Dr. Parag MoonSenior Resident, Neurology

GMC, Kota.

Taenia saginata-beef

T. s. asiatica -pig organs

T. solium primarily in pork

Cysticercosis and Taeniosis -foodbornezoonotic infections with larval or metacestodeand adult tapeworms, respectively

Larvae meat-borne (pork)

Adult stage-small intestine of the human host (obligate).

Risk factors

Poor sanitation

Intimate contact between humans and their livestock

Use of untreated or partially treated wastewater in agriculture

Uncooked or partially cooked meat

50 million people have cysticercosisworldwide.

Underestimate since many infections are not diagnosed.

Cestodes are cosmopolitan in distribution

Highly endemic in Latin America, Africa and Asia

NCC -most common cause of adult-onset seizures in developing countries

Adult form-flat, opaque white or yellowish, long segmented parasites, measuring 1 to 12 m.

Head or scolex -attachment organ

Has four suckers and a rostellum that may be armed with hooks(T. solium), or unarmed and sunken (T. saginata), or with rudimentary hooklets (Taenia saginata asiatica)

Scolex -size of a pin-head

Followed by a short and undivided region, the neck

Long chain of proglottids or segments (termed the strobila) proliferate

Strobila has the appearance of a ribbon and may consist of more than a thousand proglottids.

Posterior end of the tapeworm has the broadest, longest and oldest proglottids

Eggs are spherical

Size -20 to 50 μm

Radial appearance on light microscopy

Eggs of all taeniids are morphologically indistinguishable by light and electron microscopy.

Humans as the sole definitive host

Pigs are intermediate host.

Humans acquire taeniosis by eating undercooked or raw pork infected with cysticerci.

Acquire cystecercosis by ingesting eggs (exogenous or endogenous autoinfection)

Cellulose -small, spherical or oval, white or yellow vesicle, 0.5 and 1.5 cm

Translucent bladder wall, through which scolexcan be seen as a small solid eccentric granule.

Generally separated from host tissue by a thin collagenous capsule, within which it remains alive

Racemose -large, round or lobulated bladder circumscribed by a delicate wall

Resembles a cluster of grapes,10 to 20 cm

More common in immmunosupressed

1)Vesicular stage-cyst with a translucent vesicular wall, transparent fluid, and a viable invaginated scolex.

Little host inflammatory reaction.

2)Colloidal stage-thick vesicular wall, fluid turbid, scolex degenerates

Varying degrees of acute and chronic inflammation.

Radiography- cystic lesions with edema and enhancement and seizures are common.

3)Granular stage- thick vesicular wall, degenerated scolex, gliosis, little inflammatory host response.;

4)Calcific stage

Asymptomatic to life threatening

Can affect parenchyma, subarachnoid space, or intraventricular system,ocular,spinal

Dependant on the location, number, and stage of the cysts at presentation

Leading cause of adult-onset epilepsy in endemic areas(Latin America, Asia, Africa)

Commonly generalized tonic-clonic or simple partial

More frequent in patients with parenchymaldisease,

Can occur in patients with cysts in the cortical sulci

Usually occur when dying cyst incites an inflammatory reaction

Has been reported in cystic stage 50%–70% of patients experience recurrent

seizures

Also occur secondary to vasculitis and infarction in setting of subarachnoid disease

Calcified NCC -development and maintenance of seizures and epilepsy

Positive correlation between endemic populations with increased proportions of calcification and seizure activity.

Calcified granulomas have increased risk of ongoing seizure

Perilesional edema related to calcification occurs episodically associated with seizures

Accompanied by enhancement around the calcified focus

Appx. 23%–35%

Out of 110 patients, those with recurrent seizures, perilesional edema was noted on MRI in 50% as opposed to 9% of asymptomatic matched controls

The Lancet Neurology, vol. 7, no. 12, pp. 1099–1105, 2008

Focal neurologic signs

Related to the number, size, and location of the parasites in individuals parenchymaldisease.

