Pediatric Ascariasis

Ascaris lumbricoides, which causes ascariasis, is the largest of the round worms (nematodes), with females measuring 30 cm x 0.5 cm. It is present in the GI tract (small intestine) of 1.2–1.5 billion individuals in tropical and subtropical areas, making it the most common nematode infection in the world. The number of cases in the United States is estimated to be 4 million, with transmission occurring in the Gulf States and southern New Mexico and southern Arizona. See the image below.

The parasite is acquired through ingestion of embryonated eggs. Ascariasis is usually asymptomatic but can be complicated by several conditions, including appendicitis, bowel perforation, cholecystitis, intestinal obstruction (large numbers), malabsorption (eg, lactose, nitrogen, vitamin A), and pancreatitis. The mortality rate is 5% if complications occur. When the parasite migrates through the lung early in its parasitic cycle, it can also cause pneumonitis. The mainstays of chemotherapy include albendazole, mebendazole, and pyrantel pantoate (for alternatives, see Medication).

A lumbricoides is one of the soil-transmitted helminths (STH), a group that includes 16 worms. Many individuals are infected with 2-3 of the 3 major parasites (ie, A lumbricoides, Trichuris trichiura, and hookworm).

Table 1. Major Soil-Transmitted Helminths ^{[1, 2]} (Open Table in a new window)

Table 2. Minor Soil-Transmitted Helminths ^{[1, 2]} (Open Table in a new window)

By chronically infecting school-aged children, usually in developing countries, these parasites significantly contribute to cognitive deficits, growth stunting, mental retardation, and malnutrition. The 3 most important infections are ascariasis (A lumbricoides) , trichuriasis (T trichiura), and hookworm (N americanus and A duodenale); often, all 3 parasites can be found in a single individual. The combined disease burden of the STHs is estimated to be equivalent to malaria or tuberculosis.

Although A lumbricoides has been present in humans for many thousands of years, science only began to elucidate its biology in the 17th century, and effective chemotherapy was only developed in the late 20th century. The earliest recovered eggs are from the 30,000-year-old Upper-Paleolithic site of Arcy-sur-Cure in Yonne, France. Infertile eggs have been reported in coprolites dating to 2277 BCE from an archeological site at Los Gavilanes, Peru. Desiccated human feces from Big Bone Cave, Tennessee dating to approximately 2177 BCE contained A lumbricoides. In the Nubian aspect of the Nile River, eggs have been recovered inside a mummy dating to 2050-1750 BCE.

In 1683, Tyson discussed " Lumbricus teres …observations on the Round Worm bred in human bodies….that common Round Worm which children u[s]ually are troubled with." In 1758, Linnaeus proposed the name Ascaris lumbricoides. In 1856, Ransom reported that finding eggs in fecal samples was a reliable means of diagnosis. In 1862, Davaine concluded that ingested embryonated eggs produced ascariasis and that the infected host would produce eggs in feces that could pass the infection to another host. In the 1980s, several reviews noted the public health impact of STH infection and suggested control strategies using antihelminthic drugs, some of which were introduced in the 1960s (eg, pyrantel pantoate) and 1970s (eg, mebendazole).

The genus Ascaris is composed of 17 species. A lumbricoides has a high host specificity for humans and, rarely, for pigs. It has been reported in other hosts, including cats, chimpanzees, domestic dogs, gibbons, gorillas, guinea-pigs, lambs, macaques, monkeys, rabbits, rats, and squirrels; however, it has not been demonstrated to achieve sexual maturity or to produce fertile eggs in these hosts.

Ascaris suum has a high host specificity for domestic pigs and, rarely, humans. It has been reported in other hosts, including domestic cattle, gorillas, goats, lambs, monkeys, mice, rabbits, and rats. As with A lumbricoides, A suum has not been demonstrated to achieve sexual maturity or to produce fertile eggs in these hosts. The other 15 species of Ascaris are not reported in humans. Therefore, A lumbricoides does not have an animal reservoir.

Species in the genus Ascaris are transmitted via the fecal-oral route, primarily from ingestion of agricultural products or food contaminated with parasite eggs.

Life cycle

Life cycle data come from investigations of A suum in pigs and A lumbricoides in mice. Little is known about the interaction of A lumbricoides larvae and humans.

Humans ingest A lumbricoides eggs, which contain stage 2 larvae and measure 50-70 µm x 40-50 µm. The eggs hatch in the jejunum and release the stage 2 larvae. They then penetrate the small intestinal wall (some evidence suggests the large intestine), enter the portal venous circulation, and migrates to the liver over 2-8 days. According to data from mice, they measure 258 µm x 14 µm at this stage.

