Taenia solium

Description

Adult T. solium is a triploblastic acoelomate, having no body cavity. It is normally 2 to 3 m in length, but can become much larger, sometimes over 8 m long. It is white in colour and flattened into a ribbon-like body. The anterior end is a knob-like head called a scolex, which is 1 mm in diameter. The scolex bears four radially arranged suckers (acetabula) that surround the rostellum. These are the organs of attachment to the intestinal wall of the host. The rostellum is armed with two rows of spiny hooks, which are chitinous in nature. The 22 to 32 rotelllar hooks can be differentiated into short (130-µm) and long (180-µm) types. The elongated body is called the strobila, which is connected to the scolex through a short neck. The entire body is covered by a special covering called tegument, which is an absorptive layer consisting of a mat of minute hair-like microtriches. The strobila is divided into segments called proglottids, 800 to 900 in number. Body growth starts from the neck region, so the oldest proglottids are at the posterior end. Thus, the three distinct proglottids are immature proglottids towards the neck, mature proglottids in the middle, and gravid proglottids at the posterior end. A monoecious species, each mature proglottid contains a set of male and female reproductive systems. The numerous testes and a bilobed ovary open into a common genital pore. The oldest gravid proglottids are full of fertilised eggs,

The infective larave, cysticerci, in humans, have three morphologically distinct types. The common one is the ordinary "cellulose" cysticercus, which has a fluid-filled bladder 0.5 to 1.5 cm in length and an invaginated scolex. The intermediate form has a scolex, while the "racemose" has no evident scolex, but is believed to be larger and much more dangerous. They are 20 cm in length and have 60 ml of fluid, and 13% of patients can have all three types in the brain.

Life cycle

The life cycle of T. solium is indirect. It passes through pigs, as intermediate hosts, into humans, as definitive hosts. From humans, the eggs are released in the environment where they await ingestion by another host. Humans as the definitive hosts are directly infected from contaminated meat.

Definitive host

Humans are infected by the larval stage, the cysticercus, from measly pork. A 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. Using the scolex, it anchors to the intestinal wall. It grows in size using nutrients from the surroundings. Its strobila lengthens as new proglottids are formed at the neck. In 10–12 weeks after initial infection, it becomes an adult worm. 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 micromeres, medium mesomeres, and large megameres. Megameres develop into syncytial layer called outer embryonic membrane. Mesomeres develop into radially striated inner embryonic membrane or embryophore. Micromeres become the morula. The morula transforms into a six-hooked embryo known as oncosphere, or sometimes hexacanth ("six hooked") larva. A single gravid proglottid can contain more than 50,000 embryonated eggs. Gravid proglottids often rupture in the intestine, liberating the eggs in faeces. The intact gravid proglottids are shed off in groups of four or five. The free eggs and detached proglottids are released into the environment through peristalsis. Eggs can survive in the environment for up to two months.

Intermediate host

Pigs ingest the eggs from human faeces or vegetation contaminated with human excreta. The embryonated eggs enter the 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 get attached 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 called 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.

Humans are also accidental secondary hosts when they are infected by embryonated eggs, either by autoinfection or ingestion of contaminated food. As in pigs, the oncospheres hatch, enter blood circulation, and have a predilection for brain tissue and other soft muscle tissues. When they settle to form cysts, clinical symptoms of cysticercosis appear. The cysticercus is often called the metacestode. If they localize in the brain, serious neurocysticercosis follows.

Pathogenesis

Intestinal infection of T. solium is called taeniasis which is quite asymptomatic. Only in severe cases, conditions of intestinal irritation, anaemia, and indigestion occur, which can lead to loss of appetite and emaciation. Cysticercus is clinically pathogenic. Ingestion of T. solium eggs or proglottids which rupture within the host intestines can cause larvae to migrate into host tissue to cause cysticercosis. This is the most frequent and severe disease caused by T. solium. In symptomatic cases, a wide spectrum of symptoms may be expressed, including headaches, dizziness, and occasional seizures. 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 location of cysts is more common than cystation in other locations of the body.

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

Prevention and control

The best way to avoid getting tapeworms is to not eat undercooked pork. 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 and/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. Therefore, personal hygiene such as washing one's hands before eating is an effective measure.

Epidemiology

T. solium is found worldwide, but is more common in cosmopolitan areas. Because pigs are intermediate hosts of the parasite, completion of the life cycle occurs in regions where humans live in close contact with pigs and eat undercooked pork. Therefore, high prevalences are reported in Mexico, Latin America, West Africa, Russia, India, Pakistan, Manchuria, and Southeast Asia. In Europe it is most widespread among Slavic countries. Cysticercosis is often seen in areas where poor hygiene allows for contamination of food, soil, or water supplies. Prevalence rates in the United States have shown immigrants from Mexico, Central and South America, and Southeast Asia account for most of the domestic cases of cysticercosis. Taeniasis and cysticercosis are very rare in predominantly Muslim countries, as Islam forbids the consumption of pork. Human cysticercosis is acquired by ingesting T. solium eggs shed in the feces of a human tapeworm carrier by gravid proglottids, so can occur in populations that neither eat pork nor share environments with pigs, although the completion of the life cycle can occur only where humans live in close contact with pigs and eat pork.

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 of the families had housekeepers from Latin American countries and were suspected to be source of the infections.