Ascariasis

Ascariasis is the most common helminthic infection, with an estimated worldwide prevalence of 804 million cases in 2013.[1, 2, 3]  It is caused by Ascaris lumbricoides, which is the largest parasite from the class of nematodes commonly known as roundworms. Usually A lumbricoides or A suum infection is asymptomatic. Ascariasis is most prevalent in children of tropical and developing countries,[4] where they are perpetuated by contamination of soil by human feces or use of untreated feces as fertilizer and the water or food contaminated by the eggs is ingested.[5] For more information on ascariasis in children, see the Medscape article Pediatric Ascariasis. Symptomatic ascariasis occurs during the adult worm's intestinal or larval migration phase and may manifest as growth retardation, pneumonitis, intestinal obstruction, or hepatobiliary and pancreatic injury. Ascariasis may exist as a zoonotic infection associated with pigs and use of hog manure and is caused by Ascaris suum, [6, 7] which is very similar to Ascaris lumbricoides [8, 9] but, in most endemic areas, it is most likely transmitted from person to person.[10]

The image below depicts a roundworm that infects humans through soil contaminated by human feces.

See Common Intestinal Parasites, a Critical Images slideshow, to help make an accurate diagnosis.

Ascaris lumbricoides is the largest of the common nematodes (roundworms) that infect humans. Adult A lumbricoides are white or yellow and 15-35 cm long (Fig 9-12-1). They live 10 to 24 months in the jejunum and middle ileum of the intestine. Each day, female A lumbricoides produce 240,000 eggs (Fig 9-12-12), which are fertilized by nearby male worms. The eggs are oval, 45-70 x 35-50 microns in size with a thick outer shell. A Chinese study showed that 45% of infected persons shed only fertilized eggs, 40% shed fertilized and unfertilized eggs, and 20% shed only unfertilized eggs. Unfertilized eggs accounted for only 6-9% of eggs shed. Fertilized eggs released into favorable soil may become infectious within 5-10 days.[11] Eggs may remain viable in soil for up to 10 years. Infection occurs through oral ingestion of food or water contaminated by soil that contains embryonated eggs from human or pig feces that hatch in the small intestine within 4 days or direct ingestion of infected uncooked pig or chicken liver containing larvae. Although the eggs can persist in water treated by chemicals, they can be eradicated by boiling or filtering water sources. (Fig 9-12-12).[12, 13]

Adult worms (females 20 to 35 cm; males 15 to 30 cm) (1) live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces (2). Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks (3), depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed (4), the larvae hatch out of eggs (5), invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs (6). The larvae mature further in the lungs (10-14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed (7). Upon reaching the small intestine, they develop into adult worms (1). Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1 to 2 years.[14]

[14]  Reproduced from: Centers for Disease Control and Prevention. DPDx: Ascariasis. Available at: http://www.cdc.gov/dpdx/ascariasis/index.html.

Larvae are released from the Ascaris eggs in the small intestine within 4 days of ingestion. These larvae migrate through cecum and proximal colon and penetrate the intestinal mucosa and reach the liver via the portal circulation. They enter the heart through the hepatic veins, infiltrate the lymphatics and end up in the lungs where they mature in about 2 weeks. The mature larvae cause symptoms of pneumonitis and ascend the trachea by the cough reflex. They are swallowed by the host to mature into adult worms in the intestinal tract where each female worm lays over 200,000 eggs daily within 1 to 11 weeks of infection.[15]  Eggs are infective only if both male and female worms are present. Although the majority of worms are found in the lumen of the jejunum, they may be seen in any part of the intestine as well as ectopic sites such as the kidneys or brain. Adult worms can live up to 2 years and are passed in the stool. The worm burden increases with reinfections in endemic areas and can be as high as 200 worms per individual.[16]

A significant exposure may produce subsequent pneumonia and eosinophilia. Symptoms of pneumonitis include wheezing, dyspnea, nonproductive cough, hemoptysis, and fever. Larvae are expectorated and swallowed, eventually reaching the jejunum, where they mature into adults in approximately 65 days. Adult worms feed on digestion products of the host. Children with a marginal diet may be susceptible to protein, caloric, or vitamin A deficiency, resulting in retarded growth and increased susceptibility to infectious diseases such as malaria.[17] Large and tangled worms may cause intestinal (usually ileal), common duct, pancreatic, or appendiceal obstruction. Mean worm burden varies from more than 16 to 4 and appears related to host factors, particularly age, geophagy,[18] and immunity. Worms do not multiply in the host. For infection to persist beyond the 2-year maximum lifespan of the worms, re-exposure must occur. Some children appear to become very heavily infested, probably from multiple cumulative exposures over time and/or relative immunodeficiency.[19]

