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Intestinal Helminths

Intestinal Helminths

Potential Severity

Infections are often asymptomatic. In the immuno-compromised host, Strongyloides can progress to a fatal hyperinfection syndrome.

Helminths include the roundworms (nematodes), flukes (trematodes), and tapeworms (cestodes). These parasites are large, ranging in size from 1 cm to 10 m, and they often live in the human gastrointestinal tract without causing symptoms.

Only when the infection is very heavy or the worm migrates to an extraintesti-nal site do patients seek medical attention. Transmission to humans results in most cases from contact with human waste.

The diagnosis is generally made by examining the stool for eggs, larvae, or adult worms.

Intestinal Nematodes (Roundworms)

Nematodes can be classified into two groups. Those that gain entry to the host by egg ingestion (Trichuris, Ascaris, and Enterobius), and those that are capable of producing larvae that penetrate the skin of their host (Strongyloides and hookworm). Roundworm life cycles can also be classified into two groups. One group, Trichuris and Enterobius, attach and grow in the intestine soon after being ingested. The second group, Ascaris, Strongyloides, and hookworm, first penetrate the venous system, enter the lungs, and migrate up the bronchi to the trachea, where they are swallowed. They then take up residence in the gastrointestinal tract. These differences in life cycle account for some of the unique clinical characteristics of the various species of nematodes.

Nematodes Acquired by Ingestion Trichuris trichiura (Whip Worm)

Trichuris trichiura is one of the most prevalent helminths. More than 2 million people are estimated to be infected in the United States. This parasite is most commonly found in the rural Southeast, particularly Puerto Rico, where the moisture and temperature favor egg maturation. Worldwide, this worm causes infection mainly in poor rural communities with poor sanitation. Humans are the principal host, and infection results from ingestion of embryonated eggs. Under optimal conditions of shade and moisture, eggs excreted in the stool undergo embryonic development within 2 to 4 weeks.

Then, when ingested by humans, the larvae break out of the eggshell and penetrate the intestinal villi of the small intestine. Over 3 to 10 days, they migrate down to the cecum, and over 1 to 3 months, they develop into egg-producing adults. Most Trichuris trichiura infections are asymptomatic.

Heavy infections can result in iron deficiency and abdominal pain and tenderness. Bloody diarrhea, growth retardation, and rectal prolapse are potential complications of a heavy infection. Diagnosis is made by fecal smear. The ova has a classic lemon shape with plug-like ends. Mebendazole is a highly effective treatment and is seldom associated with side effects. Albendazole is also recommended as first-line therapy; ivermectin or nitazox-anide are efficacious alternatives.


Ascaris is the most common helminthic infection of humans, being estimated to infect more than 1 billion humans worldwide. In the United States, infections are found predominantly in the southeast, where weather conditions favor egg embryonation. Like Trichuris, Ascarisis a parasite of humans, the infection being contracted by ingesting material contaminated with human feces. Under proper temperature and moisture conditions, eggs develop into infective embryos within 5 to 10 days. When ingested, the parasites hatch in the small intestine.

Embryos then penetrate the intestinal wall and enter the venous bloodstream. On reaching the capillaries of the lung, they break into the alveoli, crawl up through the bronchi and trachea, and then are swallowed, re-entering the gastrointestinal tract, where they mature over a period of 2 months. Each mature gravid female can produce 200,000 eggs per day. As in other roundworm infections, most patients with Ascaris are asymptomatic. However, patients with high worm burdens can experience obstruction of the small intestine, accompanied by vomiting and abdominal pain. Patients may vomit worms during such attacks or may pass them in their stool. Heavy infections may also be associated with malabsorption, steatorrhea, and weight loss.

A single Ascaris worm can migrate up the biliary tree and obstruct the common bile duct, precipitating symptoms of cholecystitis, including epigastric abdominal pain, nausea, and vomiting. As the worms migrate into the lungs, some patients experience respiratory symptoms and develop pneumonia visible on chest radiographs, accompanied by peripheral eosinophilia (sometimes called Loef-fler’s syndrome). On occasion, worms can migrate to other sites in the body, causing local symptoms. Because of the large number of eggs excreted daily, this infection is easily diagnosed by stool smear. Ascaris infection is effectively cured with mebendazole. Alternative treatments include pyrantel pamoate, albendazole, and nitazoxanide. Improved sanitation is critical for controlling this infection.

Hand-washing and boiling of water have been shown to prevent reinfection. Alternatively, all school-age children in endemic areas can be treated twice or three times per year to reduce the worm burden.

