Neurocysticercosis is an infestation of the central nervous system with the larval cysts

of the pork tapeworm (Taenia solium), when a man is paratenic host of the parasite.
The infection results from ingestion of food or water contaminated with human feces
containing the parasitic eggs. Much rarely, the infection is caused by autoinoculation,
when the mature parasites are present in the small intestines, and reversed peristalsis
gives rise to regurgitation of gravid proglottides (internal auto-infestation), or by
ingestion of the eggs from one's own feces (external auto-infestation). The embryos
(oncospheres) develop from the eggs, penetrating the small intestine mucosa and
entering the circulation and subsequently different tissues and organs where
cysticerci, small tissue larvae, are developed. Cysticerci have specific affinity for the
central nervous system, eyes and striated muscles what is accounted for high
concentration of glucose or glycogen in these organs. Neurocysticercosis is the most
frequent parasitic disease of the central nervous system and the most common cause
of convulsions and hydrocephalus in the adults in endemic regions, where the
seroprevalence of disease is about 4% of population. Neurocysticercosis is classified
into six clinical syndromes: asymptomatic, parenchymal, subarachnoid,
intraventricular, spinal and ocular forms. Albendazole (benzimidazole) of 15 mg/kg/BW
during 8-28 days or praziquantel (pyrazolone quinoline) of 50-60 mg/kg/BW during 15
days (or 100 mg/kg/BW only one day) are applied for treatment of neurocysticercosis.

The presence of the adult tapeworm in the intestine can lead to malabsorption and
malnutrition in the host. The presence of the larval form of the tapeworm in extraintestinal tissues can lead to various symptoms and signs, including seizures (from
cysts in the brain), hepatomegaly (from cysts in the liver), and cough and/or
haemoptysis (from cysts in the lung).
Intestinal infection (e.g., with Diphyllobothrium latum, Hymenolepis nana, Taenia
saginata)

Larvae are ingested, oncospheres (embryos) hatch, and adult tapeworms

develop inside the human intestinal tract.

Both adult and larval forms may be present in the human intestinal tract (e.g.,
with H nana).

Adult parasites live in the human intestinal tract, and eggs and proglottids are
passed in the faeces.

H nana oncospheres penetrate the bowel mucosa and develop into cysticercoid
larvae. Larvae emerge in the bowel lumen after a period of 5 to 6 days, and
develop into adult tapeworms in the ileum. About 20 to 30 days after initial
infection, the adult begins to produce new eggs, which can be found in the
faeces and spread the infestation. [2]

Cysticercosis and neurocysticercosis

Humans develop cysticercosis by ingesting embryonated Taenia solium eggs or

gravid proglottids. Following ingestion, oncospheres hatch and infect the small
intestine or invade through the intestines and migrate to extraintestinal tissues.

A minimal inflammatory reaction may occur with T saginata, suggesting that

these tapeworms have an 'irritative' effect, perhaps causing clinical symptoms.

Embryos invade the bowel wall and the scolex (tapeworm head with suckers,
hooks, and a rudimentary body from which proglottids are produced by budding)
of the larva evaginates, attaches to the upper jejunum, and develops into an
adult worm.

Cysticerci (liquid-filled vesicles consisting of a membranous wall and a nodule

containing the evaginated scolex) develop over a period of 3 weeks to 2
months.

Larvae may form within any extraintestinal tissue. Neurocysticercosis is invasion

of the CNS.

Humans with cysticercosis are intermediate or dead-end hosts (do not transmit
infection).

Once present in the parenchyma of host organs, cysts undergo dynamic

changes. Initially cysts are vesicular and filled with clear fluid, and they may
produce host inflammatory reactions (referred to as the cystic stage). The cysts
start to degenerate and become turbid with intense inflammatory reactions in
surrounding tissue (referred to as the colloidal stage). [11] The granular stage is
next, and is characterised by further degeneration when the cyst ultimately
calcifies.