Ascaris lumbricoides suum, a swine nematode, is thought responsible for zoonotic infection. Distinguishing this worm from A lumbricoides is difficult, as it differs by only 6 (1.3%) nucleotides in the first internal transcribed spacer (ITS-1) and by 3%-4% in the mitochondrial genome sequence.[19] A suum appears to responsible for most ascariasis cases in well-developed countries with excellent sanitation (eg, Denmark,[20] United States,[9] UK[21] ). In this setting, infected persons have a low worm burden and may present with only cough, acute eosinophilia, or eosinophilic liver lesions visible on CT scans. However, a molecular genetic study from China casts doubt that infections in pigs are the cause of most human infection.[10]

Ascariasis is transmitted mainly by ingestion of food or water that has been contaminated by the fertilized infected eggs of A. lumbricoides or A. suum. Poor hand hygiene, polluted water and unsanitary food preparation play major role in reinfections in endemic areas and lingers in families and group homes with shedding of eggs by asymptomatic individuals. No immunity develops with past infections or treatment and other parasitic infections may coexist. A. suum infection is common in pig farmers and eating uncooked meat or vegetables grown in soil fertilized by pig manure.[22, 23]

Frequency

United States

In 1974, an estimated 4 million people, mainly in the southeast United States, had ascariasis. Recent estimates of ascariasis prevalence are much lower. Immigrants from countries with a high prevalence of ascariasis comprise most recent cases. In the past, it was most prevalent in the southeast United States, but after introduction of modern waste management systems and sanitation, the numbers have sharply declined.[24]

International

The prevalence of ascariasis is highest in children aged 2 to 10 years, with the highest intensity of infection occurring in children aged 5 to 15 years who have simultaneous infections with other soil-transmitted helminths, such as Trichuris trichiura and hookworm. The warm, wet climate of tropical countries with suboptimal sanitation is a very favorable environment for the transmission of helminth infections. The prevalence decreases after the age of 15 years. A Vietnamese study found that adult women living in rural areas, especially those exposed to human night soil and living in households without a latrine, were at surprisingly high risk for ascariasis.[25] In regions with soil-transmitted diseases, ascariasis tends to be more geographically dispersed than Trichuris or hookworm.[26]

The Centers for Disease Control and Prevention (CDC) estimated that that there are more than one billion cases of A. lumbricoides infection worldwide.[27, 28] Ascariasis rates in 2005 were as follows: 86 million cases in China, 204 million elsewhere in East Asia and the Pacific, 173 million in sub-Saharan Africa, 140 million in India, 97 million elsewhere in South Asia, 84 million in Latin America and the Caribbean, and 23 million in the Middle East and North Africa. Between 1990 and 2013, the disease burden of ascariasis was estimated to have decreased by 75%.[2] Survey data, however, are corrupted by lack of standardized diagnostic methods.[29]

Because the lifespan of adult worms in the intestine is only 1 to 2 years, persistent infection requires frequent re-exposure and reinfection. The frequency and intensity of infection remain high throughout life in endemic areas and pose a risk to both elderly and young persons. In a recent study in rural southwest Nigeria, the intensity of excreted eggs per gram of feces among infected persons was 2371 for Ascaris species, 1070 for hookworm, and 500 for Trichuris species, with only slightly lower rates among persons in urban areas.[30]

Estimates of disability-adjusted years of life due to ascariasis have fallen because of development and management programs during the 1990s, especially in Asia, but still constitute a significant burden in some countries. Current ascariasis-associated disability-adjusted life years (DALYs) are approximately 1 million,[2] with nonsurgical morbidity mostly associated with wasting syndrome in children.[2]

A suum infections have been seen in countries where pigs are raised and pig manure is used as a fertilizer.[12, 31]  These have been reported in China,[32]  Japan,[31] Thailand, Lao People's Democratic Republic, Myanmar,[33] the United States,[34]  and Europe.[8, 20]

