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Enterobius vermicularis causes pinworm infection (enterobiasis).
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The life cycle of E. vermicularis is shown in Figure 56–1. Infection occurs only in humans; there is no animal reservoir or vector. The infection is acquired by ingesting the worm eggs. The eggs hatch in the small intestine, where the larvae differentiate into adults and migrate to the colon. The adult male and female worms live in the colon, where mating occurs (Figure 56–2A). At night, the female migrates from the anus and releases thousands of fertilized eggs on the perianal skin and into the environment. Within 6 hours, the eggs develop into embryonated eggs (Figures 56–3A and 56–4) and become infectious. Reinfection can occur if they are carried to the mouth by fingers after scratching the itching skin.
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Pathogenesis & Clinical Findings
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Perianal pruritus is the most prominent symptom. Pruritus is thought to be an allergic reaction to the proteins of either the adult female or the eggs. Scratching predisposes to secondary bacterial infection.
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Enterobius is found worldwide and is the most common helminth in the United States. Children younger than 12 years of age are the most commonly affected group.
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The eggs are recovered from perianal skin by using the Scotch tape technique and can be observed microscopically (see Figure 56–4).
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Unlike those of other intestinal nematodes, these eggs are not found in the stools. The small, whitish adult worms can be found in the stools or near the anus of diapered children. No serologic tests are available.
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The drug of choice is albendazole, mebendazole, or pyrantel pamoate. These drugs kill the adult worms in the colon but not the eggs, so retreatment in 2 weeks is suggested. Reinfection is very common. Household members should also be treated.
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There are no specific means of prevention, but washing hands when preparing food and washing bed sheets, towels, diapers, and clothing to remove eggs are helpful.
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Trichuris trichiura causes whipworm infection (trichuriasis).
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Humans are infected by ingesting worm eggs in food or water contaminated with human feces (see Figures 56–3B and 56–5). The eggs hatch in the small intestine, where the larvae differentiate into immature adults. These immature adults migrate to the colon, where they mature, mate, and produce thousands of fertilized eggs daily, which are passed in the feces. Eggs deposited in warm, moist soil form embryos. When the embryonated eggs are ingested, the cycle is completed. Figure 56–2B illustrates the characteristic “whiplike” appearance of the adult worm.
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Pathogenesis & Clinical Findings
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Although adult Trichuris worms burrow their hairlike anterior ends into the intestinal mucosa, they do not cause significant anemia, unlike the hookworms. Trichuris may cause diarrhea, but most infections are asymptomatic.
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Trichuris may also cause rectal prolapse in children with heavy infection. Prolapse results from increased peristalsis that occurs in an effort to expel the worms. The whitish worms may be seen on the prolapsed mucosa.
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Whipworm infection occurs worldwide, especially in the tropics; more than 500 million people are affected. In the United States, it occurs mainly in the southern states.
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Diagnosis is based on finding the typical eggs (i.e., barrel-shaped [lemon-shaped] with a plug at each end) in the stool (see Figures 56–3B and 56–5).
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Albendazole is the drug of choice.
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Proper disposal of feces prevents transmission.
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Ascaris lumbricoides causes ascariasis. Ascaris larvae migrating through the lung can cause eosinophilic pneumonia (Loeffler's syndrome).
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The life cycle of A. lumbricoides is shown in Figure 56–6. Humans are infected by ingesting worm eggs in food or water contaminated with human feces (Figures 56–3C and 56–7). The eggs hatch in the small intestine, and the larvae migrate through the gut wall into the bloodstream and then to the lungs. They enter the alveoli, pass up the bronchi and trachea, and are swallowed. Within the small intestine, they become adults (Figures 56–2C and 56–8). They live in the lumen, do not attach to the wall, and derive their sustenance from ingested food. The adults are the largest intestinal nematodes, often growing to 25 cm or more. A. lumbricoides is known as the “giant roundworm.” Thousands of eggs are laid daily, are passed in the feces, and differentiate into embryonated eggs in warm, moist soil (see Figure 56–3C). Ingestion of the embryonated eggs completes the cycle.
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Pathogenesis & Clinical Findings
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The major damage occurs during larval migration rather than from the presence of the adult worm in the intestine. The principal sites of tissue reaction are the lungs, where inflammation with an eosinophilic exudate occurs in response to larval antigens. Because the adults derive their nourishment from ingested food, a heavy worm burden may contribute to malnutrition, especially in children in developing countries.
