infections of the snc · 2020-04-16 · meningitis in infants –all cardinal signs of meningitis...
TRANSCRIPT
Infections
of the SNC
1
Difine probable site of infection
•Meninges
– Acute meningitis
– Chronic meningitis
– Recurrent meningitis
• Brain
– Acute encephalitis
– Chronic encephalitis
– Space-occuring lesions
– Toxin-mediated syndromes
– Encephalopathy with systemic syndrome
– Postinfectious syndrome
•Spinal cord
– Acute encephalomielitis
– Chronic encephalomielitis
– Space-occuring lesions
– Toxin-mediated syndromes
– Postinfectious syndrome
2
Infections of the central nervous system
• Fungal: Cryptococcus, Coccidiodes, Aspergilus, Histoplasma, Candida
• Protozoal: Toxoplasmosis, Plasmodium, Amoeba, Cysticercosis
• Bacterial: Bac. men, Tbc, Neuroborreliosis, Neurosyphilis
• Virlal:
– HSV, HZV, CMV
– Encephalitis: Japanese, West Nile, St. Louis, Estern equine, California
– Mumps, Measles, Rabies, Poliomyelitis
– Slow virus: HIV, progressive multifocal leucoencephalopathy, subacute
sclerosing panencephalitis
• Prionic: Creutxfeldt-Jacob, etc
• Post-infectious diseases of the CNS:
– PANDAS (Pediatric autoimmune neuropsychiatric disorders associated
with streptococcal infections)
– Acute disseminated encephalomyelitis
– Guillain-Baree syndrome
3
4
PATHOGENESIS CNS INFECTION
5
6
7
Meningitis in infants
– All cardinal signs of meningitis (fever, vomiting, stiff neck) are rarely present.
– paradox irritability (ie, quiet when stationary, cries when held), crying, lethargy, alertness changes
– High-pitched cry
– poor feeding and/or vomiting, diarrhea
– seizures (30-40% - rarely the sole manifestation)
– altered sleeping or eating patterns.
– respiratory distress
– bulging fontanelle may be present late in disease
– hypotonia
– fever may be not present in neonates • A febrile child who is playful, smiling, or interactive is unlikely to
have meningitis in the absence of other signs/symptoms
– 6% DIC and endotoxinic schock
8
9
Meningitis in elderly patients
Older pts, immunocompromised:
fever may not be present
early behavioral problems
Cushing reflex (bradycardia, hypertension, irregular
respirations)
reduced level of consciousness (inability to answer 2
consecutive questions correctly or to follow 2 consecutive
commands, abnormal language, obtundation/coma)
papilledema
dilated pupils, anizocoria, poorly reactive
rigid posture or posturing
VI nerve palsies (abducens supplies the lateral rectus
muscle) gaze palsy
~ facial palsy
seizures
hypertermia
focal paralysis in any of the limbs or trunk
arrithmya
10
cerebral herniationSigns of raised ICP and cerebral edema:
11
12
four tubes of CSF,
each containing about 1mL of fluid
Normal CSF
• Gross appearance: clear and colorless.
• CSF opening pressure: 50–180 mmH2O
• Glucose: 40–85 mg/dL (2.8–4.4 mmol/L)
• N glucose ratio CSF : serum = 0.6 (0.3 for diabetics)
• (In term neonates, a ratio of 0.6 is considered to be abnormal)
• Protein (total): 15–45 mg/dL (albumin 2/3 of total)
• Lactate dehyrogenase: 1/10 of serum level (<35 mg/dL)
•Leukocytes (WBC):
• 0–5/µL (adults / children)
• up to 30/µL (newborns)
• Differential:
• 60–70% lymphocytes;
• up to 30% monocytes and macrophages;
• Stain: negative
•Culture: sterile
• Specific gravity: 1.006–1.009
13
Incidence of various pathogens in different age groups and with specific risk
factors for bacterial meningitis
14
Acute Community-Acquired Bacterial Meningitis
15
Healthcare-Acquired Meningitis
and Ventriculitis
= infections that complicate:
• craniotomies,
• CSF shunt,
• drain surgeries.
most common:
1. Gram-positive
• Staph. epidermidis / aureus
2.Gram-negative bac
• Escherichia coli,
• Klebsiella ,
• Pseudomonas ,
• Acinetobacter
3.anaerobes
• Propionibacterium acnes
Neiseria
meningitidis
-Acute oncet
- winter&early spring
-I peak children <5yo; II - 15-24yo
-nasopharyngitis
-meningococcemia
~ attention: Waterhouse-Friderichsen
Str. pneumonia -asplenism,
-Ig deficiency
- pneumonia
-endocarditis
-otitis media
-paranasal sinusitis
-skull fracture
Haemophilus
influenzae
age < 5 years, unvaccinated
In adults: presence of an underlying
medical disorder (sinusitis, otitis,
alcoholism, CSF leak following head
trauma)
-epiglottitis
-otitis media
-sinusitis
-traheobronh.
