Enterobiasis

For most physicians, parasitic worm infection is quite low on the list of differential diagnoses, if it is thought of at all. Parasitic infections, like tuberculosis, are complacently thought of as problems of the past--unpleasant afflictions that have vanished with outhouses and crowded living conditions. Yet, like tuberculosis and the poverty with which that disease is associated, parasites are still very much a part of our reality.

The world is fast becoming a smaller, more intimate place as the United States attracts more and more immigrants, legal and illegal, from around the globe. Substandard housing, drug abuse and homelessness are commonplace in our big cities, leading to a breakdown in hygienic standards. In rural areas, migrant laborers face the same nonhygienic conditions, coupled with inaccessible medical care. Even the more affluent of society may be affected; parasitic infections may be associated with foreign adoptions, exposure to day care centers and overseas travel. Without proper food and water precautions, some overseas travel may result in the unwitting acquisition of intestinal stowaways.

Symptoms

Parasitic helminths often produce such vague symptoms that the diagnosis is complicated. Intestinal worms are usually asymptomatic, but heavier infections may produce symptoms ranging from abdominal discomfort to severe pain. Anorexia (rather than hunger pangs, as is commonly thought), nausea, diarrhea, pruritus, rectal prolapse, and even bowel obstruction and death may occur as a result of helminth infestation.[1,2]

Allergic manifestations such as hives and eosinophilia may develop, but the latter sign is usually not striking in patients with simple intestinal infection. Sometimes the worms reveal their presence dramatically by suddenly exiting the body--even when the person is not at stool. As can be imagined, the psychologic trauma of such an event often outweighs any physical pain.[2]

Indeed, the very mention of worms, with their social stigma, may provoke fear in patients. This fear must be handled with care by the physician. Many patients, out of fearfulness, request unnecessary, excessive or repeat treatments. Other patients, unconvinced of their infection, are reluctant to take any medication unless they can see the worms in their stools.[3]

Stool Examination

The diagnostic test of choice for intestinal helminthic infection is examination of the stool for ova and parasites, which is performed by most laboratories. To obtain a urine-free specimen, stools are best collected using plastic wrap under the toilet seat. The patient then uses a spatula to select samples of the stool for preservation, preferably portions with visible mucus or blood. Any unusual-appearing element in the stool should be included in the sample. The patient takes the stool specimen to the laboratory for preparation and, occasionally, staining.[4] In some cases, especially when suspicion of intestinal helminths is high, fresh stool may be obtained by digital rectal examination and examined immediately.

Enterobiasis

Pinworms (Enterobius vermicularis) are the most common helminth seen by primary care physicians in North America. Pinworms classically present as anal pruritus in irritable, sleepless children and, unlike most other worms, are most common in temperate regions. The most severe pinworm infections occur in institutionalized patients, where spread is quite rapid; however, people of all groups and socio-economic levels may be affected. Piworms are more annoying than dangerous; many infected patients are asymptomatic. Heavier infections may cause insomnia, restlessness, vulvovaginitis, loss of appetite and intractable localized itching.[5]

Pinworms are small; the females are only about 10 mm in length (Figures 1, 2 and 3). The worms favor the ileocecal region, although they may travel throughout the intestinal tract during their one- to two-month life span. The female worm has a pin-shaped tail, from which the name is derived. At night, sexually mature worms migrate to the anus, emerge to deposit their eggs and the on the perianal skin. If not washed off, the eggs hatch, and the larvae may return to the large intestine (retroinfection). Alternatively, anal scratching contaminates the fingernails with eggs, which are then carried to the mouth. Such large numbers of microscopic eggs are produced that clothing, bedding and other surfaces in the home soon become infested. In many cases, the child's infection spreads to the entire family, although not everyone becomes symptomatic.

Pinworms are best diagnosed by examining the perianal skin rather than the stool, which is usually negative for ova and worms. To recover the eggs, a tongue blade covered with a segment of clear (not translucent) cellulose tape is placed sticky-side down over the unwashed perianal skin in the morning. Several specimens are collected on three separate mornings, taped to glass slides and taken to a laboratory for examination. The characteristic elongate, colorless eggs measure 50 to 60 [mu]m and are flattened on one side. The glistening adult worms may also be evident if the anus is examined with a flashlight very late at night or early in the morning before the patient awakes. Occasionally, pinworms are passed in the stool and can be recovered in that manner.

