145 Trichinosis

Trichinosis, also known as trichinellosis, trichinia- sis, or trichinelliasis, is a disease of humans and of other mammals infected with the nematode worm Trichinella spiralis. The pathological changes and the symptomatology of Trichinella infection are manifestations of three successive stages in the life history of the worm: (1) penetration of adult female worms into the intestinal mucosa, (2) migration of juvenile worms, and (3) penetration of juvenile worms and subsequent encystment in muscle cells.

Distribution and Incidence

Although trichinosis occurs worldwide, in humans it is found principally in the United States, Canada, and eastern Europe. It is also well known in Mexico, parts of South America, Africa, southern Asia, and the Middle East. People acquire trichinae by ingest­ing uncooked or poorly cooked meat, especially pork. Home-made sausages have caused many recent out­breaks in the United States. Hence, the prevalence of trichinosis is less in the tropics and subtropics, where less meat is consumed. Trichinosis does not occur among Hindus, Jews, and Moslems, for whom there are religious bans on eating pork.

Although the prevalence of trichinosis in human populations is low (probably 2.2 percent or less in the United States, based on autopsy surveys), epi­demic outbreaks are not infrequent. Incidence of in­fection is likely to be higher than suspected because of the vagueness of symptoms, which usually sug­gest other conditions.

Epidemiology and Etiology

T. spiralis is unusual in that a single individual animal serves as both intermediate and definitive (final) host, with the juvenile and adult worms lo­cated in different organs.

Humans acquire infections by ingesting infective juveniles, which are encysted in striated muscle of swine or other animals. The worms are freed from their cysts by gastric juices and invade the intestinal mucosa where they copulate.

Young juveniles are carried throughout the body via the arterial system. They finally reach skeletal muscle, where they penetrate individual fibers and grow in a spiral fashion, eventually becoming en­cysted by a blunt, ellipsoidal capsule of host origin. The time required for complete encapsulation is about 3 months. Calcification of the capsule begins as early as 6 months and may take up to 2 years to complete. Eventually the worms also become calci­fied, although they may remain viable for several years prior to calcification.

Not all striated muscles are parasitized to the same degree. Among muscles most heavily affected are the diaphragm, tongue, and masticatory mus­cles, intercostals, and muscles of the arms and legs.

Most mammals are susceptible to Trichinella infec­tions. Infections are maintained in nature by flesh­eating animals. Humans are regarded as accidental hosts because, barring cannibalism or the consump­tion of cadavers by other mammals, the infection reaches a dead end. Most human infections result from eating pork or pork products, but numerous fatal cases of trichinosis have been recorded from among those who eat undercooked or underfrozen bear or walrus meat.

Cooking meat is of importance in preventing trichinosis. Pork should be cooked until the pink color turns to gray. Alternatively, freezing of meat at -15^oC for 20 days will destroy all parasites.

Immunology

Trichinella infection results in the development of serum antibodies, including IgE, and cell-mediated immune responses. Resistance to reinfection has been demonstrated in experimental animals by an allergic IgE-mediated inflammatory response that expels adult worms from the intestine. Eosinophils may also play a role in immunity to Trichinella because experimental depletion of eosinophils has been shown to result in increased numbers of larvae recovered from infected animals.

Clinical Manifestations and Pathology

The first symptoms of Trichinella infection occur 1 to 2 days after ingestion of infected meat. Initial symptoms are vague and often lead to misdiagnosis, if apparent at all. As a host reacts to the waste products produced by the worms, lesions develop and enteric bacteria are introduced into them. Nau­sea, toxic diarrhea, sweating, and vomiting may occur, mimicking an acute food-poisoning syn­drome. Respiratory symptoms may follow between the second and sixth day, and last for 6 days. In addition, there may be red blotches erupting on the skin.

During the period of migration of juveniles, there are muscular pains as inflammatory processes de­velop in the muscles. Difficulty in breathing, chew­ing, and swallowing develops. Edema around the face and hands is due to endovascular and perivascu­lar inflammation. Edema around the eyes is a com­mon early sign. Lymph nodes become enlarged and tender. Enlarged parotid or sublingual glands often lead to misdiagnosis of mumps. Eosinophilia may be present but often does not occur, even in the most extreme cases. Myocarditis, peritonitis, pneumonia, encephalitis, pleurisy, meningitis, and eye damage may result from migrating juveniles. Death from myocarditis may occur at this stage.

Penetration by juveniles into muscle cells, and subsequent encystment, may result in toxic edema, cachexia, or dehydration. Blood pressure drops rap­idly, and the patient may display nervous disorders such as defects of vision, altered or lost reflexes, hallucinations, delirium, and encephalitis. Severe cases can result in death 4 to 6 weeks after infection. Death may occur as a result of toxemia, myocarditis, nephritis, peritonitis, or other complications.

It is important to recognize that most cases of trichinosis go undetected and that in milder cases no special series of symptoms may be present. Accu­rate diagnosis is made by employing muscle biopsy, pressing the tissue between glass slides, and exam­ining it under a microscope.