The larvae then migrate via the venous circulation to the pulmonary circulation and to the lungs. Here, the larvae measure 564 µm x 28 µm. They then break into the alveolar spaces, molt to the stage 3 larvae, grow to 1,700–2,000 µm, and molt to stage 4 larva, all over 4-14 days. They then ascend the trachea, are swallowed, return to the small intestine (usually intestine), molt for the final time, and develop into mature adults, all over 14-20 days. The total elapsed time in humans from the time of ingestion to development of mature adults is 18-42 days.

The size range of the mature female is 20-40 cm x 0.5–0.6 cm; the mature male is somewhat smaller at 12-25 cm x 0.3-0.4 cm. The Ascaris genus contains the largest of the nematode parasites; the migration through the tissues appears to confer this size advantage. In general, alimentary tract nematodes (700 species) that migrate through tissues grow faster.

Females produce approximately 200,000 eggs per day (134,462-358,750), although this number fluctuates. In the presence of a male, the eggs are fertilized by copulation. Female-only infections produce nonfertilized eggs that cannot become infective. Male-only infections produce no eggs. The prepatent period (time from ingestion of the egg to detection of the eggs in feces) is 67-76 days (67 d in children < 4 y). A suum infections in humans have a similar life cycle, with a prepatent period of 24-29 days.

The life span of A lumbricoides is 1-2 years. Eggs, fertilized and unfertilized, are released to the environment via feces. Unfertilized eggs do not become infective. Fertilized eggs cannot infect until they embryonate outside the human body under proper conditions. Fertile eggs have 4 layers. The outer layer, which is not always present, consists of an extruded, sticky mucopolysaccharide from the parent female worm. This provides adhesiveness thought to be advantageous, allowing the eggs to stick to many types of surfaces. The other 3 layers are secreted by the embryo and include an outer thin proteinaceous membrane, a middle protein and chitin layer that provides structural strength, and the inner ascaricide layer, which consists of protein (25%) and unsaponifiable lipid (75%). This inner ascaroside layer is selectively permeable and is important for the survival of the egg in various conditions.

To become infective, eggs must complete embryonization while in the soil. The zygote develops into a stage 1 larva and molts to a stage 2 larva within the egg shell. This occurs over 10-14 days at 28-32°C (82.4-89.6°F) and over 45-55 days at 16-18°C (60.8-64.4°F). Several factors favor survival of the egg, including the following:

• Amount of moisture in the soil (ie, clay soil vs sandy soil)

• Protection from direct sunlight (quickly kills eggs)

• Temperatures of 5-34°C (41-93.2°F): A temperatures of 40°C (104°F) is lethal. A temperature of 38°C (68.4°F) is lethal after 8 days.

• Soil humidity of more than 4%: The length of survival is 4.5 hours or less with soil humidity of less than 4%, varies at 4-50% soil humidity, and is best at more than 50% soil humidity

• Formation of stage 2 larvae in the egg

Freezing at –15°C to –12°C (0.4-5°F) for 90 days kills all eggs except those at the single blastomere stage. Depth in the soil is another major influence. Experimentally, under similar climatic conditions, eggs survive 21–29 days on the surface, 1.5 years or less at a depth of 10-20 cm, and 2.5 years or less at a depth of 40-60 cm. Eggs and infective larva can survive over winter to infect in warmer weather. Under experimental conditions, eggs have survived for 6-14 years in the soil. However, in general, eggs are expected to survive 28-84 days. In areas of endemicity, particularly where night soil (human feces) or untreated wastewater is used as fertilizer, the egg concentration is 100 eggs per gram of soil. Eggs can be spread through the soil by earthworms, insects (eg, termites), and other burrowing animals. Egg-contaminated dust can be spread by wind and can lead to human infection via inhalation and swallowing.

In endemic areas eggs contaminate numerous domestic and public sites, including the following:[2]

• Chopping boards

• Coins

• Door handles

• Dust

• Fingers

• Fingernail dirt

• Fruit

• Furniture

• Insects

• Nasal discharge

• Paper money

• Pickles

• Public baths and restrooms

• Public transportation (eg, buses)

• Public squares (eg, sand, lawns)

• School rooms

• Underclothes

• Vegetables

• Wash basins

The average number of female offspring that attain reproductive capacity (reproductive number) produced by one adult female A lumbricoides worm is 1-6.