TREATMENT

Treatment of pinworms is fairly simple, although relapses are common. Mebendazole (Vermox), one 100-mg tablet orally, is generally safe and effective, except in pregnant women.[6] A second dose 10 days later is often recommended to ensure effectiveness. The entire family should be treated to assure eradication. For symptomatic infections in pregnant women, pyrantel (Antiminth), 11 mg per kg of base (maximum dosage: 1 g), may be given in a single dose, with the same dose repeated in two weeks.[7]

Hygienic precautions involve washing infested clothing and bedding, trimming fingernails and keeping the perianal area clean. It should be emphasized to the patient that the family dog and cat are not to be blamed for this infection, since only humans are hosts to these worms.[8]

Ascariasis

Roundworms (Ascaris lumbricoides) are by far the largest and most impressive of the common parasitic nematodes, with the females measuring up to 18 inches in length. The smaller males may be distinguished by their curved tails. Roundworm infection is still reasonably common in rural southeastern United States and is frequently found in immigrants. Up to 25 percent of the world's population may be infected with a species of Ascaris.[9] Similar species infest other animals, such as Toxocara canis in dogs, Toxocara cati in cats and Ascaris suum in pigs; however, the life cycle of A. lumbricoides usually involves only humans.[8]

Ascaris eggs (Figures 4 and 5) reach the soil in feces and in two to three weeks develop into embryos, when they become infectious. If protected from heat and sun, the remarkably resistant eggs may persist in the soil for more than a decade until they are accidentally consumed.

The larval worms hatch in the intestine and penetrate the lymphatic circulation, where they are carried through the liver to the alveoli of the lungs. In the lungs, they may cause a pneumonitis, known as Loffler's pneumonia, which can be life-threatening in patients with heavy infections. The condition, however, is usually self-limited, lasting one to two weeks, with associated substernal burning, cough, wheezing, rales and fever. Perihilar infiltrates on chest radiographs, with eosinophilia, Charcot-Leyden crystals and larvae in the sputum, are characteristic at this stage.[2] Most cases, however, go undiagnosed.

The juvenile worms are coughed up, swallowed and returned to the small intestine. There they feed on intestinal contents, become sexually mature and survive for 12 to 18 months. In the gut, adult worms may aggregate, causing intestinal obstruction at the ileocecal valve. The collection of worms may be large enough to be palpated or visualized on radiographs. Sometimes worms lodge in the biliary tree, causing biliary colic, hepatitis, pancreatitis or (if they perforate the peritoneal wall) peritonitis. Fever, illness or even spicy foods may compel Ascaris to exit the body abruptly through the mouth, nose or rectum. Usually, however, only vague abdominal discomfort or nausea hint that an infection is present.[2]

TREATMENT

Roundworms are eradicated with mebendazole, 100 mg twice daily for three days.[6] (This dosage is for patients more than two years of age.) In pregnant patients, pyrantel, 11 mg per kg (maximum dosage: 1 g) may be prescribed.[7]

Pyrantel, which is also available in an over-the-counter form (Reese's Pinworm), works by inducing a neuromuscular blockade that paralyzes the worm. A third treatment option is piperazine, 75 mg per kg daily for two days (maximum daily dosage: 3.5 g). This drug is now difficult to obtain.

Any of these treatments may fail to kill migrating larvae, so a follow-up examination of stool for ova and parasites should be performed in two months. Family screening is important as well, since familial risk is increased, although not to the extent that occurs with Enterobius infection.

Trichuriasis

Whipworm (Trichuris trichiura) infestation is generally less common than Ascaris infestation, but whipworm is often found in association with Ascaris. Trichuriasis is found in southeastern states but is more common in foreign immigrants (especially children) and migrant workers. T trichiura lacks an animal reservoir, although similar whipworm species infest a variety of mammals.

Whipworm eggs require three weeks of incubation in the soil in a moist, shady place (Figures 6, 7, 8 and 9). When swallowed, the eggs hatch in the small intestine, and the larvae burrow into the intestinal wall, where they remain for about one week before re-emerging and traveling to the colon. Unlike ascariasis, trichuriasis has no pulmonary stage.

