Taeniasis and cysticercos

Taeniasis and Cysticercosis

Taeniasis and Cysticercosis

These are infections with cestode parasites in the genus Taenia. There are two species of interest: T. solium (the “pork” tapeworm) and T. saginata (the “beef” tapeworm). T. solium has a complex life cycle that can lead to humans being infected by one or multiple forms of the parasite. T. saginata has a simpler life cycle and chooses not to venture beyond the confines of the human intestine. Sometimes these various forms are referred to with names that make them sound like different species; they aren’t just different stages in the life cycle. So “taeniasis” is having the adult tapeworm and “cysticercosis” is having the larval stage (cysticerci); some people have both, or they may have just tapeworms but be at risk for developing cysticercosis later.


Taeniasis due to T. solium is acquired by humans through ingestion of tapeworm larvae (cysticerci) in undercooked pork. The larvae develop into adult tapeworms in the intestine of infected humans and produce eggs which are shed into the environment due to open defecation.

Pigs get infected by eating the parasite’s eggs from the environment. In humans, cysticercosis is caused by accidental infection with the T. solium eggs via faecal-oral route, from contaminated soil, food (mainly vegetables) or water.

Larvae (cysticerci) develop in the muscle, skin, eyes, and brain (in the central nervous system is called neurocysticercosis).

Description of illness

Intestinal infection with the adult form of the parasite (the tapeworm) is called taeniasis. Taeniasis is usually asymptomatic, although mild, non-specific abdominal symptoms including nausea, anorexia and abdominal pain are sometimes reported. Persons with intestinal taeniasis may pass readily visible worm segments (proglottids) in stool. Proglottid fragments are typically white and measure about 5 x 10 mm.

Cysticercosis is defined as infection of any tissue, usually in the central nervous system or muscle, with the larval form of the parasite. The corresponding symptoms depend on the number, location, and stage of development of the larval cysts, as well as on the host’s immune response.

Neurocysticercosis is common, occurring when the larvae encyst in the brain or other CNS tissue. Neurologic signs and symptoms can be quite variable. Seizures result from inflammation surrounding dead or dying cysts in the brain parenchyma, and occur in up to 80% of neurocysticercosis cases. Headaches— often severe and protracted—are also common and present in around 40% of cases. Hydrocephalus and increased intracranial pressure, with associated chronic or recurrent headaches, nausea and vomiting can result from blockage of cerebrospinal fluid flow by cysts and/or inflammation in the cerebral ventricles. Untreated hydrocephalus may result in sudden death due to brain herniation.


Other neurologic symptoms of neurocysticercosis include psychiatric disturbances, balance problems, cognitive impairment, visual disturbance, focal weakness or paresthesias. Cysts may also develop in skeletal muscle, skin, or other organs, but these usually cause few if any symptoms.

Reservoirs and Life Cycle

The “natural” cycle of T. solium alternates between humans and pigs. Humans get tapeworms by eating undercooked and “measly” pork, which is tissue from pigs with cysticercosis— i.e., parasite cysts had formed in their muscles (the meat) at least. (Whether they also had bad headaches is hard to say.) Once ingested, the larvae “excyst” and attach to the wall of the small intestine as baby tapeworms. Over a period of months they develop into hermaphroditic adult tapeworms that may attain several meters in length.

Taeniasis and cysticercos

Tapeworms can survive in the human intestine for many years, intermittently shedding eggs and worm fragments in stool; these are immediately infectious to both humans and pigs. If ingested, these eggs develop into larvae, invade the intestinal wall and are then carried via the bloodstream throughout the body. Eventually the larvae embed themselves in soft tissues and become encapsulated: cysticercosis.

Some people do eat pigs though, and sometimes these are pigs with cysticercosis. To summarize, while both pigs and humans can develop cysticercosis, tapeworms only develop in humans; thus, only humans can shed eggs. In other words, while the most common scenario is a pig-human cycle, it is possible (and very dangerous) to have a human-human cycle. It is not possible to have a pig-pig cycle. In other words, although not recommended for other reasons, eating pig feces is not a risk factor for cysticercosis. Eating human feces is quite another matter, as that is how both people and pigs get cysticercosis.

Interestingly, tapeworm carriers are a danger not only to other persons, but also to themselves. Since the eggs shed in stool are immediately infectious, ingestion of human feces (including your own) can lead directly to in vivo larval development (i.e., cysticercosis). The risk of auto-infection is high enough that most tapeworm carriers also have cysticercosis at some point, though often it is asymptomatic.

Signs and symptoms

Human taeniasis may cause loss of appetite, abdominal pain, nausea, diarrhoea or constipation. Human cysticercosis is often asymptomatic; however, it can cause variable clinical symptoms including visible or palpable nodules beneath the skin.

Neurocysticercosis may cause chronic headaches, blindness, epileptic seizures, and can be fatal. Typically, there are no symptoms in pigs. At examination, heavily infected pigs can show cysts in their tongue.


Simple, cost–effective and rapid diagnostic tools are still needed for detection of T. solium carriers and cases of human and porcine cysticercosis. Field-based tools include stool examination (human) and tongue palpation (pigs). They are simple and useful in highburden areas/animals. Confirmation of neurocysticercosis requires imaging. Laboratory-based tools such as serological tests for specific antibody or circulating antigen tests are useful to confirm epilepsy due to cysticercosis.


Treatment of taeniasis is simple and effective. There are two single-dose options:

• Niclosamide, adults 2 g once, children 50 mg/kg once, or

• Praziquantel, 5-10 mg/kg once

Some recommend treatment with a purgative if niclosamide is used; others do not. This is because the tapeworm can regenerate completely if the scolex is retained. (The scolex is the “head” end of the tapeworm with the hooklet structures that attach to the bowel wall.)

Niclosamide is arguably the safer drug because it is not absorbed by the GI tract and, therefore, has no activity against cysts. Inadvertently killing cysts in the CNS can cause inflammation and precipitate seizures. Unfortunately, niclosamide is not easy to get; local pharmacists will not carry it and most will tell you that it is “unavailable.” It is available from some compounding pharmacies and ACDP staff will help you get it, if required.

Praziquantel is active against both tapeworms and cysts, so one must be cautious in using it to treat tapeworms in patients who may have coexisting neurocysticercosis (NCC). Patients should be evaluated for signs and symptoms of NCC before treatment and be monitored for adverse reactions (e.g., headache and seizures) following treatment that may indicate an acute inflammatory response to dying parasites.

Cysticercosis treatment is complex and expert medical consultation is recommended. Albendazole and praziquantel are both effective against CNS cysts. Not everyone benefits from anti-helmenthic therapy, however. Cysts often do not cause symptoms until they are already dead or dying and treatment may paradoxically increase symptoms by killing viable cysts, resulting in an increased inflammatory response. Control of inflammation around dying cysts may require prolonged corticosteroid therapy. Seizures generally require anticonvulsant medications, often lifelong. Neurological intervention for excision of cysts or shunting of cerebrospinal fluid may be required.




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