A lumbricoides and A suum

Evidence suggests that these parasites are separate species, although they are closely related. A lumbricoides infects humans almost exclusively and rarely infects pigs. A suum infects pigs almost exclusively and rarely infects humans. A lumbricoides has occasionally been reported in other animals, such as bears and primates, and A suum has occasionally been reported in cattle or sheep.

Morphologically, they are essentially indistinguishable; however, several reports cite differences in the denticles as a distinguishing characteristic. The morphology of the sex chromosomes exhibits differences, suggesting that the species are different. Species differences in the internal transcribed sequences of the ribosomal DNA have been reported, allowing differentiation. Protein profiles using 2-dimensional electrophoresis reveal reproducible differences. The current consensus is that these are, in fact, different species; however, they are closely related enough biologically that data on the life cycle and pathology of A suum have been extrapolated to humans.

Pathophysiological mechanism

Adult worms move throughout the GI tract and move in and out of orifices (eg, biliary tract, pancreas, appendix, diverticula, Meckel diverticulum) and may become incarcerated, leading to obstructive pathology. The worms may die, leading to inflammation, necrosis, infection, and abscess formation. If they migrate through an existing perforation in the bowel wall secondary to tuberculosis or typhoid, they can cause a granulomatous peritonitis. Larvae during migration may be deposited in the brain, spinal cord, kidney, or other organs, leading to granuloma formation, inflammation, or infection. They may become entwined in a bolus and obstruct the small bowel; this is most common in the terminal ileum, although other, more proximal, sites have been rarely reported.

This condition may be precipitated by the administration of an antihelminthic drug (see Medication). Eggs may be deposited in the liver or biliary tract. If they gain entry to the blood, they are deposited in extraneous sites, leading to local reactions.

Only a small percentage of Ascaris infections produce serious, acute pathology; however, because about one quarter of the human population is infected, the number of cases is significant.

Immunology

Humans make antibodies in response to Ascaris antigens and infection; immunoglobulin (Ig) E is predominant.[3] The response is heterogeneous and is believed to confer some immunity. Evidence also suggests that whatever immunoprotection is conferred is not immunoglobulin-based.

Whether the presence of Ascaris infection increases risk or causes allergic disease or may have a protective effect remains controversial. Several studies demonstrate an association between Ascaris infection, seropositivity, or sensitization and allergic symptoms, sensitization, or asthma risk.[4, 5, 6, 7] Some studies demonstrate a negative association.[8, 9]

An association has been reported between egg excretion in children and increased prevalence of allergic disorders (eg, asthma) compared with children who do not excrete eggs. Because ascariasis and other helminthic infections are long-lived without producing consistently serious symptoms, a significant immunomodulatory relationship must occur between the infection and the human host, the details of which have not been fully clarified. Future research may lead to the development of vaccines and other interventions that will permit better control and treatment of this pervasive parasitic disease.

Frequency

United States

In the United States, more than 4 million individuals are believed to be infected with Ascaris species. Most infected persons are immigrants from developing countries, although the species are endemic in the southeastern United States in rural, low-income families.

During April 2010–March 2013, the Maine Department of Health and Human Services investigated multiple cases of ascariasis that had been reported by health-care providers, veterinarians, and patients. All of the cases were in persons who had lived or worked on Maine farms and had frequent exposure to pigs. After investigation, 14 persons on seven farms in Maine were identified with Ascaris infection.[10]

International

Worldwide, more than 1.4 billion people are infected with ascariasis. The distribution of cases is as follows:

• South America, Central America, and the Caribbean - 8.3%

• Africa and the Middle East - 16.7%

• Asia and the Oceania region - 75%

Ascariasis is present in at least 150 of the 218 countries in the world. Prevalence estimates widely vary among countries and within communities inside these countries.

Mortality/Morbidity

Annual mortality estimates range from 10,000-200,000. Currently, the rate is believed to be 10,000 deaths per year based on more detailed calculations.

Morbidity is proportional to the worm burden. A large majority of cases are asymptomatic. Intestinal obstruction, the most common complication of ascariasis, has been reported with as few as 4 worms. The average worm burden in numerous nonfatal case reports was 59 worms (range, 4-990); in fatal cases, the average worm burden was 659 (range, 23-1978).