Enterobius (Pinworm)

Pinworm is the most common worm infection in countries within the temperate zone. This infection is very common in children of all socioeconomic groups in the United States. Between 20 and 40 million people are estimated to be infected. The eggs of this parasite resist drying and can therefore contaminate bed linens and dust. As a result, infection in one young child can lead to infestation of the entire family.

After ingestion, the eggs hatch in the duodenum and jejunum, and the larvae mature in the cecum and large intestine. At night, gravid females migrate to perianal area, where they lay eggs and cause localized itching. When this area is scratched, eggs are trapped under fingernails and are subsequendy ingested by the host, resulting in repeated autoinfection. The major clinical manifestation is nocturnal itching of the perianal area that often interferes with sleep. This parasite rarely causes other symptoms.

Because Enterobius rarely migrates through tissue, this infection is not associated with peripheral eosinophilia. Diagnosis is made by pressing adhesive cellophane tape onto the perianal area in the early morning. Small, white, thread-like worms and eggs become attached to the tape and can be easily identified using a low-power (100X) microscope. Two doses of mebendazole or albendazole taken 2 weeks apart is curative. All symptomatic family members should be treated simultaneously.

Intestinal Helminths

Nematodes Acquired by Ingestion

  1. Tend to cause minimal symptoms and are not life-threatening.
  2. Contracted by contact with fecal material.
  3. Trichuris trichiura can cause iron-deficiency anemia;excretes lemon-shaped ova.
  4. Ascaris passes through the lung and can initially cause respiratory symptoms; can also cause biliary obstruction; excretes round,thick-walled ova.
  5. Enterobius is common in children and readily spreads by dust and contaminated linens. Diagnosed when the adhesive cellophane tape test demonstrates worms in the anal area.
  6. Mebendazole or albendazole is effective treatment.

Nematodes Acquired By Skin Penetration

Prevalence, Epidemiology, and Life Cycle

Strongyloides infection occurs less commonly than do infections involving the other roundworms; however, strongyloidiasis is widely distributed throughout the tropics and commonly infects people in the southern United States.

Because Strongyloides can cause a fatal hyperinfection syndrome in the immunocompromised host, clinicians need to be familiar with this parasite. The filariform larvae excreted in the feces are capable of penetrating the skin.

Humans become infected as a result of skin exposure to feces or soil contaminated by feces. Walking barefoot on contaminated soil is the most common way of contracting this infection. After skin penetration, the larvae enter the bloodstream and lymphatics. Subsequently, they become trapped in the lungs, where they enter the alveoli and are coughed up and then swallowed, entering the gastrointestinal tract.

The larvae mature in the upper gastrointestinal tract, where females are able to penetrate the bowel mucosa and deposit their eggs. Eggs hatch in the mucosa, releasing rhabditiform larvae that either mature within the intestine, forming filariform larvae capable of penetrating the bowel wall and causing autoinfection, or are passed in the feces. In warm moist soil, the excreted larvae can mature into the infectious form.

Because Strongyloides can re-infect the human host, an initial infection can persist for 35 to 40 years. The intensity of the infection depends not only on the initial inoculum, but also on the degree of autoinfection. In the immunocompromised host, autoinfection can be intense and can cause severe disseminated illness.

Epidemiology and Life Cycle of Strongyloides

  1. Endemic in warm areas, including the southeast United States.
  2. Larvae in soil contaminated with fecal material penetrate the skin of bare feet.
  3. Larvae enter the bloodstream, invade the lung, crawl up the bronchi to the trachea, are swallowed, and mature in the small intestine.
  4. Adult worms deposit eggs in the bowel wall where the eggs hatch.
  5. Larvae in the bowel can enter the bloodstream, causing autoinfection.
  6. Infection can persist for 35 to 40 years.

Clinical Presentation

A 60-year-old white man was admitted to the hospital for elective cardiac and renal transplantation. He had long-standing diabetes mellitus and had experienced multiple myocardial infarcts leading to severe ischemic cardiomyopathy. He had also developed end-stage diabetic nephropathy Following transplantation, he received mycophenolate mofetil, tacrolimus, and high doses of methylprednisolone.

Intestinal Helminths

One month after transplant, he suddenly developed fever and increasing shortness of breath, associated with a cough productive of clear watery sputum. Two days later, he began coughing up bloody sputum. A social history found that this patient had never smoked. He had never traveled outside of northern Florida, having lived in the area his entire life. Physical examination showed a blood pressure of 133/72 mm Hg, a pulse of 81 per minute, a respiratoryrate of 20 per minute, and a temperature of37.6°C. This patient appeared acutely ill, being short of breath on a Ventimask.