Adult whipworms are 30 to 50 mm in length, with a thread-like anterior portion and a thickened posterior section. They become sexually mature and start producing eggs in about two months but, unlike Ascaris, they can live for several years in the host's intestine. The anterior "whip" portion of these worms burrows into the intestinal lining, traumatizing it enough to cause mild chronic blood loss and even symptoms mimicking proctitis and inflammatory bowel disease. Rectal prolapse, diarrhea loss of appetite and hives are other symptoms. Adult worms are occasionally visualized on proctosigmoidoscopy performed as part of a work-up for colitis.

Treatment of trichuriasis is the same as that for ascariasis and also requires family screening and post-treatment follow-up.[10]

As with other parasitic infections, trichuriasis is most likely to occur in small children, probably because of their tendency to place dirty objects (including contaminated fingers) in their mouths. Children also tend to be more symptomatic and susceptible to infection in most cases. One study demonstrated a 29 percent prevalence of intestinal parasites in foreign children adopted by U.S. citizens.[11] Therefore, stool ova and parasite screening should always be considered in high-risk children.

Less Common Parasites

The helminths discussed in the following section are much less common in the United States but are significant in immigrants coming from tropical regions. Several studies show that these infections tend to be persistent, making early detection even more important.[3] Prevalence estimates of all intestinal parasites for U.S. immigrants range from 20 to 60 percent. Trematodes (flukes) may infect immigrants, especially those coming from the Orient; however, because trematodes are still quite uncommon in the United States, they have been omitted from the following discussion.

HOOKWORMS

Hookworm infections are caused by two related species, Necator americanus, the "New World" hookworm, and Ancylostoma duodenale, the "Old World" hookworm. In fact, both types are native throughout the tropical Eastern hemisphere, but Necator was probably transported to southeastern United States and South America by the slave trade. It is now by far the most prevalent hookworm species.[8]

Hookworm eggs (Figures 10 and 11) are more sensitive to environmental changes than eggs of other helminths. They may disintegrate or hatch with storage. The juveniles develop in the soil from eggs in feces. Following a dormant second stage, the juveniles enter moist, sandy soil and molt into infective, third-stage (filariform) larvae. The larvae, in turn, are capable of penetrating the skin (usually the bare feet) of any nearby person and causing a pruritic rash, referred to as "ground itch." The larvae migrate to the lungs and then, like Ascaris, they are coughed up and swallowed, after which they reach the small intestine.

Adult Necator hookworms are about 10 mm in length, with a hooked anterior end that they use to consume blood. A hookworm consumes 0.03 mL of blood per day. An Ancylostoma hookworm may consume up to 0.15 mL of blood per day and so may cause symptoms with far fewer worms.[10]

Iron deficiency anemia, chronic fatigue, geophagia, failure to thrive and depression are typical symptoms of hookworm infection. Whites are more susceptible to this infection than blacks.

Hookworms take only five weeks to start producing eggs but may live for 10 to 15 years. Thus, they persist long after the host has emigrated from the place of acquisition.[3,10] Treatment of hookworms consists of mebendazole, 100 mg twice daily for three days, along with iron supplementation in patients with significant anemia.[6]

STRONGYLOIDIASIS

Strongyloides stercoralis is undoubtedly one of the most versatile of all human parasites in that it may exist indefinitely as a free-living parasite with both sexes present or as a self-perpetuating parasitic population of females that reproduce through parthenogenesis (monosexual reproduction).[8] Filariform larvae are capable of penetrating intact skin and migrating through the bloodstream to the lungs, where most of the larvae are coughed up and swallowed.