Based on numerous reports in the literature, a rough estimate of the occurrence (percent of total complications) of complications is as follows:[2]

• Intestinal obstruction - 63%

• Bile duct obstruction - 23%

• Perforation, peritonitis, or both - 3.2%

• Volvulus - 2.7%

• Hepatitic abscess - 2.1%

• Appendicitis - 2.1%

• Pancreatitis - 1%

• Cerebral encephalitis - 1%

• Intussusception - 0.5%

Other sites of pathology (< 0.5%) include Meckel diverticulum, the gallbladder, ears, eyes, nose, lungs, kidneys, vagina, urethra, heart, placenta, spleen, thoracic cavity, umbilicus, pericecal mass, jejunostomy tube, and erythema nodosum. In endemic regions, ascariasis is a significant part of the differential diagnosis for intestinal obstruction, appendicitis, biliary tract disease, pancreatitis, intussusception, and volvulus.

Public health issues

A lumbricoides and other STHs have been shown to play a significant role in childhood malnutrition, which leads to growth retardation, cognitive impairment, and poor academic performance, resulting in a poorer quality of life and less ability to contribute to society. For the 3 major STHs, the disability-adjusted life years lost is 39 million years. Ascariasis accounts for 10.5 million years, hookworm infection accounts for 22.1 million years, and trichuriasis accounts for 6.4 million years. In comparison, malaria accounts for 35.7 million years.

Deworming with medications is one of many public health strategies to reduce infection rates and worm burden. Many studies demonstrate that after deworming, reinfection at the pretreatment level returns within 2-6 months, particularly, among the poor and socially disadvantaged. Several factors play a role in reinfection, including swimming in polluted rivers, absence of parent (at work) to supervise children, absence of toilet in house, running barefoot, eating without washing hands, geophagy (eating soil), eating unwashed fruits and vegetables, and chores that require contact with floors and ground.[11, 12, 13]  A study by Clarke et al reported that for hookworm and Ascaris lumbricoides, mass deworming led to a significant reduction in prevalence in children when compared to targeted deworming.[14]

 

Race

No racial predilection is recognized.

Sex

Hepatobiliary and pancreatic ascariasis (HPA) occurs with a greater frequency in women than men (76% in one series).[15] In the same series, biliary surgery was more frequent in women (77%) and was an important risk factor for HPA. No other sex association is reported.

Age

Intestinal obstruction predominates in young children (85% of cases occur in children aged 1-5 y) but can occur at any age.

HPA is more common in adults than in children. In one large series of 500 patients, the age range was 4-70 years (median, 35 y).[16]

Most individuals are asymptomatic, even in communities where the prevalence is high. The most common manifestation is asymptomatic passage of an adult worm via the rectum, particularly in children in endemic areas. Rarely, an adult in a nonendemic area who is asymptomatic passes a worm via the rectum and may not be able to recount any significant exposure history. Less frequently, a worm migrates to the oropharynx and is coughed out. Ascaris eggs are often found in the stools of asymptomatic individuals in endemic areas. Some individuals with known significant worm burdens report anorexia, abdominal discomfort, and diarrhea; however, these symptoms cannot be directly attributed to ascariasis.

Pulmonary ascariasis

Symptoms develop 1-2 weeks after infection; they vary from none to life-threatening (rare), depending on sensitization or considerable migrating worm burden. Symptoms include chest pain (burning, aggravated by cough), cough (dry), dyspnea, fever, sputum (may be blood-tinged), and wheezing.

A massive infestation can lead to Löeffler syndrome (ie, transient eosinophilia, transient lung infiltrates); ascariasis remains the most common cause of this syndrome worldwide. In areas of continuous transmission, pulmonary symptoms tend to be less evident. Urticaria is present in 15% of patients and usually develops in the first 4-5 days of illness. Symptoms last 5-10 days but have been reported to last weeks in severe cases.

Intestinal obstruction

Partial or complete obstruction secondary to an entangled worm bolus can occur at any age; however, 85% of cases occur in children aged 1-5 years and most occur at terminal ileum, although they have been rarely reported in the duodenum. The worm bolus may also cause intussusception or volvulus.[17] Severe, sharp, colicky abdominal pain with associated vomiting predominates. The vomit may contain worms. Other common symptoms include fever and diarrhea. Depending on the duration of symptoms and the presence of comorbid conditions (eg, malnutrition), the patient may present with or progress rapidly to sepsis, sepsis syndrome, and septic shock.

Complete obstruction may begin subsequent to the administration of an antihelminthic, particularly in the setting of acute abdominal pain or partial bowel obstruction. Specific concern surrounds the administration of pyrantel pamoate, which causes a spastic paralysis of the worms and accentuates the potential for an obstructive bolus. Complete obstruction has also been reported with piperazine (flaccid paralysis of worms) and mebendazole (single large dose).

In endemic countries, ascariasis accounts for 5-35% of intestinal obstruction cases, particularly in children.

