Flashcards in mass lesions: NCC and toxo Deck (42):
AKA contrast/ring-enhancing lesions caused by Infectious abscesses and common parasitic diseases of the CNS - Neurocysticercosis (NCC) and Toxoplasma gondii/Toxoplasmosis
mass lesion manifestations
ddx mass lesions: abscesses
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.
ddx mass lesions besides abscesses
mass lesions in AIDs pt
Primary or metastatic brain tumor – EBV-associated primary CNS lymphoma (PCNSL).
CMV polyradiculopathy, encephalitis, myelopathy, etc.
Taenia solium metacestodes.
NCC: most common ??
Many (annual prevalence = 50 million) people carry ??
parasitic CNS disease
cause of epilepsy in the world (Asia, Africa, Central & South America).
cysticerci (larval stage) of T. solium
Prevalence of NCC is highest in ??
Prevalence in US is increasing due to the ??
Central and South America, India and Sub-Saharan Africa.
influx of immigrants from these endemic areas.
NCC pathogenesis: pt ingests ??
Oncospheres are released in ??
develop into ??
ova (NOT cysts) or gravid proglottids.
GIT → disseminate → lodged in the CNS (brain parenchyma, meninges, ependyma, choroid plexus, etc.)
develop into cysticerci.
NCC: Parenchymal cysts:
viable for how long?
how many to be symptomatic?
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.
what causes s/s in NCC?
how long does it take?
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.
Rarely, NCC parenchymal cysts growth → ??
mass effect on brain parenchyma.
NCC: Extraparenchymal Cysts:
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).
Clinical manifestations depend on location(s) of NCC cyst(s):
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)
NCC dx: symptoms usually only occur in ??
calcified lesions evident by MRI.
another ddx mass lesions
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).
-Bacteria: S. aureus, anaerobes, L. monocytogenes, M. tb
-Chronic fungi: C. immitis or Candida albicans
one of 3 for confirmatory NCC dx
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.
In absence of one or more of these results that confirm a diagnosis of neurocystticercosis, but with imaging results that suggests the diagnosis:
*Positive serum enzyme-linked immunoelectrotransfer blot (EITB)*
*CSF WBC with differential reveals an eosinophilia as high as 15%.
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
NCC dx: Positive serum enzyme-linked immunoelectrotransfer blot (EITB) for detection of ??
sensitivity and specificity of more than 98%
serologic assay of choice for the detection of cysticercosis.
NCC tx: antiparasitic
both asymptomatic and symptomatic pts
*all destroy VIABLE cyst in CNS
other NCC tx
Corticosteroids (dexamethasone or prednisone [60 mg/d]).
Ventricular shunt for elevated intracranial pressure or hydrocephalus.
Surgery may be required to remove cysts
excellent with treatment
Toxoplasma gondii/Toxoplasmosis agent
Tissue protozoan (eucaryote)
an obligate intracellular parasite
toxo tissue-based infectious forms in humans:
Actively growing toxo trophozoite (aka tachyzoite) infect ??
any nucleated host cells
latent toxo pseudocyts found primarily in ??
how is the pseudocyst formed??
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.
rare or common in US??
2nd most common cause of ??
many person in the US are infected (about 45%).
CNS infection in AIDS pt., after HIV.
definitive host of todo??
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
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.
toxo pathogenesis is ?
Following release from oocyst or pseudocyst, protozoan spreads ??
multifocal mass lesions
hematogenously to all organs and tissues where the trophozoites infect any nucleated cells.
Intracellular proliferation of toxo leads to the ?? relasing trophs to infect of adjacent cells with intracellular proliferation and lysis relasing more trophs, eventually causing ??
rupture of infected cells
small necrotic foci
Sites where toxo lesions are found include:
CNS most common
*Tissue trophozoites form intracellular pseudocysts due to the host CMI and they persist for years.
If the host CMI response weakens/marked T-cell suppression -->??
reactivation of latent infection → pseudocysts breakdown releasing trophozoites → damage host
T cell suppressive disorders:
Reactivation diseases include:
Multifocal mass lesion or generalized seizures.
Disease in eye and/or lung.
*both can cause toxo activation
toxo manifestations are weeks → several months of progressive worsening of:
altered mental status,
cranial nerve abnormalities
focal or generalized seizures.
ddx mass lesions in immunocompromised person (i.e. AIDS pt)
Primary or metastatic brain tumor – EBV-associated primary CNS lymphoma (PCNSL),
CMV polyradiculopathy, encephalitis, myelopathy, etc.
Neuroimaging/neuroradiologic scans (contrast enhanced)
CT scan → ring enhancing lesions.
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.
toxo Serological studies:
what will not be present??
what will be present if toxo, and if absent makes dx unlikely?
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).
toxo dx: Brain biopsy and histological diagnosis with observation of ??
trophs or multiple, ruptured tissue cysts in inflammatory lesions
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.