There is no thoroughly effective treatment for trichinosis. Thiabendazole has been somewhat effec­tive, but serious side effects are known to occur. Steroids are given if myocarditis develops or if there - are central nervous system complications. However, because corticosteroid therapy will inhibit the in­flammatory reaction, an increase in larvae in the muscles will accompany this treatment.

History and Geography

Antiquity

Although knowledge of the parasite causing trichino­sis was first obtained in 1835, knowledge of the disease dates back to antiquity. Dietary laws prohib­iting the eating of swine are thought to have been engendered by the observation that human illness sometimes followed the eating of such flesh. In 1940 Asa Chandler stated: “There can be little doubt that this worm, with the pork tapeworm as an accom­plice, was responsible for the old Jewish law against the eating of pork.” Historians have surmised that Muhammad recognized that certain epidemics could have been caused by ingestion of pork, and thus followed the example of Moses in prohibiting pork consumption.

Nineteenth Century

The first person to actually see trichinae was James Paget, a 21-year-old freshman medical student at St. Bartholomew’s Hospital in London. In 1835 Paget noted a curious pathological condition in the cadaver of a middle-aged man that was brought in for study. The cadaver had “spicules of bone” in the muscles. They were so hard that they blunted the scalpel. Others had seen these gritty particles previously, but it was Paget who had natural history training and the intense desire to observe new things, and thus he was the first to note that the particle was a worm in its capsule.

Although Paget’s discovery was overshadowed by the detailed and complete memoir by Owen, Paget retained his intense spirit of scientific inquiry and published many papers on medical subjects. Later, he became Sir James Paget, one of the most distin­guished surgeons of his time.

Trichinae in animals other than humans were first noted in 1846. Joseph Leidy, a professor of anat­omy working in Philadelphia, found the worms in the extensor muscles of the thigh of a hog. Leidy had previously seen trichinae in human bodies in a dis­section room, and he could perceive no distinction in the worms from the two hosts. In 1850 Ernst Herbst, working in Gottingen, established that trichinae from meat eaten by an animal may invade its mus­cles. Herbst infected a badger with trichinous dog meat and then fed the infected badger meat to three dogs. All three dogs were infected at autopsy.

The significance of Herbst’s experiments, as well as Leidy’s observations, was not appreciated at the time because leading authorities believed that the trichinae from nonhumans were of a different spe­cies from those of humans. Herbst himself believed that trichinae were actually the larvae of filarial worms.

The problem of determining the life cycle of trichi­nae soon caught the attention of two of the leading researchers of their time, Rudolf Virchow of Berlin and Rudolph Leuckart of Giessen. Leuckart, in 1850, observed that the female intestinal trichinae are viviparous, but he believed that the trichinae were derived from the intestinal nematode Trichuris trichiura.

Verification of the life cycle of trichinae and the discovery of the pathogenesis of trichinous infections represent monumental contributions by Friedrich Albert Zenker in 1860. Zenker performed an autopsy on a 20-year-old servant girl in Dresden whose ill­ness had been diagnosed as typhoid fever. He exam­ined muscle fibers from the arm and was startled to see “dozens of trichinae, lying free in the muscle, either coiled or extended, and exhibiting the plain­est signs of life.” Other skeletal muscles examined were likewise inhabited by the worms. Upon examin­ing intestinal contents, Zenker saw sexually mature worms. It was apparent to him that the parasite underwent its entire life cycle in one and the same host.

Zenker subsequently investigated the household in which the servant girl worked, and found the parasite in sausage that had been prepared just prior to the onset of the girl’s illness. Furthermore, other members of the household who had eaten the meat had become seriously ill with the same symp­toms as shown by the Imfortunate servant girl.

Following the establishment of the details of the life cycle and pathogenesis of trichinae, several out­breaks of infection were recorded. Some 140 epidem­ics of trichinosis were noted in Europe between 1860 and 1877, in which 3,044 persons were known to have fallen ill and 231 to have died.

Beginning in 1863, examination of pork for trichinae was practiced in parts of Germany, and in 1879 a law was enacted in Prussia whereby all pork was required to be examined for trichinae. In this same year, ordinances were passed in Italy, Austria, and Hungary forbidding the importation of swine or pork products from the United States, and other coun­tries followed with similar bans. Subsequently, the U.S. Department of Agriculture, although not provid­ing for specific examination for trichinae, did specify methods for the processing of pork products that are customarily eaten raw. Such procedures will destroy the infectivity of any trichinae present. Public educa­tion, and heat treatment of the garbage used to feed hogs, have also helped to reduce the incidence of the disease in North America and Europe.

Donald E. Gilbertson

Bibliography

Blumer, G. 1939. Some remarks on the early history of trichinosis (1822—1866). Yale Journal of Biology and Medicine 11: 581—8.

Brown, Harold W., and Franklin A. Neva. 1983. Basic clinical parasitology. Norwalk, Conn.

Campbell, W. C., ed. 1982. Trichinellosis. New York.

Chandler, Asa C. 1940. Introduction to parasitology. New York.

Gould, S. E., ed. 1970. Trichinosis in man and animals. Springfield, Ill.

Reinhard, Edward G. 1958. Landmarks of parasitology. II. Demonstration of the life cycle and pathogenicity of the spiral threadworm. Experimental Parasitology 7: 108-23.