Cysticercotic encephalitis-Intracranial hypertension in patients with parenchymalNCC

Seen in children and young woman

Acute inflammatory response to massive cysticercal infection resulting in brain edema

Presents with clouding of consciousness, seizures, decreased visual acuity, headache, vomiting, and papilledema- subacute or acute in onset

Treated with mannitol and corticosteroids

May require decompressive temporal craniotomy

Not candidate for antiparasitic agents

Other causes of intracranial hypertension-large cyst displacing midline structures or obstructs the flow of CSF at aqueduct

Psychiatric manifestations-depression, psychosis

Study showed chronic inpatient psychiatric pts were more likely to have a positive serology for T. solium than healthy controls

Increased risk with pts with mental retardation

American Journal of TropicalMedicineand Hygiene, vol. 73, no. 3, pp. 504–509, 2005

Subarachnoid NCC

Seen in Sylvian fissure or basilar cisterns

Normal evolution not occur in the intraventricular or subarachnoid form

Racemose type-aberrant proliferating cestodelarvae

Local mass effect

Arachnoiditis resulting in communicating hydrocephalus secondary to chronic inflammation or fibrosis of arachnoid villi

Cysticercotic arachnoiditis can lead entrapment of cranial nerves in the inflammatory exudates.

Extraocular muscle paralysis, diplopia and papillary abnormalities

Decreased visual acuity,visual field defects

Acute aseptic meningitis-signs of meningealirritation rare

Cerebral infarction, transient ischemic attacks, brain hemorrhage

Mechanism-Cerebral arteritis, particularly with subarachnoid cysticercosis

Middle-size vessel involvement common

Vary according to size of parasites, their location inside ventricular system, and the coexistence of granular ependymitis

Lateral ventricles -syndrome of increased intracranial pressure, may be associated with focal neurological signs due to compression.

Third ventricle cysticerci -progressively worsening headaches and vomiting due to developing obstruction

May present with sudden loss of conscious from acute hydrocephalus

Paroxysmal headache and vomiting secondary to intermittent obstruction at the level of the cerebral aqueduct

Fourth ventricle-subacute hydrocephalus that may be associated with signs of brainstem dysfunction secondary to compression of fourth ventricle

Bruns’ syndrome -Fourth ventricle cyst Characterized by episodic headache,

papilledema, neck stiffness, sudden positional vertigo induced by rotatorymovements of the head, nausea and vomiting, drop attacks and loss of consciousness

Rapid recovery and long asymptomatic periods

Cysts in the third and fourth-cause of sudden death due acute obstructive hydrocephalus

Granular ependymitis

Degenerating cyst in the ventricles can result in inflammatory reaction throughout the ventricular system

Cyst fixed to the ventricular wall with strong

adhesions and fibrosis leading to hydrocephalus

Tend to have a more chronic course

1%–5% of all cases Extramedullary more common Intramedullary cysts are most common in

thoracic spine Extramedullary cysts or leptomeningeal NCC-

extension of subarachnoid disease,migratedfrom basilar cisterns

Single or may form clumps Combination of radicular pain and motor

deficits of subacute onset and progressive course

Subretinal space -progressive decrease in visual acuity

Vitreous cysts-worsening vision with perception of something moving within the eye

Anterior chamber cyst-may induce a severe iridocyclitis

Retro-ocular intraorbital cyst-decreased visual acuity due to pressure on the optic nerve

In the vesicular stagem cysticerci appear as cystic lesions within the brain parenchyma

CT and MRI –thin walled cyst well demarcated from parenchyma,lack perilesional edema and do not enhance after administration of contrast medium.

May be a bright nodule in their interior giving the lesion a “hole with dot” appearance that represents the scolex

Colloidal stage so-called “acute encephalitic phase” of NCC has intense host reaction

Appear as ill-defined lesions surrounded by edema which enhance after contrast medium administration

MRI reveals a thick and hypointense wall with marked perilesional edema

Granular cysticerci appear as nodular hyperdense lesions surrounded by edema or a rim of gliosis after contrast medium administration

Calcified (dead) cysticerci appear on CT as small hyperdense nodules without perilesional edema

Cysticerci within the basilar cisterns missed by CT scan, require MRI

Subarachnoid cysts located in the Sylvianfissure may reach 50mm or more in size;havea mulitlobulated appearance, behave as mass occupying lesions.

Hydrocephalus is most common CT finding in subarachnoid NCc.

Leptomeningeal enhancement at the base of the brain observed on MRI

Appear on CT images as cystic lesions.

Initially isodense with the CSF so not well visualized.

