Cysticercosis or Cysticercosis is an infection caused by the pork tapeworm, Taenia solium.
Infection occurs when the tapeworm larvae enter human body and form cysticerci (cysts)
. Figure. Cysticercus
The presence of cysticercerci within the human central nervous system (CNS) is called neurocysticercosis. (1)Neurocysticercosis, is the most common parasitic infection of the brain worldwide. (2)(3)
Figure. Neurocysticercosis in the parietal lobe.
Agent (classification and taxonomy)
The main cause of human cysticercosis is the larval form of Taenia solium (pork tapeworm). T.solium is a platyhelminth of the cestoidean class, the cyclophyllidea order and the taeniidae family. The common larval stage of T.solium was also known as Cysticercus cellulosae.
Synonyms – NONE
History of Discovery
The earliest refernce to tapeworms were found in the works
of ancient Egyptians that date back to almost 2000 BC. (4) The description of
measled pork in the History of Animals written by Aristotle (384-322 BC) showed
that the infection of pork with tapeworm was known to ancient Greeks as that
time (4). Recent examination of evolutionary histories of hosts and paratistes
and DNA evidence show that over 10,000 years ago, ancestors of modern humans in
Figure. ancestor of modern humans
Cysticercosis was described by Johannes Udalric Rumler in 1555; however, the connection between tapeworms and cysticercosis had not been recognized at that time. (5) Around 1850, Kuchenmeister fed pig meat containing cysticerci of T.solium to humans awaiting execution in a prison, and after they had been executed, he recovered the developing and adult tapeworms in their intestines. (4)(5)(6) By the middle of the 19th century, it was established that cysticercosis was caused by the ingestion of the eggs of T.solium. (6)
Clinical Presentation in Humans
1. Cysticercosis in muscles
Cysticerci can develop in any voluntary muscle in humans. (2) Invasion of muscle by cysticerci can cause myositis, with fever and eosinophilia, and muscular pseudohypertrophy, which initiate with muscle swelling and later progress to atrophy and fibrosis. (2) In most cases, it is asymptotic since the cysticerci die and become calcified.
Figure. Calcification in muscles due to cysticercosis.
Neurocysticercosis present in many forms, depending on the localization of the cysts and disease activity. (2) 60% of the patients with cysticerci are found to have them in the brain. (2) As the stage of cysticerci reflect the sign, symptoms and treatment of neurocysticercosis, it is important to understand the natural history of CNS cysts. (3) In the case of cysticerci in the brain parenchyma, four major stages have been classified: (3)
In stage 1, immature cysts appear within 1-4 weeks during which the oncosphere lodges to the brain and finally expands into a cyst. It is mainly asymptomatic, although flu-like illness, rare seizures, rare increased intracranial pressure from massive infestation has been recorded. (3)
In stage 2, the cysticerci become mature and viable about 2 months after egg ingestion. The cyst possess a protoscolex with the cyst bladder and causes no or minimal surrounding inflammation or edema. The cysticerci also down-regulates host cellular immunity. Stage 2 cysts are also asymptomatic, and can persist for more than 10 years. (3)
Figure. CT scan of the brain shows: multiple cysts in vesicular, some cyst in colloidal stage (stage 3) surrounded by perilesional edema, and calcified lesions on both cerebral hemisphere.
Stage 3 possess colloid or degenerating cysts with thick cystic fluid, thickened capsule, and appear two to 10+ years after the cyst becomes mature. The cyst no longer prevents a host immune response and its antigens leak from the bladder wall. The intense inflammation is provoked around the degenerating cyst. Most patients bearing stage 3 develop clinical signs and symptoms such as seizures, occasional focal neurological signs, headaches, nausea, vomiting, lethargy from increased intracranial pressure and altered mental status. (3)
Figure. Parenchymal cysticercosis: the uneven development of cysticerci as vesicular stage (stage 2) (arrow) and colloidal stage (stage 3) (arrow head) and other granular colloid phase (star).
