnosed BPPV
• Over late summer, patient and family noticed progressive

slurred speech, double vision, diffuse weakness, and gait instability

Case Three

• Admitted to local hospital and

diagnosed with cerebellar and pontine strokes

• Started on aspirin/clopidogrel,

statin, anti-hypertensives and discharged to acute rehab where his deficits worsened

• Readmitted to local hospital 

MRI with progressive abnormalities, LP recommended but patient refused until transfer to UCSF

Case Three

• Social history/exposures
• Married, two adult children
• Born in central California where he currently lives with wife
• Works in a “government desk job”
• Occasional alcohol use; 10 pack-year smoking history, quit 20

years ago

• No history of incarceration or homelessness
• Avid hiker, spends a lot of time outdoors; no known recent tick or

mosquito bites

• Has traveled to China, Japan, and Thailand; no recent

international travel

Case Three

• Exam: Awake, intermittently follows commands. Eyes
• pen spontaneously. Pupils equal and sluggishly reactive

to light. Minimal preserved volitional upgaze and downgaze but otherwise complete ophthalmoplegia. Intermittent slow left beating nystagmus. No corneal

• reflexes. Severe bifacial LMN weakness. No cough, no

gag reflex. Diffuse weakness in all four extremities.

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Case Three

• 51-year-old man with hypertension and

hypercholesterolemia who presents with impaired pupillary response, ophthalmoplegia, bifacial weakness, and quadriplegia concerning for a subacute, progressive rhombencephalopathy.

What is the most likely diagnosis?

• A. Listeria meningoencephalitis
• B. Enterovirus meningoencephalitis
• C. West Nile virus meningoencephalitis
• D. Progressive multifocal

leukoencephalopathy (PML)

• E. Botulism

Listeria meningoencephal... Enterovirus meningoenc... West Nile virus meningo... Progressive multifocal le... Botulism

27% 10% 3% 16% 45%

Pathogens that can cause brainstem encephalitis

• Viruses
• Enterovirus (EV71, EV68)
• Flaviviruses (WNV, JEV)
• HSV (1>2)
• EBV
• HHV-6
• Bacteria/Mycobacteria
• Listeria
• Tuberculosis
• Brucella
• Non-infectious (immune-mediated, paraneoplastic,

malignancy)

• MS, Behcet’s, lymphoma, and many others

Solomon Pract Neurol 2007, Moragas Medicine 2011

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A critical lab value returns…

Case Three

• HIV Ag/Ab test sent upon arrival to UCSF was positive:

CD4 46 (10%), VL 123,437 copies/mL

• Quantiferon Gold negative, serum toxoplasma IgM/IgG,

CrAg, RPR negative

• Lumbar puncture
• WBC 0, RBC 0, protein 21, glucose 65; OCB >5
• VDRL, CrAg negative
• HSV 1/2, VZV, enterovirus, JCV, EBV, CMV, HHV-6 PCR pending

Case Three

• 51-year-old man with

hypertension, hypercholesterolemia, and newly diagnosed HIV (CD4 46 cells/mm3, viral load 123K) presents with subacute, progressive rhombencephalopathy

PML, next case? Or, not so fast?

• A. I think PML is likely based on the

presentation and imaging, but the lack of a pleocytosis is unusual for PML.

• B. I think PML is likely based on the imaging

and CSF profile, but the CD4 count of <50 is unusual for PML.

• C. I think PML is likely based on the

presentation and CSF profile, but the brainstem involvement is unusual for PML.

• D. It all fits with PML.

I t h i n k P M L i s l i k e l y b a s e . . . I t h i n k P M L i s l i k e l y b a s e . . . I t h i n k P M L i s l i k e l y b a s e . . . I t a l l f i t s w i t h P M L .

4% 30% 60% 5%

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Case Three

• CSF JCV PCR returned at >100 million

copies/mL

Progressive multifocal leukoencephalopathy (PML)

https://library.med.utah.edu/WebPath/TUTORIAL/AIDS/AIDS076.html

Progressive multifocal leukoencephalopathy

• Demyelinating disease caused by reactivation of JC virus

infection

• Subacute, progressive decline over weeks to months w/

focal deficits

• Immunocompromised populations at risk: HIV, solid organ

and hematopoietic stem cell transplant, hematological malignancy, chemotherapy, patients receiving monoclonal antibodies (e.g., natalizumab, rituximab)

• CSF profile usually normal
• Very mild lymphocyte-predominant pleocytosis in <25% of patients
• Mildly elevated protein in up to 20-30% of patients

Cinque AIDS 1997; Tan Lancet Neurol 2010, Berger Cleve Clin J Med 2011, Berger et al. Neurology 2013, Marzocchetti et al. J Clin Microbiol 2005 Antinori,J Neurovirol 2003;

How good is CSF JCV PCR?