Mortality/Morbidity

Most A lumbricoides or A suum infections are asymptomatic especially in adults. Severe, symptomatic ascariasis is most common in children. Intestinal obstruction caused by heavy worm burden (≥60) is the most common presenting manifestation of disease. An estimated 2 per 1000 infected children develop intestinal obstruction per year.[35] Among children aged 1 to 12 years who presented to a Cape Town hospital with abdominal emergencies between 1958-1962, symptomatic A lumbricoides infection was responsible for 12.8% of cases, with 68% of those due to intestinal obstruction, usually at the terminal ileum. The peak incidence was at age 2 years in a series from Colombia and age 4.8 years in a series from Turkey.

The prevalence of infection in Vietnam is estimated at 44.4%, more commonly in the northern peri-urban and rural areas of the country.[36] In Vietnam, vegetable cultivation using night soil fertilizer places adult women at especially high risk. Children with chronic ascariasis may experience decreased growth and development due to decreased food intake.

The disease is commonly symptomatic during the early phase larval migration stage with pulmonary symptoms and in late-phase adult worm intestinal stage and manifests as intestinal, hepatobiliary, or pancreatic symptoms. Within weeks of new infection, pulmonary manifestations may be seen but are uncommon in patients from endemic areas or reinfections. This was demonstrated by a study of 13,00 patients in and endemic region of Columbia with only 4 cases of Loeffler syndrome.[37, 38, 39]

Adults with ascariasis are more likely to develop biliary complications due to migration of adult worms, possibly provoked by other illnesses such as malarial fever. In Damascus, of 300 adults referred for complications of ascariasis between 1988 and 1993, 98% had abdominal pain, 4.3% had acute pancreatitis, 1.3% had obstructive jaundice, and 25% had worm emesis. Twenty-one to 80% of patients had undergone previous cholecystectomy or endoscopic sphincterotomy.

Because of improved access to care and availability of ultrasonography, biliary ascariasis has been increasingly recognized and reported from endemic areas.[40] In Kashmir, it may account for up to 36% of patients presenting with biliary or pancreatic disorders and is reported to cause 20% of biliary disease in the Philippines.[40]  A review of biliary ascariasis suggests that this association may be causative as a result of dilatation of the common bile duct and elevation of cholecystokinin levels with resultant relaxation of the sphincter of Oddi.[41]

A report from India indicated that, of consecutive patients diagnosed with biliary ascariasis, 80% presented with recurrent abdominal pain, 30% with acute cholecystitis, 25% with obstructive jaundice, 25% with cholangitis, only 5% with pancreatitis, 5% with perforated viscus, and 5% with hepatolithiasis. Only 25% of the Indian patients required surgery, and conservative medical therapy with oral anthelminthics has recently been recommended.[40]

A postcholecystectomy syndrome of pain and jaundice is frequently due to ascariasis in endemic areas, presumably owing to enhanced patency of the biliary system after surgical or endoscopic sphincterotomy.[42]

Intestinal obstruction, usually of the terminal ileum in children, is the most commonly attributed fatal complication, resulting in 60,000 deaths per year.[3] Besides direct obstruction of the bowel lumen, toxins released by live or degenerating worms may result in bowel inflammation, ischemia, and fibrosis.

Age

See International and Mortality/Morbidity.

Universal treatment is effective in endemic areas regardless of asymptomatic infections. However in non-endemic areas, screening or empiric treatment is based on the high pretest probability, especially in patients with history of travel to endemic areas or exposure to infected populations. Immediate cure rates after single-dose albendazole in South Africa were 95%, with egg reduction rates of more than 99%.[43]

Most treated patients become reinfected within months unless they are relocated to an area of significantly improved sanitation.

Because of the limited (2-year) lifespan of the disease, education on hand hygiene, fecal waste disposal, and general public health could be instrumental in breaking the cycle of infection in households and communities.[3]

Early symptoms of ascariasis, during the initial lung migration (first 10-14 days after ingestion) include cough, dyspnea, wheezing, urticaria, hemoptysis, and chest pain.[2] This may be seasonal after rains in some countries, such as Saudi Arabia. Returning travelers could also present with Loeffler syndrome of eosinophilic pneumonia if exposed in a high-risk environment.