At stage 4, the cyst is calcified. The surrounding inflammation drops since the dead cyst no longer produces foreign antigens. Common clinical features includes persistent non-provoked seizures although most of the patients are asymptomatic. (3)
In meningeal cysticercosi, cysticerci often do not develop into typical cysts, and become racemose lacking a scolex and becoming lobes in thin-walled bladders. (3) These cysts increase and slowly leak their antigen into the subarachnoid CSF producing meningitis and can further develops into arachnoiditis, which may lead to obstructive hydrocephalus, cranial nerve involvement, intracranial hypertension, arterial thrombosis and stroke. (2)(3)
In intraventricular Cysticercosis, the cyst occurs in the lateral, third or fourth ventricles which may be asymptomatic or if they block the flow of CSF, they may cause increased intracranial pressure. (3)
Figure. MRI scan of Ventricular Cyst with Scolex http://www-lab.biomedicas.unam.mx/cistimex/Galeria/Cap2_Page_27_Image_0001.jpg)
3. Ophthalmic Cysticercosis
In some cases, cysticerci may be found in the globe, subconjunctiva, extraocular muscles, and subconjunctiva (2)(3). Depending on the location, they may cause visual difficulties that fluctuate with eye position, retinal edema, hemorrphage, a decreased vision or even a visual loss (2)(3).
Figure. Right eye showing smooth, horizontally oval subconjunctival swelling. http://www.bhj.org/journal/2002_4404_oct/images/fig1_693.jpg
4. Subcutaneous Cysticercosis
Subcutaneous cysts are in the form of firm, mobile nodules, occurring mainly on the trunk and extremities (8). Patients with subcutaneous nodules sometimes feel painful (8).
Figure. Multiple subcutaneous nodules on the chest wall and calcified lesions on chest X-ray.
Humans can be transmitted by ingesting the eggs or larvae from eating undercooked pork that contains viable cysticercosis larvae or from fecally contaminated food or water. (1-3) The adult tapeworm develops in humans after the ingestion of infected meat; however cysticercosis occurs after the ingestion of eggs, either from external sources or from their own feces (2).
Figure. Pig heart with vesicular cysticerci.
Pigs get infected with cysticerci when they ingest human feces.
Figure. Pig eating feces.
Humans and Pigs are reservoirs.
Months to years(10+ years)
T.solium worms may reach a length of several meters (2). The scolex has four suckers , and a double crown of prominent hooks, which attach to the intestinal mucosa. (2)
Figure. Scolex found in the electron microscope.
Taenia solium eggs are spherical and 30-40 nm in diameter. (3)
Figure. T.solium egg in the electron scanning microscope.
The cysticercus larva completes development in about 2 months. (2)It is semitransparent, opalescent white, and elongate oval in shape and may reach a length of 0.6 to 1.8 cm (2).
Figure. Life cycle of cysticercosis
As seen from the diagram, the life cycle involves humans as a definite host and pigs as an intermediate host. Pigs ingest contaminated food or water that contains eggs or proglottids from human’s feces. The ova develop into cysticercus in pig muscles. Human becomes infected when they ingest raw or undercooked “measly pork” that contains viable cysticercus. Upon reaching the small intestine, the scolex attaches to the intestinal wall and continue to grow a chain of proglottids. T.solium releases three to six proglottids/day, bearing 30,000-70,000 eggs per proglottids into the intestine. (3) Nearly 250,000 eggs are passed daily into the human feces and to the environment and the cycle continue (3).
Infection with cysticercus occur after humans consume the ova through self-infection via the fecal-oral route or the ova from exogenous sources. (2) Humans, in this case, are intermediate hosts (3). The ova are digested in the stomach and release oncosphere which penetrate intestinal wall and reach the bloodstream (1). These oncospheres develop into cysticerci in any organ but common in brain, subcutaneous tissue or eyes (2)(3).
The traditional method of demonstrating T.solium eggs in stool samples diagnose only taeniasis (1). Though the presence of T.solium eggs or proglottids in the feces does not necessary mean the infection with cysticercus, those patients should be evaluated serologically since autoinfection via fecal-oral route, can potentially result in cysticercosis (1).