Can be inferred from distortions of the ventricular system causing asymmetric or obstructive hydrocephalus

Well visualized by MRI particularly using FLAIR techniques

Ventricular migration sign move within ventricular cavities in response to movements of patients’ head a phenomenon best observed with MRI

CT -symmetrical enlargement of the cord (intramedullary cysts)

Pseudoreticular formations within the spinal canal (leptomeningal cysts).

MRI -intramedullary cysticerci to be ring enhancing lesions that have eccentric hyperintense nodule representing the scolex.

Myelography in spinal leptomeningealcysticercosis shows multiple filling defects in column of contrast material corresponding to each cyst

Electroimmunotransfer blot (ETIB) using partially purified antigenic extracts

Specificity 100% & sensitivity 94%–98% in two or more cystic or enhancing lesions

False negative results in patients with single intracranial cysticerci

Detection of circulating parasite antigen reflects presence of live parasites, ongoing viable infection, permit quantitative verification of successful treatment

Monoclonal antibody-based ELISA to detect T. solium antigens in urine

Sensitivity of urine antigen detection for viable parasites was 92%, which decreased to 62.5% in patients with a single cyst.

Only calcified cysticercosis were urine antigen negative

Indirect haemagglutination tests

Lymphocyte transformation test (LTT) has sensitivity of 93.7% and specificity of 96.2%

Single cyst infection sensitivity of test was 87.5%

For Parenchymal Disease-Praziquantel and albendazole are antiparasitic agents

Efficacy 60%-85%

Greater cyst reduction with albendazoleadministration

Praziquantel dose-50 mg/kg/d for 2 weeks

Albendazole dose-15mg/kg for four weeks later reduced to 15 days then to one week

Between second and fifth day of treatment-exacerbation of neurologic symptoms attributed to inflammation secondary to killing of cysticerci

Steroids used in conjunction to control resulting edema

Steroids decrease the plasma level of praziquantel,but not albendazole

Oral prednisolone preferred

Started 2-3 days before cysticidal therapy and continued for 7-10 days along with cysticidal therapy

High dose corticosteroids in cysticercoticencephalitis

Whether provoked or acute symptomatic seizures and unprovoked seizures

Acute symptomatic seizures patients may be treated only for duration of acute condition

No guideline regarding duration

Unprovoked seizures-2 years seizure free period

SSECTG-monitor cyst activity with neuroimaging(6months) and to continue AED until resolution of the acute lesion.

Resolved then AED may be tapered off over next 12 weeks

1. Ventricular, subarchanoid cysts-neuroendoscopic removal

2. Giant cysticerci

3. Hydrocephalus

4. Cysticercoid enchephalitis with raised ICT may require temporal hemicraniotomy.

Current consensus guidelines for treatment of neurocysticercosis. Clin Microbiol Rev 2002; 15: 747-756

Cochrane Database review on drugs for treating NCC concludes that there is insufficient evidence to assess whether cysticidal therapy in NCC is associated with beneficial effects

Depends on degree of infection and host response to parasite

85% with a SCCG have good seizure outcome following resolution of lesion

With more than two seizures, breakthrough seizures, whose follow-up CT scan shows a calcific granuloma have a higher risk of recurrence

Eradication of swine cysticercosis through improved animal husbandry and meat inspection procedures

No vaccine developed

Thanks

Neurocysticercosis: Management Issues;Tarun Dua,S. AnejaIndian Pediatrics 227-236 Volume 43;march 17, 2006

Human Cysticercosis And Indian Scenario: A Review ;KASHI NATH PRASAD Et Al. J. Biosci. 33(4), November 2008, 571–582

Diagnostic criteria for neurocysticercosis: Some modifications are needed for Indian patients; Ravindra Kumar Garg: Neurology India June 2004 Vol 52 Issue 2

Neurocysticercosis – Indian Scenario; G. Singh, M. Sappal; Medicine Update 2012 Vol. 22

Neurocysticercosis: Revisited; K.Kulkantrakorn; J INFECT DIS ANTIMICROB AGENTS Jan.-Apr. 2005

Diagnosis and Treatment of Neurocysticercosis;C. Coyle, H. Tanowitz; Interdisciplinary Perspectives on Infectious Diseases Volume 2009, 9 pages

WHO/FAO/OIE Guidelines for the surveillance, prevention and control of taeniosis/cysticercosis 2005