-pneumonia
-CSF leak following head trauma
Listeria
monocytogenes
-neonates >3 d & <3mo
-adults >50-60 yo, cancer, diabetis
-food-borne: milk products; vegetables,
undercooked meat, soft cheese
-grow at refrigerator temperatures
+/- gastrointestinal symptoms
-20% no neck stiffness
-multiple CN deficits: VI, VII
-CSF:1/3 - limph, 2/3 neutro
16
Clinical criteria for the etiological diagnosis of meningitis
CSF findings suggestive of bacterial meningitis:
• High WBC 1000–5000 cells/mm3 (100-100,000 cells/mm3)
• low: head trauma, brain abscess, neurosurgery, AIDS
• low WBC count (<20 cells/µL+ high bacterial load = poor prognosis)
• PMN predominance >80-90%
• early in mening. <24-36 ho lymph. predom. (60-70%)
• Low glucose <40 mg/mL, ratio <0.4
• Impaired transport from blood, decreased gluc. receptor expression,
• ↑ anaerobic glycolysis by leucocytes & brain cells
• High protein >100 to 500 mg/dL (N = 45-60 mg/dL)
• Gram staining pos: 70-85% without previous atb; 40-60% with
• ↑ CSF lactate concentrations:
recommend. in postoperative neurosurgical pts initiate empirical atb if lactate >4.0 mmol/L
↑ serum polypeptide procalcitonin polypeptide = in pts with severe bac. Inf.17
18
Test Turnaround
time
Result
interpretation
Advantages Disadvantages
Microscopic
examination
0.5–1 hours Direct if
correlated with
symptoms
Rapid. Poor sensitivity and
specificity; special skills
are needed for
interpretation
Rapid
antigen
15–30 min Direct if
correlated with
symptoms
Rapid False positive results
Culture 2–14 days Definite For phenotypic
drug
susceptibility
testing
Time-consuming; poor
sensitivity; limited
microorganisms are
culturable
Serology 2–8 hours Indirect Automation Results are generally
retrospective; cross-
reactions;
immunosupressed host
may be unable to mount
a response
Molecular
diagnostic
2–8 hours Direct without
knowing
microbial viability
High sensitivity
and specificity
Not the test of cure;
clinical relevance need
to be determined
Laboratory methods used for diagnosis of CNS infections
19
CSF Gram stain: sensitivity 60-90%
CSF concentration of bac. Pos stain
103 colony-forming units/mL 25%
103 – 105 CFU/mL 60%
>105 97%
pos Gr stain
Str. pneumoniae 90%
H.influenzae 86%
N. meningitidis 75%
gram-neg bacilli, 50%
Listeria m. 30%
Bacterial Meningitis Empiric Therapy
Younger than 1
month:
group B Strept (GBS),
E.coli, Listeria monocytogen.,
Klebsiella species.
Ampicillin + cefotaxime /
+aminoglycoside
(gentamicin / tobramycin)
One to 23 months Neisseria meningitidis
Strepto. pneumoniae,
group B Strept (GBS), E coli.
Haemophilus influenzae type b,
Vancomycin +
Ceftriaxone /Cefotaxime
Neisseria men.:benzylpen. /
ceftriaxone / cefotaxime)
Two to 50 years: N meningitides
S pneumoniae
Vancomycin +
Ceftriaxone /Cefotaxime
Older than 50
years:
S pneumoniae, N meningitidis,
L monocyt., aerobic gr-neg rods
Ampicillin + Vancomycin +
Ceftriaxone / Cefotaxime
Immunocompr. S pneumoniae, N meningitidis,
Listeria species, anaerob Gr-neg
Ampicillin + Vancomycin +
Ceftriaxone / Cefotaxime
Basilar skull
fracture
S pneumoniae, H influenzae
Strept. pyogenes
Vancomycin +
Ceftriaxone /Cefotaxime
Penetrating
trauma
neurosurgery
Staph aureus / epidermidis,
aerobic gram-neg bacilli.