In CDC’s immunoblot assay, cysticercosis-specific antibodies can react with structural glycoprotein antigens from the larval cysts of T.solium (1). Therefore, the serum samples from patients with other microbial infections do not react with any of the T.solium derived antigens. The positions of the seven diagnostic glycoproteins are marked and selected based on how fast they can move in SDS-PAGE. The test is so far 100% specific and has higher sensitivity than any other immunoassay systems.
Figure. Typical antibody reactions in CDC’s immunoblot for cysticercosis.
Neuroimaging with CT or MRI is the most useful method to diagnose neurocysticercosis (3). CT scan shows both calcified and uncalcified cysts, as well as distinguishing active and inactive cysts (2). MRI can detect intraventricular cysts while CT scan cannot (3).
Management and Therapy
Treatment includes medical drugs such as antihelminthic drugs and corticosteroids or surgical removal of the cyst. Surgical treatment includes direct excision of ventricular cysts, shunting procedures, and removal of cysts via endoscopy (2)(3). Albendazole is preferable over praziquantel due to its lower cost and corticosteroids and anticonvulsants do not reduce CSF and brain drug levels (3). Moreover, the results from meta-analysis study have shown that albendazole is more effective than praziquantel in terms of clinically important outcomes in patients with neurocysticercosis (9)
In the case of brain parenchymal cysticercosis, treatment depends on the stage of cyst development. In immature cyst stage (stage 1), high-dose corticosteroids are administered to reduce the edema but antihelminth drugs have been found to be harmful (3). Vesicular or viable cysts (stage 2) are often asymptomatic, and usually are not treated with antihelminth drugs, while surgical removal of the cyst, along with albendazole is indicated in the colloid cyst stage (stage 3) (3). No antihelminthic treatment is administered in dead calcified cysts stage (stage 4) (3).
In the case of cysts in globe, surgical cyst removal is necessary, while antihelminth drug with steroids alone might be sufficient to treat cysts outside globe (3). Treatment recommendations for subcutaneous cysticercosis includes surgery, praziquantel and albendazole (8).
is highly endemic in Central and South America, and some parts of Africa and
Public Health and Prevention Stategies
Cysticercosis is considered as “tools-ready disease” according to WHO (12). International Task Force for Disease Eradication in 1992 reported that cysticercosis is potentially eradicable (13). It is feasible because there are no animal reservoirs besides humans and pigs and T.solium. The only source of T.solium infection for pigs is from humans, a definite host (11). Theoretically, breaking the life cycle seems easy by doing Figure. Life cycle of cysticercosis (http://www.dpd.cdc.gov/dpdx/images/ParasiteImages/A-F/Cysticercosis/Cysticercosis_LifeCycle.gif)
intervention strategies from various stages in the life cycle (11).
(a) Massive chemotherapy treatment of infected humans, improving sanitation and education humans are major ways to discontinue the cycle at step 1, in which eggs from human feces are transmitted to other humans and/or pigs.
(b) Cooking of pork or freezing them and inspecting meat are effective means to cease the life cycle at step 3.
(c) The management of pigs by treating them or vaccinating them is another possibility to intervene step 4 of the life cycle.
Intervention by concurrent treatment of humans and pigs
The intervention strategies to eradicate cysticercosis includes surveillance of pigs in foci of transmission and massive chemotherapy treatment of humans (13). In reality, control of T.solium by a single intervention, for instance, by treating only human population will not work because the existing infected pigs can still carry on the cycle (14). The proposed strategy for eradication is to do multilateral intervention by treating both human and porcine populations (14). It is feasible because treatment pigs with oxfendazole have been shown to be effective and once treated, they are protected from further infections for at least 3 months (15).
Even with the concurrent treatment of humans and pigs, the complete eliminate is hard to achieve. In one study conducted in 12 villages in Peru, both humans and porcine are treated with praziquantel and oxfendazole, with the coverage of more than 75% in humans and 90% in pigs (16) The result shows a decreased in prevalence and incidence in the intervention area; however the effect did not complete eliminate T.solium. The possible reason includes the incomplete coverage and re-infection. (17) Even though T.solium could be eliminated through mass treatment of human and porcine population, it is not sustainable (14). Moreover, both tapeworm carriers of humans and pigs tend to spread the disease from endemic to non-endemic areas resulting in periodic outbreaks of cysticercosis or outbreaks in new areas (14)(18)(19).