An examination of ears, nose, and throat was unremarkable. The patient’s neck was supple, without lymphadenopathy. Coarse breath sounds were heard bilaterally in the lungs, and the midline sternal wound was clean and without drainage. The heart showed normal SI and S2, with no murmurs, rubs, or gallops. The abdomen was soft and nontender. No organomegaly was noted, and bowel sounds were normal. Some leg edema was noted (3 + in the left lower leg, and 1 + in the right lower leg), but pedal pulses were intact. A neurologic exam uncovered no focal deficits. The patient was able to follow simple commands.

A laboratory workup showed a white blood cell count of 3700/mm3, with 85%, neutrophils. 5.4% lymphocytes, 2% eosinophils, 0.6% basophils, and 4.4% monocytes. Hematocrit was 29%, and platelet count was 301,000/mm3. Serum sodium was 137 mEq/L, and liver function tests were within normal limits. Arterial blood pH was 7.02, with a Paco2 of 59 mm Hg, a Pao2 of 51 mm Hg, an HC03 of 15 mEq/L, and oxygen saturation of 66% (Fio2 95%).

A chest radiograph revealed diffuse bilateral parenchymal opacities consistent with pulmonary edema. A computed tomography scan of the chest showed diffuse reticular interstitial infiltrates consistent with pulmonary edema and two subsequent bronchoscopy exams revealed no pathogens.

Diffuse alveolar hemorrhage was observed. Despite treatment with voriconazole, ganciclovir, and broad-spectrum antibiotics, the patient became hypotensive and remained hypoxic, dying 7 days after the onset of his acute respiratory illness. All blood cultures and sputum culture were negative for pathogens. At autopsy numerous Strongyloides stercoralis filariform larvae were found to be present within the alveolar spaces, alveolar septa, and connective tissue.

Occasional filariform larvae were also seen within the sinuses of the hilar lymph nodes and were iden tided within the myocardial in terstitium. Filariform larvae were seen within the walls of the esophagus, stomach, small bowel, and colon, with the heaviest infestation being observed in the colon.

As observed with other roundworm infections, most patients with Strongyloides have no symptoms when they harbor only a small number of worms. Heavier infestations can cause symptoms associated with the parasite’s life cycle. When the filariform larvae first penetrate the skin, they can cause itching and a papular erythematous rash. Migration into the lungs can cause respiratory symptoms, pneumonia, and peripheral eosinophilia (Loeffler’s syndrome).

Once Strongybides takes up residence in the gastrointestinal tract, the parasite can cause burning abdominal pain that mimics peptic ulcer disease or a colicky abdominal pain that mimics gallbladder disease.

Abdominal pain may be associated with diarrhea and the passage of mucus. Malabsorption, nausea, vomiting, and weight loss may also be present. Because the female worm penetrates the bowel mucosa and the filariform larvae can migrate through the bowel wall, the host responds by producing eosinophils, and peripheral eosinophilia is a prominent finding in strongyloidiasis.

When larvae penetrate the perianal area, a localized snakelike urticarial rash may be seen. A generalized urticarial rash may also be seen. As illustrated by case 3, when asymptomatic individuals who harbor small numbers of organisms receive immunosuppressants such as high-dose corticosteroids, or develop depressed cell-mediated immunity because of severe malnutrition or AIDS, the level of autoinfection can increase markedly, resulting in a hyperinfection syndrome.

Symptoms may include diffuse pulmonary infiltrates, severe abdominal pain, meningitis, and gram-negative sepsis, the latter manifestation being the result of filariform larvae compromising the integrity of the bowel wall. Other clinical manifestations can include hemoptysis and a skin rash.

Periumbilical purpura, diffuse nonpalpable purpura, angioedema, or erythroderma mimicking a drug-related allergic eruption have all been described. As in case 3, eosinophilia is usually absent in the hyperinfectionsyndrome. When an immunocompromised patient presents with this clinical constellation and was raised in the rural south or previously lived in a tropical region, hyperinfection with Strongybides needs to be considered.

Clinical Presentation of Strongybides

  1. Many patients are asymptomatic.
  2. Skin penetration can cause an itchy, erythematous rash.
  3. Lung invasion can produce Loeffler’s syndrome (cough, wheezing, pneumonia,and eosinophilia).
  4. Heavy infection can cause abdominal pain and eosinophilia.
  5. Treatment with high-dose steroids can cause a fatal hyperinfection syndrome (accelerated autoinfection).
  6. Hyperinfection causes diffuse pneumonia, meningitis, abdominal pain, and gram-negative sepsis, hemoptysis,and skin rashes. Eosinophilia is absent.

Diagnosis and Treatment of Strongyloidiasis

  1. Diagnosis is difficult. (Stools do not contain ova.)
  2. Larvae are found inthestool; duodenalendoscopy may be required.
  3. Peripheral eosinophilia may the only finding.
  4. Treat asymptomatic infections.
  5. Ivermectin is the drug of choice.