Neurocysticercosis can be parenchymal or extraparenchymal. Parenchymal

disease used to be referred to as active (when the larvae is viable) and inactive
(when the larvae is calcified), but that classification is no longer applicable. MRI
studies have documented that patients with neurocysticercosis seizures, and
calcified lesions often have associated contrast enhancement and oedema.
There has been increasing evidence that perilesional oedema, which occurs
episodically, is associated with seizures. There is no evidence to suggest these
lesions are associated with viable parasites. Instead, they may be caused by the
release of antigens from the calcified granuloma in restimulation of host
inflammation.

Extraparenchymal neurocysticercosis includes involvement of the subarachnoid

space, the ventricles, the spinal cord, and/or the eye.

Another form of neurocystercosis is referred to as racemose disease. It generally

occurs when subarachnoid or intraventricular cysts proliferate in spite of scolex
degeneration, provoking intense inflammatory responses from hosts.

Mixed neurocysticercosis involves both parenchymal and extraparenchymal

disease

http://bestpractice.bmj.com/bestpractice/monograph/358/basics/pathophysiology.html

Taenia solium Neurocysticercosis

http://web.stanford.edu/group/parasites/ParaSites2010/Adnan_and_Rehan_Syed
/Parasites%20and%20Pestilence%20Paper_ParaSites%20Submission%20for
%20Carlos%20Seligo_Rehan%20Syed%20and%20Adnan%20Syed.htm
Taenia solium, also known as the pork tapeworm, can cause disease in humans
when ingested[26]. Ingestion of infective larvae or cysticerci in undercooked or
cured pork results in the development of adult worms within the new hosts
intestines. However, ingestion of viable eggs instead involves the disintegration
of the eggs outer shell in the intestines, allowing the embryo or oncosphere to
penetrate the intestinal wall and enter the bloodstream. Once in circulation,
these may settle in many types of tissue. Sometimes they are able to pass
through the blood-brain barrier and enter the CNS. The mechanism for
bypassing the blood-brain barrier is not fully understood, and while some
suspect enzymes may weaken this barrier, others believe special permeability
allows passage without damaging the barrier [27]. Once inside the CNS, the
parasites settle and begin to develop into cysts.

Brain parenchymal cysticercosis.

(Biocrawler)
Neurocysticercosis
The development and persistence of living fluid-cysts (metacestodes) within the
CNS is known as active neurocystercosis, and is the most common parasitic CNS
infection worldwide[28]. Symptoms of neurocysticercosis are largely caused by
the direct growth of these cysts on cerebral parenchyma or growth in and
blockage of cerebrospinal fluid-filled cavities. Once formed into cysts within the
CNS, the metacestodes are significantly more shielded from the immune
response than when in their egg or larval stages. Living within the immuneprivileged CNS grants the cysts some protection, but they must still confront the
hosts immune response as it strengthens. However, the cysts have developed
several sophisticated mechanisms to evade and even exploit this immune
response.
T. solium metacestodes are closely associated with suppression of the hosts
immune response, particularly of CD4+ T cells in the peripheral blood through
apoptosis[29]. Cysts may be able to protect themselves from the innate immune
system by directly inhibiting neutrophil and eosinophil function, as the white
blood cells have been seen enveloping metacestodes with no signs of harm [30]. It
is suspected that this may be achieved by preventing the attacking cells from
producing key proteins or by blocking their ability to target the cysts. Other
studies have shown increased host immunoglobulin levels around living cysts
compared to dead ones, suggesting that living cysts use these to disguise
themselves as host cells from the humoral immune response [31]. It is even
thought that T. solium cysts may stimulate T-cells to form immunoglobulins that

can then be digested as a primary protein source. As such, these metacestodes

are both protected from much of the immune response and can selectively
elevate aspects of the response for their own benefit.