Hepatobiliary and pancreatic ascariasis and other GI diseases

Migrating adult worms (most common), worm fragments, or eggs can cause acalculous cholecystitis, ascending cholangitis, appendicitis, biliary colic, gastric hemorrhage, granulomatous peritonitis, liver abscess, Meckel diverticulum inflammation, obstructive jaundice, pancreatitis, and peritonitis and/or peritoneal granulomatosis (ie, ductal and/or intestinal perforation or migration through perforation secondary to typhoid or tuberculosis). Imaging with CT scanning and ultrasonography reveals the etiology in many cases. The etiology may not be apparent until endoscopic retrograde cholangiopancreatography (ERCP) or surgery is performed.[18]

Extra-GI conditions

Worms may migrate to the upper respiratory tract (ie, throat, nose, lacrimal ducts, and inner ear); to the vagina; and to the kidney, ureter, and bladder (via the vagina).

Experimental studies report that the migrating larvae can enter many tissues, including the brain, kidney, and lymph nodes, but cannot survive. Several case reports have suggested encephalopathy secondary to Ascaris larvae.

Pulmonary ascariasis

In most cases, the lungs are clear or wheezing may be observed. In more severe cases, including ascaris pneumonia, a fever (≤ 102ºF), rales, and wheezing may be observed. Dullness to percussion and bronchial breathing are rare, even in severe cases. Signs may persist for several days.

Intestinal obstruction or partial obstruction

The patient appears ill, often with abnormal vital signs (eg, tachycardia, fever) and may be actively vomiting and reporting severe abdominal pain. The abdomen is moderately-to-severely tender in a diffuse or localized pattern, usually on the right side. A palpable mass (worm bolus) may be observed. Assess for increasing pain, tachycardia, tachypnea, fever, abdominal tenderness, and vomiting, all of which may indicate progression of the obstruction, the development of sepsis, or perforation.

Hepatobiliary disease

Upon presentation, the patient may appear ill, may have abnormal vital signs (eg, tachycardia, tachypnea, fever), and may be actively vomiting. These patients usually report abdominal pain (mild, moderate, or severe). Depending on the pathology, the symptoms may rapidly progress rapidly over hours, as follows:

• Biliary colic: Fever and jaundice are often absent; the worms are usually in the ampullary orifice, and removal results in rapid improvement.

• Acalculous cholecystitis: Pain and tenderness in right upper quadrant are reported. Jaundice may or may not be present. The pain often radiates to the back on the right (see Cholecystitis).

• Ascending cholangitis: The patient is usually critically ill with fever, tachycardia, tachypnea, jaundice, severe pain, and severe right upper quadrant or diffuse abdominal tenderness. The liver is tender and enlarged.

• Pancreatitis: Moderate or severe pain and tenderness in the epigastrium and the left upper quadrant is reported, along with associated vomiting of varying intensity. The pain often radiates to the back on the left (see Pancreatitis and Pancreatic Pseudocyst).

• Hepatic abscess: Severe pain and tenderness is reported in the right upper quadrant. The liver is tender and enlarged.

Ascariasis is caused by ingestion of an embryonated A lumbricoides egg or embryonated A suum egg (see Pathophysiology). Whether A suum and A lumbricoides are separate species remains controversial; however, evidence suggests that they may be distinct entities.

Adult worms may be coughed out, vomited, or passed via the rectum and studied.

A microscopic examination finding of eggs in the feces confirms the diagnosis. This is performed using a direct method (stool mixed with saline) or after concentrating the stool. The Kato-Katz method is the preferred method. Fertilized eggs are easier to identify than unfertilized eggs and decorticate eggs, which are infrequently produced and lack the outer covering. Male-only ascaris infections produce no eggs. Microscopic examination of gastric contents may reveal larvae and eggs. Microscopic examination of sputum may reveal larvae.

Eosinophilia (5-12%) may occur, particularly during the lung migration phase, and can be as high as 50% in ascaris pneumonia.

Serology is used for epidemiological purposes and is not useful for diagnostic purposes.

Chest radiography

According to Löeffler, "The x-ray shadows are variable, unilateral or bilateral, fleecy or dense and small and round or big and irregular; they may be very extensive. They usually appear within three days and disappear in about 10-12 days." Follow-up radiography several months after the acute illness reveals no residual abnormalities.

Abdominal ultrasonography

This is the study of choice for imaging Ascaris worms in the biliary tree. Worms may be single, multiple, in bundles, and moving during the examination.