• Specificity 92-100%
• Sensitivity 75 to 95% but may be as low as 58% in

current era of effective ART

• Sensitivity may be LOWER for patients
• On ARVs or intermittently on ARVs
• With higher CD4 counts
• With PML-IRIS
• With non-HIV/AIDS related PML
• If PCR is negative, worth repeating LP and repeating

JCV PCR if suspicion is high enough

Cinque AIDS 1997; Antinori J Neurovirol 2003; Marzochetti J Clin Micro 2005

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PML imaging

• Typical locations: Subcortical

white matter, brainstem, cerebellum

• T2/FLAIR hyperintense and T1

hypointense lesions

• Not necessarily multifocal  up

to half of cases demonstrate isolated lesion

• Mass effect, edema and

enhancement are uncommon

Tan Lancet Neurol 2012

Treatment of PML

• Initiate or optimize antiretroviral therapy (ART) for HIV-

associated PML  often see 1-3 month period of continued progressive decline even after systemic response to ART

• Withdraw immunosuppressing drugs when feasible for non-

HIV-associated PML

• Discontinue natalizumab and start plasma exchange for

patients with natalizumab-associated PML

• Many treatments with limited or anecdotal data: IL-7, IFN-α,

cytarabine, cidofovir, mirtazapine, mefloquine, maraviroc

Marra AIDS 2002; Hall NEJM 1998, Aksamit J Neurovirol 2001, Royal 2003, Berger 1992, Clifford J Neurovirol 2013

• One case series and two letters published in NEJM in 2019 on

use of pembrolizumab and nivolumab, two monoclonal Abs (“immune checkpoint inhibitors”) that target PD-1 (programmed cell death protein 1), a marker of T-cell exhaustion

• PD-1 expression elevated on CD4 and CD8 T cells of PML

patients

• Inhibition of PD-1 shown to improve cellular immune response

to JC virus (e.g., T cell proliferation and cytokine production)

Cortese NEJM 2019, Walters NEJM 2019, Rauer NEJM 2019

Neuro-Infectious Diseases 201: Beyond the Basics 10 patients total; CSF JCV copy number 63 to 119,000 copies/mL 1 variable immunodeficiency w/ diffuse large B-cell lymphoma, 2 with lymphoma, 2 with HIV, 2 with CLL, 3 with idiopathic lymphopenia 7 of 10 with stabilization or reduction in size of lesions on MRI and decrease in CSF JCV copy number 3 of 10 had no clinical benefit, 2 of whom developed progressive disease and died from PML Enthusiasm tempered by previous reports of PML complicating use of PD-1 inhibitors in cancer patients larger clinical trial needed Neuro-Infectious Diseases 201: Beyond the Basics

Cortese NEJM 2019, Walters NEJM 2019, Rauer NEJM 2019

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• Three patients with CSF JCV PCR+ PML treated with “off-the-shelf”

banked BK virus (genetically similar family member of JCV) specific, partially HLA matched T cells

• Reduction in CSF JCV copy number after first infusion with stabilization
• r improvement of clinical symptoms and reduction in MRI lesions or

changes c/w IRIS

• 2 patients cleared CSF JCV after additional infusions with good clinical
• utcomes; 1 patient stabilized but opted to enter hospice due to

neurologic disability

Muftuoglu NEJM 2018

Neuro-Infectious Diseases 201: Beyond the Basics

Key learning points

• HIV testing should be sent in anyone presenting with

meningitis, encephalitis, encephalopathy, or other signs/symptoms of a potential neuroinfectious disease, even if you do not think they have (or they deny) risk factors

• CSF profile is usually stone cold normal in PML
• CSF JCV PCR sensitivity may be lower in persons with HIV on

ART or in persons with higher CD4 counts

• Interesting recent data that monoclonal antibodies to PD-1 and

“off-the-shelf” partially HLA-matched BK virus-specific T cells may be effective in treating PML

THANK YOU

Questions, comments, suggestions: felicia.chow@ucsf.edu

Extra slides

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https://www.who.int/news-room/fact-sheets/detail/taeniasis-cysticercosis

Stages of NCC

Garcia et al. NEJM 2004

Location of intraventricular cysts

• Cysts can be found

anywhere in the ventricular system

• Fourth ventricle most

common location of cysts (~50%), followed by third and lateral ventricles (10- 33%) and cerebral aqueduct (<10%)

• Multiple ventricular cysts

frequently seen

Nash et al. Am J Trop Med Hyg 2018

a: T2 b: FLAIR c + d: FIESTA

Neyaz et al. Neurol India 2012

FIESTA/CISS and SWI to detect IV cysts

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Nash et al. Am J Trop Med Hyg 2018

• Reviewed all NCC cases seen at NIH between 1985 and 2017 

20% with intraventricular cysts

• Median time from leaving residence in endemic country to

presentation 6.5 years (0.17-16 years)

• Hydrocephalus (74%), ventriculitis + periventricular edema (30%)
• 61% underwent surgical removal of cyst, usually by suboccipital

craniotomy

• Four patients did not receive any antiparasitic therapy after removal of

cysts without recurrence “We suggest antiparasitic drugs with corticosteroid therapy following shunt insertion to decrease subsequent shunt failure in patients in whom surgical removal of isolated intraventricular cysts is not possible (weak, low), but neither after successful removal of intraventricular cysts (weak, low)” “Recent data have noted that when cysts are successfully removed...if imaging studies are negative, outcomes are excellent without further antiparasitic therapy (T. Nash, unpublished observations).”

White et al. Clin Infect Dis 2018

Case One

• Negative studies from CSF
• Fungal and mycobacterial culture
• Beta-d-glucan
• Universal bacterial, fungal, and mycobacterial PCR
• Metagenomic sequencing negative for DNA virus, RNA virus,

bacteria, fungi, parasites

• Negative serologies from blood
• Brucella, Coxiella, and Bartonella

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