Abdominal pain or discomfort, distension, colic, nausea, anorexia, and intermittent diarrhea may be manifestations of partial or complete intestinal obstruction by adult worms during the late phase of infection six to eight weeks after egg ingestion. Adult worms are passed in the stool and can be seen on stool examination.

Jaundice, nausea, vomiting, fever, and severe or radiating abdominal pain may suggest cholangitis, pancreatitis, hepatic abscess, or appendicitis.

Within 1 to 2 weeks of new infection following egg ingestion, Ascaris larvae migrate through lungs causing eosinophilic pneumonitis. This is known as the Loeffler syndrome. Parasitic infections with Strongyloides stercolis, Ancylostoma duodenale, Necator americanus, Toxocara, schistosomiasis, and lymphatic filariasis can present with a similar pathological presentation. Patients may present with fever, dry cough, dyspnea, wheezing, and urticaria that subsides within 5 to 10 days. Rales, wheezes, and tachypnea may develop during pulmonary migration, particularly in persons with a high worm burden. Urticaria and fever may also develop late in the migratory phase.

Abdominal distension is nonspecific, but is common in children with ascariasis.

Abdominal tenderness, especially in the right upper quadrant, hypogastrium, or right lower quadrant, may suggest complications of ascariasis.

Evidence for nutritional deficiency due to ascariasis is strongest for vitamins A and C, as well as for protein, as indicated by albumin and growth studies in children observed prospectively. Some studies have not confirmed nutritional or developmental delay due to ascariasis.

Complications of ascariasis are related to worm burden and location of the relatively large nematode. They include acute abdomen, upper GI bleeding, small-bowel obstruction, volvulus and intussusception, peritonitis, biliary colic, acute cholecystitis, acute pancreatitis, acute cholangitis, and hepatic abscess. As such, ascariasis could be considered a potential cause of surgical emergency in endemic areas.[2]

Stool examination for ova andparasites:

Visualization of large, brown 60 µm X 50 µm trilayered eggs is confirmatory. However, stool examination may be negative for ova for up to 40 days after infection because of the time needed for migration and maturation of the worm. The outer surfaces of fertilized eggs have an uneven mucopolysaccharide coat. Other parasitic coinfections can also be detected and are common. However, it may take 40 days for eggs to appear in the stools and if only infested with male worms, there may be no eggs at all.

Adult A lumbricoides worms can be visualized in the stool or the patient may notice them when passed. Mature worms are 35 cm long (females 20 to 35 cm; males 15 to 30 cm) and 6 mm in diameter. The worms are white or pink and are tapered at both ends.

Sputum examination:

Ascaris larvae may be observed in microscopic wet preparations of sputum during the pulmonary migration phase.

CBC with differential:

Results will reveal peripheral eosinophilia during the tissue migration phase of the infection. It may take weeks to resolve, but can be masked with the administration of steroids. It is more likely in the early lung phase than the late phase.[31, 37]

Serological tests:

Serum IgG and IgE are elevated during early infection, but this finding is not clinically useful.

Radiologists practicing in Europe and North America should be familiar with unexpected but specific abnormalities associated with parasitic disease, especially in this age of increasing migration and tourism.[44]

Chest radiographs/CT chest: Images may show fleeting opacities during pulmonary migration. Bilateral, round infiltrates or ground glass opacities with ill-defined margins with variable sizes ranging from several millimeters to centimeters may be seen in patients with high eosinophilia. Infiltrates may show migratory pattern or become confluent as the worms move in the lung tissue.

Abdominal radiographs/ CT abdomen/ MRI: Plain radiographs may show aggregated worms in the intestine, especially in children. A whirlpool pattern of intraluminal worms may be visible. Narrow-based air fluid levels without distended loops of bowel on upright plain films suggest partial obstruction. Wide-based air fluid levels with distended loops suggest complete obstruction. Barium swallow study may also reveal adult worms as filling defects or if ingested by worms show their alimentary canal.[16]  Worms have been increasingly identified in the biliary duct or gallbladder with ultrasonography and CT scanning.[45] Liver granulomata due to A suum infection have been described as ill-defined, 3- to 35-mm, nodular- or wedge-shaped lesions in the periportal or subcapsular regions.