Cacing dewasa hidup di dalam tubuh manusia pada usus halus. Cacing dewasa melepaskan
segmen gravid paling ujung yang akan pecah di dalam usus sehingga telur cacing dapat dijumpai
pada feses penderita. Apabila telur cacing yang matur mengkontaminasi tanaman rumput atau pun
peternakan dan termakan oleh ternak seperti babi, telur akan pecah di dalam usus hospes perantara
dan mengakibatkan lepasnya onkosfer. Dengan bantuan kait, onkosfer menembus dinding usus,
masuk ke dalam aliran darah, lalu menyebar ke organ-organ tubuh babi, terutama otot lidah, leher,
otot jantung, dan otot gerak . Dalam waktu 60-70 hari pasca infeks, onkosfer berubah menjadi larva
sistiserkus yang infeksius.10
Manusia terinfeksi dengan cara makan daging babi mentah atau kurang masak, yang mengandung
larva sistiserkus (Ideham dan Pusarawati, 2007; Wandra et al., 2007; Tolan, 2011). Di dalam usus
manusia, skoleks akan mengadakan eksvaginasi dan melekatkan diri dengan alat isapnya pada
dinding usus, lalu tumbuh menjadi cacing dewasa dan kemudian membentuk strobila. Dalam waktu
5-12 minggu atau 3 bulan, cacing Taenia solium menjadi dewasa dan mampu memproduksi telur.
Seekor cacingTaenia solium dapat memproduksi 50.000 sampai 60.000 telur setiap hari.11
Proglotid yang telah lepas, telur atau keduanya akan dilepaskan dari hospes definitif (manusia) dalam
bentuk feses. Kemudian babi akan terinfeksi jika pada makanannya telah terkontaminasi dengan telur
yang berembrio atau proglotid gravid.12
Manusia juga dapat menjadi hospes perantara untuk Taenia solium (sistiserkorsis).Hal ini dapat
terjadi apabila manusia termakan telur dari cacing tersebut dari hasil ekskresi manusia. Teori lainnya
adalah autoinfeksi. Namun, teori ini belum dibuktikan. Jika terdapat cacing pita dewasa pada usus,
peristaltik yang berlawanan pada gravidproglotid akan menyebabkan proglotid bergerak secara
retrograd dari usus ke lambung. Telur hanya dapat menetas apabila terpapar dengan sekresi gaster
diikuti dengan sekresi usus sehingga setelah terjadi peristaltik yang bersifat retrograd, onkosfer akan
menetas dan menembus dinding usus, mengikuti aliran kelenjar getah bening atau aliran darah.Larva
selanjutnya akan bermigrasi ke jaringan subkutan, otot, organ viseral, dan sistem saraf pusat dan
membentuk sistiserkus. Sistiserkosis dapat terjadi pada berbagai organ dan gejala yang timbul
tergantung dari lokasi sistiserkus. Proglotid dari Taenia soliumkurang aktif dibandingkan
dengan Taenia saginata sehingga kemungkinan untuk ditemukan pada lokasi yang tidak seharusnya
lebih jarang

Sistiserkus pada kebanyakan organ biasanya tidak atau sedikit menimbulkan reaksi jaringan. Suatu
penelitian post mortem menyebutkan bahwa 80% dari seluruh kasus sistiserkosis asimptomatik.
Akan tetapi, kista yang telah mati pada sistem saraf pusat dapat menimbulkan respon jaringan yang
berat. Infeksi pada otak (sistiserkosis serebri) dapat menimbulkan gejala yang berat, akibat dari
efek massa dan inflamasi yang disebabkan oleh degenerasi sistiserkus dan pelepasan antigen.
Sistiserkus dapat juga menginfeksi sumsum tulang belakang, otot, jaringan subkutan, dan mata.13

Perubahan yang terjadi berhubungan dengan stadium peradangan. Dalam stadium koloidal, kista
terlihat sama dengan kista koloid dengan materi gelatin dalam cairan kisat dan degenerasi hialin dari
larva. Dalam stadium granular-nodular, kista mulai berkontraksi dan dindingnya digantikan dengan
nodul fokal limfoid serta nekrosis. Akhirnya, pada stadium kalsifikasi nodular jaringan granulasi
digantikan oleh struktur kolagen dan kalsifikasi.13

