Taenia solium

Humans are colonised by the larval stage, the cysticercus, from undercooked pork or other meat. Each microscopic cysticercus is oval in shape, containing an inverted scolex (specifically "protoscolex"), which everts once the organism is inside the small intestine. This process of evagination is stimulated by bile juice and digestive enzymes (of the host). Then, the T. Solium lodges in the host’s upper intestine by using its crowned hooks and 4 suckers to enter the intestinal mucosa. Then, the scolex is fixed into the intestine by having the suckers attached to the villi and hooks extended. It grows in size using nutrients from the surroundings. Its strobila lengthens as new proglottids are formed at the foot of the neck. In 10–12 weeks after initial colonization, it is an adult worm.[12] The exact life span of an adult worm is not determined; however, evidences from an outbreak among British military in the 1930s indicate that they can survive 2 to 5 years in humans.[13][14]

As a hermaphrodite, it reproduces by self-fertilisation, or cross-fertilisation if gametes are exchanged between two different proglottids. Spermatozoa fuse with the ova in the fertilisation duct, where the zygotes are produced. The zygote undergoes holoblastic and unequal cleavage resulting in three cell types, small, medium and large (micromeres, mesomeres, megameres). Megameres develop into a syncytial layer, the outer embryonic membrane; mesomeres into the radially striated inner embryonic membrane or embryophore; micromeres become the morula. The morula transforms into a six-hooked embryo known as an oncosphere, or hexacanth ("six hooked") larva. A gravid proglottid can contain more than 50,000 embryonated eggs. Gravid proglottids often rupture in the intestine, liberating the oncospheres in faeces. Intact gravid proglottids are shed off in groups of four or five. The free eggs and detached proglottids are spread through the host's defecation (peristalsis). Oncospheres can survive in the environment for up to two months.[5][15]

Pigs are the most common host who ingest such eggs in traces of human faeces, mainly from vegetation contaminated with it such as from water bearing traces of it. The embryonated eggs enter intestine where they hatch into motile oncospheres. The embryonic and basement membranes are removed by the host's digestive enzymes (particularly pepsin). Then the free oncospheres attach on the intestinal wall using their hooks. With the help of digestive enzymes from the penetration glands, they penetrate the intestinal mucosa to enter blood and lymphatic vessels. They move along the general circulatory system to various organs, and large numbers are cleared in the liver. The surviving oncospheres preferentially migrate to striated muscles, as well as the brain, liver, and other tissues, where they settle to form cysts — cysticerci. A single cysticercus is spherical, measuring 1–2 cm in diameter, and contains an invaginated protoscolex. The central space is filled with fluid like a bladder, hence it is also called bladder worm. Cysticerci are usually formed within 70 days and may continue to grow for a year.[16]

Humans are also accidental secondary hosts when they are colonised by embryonated eggs, either by auto-colonisation or ingestion of contaminated food. As in pigs, the oncospheres hatch and enter blood circulation. When they settle to form cysts, clinical symptoms of cysticercosis appear. The cysticercus is often called the metacestode.[17]

Taeniasis is infection in the intestines by the adult T. solium. It generally has mild or non-specific symptoms. This may include abdominal pain, nausea, diarrhea and constipation. Such symptoms will arise when the tapeworm has fully developed in the intestine, this would be around eight weeks after the contraction (ingestion of meat containing cysticerci).[18]

These symptoms could continue until the tapeworm dies from the course of treatment but otherwise could continue for many years, as long as the worm lives. If untreated it is common that the infections with T. solium last for approximately 2–3 years. It is possible that infected people may show no symptoms for years.[18]

Ingestion of T. solium eggs or egg-containing proglottids which rupture within the host intestines results in the development and subsequent migration of larvae into host tissue to cause cysticercosis. In pigs, there are not normally pathological lesions as they easily develop immunity.[19] But in humans, infection with the eggs causes serious medical conditions. This is because T. solium cysticerci have a predilection for the brain. In symptomatic cases, a wide spectrum of symptoms may be expressed, including headaches, dizziness, and seizures. Brain infection by the cysticerci is called neurocysticercosis and is the leading cause of seizures worldwide.[14][20]