Computed tomography (CT) scanning or magnetic resonance imaging (MRI) may demonstrate worms in the bowel. CT or MRI may demonstrate adult Ascaris worms in the liver or bile ducts in case of hepatobiliary disease. Magnetic resonance cholangiopancreatography (MRCP) may detect adult worms in bile or pancreatic ducts. Ultrasonography can also be useful for demonstration of hepatobiliary or pancreatic infestations.

Endoscopic retrograde cholangiopancreatography (ERCP) has become a commonly used procedure for both diagnosis of ascariasis and removal of worms from the biliary tract. The ease of diagnosis and therapy in the same setting makes ERCP particularly valuable when used with real-time ultrasonography. The combined procedures yield a sensitivity of nearly 100%.[41]

Specific patient and community-wide public health approaches to ascariasis should be coordinated. Individual patient deworming can prevent surgical and nutritional complications and can serve as an opportunity to investigate, educate, and treat other family members and neighbors. Community- and school-based epidemiological deworming programs should be administered under WHO guidelines and would be subject to diagnostic methods used to determine pretherapy and posttherapy prevalence. Newer highly sensitive diagnostic methods instead of classic stool sampling would be most useful for communities with moderate (30%-70%) prevalence, rather than very high or low prevalence,[46] whereas they may be more useful for screening in adults, who have lower worm burden and lower prevalence than children.[4]

In an area with high prevalence of soil-transmitted helminth infection, intestinal ascariasis should be suspected in patients with nonspecific abdominal discomfort, anorexia, nausea, or vomiting with or without the intestinal, biliary or pancreatic complications. The diagnosis is established via stool microscopy for ova or parasites. If the patient has suspected intestinal obstruction, radiographic imaging can reveal the etiology.

 

Early phase:

Management of pulmonary manifestations in the early phase of Ascaris infection consists of supportive care with inhaled bronchodilators for wheeze and cough or systemic corticosteroids for severe pneumonitis. However, it is imperative to rule out Strongyloides by examination of sputum and stool for Strongyloides larvae and serologic testing due to concern of Strongyloides hyperinfection syndrome-associated multiorgan system dysfunction and septic shock secondary to steroid administration.

Anthelminthic therapy is generally not administered during the pulmonary phase and is delayed to 2 months after resolution of pulmonary symptoms, because the efficacy of drugs against larvae in the lungs is uncertain.

Late phase:

Management of intestinal manifestations in the late phase of Ascaris infection include management of the individual presentation or complications such as intestinal obstruction, malnutrition, hepatobiliary involvement, and pancreatitis.

Malnutrition

Due to high parasitic burden, ascariasis results in malnutrition secondary to poor intestinal absorption of lactose, proteins and vitamins A and C. This is seen as growth retardation and poor cognitive development in young children, with improvement seen after treatment. However, due to the demographics of the disease in areas with poor housing and sanitation, there are socioeconomic factors that confound the nutritional deficiencies as well.[47]

Hepatobiliary and pancreatic involvement

Ascariasis can cause obstructive jaundice, ascending cholangitis, biliary colic, biliary strictures, liver abscesses, and bile duct perforation with peritonitis during the migration phase of the adult worms. It can also cause acalculous cholecystitis due to parts of dead worms serving as a nidus for biliary stones; this results in recurrent pyogenic cholangitis if present in the bile duct or pancreatitis if obstructing the pancreatic duct. This accounts for about a third of the biliary and pancreatic disease.[48]

Other manifestations

Migration of worms outside the gastrointestinal tract may produce atypical presentation including ectopic sites such as the mouth, nose, esophagus, lungs, lacrimal ducts, umbilicus, inguinal canal, or skin. This is unusual and is seen in physiological stress associated with febrile illness, anthelmintic medications, starvation, or other acute serious illness.

 

Because of the risk for complications, patients with ascariasis who have other concomitant helminthic infections should always undergo treatment for ascariasis first. Medical therapy is usually not indicated during active pulmonary infection, because dying larvae are considered a higher risk for significant pneumonitis. Pulmonary symptoms may be ameliorated with inhaled bronchodilator therapy or corticosteroids, if necessary. Initial treatment for uncomplicated disease is anthelminthic therapy. If other parasitic coinfections are detected, they will have to be treated as well. It is important to note that treatment does not prevent reinfection and if eggs or worms are detected after treatment, the patient should repeat the course. These anthelminthic agents are active against adult worms but not against larvae and may not be effective until all the worms are mature.