Gejala timbul tergantung dari jumlah dan lokasi larva. Neurosistiserkosis merupakan bentuk
sistiserkosis yang menyerang sistem saraf pusat dan paling membahayakan. Pada kasus tertentu,
gejala yang timbul mungkin timbul sangat lambat, tetapi progresif. Namun, dapat juga gejala timbul
secara tiba-tiba akibat obstruksi cairan serebrospinal akibat adanya sistiserkus yang melayanglayang di dalam cairan. Gejala yang paling sering adalah sakit kepala kronik dan kejang atau
epilepsi (70-90%). Gejala lainnya yang mungkin timbul adalah peningkatan tekanan intrakranial,
hidrosefalus, tanda neurologis fokal, perubahan status mental, mual, muntah, vertigo, ataxia,
bingung, gangguan perilaku, dan demensia progresif, dan sakit kepala kronik. Sedangkan apabila
neurosistiserkosis menyerang sumsum tulang belakang dapat menyebabkan kompresi,transverse
myelitis, dan meningitis. Namun kasus ini jarang.2,13,14
Adapun bentuk manifestasi klinis dari sistiserkosis terbagi atas 4 :
a. Infeksi inaktif, ditandai dengan penemuan residu infeksi aktif sebelumnya (kalsifikasi
intraparenkimal). Gejala yang timbul: sakit kepala, kejang, psikosis.

b. Infeksi aktif, terdiri atas neurosistiserkosis parenkim aktif dan ensefalitis sistiserkal.
c. Neurosistiserkosis ekstraparenkimal yang memiliki bentuk neurosistiserkosis ventrikular.
d. Bentuk lain: sistiserkosis spinal, sistiserkosis oftalmika, penyakit serebrovaskular, dan lain-lain.13
Pada mata (sistiserkosis oftalmika), sistiserkus paling sering ditemukan pada vitreous humor,
rongga subretina dan konjungtiva. Gejala yang umum adalah kaburnya penglihatan atau
berkurangnya visus, rasa sakit yang berat, sampai buta. Sistiserkus di otot biasanya asimptomatik.
Namun, dalam jumlah banyak dapat menimbulkan pseudohipertrofi, miositis, nyeri otot, kram, dan
kelelahan. Larva di jantung menimbulkan gangguan konduksi dan miokarditis.14

Pada kulit, sistiserkus mungkin dapat terlihat sebagai nodul subkutan. Larva juga dapat
menyebabkan vaskulitis atau obstruksi arteri kecil yang menimbulkan stroke. Akan tetapi, hal ini
jarang terjadi.1

Center for Food Security and Public Healt (CFSPH), 2005. Taenia Infections Available
from: http://www.ivis.org/advances/Disease_Factsheets/taenia.pdf
Sutanto,Inge dkk. 2008. Buku Ajar Parasitologi Kedokteran Edisi Keempat, Jakarta :
Balai Penerbit FKUI

Tolan,
R.W.
2011.
Taenia
Infection.
Available
from:
[Accessed
1
May
2014].http://emedicine.medscape.com/article/999727-overview#a0104
12. Wandra T., Margono, S.S., Gafar, M.S., Saragih, J.M., Sutisna, P., Dharmawan, N.S., et al., 2007.
Taeniasis/Cysticercosis in Indonesia 1996-2006. Southeast Asian J Trop Med Public Health 38 (1):
140-143.
13. Wiria, A.E., 2008. Sistiserkosis. Buku Ajar Parasitologi Kedokteran edisi ke- 4. Jakarta: Fakultas
Kedokteran Universitas Indonesia, 86-89

http://journals.lww.com/infectdis/Citation/1997/06060/Neurocysticercosis__Pathophysi
ology,_Diagnosis,.2.aspx