Vaccine against porcine cysticercosis
Given the fact that pigs are part of a life cycle, vaccination of pigs is another feasible intervention to eliminate cysticercosis. Research studies have been focusing on vaccine against cestode parasites, since many immune cell types are found to be capable of destroying cysticercus (20). Many vaccine candidates are extracted from antigens of different cestodes such as T.solium, T.crassiceps, T.saginata, T.ovis and target at oncospheres and/or cysticerci (20-23). In 1983, Molinari et.al reported the first vaccine candidate against porcine cysticercosis using antigen from cysticercus cellulosae drawn out from naturally infected (23). Recently, vaccines extracted from genetically engineered 45W-4B antigens have been successfully tested to pigs in an experimental condition. (22)This type of vaccine can protect against cysticercosis in both Chinese and Mexican type of T.solium. However, it has not been tested in endemic field conditions, which is important because the realistic condition in the field differ greatly from experimental condition, and this can result in a great difference in the chances of infection and immune reaction (20).
The S3PVAC Vaccine
vaccine constituted by 3 peptide synthetically produced (S3Pvac) has proven its
efficacy in natural conditions of transmission (24). The S3PVAC vaccine so far,
can be considered as the best vaccine candidate to be used in endemic areas
Figure. Three peptides present in different stages of T.solium
pigs from rural villages in
Limitations of vaccines
Even though vaccines have been successfully generated, the feasibility of its production and usage in rural free ranging pigs still remains a challenge. If a vaccine is to be injected, the burden of work and the cost of vaccine administration to pigs will remain high and unrealistic (20). The incentives of using vaccines by pig owners will decrease if the vaccine administration to pigs takes time by injecting every single pig in their livestock. An oral vaccine is proposed to be more effective in this case as it can be easily delivered to the pigs with the food, though no one has ever achieved it yet (20).
Other types of interventions and Limitations
Cysticercosis can also be prevented by routine inspection of meat and condemnation of measly meat by the local government (28). However, in areas where food is scare, cyst-infected meat might be considered as wasted since pork can provide high quality protein (29). At times, infected pigs are consumed within the locality or sold at low prices to traffickers who take the uninspected pigs at urban areas for sale. (30)
Giving health education about cysticercosis is a good strategy to change human’s behavior. However, education does not result in dramatic changes in behavior, since other social and economic factors also play a role (14).
Current efforts to combat cysticercosis
Center for Disease Control (CDC) gives
support and collaboration in research and control activities through formal
designation of the Division of Parasitic Diseases (NCID, CDC) as WHO/CDC
Collaborating Center for Cysticercosis and Taeniasis (31). Moreover, the
cysticercosis working group in Europe works in collaboration with WHO/FAO
Collaborating Center for Parasitic Zoonoses in
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(8) Wortman PD. “Subcutaneous cysticercosis” J Am Acad Dermatol. 1991 (2 Pt 2): 409-14.
(9) Dimitrios K. Matthaiou, Georgios Panos, Eleni S. Adamidi,Matthew E. Falagas “Albendazole versus Praziquantel in the Treatment of Neurocysticercosis: A Meta-analysis of Comparative Trials” PLoS Negl Trop Dis. 2008 March; 2(3): e194.
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(21) Flisser A, Gauci CG, Zoli A, Martinez-Ocana J, Garza-Rodriguez A, Dminguez-Alpizar J L, Maravilla P, Canul RP, Avila G, Aguilar-Vega L, Kyngdon C Geerts S, Lightowlers MW. 2004 “Induction of Protection against Porcine Cysticercosis by Vaccination with Recombinant Oncosphere Antigens” Infect Immun. 72(9): 5292-5297.
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(27) E-mail interview with Edda Sciutto. Feb 26 2009.
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