Vancomycin +
Cefepime / ceftazidime /
meropenem
Cerebrospinal
fluid (CSF) shunt:
Staph epidermidis / aureus,
aerobic gr-neg bacilli,
Propionibacterium acnes.
Vancomycin +
Cefepime / ceftazidime /
meropenem
21
22
Adjunctive dexamethasone therapy
• Dexametazon (not Metilprednisolon)– I dose 10-20 min prior atb / at least concomitent
(dexamethasone treatment can still be started up to 4 h after the firstdose of antibiotics)
– 0,15 mg/kg q6h (adults 8-12mg primary, then 4-8mg q6h)– length 2 - 4 days– not recommended in treatment of edema secondary to
stroke or haemorrhage)– not recommended in neonates concern regarding effects
on neurodevelopment– The guideline advises to consider discontinuation of
dexamethasone if pathogens otherthan S. pneumoniae or H. influenzae are identified.
23
“For infants and children 6 weeks of age and older, adjunctive therapy with
dexamethasone may be considered after weighing the potential benefits and
possible risks. Experts vary in recommending the use of corticosteroids in pneumococcal
meningitis; data are not sufficient to demonstrate clear benefit in children”
24
25
COMPLICATIONS OF SEPTIC MENINGITIS
1.Cerebral edema (may lead to herniation)
2.Subdural effusion or empyema
3.Vasculitis
• Arteritis (stroke)
• Cortical venous thrombosis (stroke, seizures)
• Venous sinus thrombosis (increased intracranial
pressure)
4.Hydrocephalus
5.Cranial nerve palsies
6.Disseminated intravascular clotting
7.Lactic acidosis
8.Inappropriate ADH secretion
9.Diabetes insipidus
10.Residual findings
• Cranial nerve palsies
• Mental retardation
• Seizures
26
Chemoprophylaxis for high- risk contacts
27
Aseptic meningitis
28
CAUSES OF ASEPTIC MENINGITIS / MENINGOENCEPHALITIS
Viral (Enteroviruses, HSV, VZV, EBV, CMV, HIV, Mumps, LCMV
(lymphocytic choriomeningitis virus), Arbovirus
Bacterial:
• Mycobacterium tuberculosis, MAC,
• Treponema pallidum,
• Brucella,
• Borrelia,
• Rickettsial infections
Fungal meningitis
Protozoal or helminthic infections
Sarcoidosis
Noninfectious causes
• Chemical meningitis (after pneumoencephalography, myelogram,
cisternogram, spinal anesthesia, intrathecal therapy, etc.)
• Toxins (lead, arsenic)
• Tumors
• Demyelinating disease
• Vascular diseases (Vasculitis / Stroke / Subarachnoid hemorrhage)
Enteroviruses
coxsackievirus gr.A 2,4,7,9, gr.B 2-5, echovirus 4,6,9,11,30, enterovirus 71
transmission: hand-to-mouth contact & rarely: respiratory and fecal routes.
temperate climates spring – autumn, outbreaks / sporadic
acute onset of nonspecific febrile illnesses, ~ diphasic pattern
associated findings: sore throat; maculo-papular / hemorrhagic rash;
diarrhoea & abdominal pain; muscle pains & joint aches; very rarely - acute
flaccid paralysis.
•self-limited and resolves in 1-2 weeks.
•~Rombencephalitis (echo 71) myoclonus, sleep disturbance, ataxia
•~Diffuse encephalitis; ~Paralytic syndromes
CSF:
WBC 500- 2,000/mm3
limph. predom. 80-90%
~ first 1-2 days >PMN
glucose – N (↓ in severe)
protein – N / mildly elevated
ARN of enterovirus by PCR from CSF
Stool isolation = misleading can be excreted 12-17 we after inf.29
HSV 1 encephalitis
Patients do not usually have concurrent cold
sores or genital herpes.
• There is often a prodrome for several days
– headache, fever, lethargy, somnolence,
– personality changes (involvement of the
limbic system)
– difficulty with recent memory (involv. temporal
lobe (hippocampi),
– decreased or lost sense of smell (anosmia)
(involv. olfactory bulbs).