Abdominal CT scanning[19, 20]

An alternative study to abdominal ultrasonography. A thin line of dye is occasionally seen within the corpus of a worm that has swallowed dye. Within the biliary tree, the worm is more easily visualized on an unenhanced scan. Double-contrast abdominal CT scanning is an excellent study for the evaluation of a patient who presents with acute abdominal symptoms suggestive of intestinal obstruction or another surgical emergency.

Magnetic resonance cholangiopancreatography (MRCP)[21]

This is an alternative to abdominal ultrasonography when it is not feasible, as is the case in some pregnant women. It is good for a general evaluation of the pancreatobiliary organs. It is an alternative to abdominal CT scanning when radiation exposure is to be avoided.

Pulmonary disease

Most cases are asymptomatic.

Most symptomatic cases are mild and self-limited (days) and do not require therapy.

Bronchospasm can be managed with conventional therapy.

Severe cases can be managed with systemic steroids and oxygen supplementation.

Partial small bowel obstruction

In the absence of signs of toxicity (eg, fever, tachycardia, protracted vomiting, peritoneal signs), persisting abdominal pain, or a palpable mass in the same site for more than 24 hours, several conservative management strategies, including supportive care, have proven efficacious. Some of these strategies are as follows:

Intravenous fluids and nasogastric tube with or without an antispasmodic (antimuscarinic)

Intravenous fluids, nasogastric tube, and antibiotics (eg, metronidazole, aminoglycoside, penicillin) with or without an antihelminthic after resolution of symptoms

Saline enema with or without an antispasmodic: Saline enemas are effective in children because 80% have an incompetent ileal-cecal sphincter.

Racine or mineral oil (15-30 mL via nasogastric tube) in conjunction with an antihelminthic: A low dose is used to allow worm death over few days. Several reports note that administration of antihelminthics in patients with partial bowel obstruction can precipitate complete obstruction.

Gastrografin (15-30 mL) via nasogastric tube: The hyperosmolar action results in increased fluid around worms, which favors their separation.

In the presence bowel obstruction, persisting or worsening abdominal pain, or sepsis, surgical intervention is warranted (see Surgical Care).

Hepatobiliary and pancreatic ascariasis

This typically manifests as biliary colic, acalculous cholecystitis, ascending cholangitis, pancreatitis, or hepatic abscess. Ascariasis is a common cause of these conditions in endemic countries.

Aggressive antibiotic therapy for suspected infection and early ERCP to remove the worms are highly efficacious together in the treatment of HPA. During ERCP, worms are sometimes observed to be moving into and out of the duct orifices. Worms are directly removed; when they are out of reach, they can be flushed out with rapid injection of 5-10 mL of diluted dye (eg, 10% Urograffin) into the duct. The entire worm must be removed because fragments lead to infection, granulomas, or stone formation.

After abdominal symptoms improve, antihelminthics can be administered. In one series, the ERCP complication (cholangitis, hypotension) rate was 6%.[15]

In endemic regions, ascariasis is a major etiology for conditions that require acute surgical intervention, including the following:

• Intestinal obstruction

• Appendicitis

• Volvulus

• Intussusception

• Ischemic bowel

• Hepatobiliary obstruction (if ERCP has failed or is unavailable)

• Failure of conservative management of partial bowel obstruction

• Severe abdominal pain or tenderness with signs of toxicity

• Persisting or worsening abdominal pain

• Severe abdominal pain with a palpable mass in the same site for longer than 24 hours

Surgical procedures used in the management of the bowel obstruction secondary to ascariasis include the following:

Milking the worms through the ileo-cecal valve: This is recommended for a worm bolus in the distal ileum. Milking proximal boluses may cause damage to the bowel. This process has been facilitated by oral administration of mineral oil (15-30 mL).

Enterotomy to remove the bolus if milking is unsuccessful

Segmental resection of damaged bowel with or without temporary ostomy, as needed: Anastomosis should be 2-layers and end-to-end to prevent residual worms from migrating through the anastomosis into the peritoneal cavity, which has been reported.

Surgeon

Any patient with acute abdominal pain and tenderness suggestive of an acute surgical process warrants a surgical consultation. If a double-contrast (ie, oral and intravenous dye) CT scan can be performed and the patient is not toxic or septic, the consultation may be deferred until the results of the scan are available. If the patient is toxic or septic, the surgical consultation should take place immediately.

Critical care specialist

Any patient who appears to be septic may qualify for early goal-directed therapy.

