T
tapeworm
name for the parasitic flatworms forming the class Cestoda. All tapeworms spend the adult phase of their lives as parasites in the gut of a vertebrate animal (called the primary host). Most tapeworms spend part of their life cycle in the tissues of one or more other animals (called intermediate hosts), which may be vertebrates or arthropods.
Anatomy and Function
An adult tapeworm consists of a knoblike head, or scolex, equipped with hooks for attaching to the intestinal wall of the host (which may be a human), a neck region, and a series of flat, rectangular body segments, or proglottids, generated by the neck. The chain of proglottids may reach a length of 15 or 20 ft (4.6–6.1 m). Terminal proglottids break off and are excreted in the feces of the host, but new ones are constantly formed at the anterior end of the worm. As long as the scolex and neck are intact the worm is alive and capable of growth. A rudimentary nervous system and excretory system run the length of the worm, through the proglottids. However, there is no digestive tract; the worm absorbs the host's digested food through its cuticle, or outer covering.
Reproduction
Each proglottid contains a complete set of male and female reproductive organs that produce the sex cells. Fertilization is internal; in most species cross fertilization between two adjacent worms is necessary, but in a few species self-fertilization may occur between two proglottids of the same worm, or within the same proglottid. In some species the fertilized eggs are shed continuously and leave the host's body in the feces; in others the fertilized eggs are stored until the proglottid is filled with them and the entire proglottid is then shed. The eggs develop into embryos with a hard outer shell; these do not hatch until they are eaten by a suitable intermediate host.
Humans as Tapeworm Hosts
Human tapeworm infestations are most common in regions where there is fecal contamination of soil and water and where meat and fish are eaten raw or lightly cooked. In the case of the human tapeworm most common in the United States (the beef tapeworm, Taenia saginata) the usual intermediate host is a cow, which ingests the proglottid while drinking or grazing. The round-bodied embryos, equipped with sharp hooks, hatch and bore through the cow's intestinal wall into the bloodstream, where they are carried to the muscles. Here each embryo encloses itself in a cyst, or bladder; at this stage it is called a bladder worm. During the bladder worm stage the embryo develops into a miniature scolex; it remains encysted until the muscle is eaten by a primary host, in this case a human. If the scolex has not been killed by sufficient cooking of the meat, it sheds its covering and attaches to the intestinal wall, where it begins producing proglottids.
A human tapeworm common in Mexico, the pork tapeworm (T. solium), has a similar life cycle, with a pig as the usual intermediate host. The fish tapeworm, Diphyllobothrium latum, transmitted to humans from fish, especially pike, is common in Asia and in Canada and the northern lake regions of the United States. This tapeworm has a more elaborate life cycle, involving both a fish and a crustacean as intermediate hosts. The dwarf tapeworm, Hymenolepsis nana, is transmitted through fecal contamination and is common in children in the southeastern United States. There are also several tapeworms for whom humans the usual intermediate host; among these, the dog tapeworm, Echinococcus granulosis, spends its adult phase in the intestines of dogs.
Consequences of Infestation
Intestinal tapeworm infestation frequently occurs without symptoms; occasionally there is abdominal discomfort, diarrhea, constipation, or weight loss. The presence of tapeworm proglottids in clothing, bedding, or feces is the usual sign of infestation. Treatment is with quinacrine hydrochloride (Atabrine) or niclosamide, which kill the worm.
The most serious tapeworm infestation in humans is caused by the ingestion of T. solanum eggs through fecal contamination, which results in the person serving as the intermediate, rather than the primary, host. The embryos migrate throughout the body, producing serious illness if they lodge in the central nervous system. The embryos of the dog tapeworm encyst in various internal organs of humans, most commonly in the liver. The cysts produced by these embryos are called hydatid cysts, and the infestation of the liver is called hydatid disease.
tartar, dental
precipitate of saliva that accumulates around teeth at the gum line. Composed primarily of calcium salts, tartar forms as a hard brownish substance that irritates gums and causes them to recede. Inflammation of this tissue may lead to the recession and infection of the bones in which teeth are imbedded and result in the loosening and loss of teeth. As symptoms may not become apparent until serious damage has occurred, periodic dental visits for the removal of tartar are recommended.
Tay-Sachs disease
rare hereditary disease caused by a genetic mutation that leaves the body unable to produce an enzyme necessary for fat metabolism in nerve cells, producing central nervous system degeneration. The disease is named for a British ophthalmologist, Warren Tay, who first described the disease, in 1881, and a New York neurologist, Bernard Sachs, who first described the cellular changes and the genetic nature of the disease, in 1887. In infants, it is characterized by progressive mental deterioration, blindness, paralysis, epileptic seizures, and death, usually between ages three and five. Late-onset Tay-Sachs occurs in persons who have a genetic mutation that is similar but allows some production of the missing enzyme. There is no treatment for Tay-Sachs.