• Rapid progression to severe CNS dysfunction:
seizures , focal weakness, cranial nerve defects,
aphasia, hemiparesis
• 20% atypical form: without focal features
• Meningeal signs may not be present
• Papilledema 20%
• Mortality 60–80% untreated.
30
HSV-1 encephalitis
CSF:
• WBC 50-500 (mean of 200 cells/mm3)
• Lymphocytes 80-90%
• RBCs (negative early; present later 10-500/mL)
• midly elevated protein (60-700 mg/dL, average 100)
• normal // mildly decresed glucose (30-40 mg/dL)
• large granular plasma cells (Mollaret cells) seen by Papanicolaou stain
• CSF Ab > serum Ab to HSV-1, not detected until 2 wks
• PCR can be neg in early stages, repeat 3-7 days– 80% - edema and mass effect
– 90% - evidence of temporal lobe involvement
attack a set of interconnected brain structures responsible for the integration of emotion, memory, complex behavior ("limbic system“) 31
HSV-1 encephalitis CT - hypodense lesions in:
•temporal lobes,
•inferior frontal lobes,
•insula,
•predilection for the medial temporal lobes with a sharp transition
MRI -` high signal on T2-weighted scans
` beginning unilaterally, progressing to bilateral` exaggerated signal does not extend beyond the insular cortex (thin arrow),
` but does involve the cingulate gyrus (thick arrow).
foci of hemorrhage occasionally can be observed
32
HSV-1 encephalitis
HSV encephalitis should be considered in any patient with: – a progressively deteriorating level of consciousness,
– fever,
– abnormal CSF,
– focal neurological abnormalities in the absence of any other causes
Treatment:
– Acyclovir, IV, 10 mg/kg q8h for 14–21 days.
– Valacicolvir (expensiv)
– Foscarnet (in severe aciclovir-resistant)
– Administer each dose slowly over 1 hour.
– Crystal-induced nephropathy may occur >> adequately hydrating the patient (eg, 1 mL fluid per day for each 1 mg/d of acyclovir)
• Combating the host inflammatory response with steroids33
Recurrent benign lymphocytic (Mollaret‘s) meningitis
• Age range 5 - 57 years
• Sudden oncet of 3 - 10 episodes of fever + men. signs
• Episodes lasts 2 - 5 days, with spontaneous recovery.
• ½ of pts have transient neurologic manifestations (including seizures,
hallucinations, diplopia, and cranial nerve palsies).
• CSF: hundreds to thousands cells, mixed lymph. and PMN, and large cells
(Mollaret's) cells, protein mildly elevated, glucose N.
• Causative agent: HSV-2 in the majority of cases (PCR)
• Treatment with acyclovir may be beneficial in:
– decreasing the severity
– decreasing the duration of attacks
– preventing further episodes.
34large monocytes with variable shapes
of nuclei (Mollaret's cells)
35
Virus Family Reservoir Primary Vector Distribution
Flaviviridae
Japanese encephalitis Birds, Pigs Culex mosquito SE Asia, Pacific Rim
Murray Valley enceph. Birds Culex mosquito Australia
St. Louis enceph. Birds Culex mosquito Americas
West Nile Virus Birds Culex, Aedes North America, Africa,
Europe, Asia, Australia
Bunyaviridae
California enceph. Rodents, rabbits Aedes mosquito North America
La Crosse virus Chipmunks,
squirrels
Aedes North America
Rift Valley fever Sheep, cattle Aedes, Culex Africa
Toscana virus Bats, humans Phlebotomine flies Europe
Alphaviridae (Togaviridae)
Chikungunya virus Primates, humans Aedes Africa, India, SE Asia
Eastern equine enceph. Birds Aedes Americas
Venezuelan equine
encephalitis virus
Rodents, horses Aedes Americas
Western equine
encephalitis virus
Birds, mammals Culex North America36
Major etiological agents of arboviral meningo-encephalitis
37
West Nile virus (WNV)
• first identified in the West Nile subregion of Uganda,
• now endemic in temperate and tropical regions throughout the world, c
• yearly outbreaks of encephalitis, more likely to occur in adults
• mortality rate 5 - 10 %
• can be transplacentally transmitted during pregnancy
• cause symptomatic inf. in adults, especially chronically ill, immunosup., or elderly
• > 90 % rate of survival with ~50 % incidence of cognitive disturbance
• WNV can spread:i. along neurons via retrograde axonal microtube-mediated transport, than
ii. hematogenous spread
• Neuronal damage and loss can occur by either direct arboviral infection or indirectly
by uncontrolled immune responses to the replicating virus
• Neuronal degeneration, necrosis, and apoptosis
• There are currently no approved antiviral medications for the treatment of neurologic
infections with arboviruses.