GI specialist

Any patient who is diagnosed with HPA or in whom a high index of suspicion for this diagnosis is noted warrants an immediate GI consultation for emergent ERCP. This procedure is often both diagnostic and therapeutic, with removal of the offending worm and relief of the obstruction.

Advise patients with known ascariasis to avoid peppery and spicy foods because they induce increased worm migration.

Several drugs are efficacious for the treatment of ascariasis, including the asymptomatic intestinal phase; this involves the periodic deworming of children (symptomatic and asymptomatic), a reduction of the public health burden in selected communities, treatment during the pulmonary phase (rarely), and treatment of complications of the infection (some but not all).

The drugs of choice in the United States include pyrantel pamoate and the benzimidazoles, albendazole and mebendazole. The efficacy for albendazole, mebendazole, and pyrantel is 88%, 95%, and 88%, respectively. For hookworm, a common infecting STH, the efficacies for the same medications are 72%, 15%, and 31%, respectively; therefore, using albendazole is more efficacious, when a coinfection of ascaris and hookworm is suspected.

In general, antihelminthic drugs are not recommended in patients from endemic areas (areas with large worm burdens) who have acute abdominal pain, with or without partial bowel obstruction, because of the risk of precipitating complete obstruction. This complication has particularly been associated with pyrantel pamoate, which causes a spastic (depolarizing) paralysis of the worms, increasing the potential for worm bolus formation; however, this complication has also been reported in association with piperazine, mebendazole, and albendazole. In cases with acute abdominal symptoms, conservative treatment is best and the antihelminthic should be administered after symptoms subside (see Medical Care).

In pregnancy, the drug of choice is pyrantel pamoate. It is recommended in symptomatic cases only and should be administered after the symptoms subside in response to conservative therapy (see Medical Care).

Two other alternative medications with demonstrated efficacy in the treatment of ascariasis include nitazoxanide, which was approved by the US Food and Drug Administration (FDA) in December 2002 for treatment of Giardia lamblia and Cryptosporidium parvum in patients aged 1-11 years, and levamisole, which was FDA approved in June 1990 for use in treatment of colon cancer and although has demonstrated efficacy in the treatment of ascariasis since at least the early 1980s.

Albendazole has the advantages of pediatric dosing for individuals younger than 2 years, good tolerability, and efficacy in the treatment of ascariasis, hookworm infection, pinworm infection, strongyloidiasis, and trichuriasis. Nitazoxanide has similar efficacy, but dosing has not been established in patients younger than 1 year.

The World Health Organization (WHO) recommends 4 drugs in STH control programs (ie, ascariasis, hookworm infection, pinworm infection, strongyloidiasis, and trichuriasis): albendazole, levamisole, mebendazole, and pyrantel embonate.[22, 23] All four have a cure rate of more than 90% in patients with ascariasis. Albendazole has a 60-90% cure rate for hookworm infection, 20-90% for strongyloidiasis and trichuriasis, and more than 90% for pinworm infection. Mebendazole is somewhat less efficacious. Levamisole is somewhat less efficacious for hookworm infection (20-90% cure rate) but significantly less so (20-60% cure rate) for pinworm infection, strongyloidiasis, and trichuriasis. Pyrantel embonate has poor efficacy (0-20% cure rate) for strongyloidiasis and trichuriasis.

In developing countries, many patients (50-92%) with acute abdominal symptoms compatible with partial and/or subacute bowel obstruction and a high degree of suspicion for ascariasis as the etiology (5-35% of all obstructions) respond to conservative measures without requiring surgery or progressing to sepsis (see Medical Care).

Class Summary

Parasite biochemical pathways are different from the human host; thus, toxicity is directed to the parasite, egg, or larvae. Mechanism of action varies within the drug class.

Mebendazole (Emverm)

Causes worm death by selectively and irreversibly blocking uptake of glucose and other nutrients in susceptible adult intestine where helminths dwell. Causes slow immobilization and death of organisms. Administration over 3 d reduces risk of worm bolus formation. Available as a 100-mg chewable tablet that can be swallowed whole, chewed, or crushed and mixed with food.

Albendazole (Albenza)

Broad-spectrum anthelmintic agent effective against Ascaris species, hookworm, tapeworm, liver fluke, and pinworms. Decreases ATP production in worm, causing energy depletion, immobilization, and finally death.

Pyrantel pamoate (Antiminth, Pin-Rid, Pin-X)

Depolarizing neuromuscular blocking agent. Inhibits cholinesterases, resulting in spastic paralysis of worm. Poorly absorbed from GI tract and partially metabolized in liver.