Strongyloidiasis may persist for many decades (more than 40 years) in the small intestine.[10] Strongyloides eggs usually hatch into rod-shaped larvae before passage (Figures 12, 13 and 14). Hookworm larvae resemble Strongyloides larvae; they can be distinguished by their longer buccal capsule. Unlike hookworm larvae, Strongyloides larvae may molt rapidly (within one to three days) to a filariform stage that is capable of penetrating the anal skin or intestinal mucosa, perpetuating the infection without a ground phase. Thus, Strongyloides can also be spread as a sexually transmitted disease, particularly with homosexual or anal-oral contact. It is usually the presence of live larval worms, not eggs, in the stool that leads to the diagnosis of Strongyloides infection. Persistent unexplained eosinophilia in a patient from a region where Strongyloides infection is endemic should prompt further investigation (including serologic testing), since negative stool specimens do not rule out this infection.[13]

Symptoms of strongyloidiasis are usually absent but may include pruritus during skin penetration, pneumonia (some worms are capable of reproducing in the lungs and may appear in sputum), abdominal cramping and colitis. As in some other parasitic infections, host immune response helps keep the parasite in check. If host immunity is compromised, as in persons who have acquired immunodeficiency syndrome or who are receiving corticosteroid therapy, hyperinfection may occur, leading to death.[14]

Treatment of strongyloidiasis is more problematic than treatment of many other parasitic infections and requires thiabendazole (Mintezol), 25 mg per kg twice daily (maximum daily dosage: 3 g) for two days for adults and children, or five days if infection is disseminated. Side effects are common and include dizziness, nausea, malodorous urine and occasional hallucinations.[6,10] Ivermectin (Mectizan) may be a less toxic alternatative treatment for Strongyloides infection.[6,13]

TAPEWORMS

Several species of tapeworms, or cestodes, create problems throughout the world. In the United States, the most common tapeworm in adults is Taenia saginata, the beef tapeworm, which is transmitted through consumption of inadequately cooked beef.[15] Taenia eggs (Figures 15, 16, 17,18 and 19), after being passed in human feces, are consumed by cattle, where they develop into bladder worm (cysticerci) in the animal's flesh. When undercooked infected beef is consumed, cysticerci rapidly develop into large tapeworms, 10 to 15 feet in length, in the human gut. Diagnosis is made on the basis of active or passive passage of ribbon-like tapeworm segments from the rectum or by the discovery of the eggs in a stool or perianal specimen.[8]

The related Taenia solium, or pork tapeworm, has a similar life cycle but affects swine rather than cattle. While much less common than T. saginata, T. solium is far more dangerous, since its eggs, if ingested, can produce cysticercosis, the invasion of human tissue by developing larval forms. In severe cases, the larvae may invade the central nervous system, giving rise to neurocysticercosis.

T. solium is found in Central and South America, and immigrants from these regions may be at risk of cysticercosis, particularly neurocysticercosis.[16] Patients with neurocysticercosis frequently present with seizures. This diagnosis should be considered in the evaluation of a patient from Central or South America with a new-onset seizure disorder.

The fish tapeworm, Diphyllobothrium latum, is still occasionally transmitted through the consumption of undercooked fish, especially fish from the Great Lakes region. The eggs hatch in water, and the resulting larvae are consumed by minute fresh-water crustaceans (copepods), which are in turn eaten by ever larger fish. The parasite survives passage into each new host and finally enters a fish-eating human, where it grows into an adult up to 30 feet long. Occasionally, megaloblastic anemia develops in the infected person; this worm is capable of depleting the host's store of vitamin [B.sub.12].[8,17]

Perhaps the most common tapeworm in the United States, at least in children, is the dwarf tapeworm, Hymenolepis nana. This tapeworm, 1 inch in length, does not require an intermediate host; the eggs are capable of directly infecting humans. Consumed eggs hatch and develop into tiny cysticercoids in the intestinal villi. The adults emerge into the small intestine and begin laying eggs, which may continually autoinfect the patient through fecal-oral contact. Mice also serve as a reservoir for the adult worms and accidental ingestion of food contaminated with mouse droppings may spread the infection.

H. nana infection is persistent and may cycle in immigrant children for years after their arrival in the United States.[3] Fortunately, considerable evidence indicates that host immune responses limit or at least contain the extent of this infection in humans.[8]

All of these tapeworms respond to treatment with either praziquantel (Biltricide) or niclosamide (Niclocide). Praziquantel, 5 to 10 mg per kg as a single dose for adults and children, is used to eradicate Taenia and fish tapeworm infections. A single dose of 25 mg per kg is recommended for H. nana infection. The adult dosage for niclosamide is four 500-mg chewable tablets (2 g) as a single dose for Taenia and fish tapeworm infection. The pediatric dosage for Taenia and fish tapeworm infection is two tablets for children weighing 11 to 34 kg, and three tablets for those weighing more than 34 kg. Vitamin [B.sub.12] supplementation may also be necessary to correct the megaloblastic anemia that occurs in patients with D. latum infections.

