mass lesions: NCC and toxo

Question 1

Mass lesions

Answer 1

AKA contrast/ring-enhancing lesions caused by Infectious abscesses and common parasitic diseases of the CNS - Neurocysticercosis (NCC) and Toxoplasma gondii/Toxoplasmosis

Question 2

mass lesion manifestations

Answer 2

Fever.
Severe headaches.
Seizures.

Question 3

ddx mass lesions: abscesses

Answer 3

S. aureus is most common single pathogen.
Mixed anaerobic infections account for @1/2 of all cases:
Mostly G- rods and G+ cocci.
L. monocytogenes or M. tb
Fungi: Coccidioides immitis, Candida albicans.

Question 4

ddx mass lesions besides abscesses

Answer 4

Neurocysticercosis.
Echinococcus.
Toxoplasmosis.

Question 5

mass lesions in AIDs pt

Answer 5

HAD
Primary or metastatic brain tumor – EBV-associated primary CNS lymphoma (PCNSL).
Toxoplasmosis encephalitis
PML
Cryptococcal meningoencephalitis
CMV polyradiculopathy, encephalitis, myelopathy, etc.

Question 6

NCC agent

Answer 6

Taenia solium metacestodes.

Question 7

NCC: most common ??

Many (annual prevalence = 50 million) people carry ??

Answer 7

parasitic CNS disease
cause of epilepsy in the world (Asia, Africa, Central & South America).

cysticerci (larval stage) of T. solium

Question 8

Prevalence of NCC is highest in ??

Prevalence in US is increasing due to the ??

Answer 8

Central and South America, India and Sub-Saharan Africa.

influx of immigrants from these endemic areas.

Question 9

NCC pathogenesis: pt ingests ??

Oncospheres are released in ??

develop into ??

Answer 9

ova (NOT cysts) or gravid proglottids.

GIT → disseminate → lodged in the CNS (brain parenchyma, meninges, ependyma, choroid plexus, etc.)

develop into cysticerci.

Question 10

NCC: Parenchymal cysts:
viable for how long?

how many to be symptomatic?

Answer 10

Mature, living cysticerci are viable for 2→10y, during which time they suppress the host immune response and the host is usually asymptomatic (with a few cysts);
6→10 or more can be symptomatic.

Question 11

what causes s/s in NCC?

how long does it take?

Answer 11

As cysticercus begins to die, they leak antigens → an intense inflammatory response (with perilesional edema) & fibroblast form capsule around cyst → the host manifests with signs and symptoms

Cyst degeneration takes 6→18 months.

Question 12

Rarely, NCC parenchymal cysts growth → ??

Answer 12

mass effect on brain parenchyma.

Question 13

NCC: Extraparenchymal Cysts:

Answer 13

A few (@10%) oncospheres lodge in ventricles, subarachnoid space or meninges develop into atypical cysts (greatly enlarged) → obstruction of CSF pathway → may cause focal neurological signs or increased cranial pressure (hydrocephalus).

Question 14

Clinical manifestations depend on location(s) of NCC cyst(s):

Answer 14

Focal or generalized tonic-clonic seizures.
Neurological deficits/focal signs (hemiparesis, visual loss, paraparesis).
AMS (dementia, confusions, stupor).
Symptoms of elevated intracranial pressure (headaches, if cyst is blocking ventricles)

Question 15

NCC dx: symptoms usually only occur in ??

Answer 15

calcified lesions evident by MRI.

Question 16

another ddx mass lesions

Answer 16

Neurocysticercosis (Taenia solium).
Cystic Echinococcosis-hydatid cyst (Echinococcus granulosus or multilocularis)
Raccoon Round Worm Encephalitis/Baylisascariasis (Baylisascaris procyonis)
Toxocaria (Toxocaria cannis or cati)
Toxoplasmosis (Toxoplasma gondii).
Abscess:
-Bacteria: S. aureus, anaerobes, L. monocytogenes, M. tb
-Chronic fungi: C. immitis or Candida albicans

Question 17

one of 3 for confirmatory NCC dx

Answer 17

Histological demonstration of parasite from biopsy of brain or spinal chord

Cystic lesion showing the scolex on CT scan or MRI

Direct visualization of retinal parasites by fundoscopic exam

*Note: Live cysts are non contrast-enchancing but dying-dead cysts are contrast-enchancing.

Question 18

In absence of one or more of these results that confirm a diagnosis of neurocystticercosis, but with imaging results that suggests the diagnosis:

Answer 18

Positive serum enzyme-linked immunoelectrotransfer blot (EITB)
*CSF WBC with differential reveals an eosinophilia as high as 15%.
*Pt s/s
EEG changes focal discharge, sharp spike, slow wave) indicate active seizure focus
Hx of travel, etc to endemic area
documented fam infestation
resolution of cysts post-td
documented extra-CNS cysticercosis

Question 19

NCC dx: Positive serum enzyme-linked immunoelectrotransfer blot (EITB) for detection of ??

Answer 19

anticysticercal antibodies
sensitivity and specificity of more than 98%
serologic assay of choice for the detection of cysticercosis.