38
Tick-borne encephalitis (Flavivirus)
•Scandinavia; W & C Europe; Asia
•bite of ixodes ticks, incub 7-14 (4-28) days
•unpasteurized dairy products cows, goats, sheeps
•I phase: 2-10 days, t0, pseudoinflu., GI simptoms
•Asimptomatic: 1-33 days
•II phase: meningoencephalitis, encephalomyelitis,
encephaloradiculitis
•far eastern subtype - monophasic, no asymptom
•no specific antiviral therapy for TBE.
39
Lymphocytic Choriomeningitis Virus (LCMV = arenavirus)
•main reservoir: house mouse, but also hamsters and domestic mice
•infection by:
– inhaling aerosolized particles of rodent urine, feces, or saliva,
– ingesting contaminated food
– contamination of mucus membranes with infected body fluids,
– directly exposing cuts or other open wounds to virus-infected blood.
– mouse and hamster bites
•Incubation 1 - 2 weeks.
•Infection in people:
– often subclinical;
– “influenza-like symptoms” ;
– meningitis (stiff neck, fever, headache, malaise, muscular pain)
– Orhitis, myocarditis, arthritis, maculopapular rash
•Pregnant women to the fetus:
– fetal or neonatal death
– hydrocephalus, or psychomotor retardation
– chorioretinitis 40
Specific therapy viral meningitis
• HSV: Aciclovir, valaciclovir, foscarnet in severe aciclovir-
resistant
• HZV: acyclovir, ganciclovir an alternative
• CMV: I line: ganciclovir, valganciclovir, II line: foscarnet,
cidofovir
• EBV: acyclovirnot recommended; corticosteroids beneficial
• HHV 6: ganciclovir or foscarnet
• Influenza virus: oseltamivir
• Measles virus: ribavirin
• West Nile virus: ribavirin is not recommended
• St. Louis encephalitis virus: IFN-2a
41
• HIV/AIDS
42
43
44
45
HIV encephalopathy
• is a diagnosis of exclusion
• Damage occurs mainly in the subcortical gray matter, especially - basal
ganglia
• Neurologic deficits usually progress insidiously we - mo
Early signs:
• Cognitive
– forgetfulness associated with slowed mental
– Decreased attention / concentration
– Inability to perform complex task
• Motor
– Poor balance
– loss of fine motor skills (e.g. tremors, clumsiness)
– loss of balance and leg weakness
– progressive loss of mobility
• Behavioral
– apathy and social withdrawal (mistakenly diagnosed as
depression)46
HIV encephalopathy in children (younger than 15 years)
47
• diffuse enlargement of the lateral
ventricle
• cortical sulci are prominent given the
age of the subject
• hyperintense signal throughout the
periventricular white matter
• small children basal ganglia
calcification
• excluding other causes
HIV encephalopathy
48
49
Tuberculous meningitis (TBM) risk factors:
HIV, excessive alcohol use, diabetes, weakened immune system prior tbc history: 50% of children, 10% of adults primary focus on Rx = 30% Formation of small subpial or subependymal foci of metastatic
caseous lesions (Rich focus) ruptures into the subarachnoid spaceTubercles rupturing into the subarachnoid space = meningitis.Tubercles deeper in the parenchyma = tuberculomas /abscesses.
Thick gelatinous exudate infiltrates the cortical / meningeal vessels inflammation, obstruction, infarction.
Tuberculomas
Tuberculous meningitis (TBM)
– duration of symptoms prior to diagnosis 2- 3 weeks• low-grade fever• intermittent headache• light sensitivity• behavioral changes, lethargy, agitation, coma
– mening. Signs + / +++– cranial nerve palsies (CN VI; III, VII)Basal meningitis CN III, VI, VII, eventually leading to obstructive
hydrocephalus from obstruction of basilar cisterns.