Piperazine citrate (Vermizine)

No longer available in the United States. Causes flaccid paralysis of the helminth by blocking response of Ascaris species worm to acetylcholine; thus, expels the worm by normal intestinal peristalsis. Readily absorbed from GI tract, partially degraded in vivo, and excreted in urine. Exhibits wide therapeutic index.

The dose of piperazine citrate is expressed in terms of piperazine hexahydrate. For example, piperazine hexahydrate 250 mg = the anhydrous form of piperazine citrate 275.75 mg. The PO solution is equivalent to 500 mg/5 mL of piperazine hexahydrate. The dosage for piperazine (granules) solution, susp, and tabs are not interchangeable.

Ivermectin (Stromectol)

Binds selectively with glutamate-gated chloride ion channels in invertebrate nerve and muscle cells, causing cell death. Half-life is 16 h; metabolized in liver.

Levamisole (Ergamisol)

Not available in the United States. L-isomer of tetramisole, a potent anthelmintic. Has demonstrated a broad range of pharmacologic activities, some of which include the modulation of the immune system. Restores immune function and stimulates T-cell activation and proliferation, monocyte function and neutrophil chemotaxis, adhesion, and mobility.

Nitazoxanide (Alinia)

Elicits antiprotozoal activity by interference with pyruvate:ferredoxin oxidoreductase (PFOR) enzyme–dependent electron transfer reaction, which is essential to anaerobic energy metabolism. Available as a PO suspension (20 mg/mL).

Prevention consists of improved sanitation and education about the disease. In endemic areas, school screening has demonstrated effectiveness in detection and early treatment of asymptomatic carriers.[24] Benefits in health and educational performance have been reported with large-scale treatment of school-aged children every 6 months in countries where ascariasis is a public health problem.

The WHO ranks STH infections as the prime cause of infectious disease in children aged 5-14 years. Three strategies have been identified to control STH infections: chemotherapy, health education, and sanitation. Sanitation in developed countries is currently too expensive to be provided to the more than 2 billion people who lack safe disposal of their feces. In terms of education, better-educated households have better health. Specifically regarding STH, studies in Sri Lanka demonstrate that the more education mothers receive, the lower the prevalence of STH infection in their children. The challenge is to educate communities without clashing with local customs and cultures.

That leaves chemotherapy as the current mainstay for control of STH infection, although this strategy is limited by the enormous ongoing burden of environmental contamination. The goal is to reduce the intensity of STH infections in the community. Three chemotherapy strategies have been field tested for reducing the intensity of STH infections in the community: universal/mass treatment (all ages, both sexes, no exceptions),[25] targeted treatment (defined age, sex, or other identifier), and selected treatment (current diagnosis of STH infection). Only universal and targeted treatments are effective. Selected treatment does have a role, although it does not reduce community STH infection intensity. Treatment delivered to children through the schools at intervals of a year, 6 months, 4 months, or 3 months has been shown to be effective. When given every 3 months to children in one study, a significant decrease in adult intensity was noted, as well.

Complications include the following:

• Intestinal obstruction: In some instances, treatment that involves an antihelminthic in an asymptomatic individual who is passing Ascaris eggs or who is involved in a mass treatment program precipitates partial or complete bowel obstruction. This situation cannot be predicted. If the patient has abdominal (nonsurgical) pain that may be related to ascariasis, conservatively treating the patient without administering an antihelminthic until the symptoms abate and then treating with antihelminthics under close observation is judicious (see Medical Care). Untreated intestinal obstruction may lead to bowel necrosis, peritonitis, sepsis, and death.

• Volvulus

• Intussusception

• Hepatobiliary disease

• Pancreatitis

• Appendicitis

• Bowel perforation

• Peritonitis

• Sepsis, sepsis syndrome, septic shock

• Ascaris pneumonia

• Löeffler syndrome

• Asthma exacerbation

• Encephalitis

• Other ectopic migration (see Mortality and Morbidity)

Prognosis is excellent for the treatment of asymptomatic ascariasis. In some instances, a second treatment may be necessary to completely clear the worms. This has been demonstrated to significantly reduce the number of complications. The concern in endemic countries is that reinfection will occur.

In children in endemic countries, treatment results in demonstrated improvement in cognitive development, school performance, and weight gain.

The prognosis is good for patients with partial bowel obstruction who do not have toxicity and who are nonseptic, provided the patient is treated early with conservative management (see Medical Care).

The prognosis in patients with bowel obstruction who do not have toxicity or sepsis is good if the patient is treated early with appropriate surgical intervention (see Surgical Care).