In more severe cases, dementia or hypertension can occur due to perturbation of the normal circulation of cerebrospinal fluid. (Any increase in intracranial pressure will result in a corresponding increase in arterial blood pressure, as the body seeks to maintain circulation to the brain.) The severity of cysticercosis depends on location, size and number of parasite larvae in tissues, as well as the host immune response. Other symptoms include sensory deficits, involuntary movements, and brain system dysfunction. In children, ocular cysts are more common than in other parts of the body.[4]

In many cases, cysticercosis in the brain can lead to epilepsy, seizures, lesions in the brain, blindness, tumour-like growths, and low eosinophil levels. It is the cause of major neurological problems, such as hydrocephalus, paraplegy, meningitis, convulsions, and even death.[21]

Stool tests commonly include microbiology testing – the microscopic examination of stools after concentration aims to determine the amount of eggs. Specificity is extremely high for someone with training but sensitivity is quite low because the high number of eggs in small amounts of sample.[22]

Stool tapeworm antigen detection: Using ELISA increases the sensitivity of the diagnosis. The downside of this tool is it has high costs, an ELISA reader and reagents are required and trained operators are needed.[22]

Stool PCR: This method can provide a species-specific diagnosis when proglottid material is taken from the stool. This method requires specific facilities, equipment and trained individuals to run the tests. This method has not yet been tested in controlled field trials.[22]

Serum antibody tests: using immunoblot and ELISA, tape-worm specific circulating antibodies have been detected. The assays for these tests have both a high sensitivity and specificity.[22]

The best way to avoid getting tapeworms is to not eat undercooked pork or vegetables contaminated with feces. Moreover, a high level of sanitation and prevention of faecal contamination of pig feeds also plays a major role in prevention. Infection can be prevented with proper disposal of human faeces around pigs, cooking meat thoroughly or freezing the meat at −10 °C for 5 days. For human cysticercosis, dirty hands are attributed to be the primary cause, and especially common among food handlers.[16]

Treatment of cysticercosis must be carefully monitored for inflammation reactions to the dying worms, especially if they have moved into the brain. In some cases the worms can be surgically removed, and in others albendazole with steroids is given to reduce the inflammation.

A vaccine to prevent cysticercosis in pigs has been studied. The life-cycle of the parasite can be terminated in their intermediate host, pigs, thereby preventing further human infection. The large scale use of these vaccine, however, is still under consideration.[23]

T. solium is found worldwide, but its two distinctive forms rely on eating undercooked pork or on ingesting feces-contaminated water or food (respectively). Because pig meat is the intermediate source of the intestinal parasite, rotation of the full life cycle occurs in regions where humans live in close contact with pigs and eat undercooked pork. However, humans can also act as secondary hosts, which is a more pathological, harmful stage triggered by oral contamination. High prevalences are reported among many places with poorer than average water hygiene or even mildly contaminated water especially with a pork-eating heritage such as Mexico, Latin America, West Africa, Russia, India, Manchuria, and Southeast Asia.[24] In Europe it is most common in pockets of Slavic countries and among global travelers taking inadequate precautions in eating pork especially.[6][25]

The secondary host form, human cysticercosis, predominates in areas where poor hygiene allows for mild fecal contamination of food, soil, or water supplies. Rates in the United States have shown immigrants from Mexico, Central and South America, and Southeast Asia bear the brunt of cases of cysticercosis caused by the ingestion of microscopic, long-lasting and hardy tapeworm eggs.[26] Rates of T. solium cysticercosis in West Africa are not affected by any religion.[27]

For example, in 1990 and 1991 four unrelated members of an Orthodox Jewish community in New York City developed recurrent seizures and brain lesions, which were found to have been caused by T. solium. All had housekeepers from Mexico, some of whom were suspected to be the source of the infections.[28][29]