Question 20

NCC tx: antiparasitic

Answer 20

both asymptomatic and symptomatic pts

Niclosamide
Albendazole
Praziquantel
*all destroy VIABLE cyst in CNS

Question 21

other NCC tx

Answer 21

Anticonvulsant.
Corticosteroids (dexamethasone or prednisone [60 mg/d]).
Ventricular shunt for elevated intracranial pressure or hydrocephalus.
Surgery may be required to remove cysts

Question 22

NCC px

Answer 22

excellent with treatment

Question 23

Toxoplasma gondii/Toxoplasmosis agent

Answer 23

Tissue protozoan (eucaryote)
an obligate intracellular parasite

Question 24

toxo tissue-based infectious forms in humans:

Answer 24

trophozoite

latent pseudocyst

Question 25

Actively growing toxo trophozoite (aka tachyzoite) infect ??

Answer 25

any nucleated host cells

Question 26

latent toxo pseudocyts found primarily in ??

how is the pseudocyst formed??

Answer 26

the brain and muscle –

T. gondii cannot form a true cyst as per T. solium (a helminth) cysticerci.
The pseudocyst is formed by the host immune system response to the trophozoite. Clinical implication is with respect to reactivation due to specific immunosuppression.

Question 27

toxo epi:
rare or common in US??

2nd most common cause of ??

Answer 27

many person in the US are infected (about 45%).

CNS infection in AIDS pt., after HIV.

Question 28

definitive host of todo??

intermediate host?

Answer 28

Definitive host is the cat:
mature oocyst are produced in the protozoan life cycle in the cat. Oocyst divids into two sporocysts, each containing two elongate sporozoites.

Intermediate host include many animals – including humans

Question 29

toxo transmission

Answer 29

Ingestion of tissue pseudocysts in undercooked or uncooked meat (esp. pork or lamb) is primary mode.

Inhalation or ingestion of mature oocyst (passed in feces of cat).

Other: Transplacental, blood transfusion, organ transplant.

Question 30

toxo pathogenesis is ?

Following release from oocyst or pseudocyst, protozoan spreads ??

Answer 30

multifocal mass lesions

hematogenously to all organs and tissues where the trophozoites infect any nucleated cells.

Question 31

Intracellular proliferation of toxo leads to the ?? relasing trophs to infect of adjacent cells with intracellular proliferation and lysis relasing more trophs, eventually causing ??

Answer 31

rupture of infected cells

small necrotic foci

Question 32

Sites where toxo lesions are found include:

Answer 32

CNS most common
eye
lung
muscle

*Tissue trophozoites form intracellular pseudocysts due to the host CMI and they persist for years.

Question 33

If the host CMI response weakens/marked T-cell suppression –>??

Answer 33

reactivation of latent infection → pseudocysts breakdown releasing trophozoites → damage host

Question 34

T cell suppressive disorders:

Reactivation diseases include:

Answer 34

AIDS
transplant pts
Hodgkin’s disease

Diffuse encephalitis.
Multifocal mass lesion or generalized seizures.
Disease in eye and/or lung.

*both can cause toxo activation

Question 35

toxo manifestations are weeks → several months of progressive worsening of:

Answer 35

altered mental status,
weakness,
cranial nerve abnormalities
neuropsychiatric disorders,
focal or generalized seizures.

Question 36

ddx mass lesions in immunocompromised person (i.e. AIDS pt)

Answer 36

HAD,
Primary or metastatic brain tumor – EBV-associated primary CNS lymphoma (PCNSL),
Toxoplasmosis encephalitis
PML,
Cryptococcal meningoencephalitis,
CMV polyradiculopathy, encephalitis, myelopathy, etc.

Question 37

toxo dx

Answer 37

CD4+ count

Question 38

Neuroimaging/neuroradiologic scans (contrast enhanced)

Answer 38

CT scan → ring enhancing lesions.

MRI:
Contrast enhancing lesions after administration of gadolinium.
multiple bilateral cerebral lesions in the juxtacortical and basal ganglia areas.
ganglia and are hypodense with ring-enhancement.
Cerebral Toxoplasmosis - Deep central gray nuclei or lobar gray-white junction.
Other sites: posterior fossa, cerebral cortex, and periventricular white

Negative thallium-201 single-photon emission CT (SPECT) scan.

Question 39

toxo Serological studies:
what will not be present??

what will be present if toxo, and if absent makes dx unlikely?

Answer 39

IgM will not be present – disease is reactivation.

Absence of anti-Toxoplasma IgG makes a diagnosis of toxoplasmosis unlikely, even in an pt with advanced HIV/AIDS (90% are toxoplasmosis IgG seropositive).

Question 40

toxo dx: Brain biopsy and histological diagnosis with observation of ??

Answer 40

trophs or multiple, ruptured tissue cysts in inflammatory lesions

Question 41

toxo tx

cure??

Answer 41

2→4 months of a combination of sulfonamides (sulfadiazine) or clindamycin plus pyrimethamine.

only treats trophozoites, (i.e., active disease) not latent infection of pseudocysts, so it not a cure, hence in immunosuppressed patient, prophylaxis after disease is lifelong.

Question 42

toxo prevention

Answer 42

Pregnant women, Advanced HIV patients, SOT patients on immunosuppressive therapy, etc. should be instructed to avoid cats, cat feces and Cook pork well, not pink.