Diagnosis and Treatment

Because the eggs usually hatch in the gastrointestinal tract, Strongybides ova are rarely seen on stool smear. Diagnosis depends on identifying rhabditiform larvae in the feces or duodenal fluid. Diagnosis requires expertise, because hookworm larvae can easily be misdiagnosed as Strongybides.

At least three stools need to be examined under a low-power (100X) microscope; if results are negative, endoscopy should be considered. The ELISA serum test is sensitive and specific, but it cannot differentiate recent from past infection.

In the Strongybides-inkcted immunocompromised host, the ELISA test may be negative. An important clue is the presence of peripheral eosinophilia, which may increase to between 10% and 20% of peripheral White blood cells. However, lack of eosinophilia, particularly in the hyperinfection syndrome, does not exclude the diagnosis of strongyloidiasis. Ivermectin for 2 days is curative in most cases.

Albendazole can be given as alternative therapy. Because of the potential danger of severe autoinfection, all patients with Strongybides, even asymptomatic patients, should be treated. Patients who develop the hyperinfection syndrome should be treated for a minimum of 7 days. However, despite treatment, the mortality associated with this syndrome remains high.

Patients with a past history of Strongybides or unexplained eosinophilia should therefore be thoroughly examined, tested, and treated before receiving immunosuppressive therapy.


Prevalence, Epidemiology, and Life Cycle of Hookworm

Hookworm (Ancylostoma duodenale and Necator americanus) has been estimated to infect nearly one quarter of the world’s population, being found throughout the tropical and subtropical zones. Infection is prevalent in areas where untreated human feces are allowed to contaminate the soil, and people walk barefoot. Necator americanus (“New World hookworm”) is found primarily in the Western hemisphere, but also in southern Asia, Indonesia, Australia, and Oceania. Ancylostoma duodenale (“Old World hookworm”) is found predominantly in the Mediterranean region, northern Asia, and the west coast of South America. As a result of sanitary waste disposal policies in the United States, hookworm infection has a low prevalence, being found primarily in the southeast. The life cycle of hookworm is very similar to that of Strongyloides. Like Strongyloides, the hookworm filariform larvae penetrate the skin, enter the bloodstream and lymphatics, pass into the lung, migrate up the bronchi to the trachea, are swallowed, and finally take up residence in the upper small intestine. They attach by means of a buccal capsule that is used to suck blood from the host. A single Necator americanus worm can remove 0.03 mL of blood daily, and a single Ancylostoma duodenale worm, 0.2 mL. Worldwide, hookworm is a major cause of iron deficiency anemia. It is responsible for an estimated blood loss of 7 million liters daily — the total blood volume of more than 1 million people! The life cycle of the hookworm also differs from that of Strongyloides in several important ways, and the differences account for hookworm’s milder clinical manifestations. The Strongyloides ova mature quickly, hatching in the bowel wall of the host; hookworm ova mature more slowly, requiring several days of incubation in warm, moist, shady soil. As a result, human hookworm infestation is confined to geographic areas with a warm climate. The longer maturation time for hookworm eggs also means that autoinfection does not occur and that infection by fresh feces is not possible.

Clinical Presentation

When hookworm larvae penetrate the skin they can cause intense pruritus, sometimes called “ground itch.” Itching is associated with local erythema and a papular rash at the site of penetration. As is observed with both Ascaris and Strongyloides, respiratory symptoms and patchy pneumonia associated with peripheral eosinophilia (Loffler’s syndrome) can develop as the worm penetrates the lung. The abnormalities most commonly associated with hookworm are iron deficiency and protein malnutrition. These abnormalities depend both on the worm burden on the nutritional status of the patient. Other complaints may include abdominal pain, diarrhea, and weight loss.

Diagnosis and Treatment

Adult female worms release between 10,000 and 20,000 worms daily, making diagnosis by stool smear simple. The eggs are readily seen using a low-power (100X) microscope. Quantitation of the egg count allows for an estimate of the worm burden. Mebendazole for 3 days is usually curative.

About Hookworm (Necator americanus and Ancylostoma duodenale)

  1. Larvae from the soil penetrate the skin, causing a pruriticrash.
  2. Larvae pass through the lung and can cause Loffler’s syndrome.
  3. Eggs hatch outside of the host in soil (no autoinfection).
  4. Adult worms attach to bowel wall and suck blood.
  5. Iron deficiency anemia is the most common manifestation.
  6. The diagnosis is readily made from observation of ova in the stool.
  7. Mebendazole is the treatment of choice.
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