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Most infections are asymptomatic. Ascaris pneumonia with fever, cough, and eosinophilia can occur with a heavy larval burden (Loeffler's syndrome). Abdominal pain and even obstruction can result from the presence of adult worms in the intestine.
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Ascaris infection is very common, especially in the tropics; hundreds of millions of people are infected. In the United States, most cases occur in the southern states.
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Diagnosis is usually made microscopically by detecting eggs in the stools. The egg is oval with an irregular surface (see Figures 56–3C and 56–7). Occasionally, the patient sees adult worms in the stools.
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Proper disposal of feces can prevent ascariasis.
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ANCYLOSTOMA & NECATOR
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Ancylostoma duodenale (Old World hookworm) and Necator americanus (New World hookworm) cause hookworm infection.
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The life cycle of the hookworms is shown in Figure 56–9. Humans are infected when filariform larvae in moist soil penetrate the skin, usually of the feet or legs (Figures 56–2E and 56–10). They are carried by the blood to the lungs, migrate into the alveoli and up the bronchi and trachea, and then are swallowed. They develop into adults in the small intestine, attaching to the wall with either cutting plates (Necator) or teeth (Ancylostoma) (Figures 56–2D, F, and G, and 56–11). They feed on blood from the capillaries of the intestinal villi. Thousands of eggs per day are passed in the feces (Figures 56–3D and 56–12). Eggs develop first into noninfectious, feeding (rhabditiform) larvae and then into third-stage, infectious, nonfeeding (filariform) larvae (see Figure 56–2E), which penetrate the skin to complete the cycle.
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Pathogenesis & Clinical Findings
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The major damage is due to the loss of blood at the site of attachment in the small intestine. Up to 0.1 to 0.3 mL per worm can be lost per day. Blood is consumed by the worm and oozes from the site in response to an anticoagulant made by the worm. Weakness and pallor accompany the microcytic anemia caused by blood loss. These symptoms occur in patients whose nutrition cannot compensate for the blood loss. “Ground itch,” a pruritic papule or vesicle, can occur at the site of entry of the larvae into the skin. The human hookworms also cause cutaneous larva migrans. Pneumonia with eosinophilia can be seen during larval migration through the lungs.
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Hookworm is found worldwide, especially in tropical areas. In the United States, Necator is endemic in the rural southern states. Walking barefooted on soil predisposes to infection. An important public health measure was requiring children to wear shoes to school.
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Diagnosis is made microscopically by observing the eggs in the stools (see Figures 56–3D and 56–12). Occult blood in the stools is frequent. Eosinophilia is typical.
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The drug of choice is albendazole, mebendazole, or pyrantel pamoate.
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Disposing of sewage properly and wearing shoes are effective means of prevention.
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Strongyloides stercoralis causes strongyloidiasis.
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The life cycle of S. stercoralis is shown in Figure 56–13. S. stercoralis has two distinct life cycles, one within the human body and the other free-living in the soil. The life cycle in the human body begins with the penetration of the skin, usually of the feet, by infectious (filariform) larvae (see Figures 56–2I and 56–10) and their migration to the lungs. They enter the alveoli, pass up the bronchi and trachea, and then are swallowed. In the small intestine, the larvae molt into adults (see Figure 56–2H) that enter the mucosa and produce eggs.
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The eggs usually hatch within the mucosa, forming rhabditiform larvae (see Figure 56–2J) that are passed in the feces. Some larvae molt to form filariform larvae, which penetrate the intestinal wall directly without leaving the host and migrate to the lungs (autoinfection). Filariform larvae can also exit the anus and reinfect through the perianal skin. In immunocompetent patients, this is an infrequent, clinically unimportant event.
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However, in immunocompromised patients (e.g., those who have acquired immunodeficiency syndrome [AIDS] or are taking high-dose corticosteroids or tumor necrosis factor [TNF] inhibitors) or patients who are severely malnourished, autoinfection can lead to massive reinfection (hyperinfection), with larvae passing to many organs and with severe, sometimes fatal consequences. Reinfection can also occur in those infected with human T-cell lymphotropic virus (HTLV) because their ability to mount a protective T-cell response is diminished.