– seizures especially in children and elderly people– ophthalmoscopic – papilloedema
Tuberculous meningitis (TBM)CSF:
– Pleocytosis in hundreds 50 – 500 WBC/ml (< 750)
– 60- 80% lymphocytes (PMN ~ predominate first 10 days) – protein: N raised (>1.0 g/L), spider-web clot– low glucose <40 mg/dL, ratio CSF/blood <0.5– low chloride
– Ziehl-Neelsen 10% (acid-fast bacillus )
– acellular CSF in elderly, HIV / AIDS pts
– PCR CSF low sensitivity
– Culture for M.tbc 3-6 weeks
• Once specific therapy has begun, a so-called therapeutic paradox may occur
and is characterized by clinical worsening and by a shift of the CSF
lymphocytic pleocytosis into a polymorphonuclear response. It must not be
interpreted as a failure in treatment
52
Tuberculous meningitis
• exudate in the basal cisterns
• basilar meningeal thickening
• infarcts in the middle cerebral
artery territory
• edema
• hydrocephalus
• tuberculoma formation
Post-contrast MRI:
basal cistern enhancement:
more prominent on
contrast enhanced T1-W image53
Criptococcal neoformans / gattii var neoformans infection
immunosuppressed hosts
54
asymptomatic or
symptomatic
pneumonia
environmental exposure
worldwide distribution
no human to human transmission
55
Criptococcal meningitis
• subacute illness (>2we), low grade fever
• confusion, change in behavior
• cranial nerve palsies and papilledema
• less often altered mental status
• mortality rate of meningitis 6-25%
• 2/3 - without signs of meningeal irritation
Associated signs:
• Skin lesion
• Oral ulcers
• Myocarditis
• Pulmonary involv. 1/3
• GI
56
Cryptococcal meningitis CSF:
• pleocytosis (20-500 cells),
• lymphocytes 80-90%
• reduced glucose in severe cases,
• elevated protein level
• CSF opening pressure elevated
• cryptococcal antigen test 90% sensitive
• India ink and specific fungal culture.
Yeast are identified through the halo effect because of the glucuronoxylomann
capsule
DD. Aspergillus and related fungi result in neutrophilic meningitis.57
58http://www.hivwebstudy.org/cases/ois-treatment/39-year-old-headache-fever-and-
confusion-text-added-andrew-draft
Cerebral toxoplasmosis
• 3% to 40% of pts CD4 counts < 200 cells/mm3
• most cases - reactivation of a previously acquired toxo
• clinical manifestations – headache (55%),
– confusion (52%),
– fever (47%),
– lethargy (43%),
– seizures (29%).
– focal neuro signs 69%: hemiparesis, ataxia, cranial nerve palsies
• CSF examination in toxoplasmosis is nondiagnostic
• CSF: Ab to Toxo are not sensitive for Toxo encephalitis
• MRI is more sensitive than CT
59
MRI is more sensitive than CT m
multiple ring-enhancing lesion surrounded by variable degrees of vasogenic edema
predilection for cortex and deep gray-matter structures such as the basal ganglia
cerebellum and brain stem are less commonly involved
Cerebral toxoplasmosis
MRI T1 weight + gadolinium
60
61
62
63
Progressive multifocal leukoencephalopathy (PML)
• JC virus (papovavirus)
• enter the body via the respiratory or oral route
• becomes latent in kidneys, lymphoreticular tissues, brain
• primary infection is asymptomatic
• HIV reactivation of the endemic JC
• Viral particles carried to CNS via B-lymph. In systemic dissem.
• infection of oligodendrocytes
• leads to demyelination dL 4-6 mo. If +HAART 2 years
• insidious onset and steady progression of focal symptoms:
• behavioral, speech, cognitive, motor, visual impairment.
•multifocal nature of the disease,
•evolves over several weeks
• PML more rapid progression than AIDS dementia complex
•Pts with more preserved immune slower progression
• As lesions expand manifest. worsen, involve larger territory
•Seizures a rare manifestation of PML (if + = demyelinating
lesions immediately adjacent to the cortex)
64
Primary Central Nervous System Lymphoma
MRI after the administration of intravenous contrast
T1 T2
single or multiple
focal ring and/or nodular enhancing mass lesion(s)
with surrounding edema
primary CNS lymphoma resembles toxoplasmosis in 50-80% of the cases
Rapid progression of the mass(es) on serial imaging studies also favor lymphoma 65