Course of the Disease
The enzyme involved in Tay-Sachs is called hexosaminidase A. Its absence allows a lipid called GM2 ganglioside to build up in the brain, destroying the nerve cells. The process starts in the fetus; the disease is clinically apparent in the first few months of life. Initial symptoms vary, but usually include a general slowing of development and loss of peripheral vision. By the age of one, most children are experiencing convulsions. The damage to the nervous system progresses inexorably, bringing with it an inability to swallow, difficulty in breathing, blindness, mental retardation, and paralysis.
In late-onset Tay-Sachs, which is often misdiagnosed, the symptoms (ataxia, dysarthria, and muscle weakness) usually become apparent late in childhood or early in adulthood. About 40% of the patients display symptoms of bipolar disorder. Life expectancy does not appear to be affected.
Genetic Basis and Screening
Tay-Sachs disease occurs primarily among Jews of Eastern European descent but is also found in French Canadians whose roots are in the St. Lawrence region, certain Cajuns in Louisiana, and some Amish communities. Tay-Sachs is an autosomal recessive disorder; a person must have two defective genes (one from each parent) in order for the disease to occur. Carriers, people with only one gene for the disorder, are physically unaffected. When both parents are carriers, each child has a 25% chance of getting the disease. If only one parent is a carrier, there is no chance that the child will get the disease, but there is a 50% chance that the child will be a carrier. The gene may be carried by many generations without a manifestation. For this reason, plus the historical lack of accurate diagnosis and routinely high infant mortality of past generations, there is often no known family history of the disease.
Genetic screening for the disease has been possible since the early 1970s and is encouraged in high-risk populations. Blood tests of carriers reveal a reduced amount of the hexosaminidase A. If a couple elects to go forward with a pregnancy, fetal status (again utilizing hexosaminidase A levels) can be ascertained via chorionic villus sampling or amniocentesis. Genetic screening and counseling has greatly reduced the incidence of the disease.
tetanus
acute infectious disease of the central nervous system caused by the toxins of Clostridium tetani. The organism has a widespread distribution and is common in the soil, human and animal feces, and the digestive tracts of animals and humans; however, the toxin is destroyed by intestinal enzymes. Infection with the tetanus bacillus may follow any type of injury, whether incurred indoors or out, including nail puncture wounds, insect bites, splinter injuries, gunshot wounds, burns, lacerations, and fractures. Deep puncture wounds are most dangerous, since the bacillus thrives in an anaerobic environment.
The tetanus toxin, one of the most potent poisons known, acts on the motor nerves and causes muscle spasm at the site of infection and in other areas of the body. The most frequent symptom is stiffness of the jaw (lockjaw) and facial muscles. Difficulty in breathing and severe convulsions may ensue. The mortality rate is very high, especially in the very young and the aged; overall it is about 40%. Treatment with tetanus antitoxin should be started promptly in conjunction with human immune globulin. It is preferable, however, to prevent the disease by active immunization (including booster shots) with tetanus toxoid (see vaccination).
tetany
condition of mineral imbalance in the body that results in severe muscle spasms. Tetany occurs when the concentration of calcium ions (Ca++) in extracellular fluids such as plasma falls below normal. The nervous system becomes increasingly excitable, and nerves discharge spontaneously, sending impulses to skeletal muscles and causing spasmodic contractions. Mild tetany is characterized by tingling in the fingers, toes, and lips; acute tetany, consisting of severe muscular contractions, tremors, and cramps, can result in death. Abnormally low extracellular calcium ion concentration can result from failure of the parathyroid glands to release parathyroid hormone, the substance responsible for the regulation of calcium concentration in the body; a deficiency in vitamin D, which facilitates calcium ion absorption from the gastrointestinal tract; or alkalosis, an excessively alkaline state of body fluids resulting from persistent vomiting, rapid breathing, or excess activity of the hormone aldosterone. Most forms of tetany can be treated with calcium, vitamin D, and a controlled diet. Muscle tetany is also caused by the pathogenic bacterium Clostridium tetani in the disease tetanus.
thrombosis
obstruction of an artery or vein by a blood clot (thrombus). Arterial thrombosis is generally more serious because the supply of oxygen and nutrition to an area of the body is halted. Thrombosis of one of the arteries leading to the heart (heart attack; see infarction) or of the brain (stroke) can result in death and, in a vessel of the extremities, may be followed by gangrene. Acute arterial thrombosis often results from the deposition of atherosclerotic material in the wall of an artery, which gradually narrows the channel, precipitating clot formation (see arteriosclerosis). A thrombus that breaks off and circulates through the bloodstream is called an embolus.
thrush
in medicine, infection caused by the fungus Candida albicans, manifested by white, slightly raised patches on the mucous membrane of the tongue, mouth, and throat. The mucous membrane beneath the patches is usually raw and bleeding. The overgrowth of this fungus results when the balance in the normal oral microbe population is disturbed by antibiotic therapy or disease. It occurs most frequently in infants, in adults suffering from chronic illnesses, in the debilitated, in the immunosuppressed, and in individuals on long-term antibiotic, corticosteroid, or antineoplastic therapy. It is often an early symptom of AIDS. Treatment is with antifungal drugs, such as nystatin.