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If larvae are passed in the feces and enter warm, moist soil, they molt through successive stages to form adult male and female worms. After mating, the entire life cycle of egg, larva, and adult can occur in the soil. After several free-living cycles, filariform larvae are formed. When they contact skin, they penetrate and again initiate the parasitic cycle within humans.
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Pathogenesis & Clinical Findings
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Most patients are asymptomatic, especially those with a low worm burden. Adult female worms in the wall of the small intestine can cause inflammation, resulting in watery diarrhea. Larvae in the lungs can produce a pneumonitis similar to that caused by Ascaris. Pruritus (ground itch) can occur at the site of larval penetration of the skin, as with hookworm. S. stercoralis also causes cutaneous larva migrans.
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Autoinfection can result in chronic strongyloidiasis characterized by intermittent abdominal pain, fluctuating rashes, and intermittent eosinophilia. In hyperinfection, the penetrating larvae may cause sufficient damage to the intestinal mucosa that sepsis caused by enteric bacteria, such as Escherichia coli and Bacteroides fragilis, can occur.
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Strongyloidiasis occurs primarily in the tropics, especially in Southeast Asia. Its geographic pattern is similar to that of hookworm because the same type of soil is required. In the United States, Strongyloides is endemic in the southeastern states.
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Diagnosis depends on finding larvae, rather than eggs, in the stool (see Figure 56–10). As with many nematode infections in which larvae migrate through tissue, eosinophilia can be striking. Serologic tests are useful when the larvae are not visualized. An enzyme immunoassay that detects antibody to larval antigens is available through the Centers for Disease Control and Prevention (CDC) in Atlanta.
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Ivermectin is the drug of choice. Albendazole is an alternative drug.
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Prevention involves disposing of sewage properly and wearing shoes. To prevent Strongyloides hyperinfection in patients scheduled to receive immunosuppressive drugs (e.g., corticosteroids, TNF inhibitors) and who have lived in an area of Strongyloides endemicity, serologic tests to determine whether antibodies to Strongyloides are present should be performed. If antibodies are found, the patient should be treated with ivermectin before immunosuppression is undertaken, if possible.
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Trichinella spiralis causes trichinosis. T. spiralis is also called the trichina worm.
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The life cycle of T. spiralis is shown in Figure 56–14. Any mammal can be infected, but pigs are the most important reservoirs of human disease in the United States (except in Alaska, where bears constitute the main reservoir). Humans are infected by eating raw or undercooked meat containing larvae encysted in the muscle (see Figure 56–2K). The larvae excyst and mature into adults within the mucosa of the small intestine. Eggs hatch within the adult females, and larvae are released and distributed via the bloodstream to many organs; however, they develop only in striated muscle cells. Within these “nurse cells,” they encyst within a fibrous capsule and can remain viable for several years but eventually calcify (Figure 56–15).
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The parasite is maintained in nature by cycles within reservoir hosts, primarily swine and rats. Humans are end-stage hosts, because the infected flesh is not consumed by other animals.
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Pathogenesis & Clinical Findings
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A few days after eating undercooked meat, usually pork, the patient experiences diarrhea followed 1 to 2 weeks later by fever, muscle pain, periorbital edema, and eosinophilia. Subconjunctival hemorrhages are an important diagnostic criterion. Signs of cardiac and central nervous system disease are frequent, because the larvae migrate to these tissues as well. Death, which is rare, is usually due to congestive heart failure or respiratory paralysis.
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Trichinosis occurs worldwide, especially in Eastern Europe and West Africa. In the United States, it is related to eating home-prepared sausage, usually on farms where the pigs are fed uncooked garbage. Bear and seal meat are also sources. In many countries, the disease occurs primarily in hunters who eat undercooked wild game.
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Muscle biopsy reveals larvae within striated muscle (see Figures 56–2K and 56–15). Serologic tests, especially the bentonite flocculation test, become positive 3 weeks after infection.
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There is no effective treatment for trichinosis when the larvae have infected the muscle, but for patients with severe symptoms, steroids plus albendazole can be useful. Mebendazole is effective against the adult intestinal worms early in infection.
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The disease can be prevented by properly cooking pork and by feeding pigs only cooked garbage.