Niclosamide has been suggested as a possible therapy for pregnant women after the first trimester.[7] As treatment for H. nana infection, niclosamide is given in a single dose of four 500-mg chewable tablets, followed by two tablets each day for six days for adults and children weighing more than 34 kg, and one tablet each day for six days for children weighing 11 to 34 kg.[6]

Final Comment

With the exception of Enterobius, helminthic infections in the developed world declined with the regular use of flush toilets and proper disposal of human feces. Effective plumbing rather than effective medical treatment is the real line of defense against these amazingly versatile pathogens. However, global events continue to bring many people from endemic regions into our medical practices. The plurality of U.S. society mandates an understanding of helminth infections and treatment, including the importance of cleaning and cooking food thoroughly to prevent infection.

REFERENCES

[1.] Jones JE. Signs and symptoms of parasitic diseases. Prim Care 1991;18:1-12. [2.] Tietze PE, Tietze PH. The roundworm, Ascaris lumbricoides. Prim Care 1991;18:25-41. [3.] Molina CD, Molina MM, Molina JM. Intestinal parasites in southeast Asian refugees two years after immigration. West J Med 1988;149:422-5. [4.] Ware BR, Jones JE. The office diagnosis of common intestinal parasitic diseases. Prim Care 1991;18:185-93. [5.] Russell LJ. The pinworm, Enterobius vermicularis. Prim Care 1991;18:13-24. [6.] Drugs for parasitic infections. Med Lett Drugs Ther 1993;35:111-22. [7.] Tietze PE, Jones JE. Parasites during pregnancy. Prim Care 1991;18:75-99. [8.] Schmidt GD, Roberts LS. Foundations of parasitology. 4th ed. St. Louis: Times Mirror/Mosby College Publishing, 1989. [9.] Bratton RL, Nesse RE. Ascariasis. An infection to watch for in immigrants. Postgrad Med 1993;93 (1):171-3,177-8. [10.] Walden J. Parasitic diseases. Other roundworms. Trichuris, hookworm, and Strongyloides. Prim Care 1991;18:53-74. [11.] Jenista JA, Chapman D. Medical problems of foreign-born adopted children. Am J Dis Child 1987; 141:298-302. [12.] Salas SD, Heifetz R, Barrett-Connor E. Intestinal parasites in Central American immigrants in the United States. Arch Intern Med 1990;150:1514-6. [13.] Wiest PJ. Eosinophilia in a Cambodian refugee. Patient Care 1994;28:78-82. [14.] Yoshimoto CM. Strongyloides infection in Hawaii: an imported case. Hawaii Med J 1993;52:59-61,76. [15.] Schantz PM, McAuley J. Current status of food-borne parasitic zoonoses in the United States. Southeast Asian J Trop Med Public Health 1991; 22(Suppl):65-71. [16.] Ehnert KL, Roberto RR, Barrett L, Sorvillo FJ, Rutherford GW 3d. Cysticercosis: first 12 months of reporting in California. Bull Pan Am Health Organ 1992;26:165-72. [17.] Curtis MA, Bylund G. Diphyllobothriasis: fish tapeworm disease in the circumpolar north. Arctic Med Research 1991;50(1):18-24.

Figures 7, 8 and 9 courtesy of Daniel Conner, M.D., Department of Pathology, Georgetown University School of Medicine, Washington, D.C. Figures 2, 3, 5, 11, 12, 13, and 16 through 19 courtesy of John Hall, Ph.D., Department of Microbiology, West Virginia University School of Medicine, Morgantown.

The Author

GREGORY JUCKETT, M.D. is an assistant professor in the Department of Family Medicine at West Virginia University School of Medicine, Morgantown. He is a graduate of Pennsylvania State University College of Medicine, Hershey, and completed a three-year residency in family medicine at the Medical University of South Carolina College of Medicine, Charleston.

Address correspondence to Gregory Juckett, M.D., Box 9247, Robert C. Byrd Health Sciences Center, West Virginia University School of Medicine, Morgantown, WV 26506.

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