Albendazole 400 mg one dose orally is the drug of choice for ascariasis in stable patients older than 12 months with uncomplicated infection.[2] A 2012 study from Indonesia showed that albendazole provided statistically significant better sterilization of Ascaris eggs than mebendazole but equivalent cure rates and egg reduction rates.[49] A 2017 systematic review and meta-analysis of 34 studies demonstrated a 95.7% cure rate with single-dose albendazole.[50] Ascariasis commonly coexists with whipworm infection, which appears to be most susceptible to triple-dose mebendazole.[51] Albendazole is not recommended during pregnancy; pyrantel pamoate is the drug of choice in these cases. Adverse effects include transient gastrointestinal discomfort, headache, and, rarely, leukopenia.

Mebendazole (100 mg bid for 3 days or 500 mg orally single dose) is alternative therapy. Mebendazole is not recommended during pregnancy; pyrantel pamoate is the drug of choice in these cases. Randomized clinical trials indicate high cure rates with single doses of albendazole and mebendazole, but this is insufficient for treatment of concomitant hookworm or Trichuris infection.

Ivermectin can be given as an alternative in a dose of 150-200 micrograms/kg bodyweight.[2]

Paralyzing vermifuges (eg, pyrantel pamoate, ivermectin) should be avoided in patients with complete or partial intestinal obstruction, because the paralyzed worms may necessitate or further complicate surgery. Pregnant women can be safely treated with a single dose of pyrantel pamoate (11 mg/kg up to 1g). Adverse effects include gastrointestinal disturbances, headaches, rash, and fever.

In the setting of mass treatment, the WHO allows use of albendazole for pregnant women in the second and third trimesters. [52]  Ivermectin (200 mcg/kg single dose) causes paralysis of adult worms.

Vitamin A supplementation improved growth development of children in Zaire; deworming did not improve growth development in this study.[53]

Retreatment: Drug therapy affects only adult worms. If the patient lives in an endemic area or has recently relocated, he or she may still be carrying larvae that are not yet susceptible. Such patients should be re-evaluated in 3 months and retreated if stool ova persist. In endemic areas, reinfection rates approach 80% within 6 months.

Nitazoxanide, a drug used primarily for protozoal infection, was shown to have 89% clinical efficacy for the treatment of ascariasis in rural Mexico, and may offer a future alternative to other medications.[54]

Compliance with antiparasitic drugs, especially at the community level, has emerged as a concern, particularly for the effectiveness of community-wide therapy.[29, 55]

Newer agents are being developed because of concern for emergence of resistance potentially associated with mass deworming campaigns.[56]

Intestinal obstruction:

Ascaris infection with a high worm burden can cause acute intestinal obstruction by obstructing the bowel lumen; this is most commonly seen at the ileocecal valve, but migrating worms can also cause appendicitis. In endemic regions, it is the most common cause of acute abdominal surgical emergencies accounting for about 35 percent of all bowel obstructions. Out of these obstructions, approximately 85 percent of are seen in children younger than 5 years with an overall incidence of approximately one in 500. Symptoms include melena, anemia, colicky abdominal pain, vomiting, and constipation. Emesis or stool may contain worms. In some cases, an abdominal mass that changes in size and location may be appreciated on serial physical examinations. Other complications associated with A. lumbricoides intestinal obstruction include volvulus, ileocecal intussusception, gangrene, and intestinal perforation.[57, 16, 23]

Conservative (nothing by mouth, nasogastric suction and repletion of fluids and electrolytes) management of partial intestinal obstruction and biliary ascariasis is usually effective but might be more quickly accomplished with orally administered contrast medium.[2] A controlled trial from Pakistan found that, in patients without peritonitis, hypertonic saline enemas relieved obstruction more quickly (1.6 d vs 3.4 d) and resulted in shorter hospital stays (4 d vs 6 d) than intravenous fluids alone. A recent study from India demonstrated that conservative therapy was successful in 19 of 22 (89%) children with intestinal obstruction. The regimen used consisted of no oral intake, intravenous fluids, antibiotics, piperazine salt per nasogastric tube, and glycerine plus liquid paraffin emulsion enemas.[35]  Anthelminthic therapy should be administered when the acute obstruction is relieved.

Recommended criteria for surgical exploration include the following:

• Passage of blood per rectum

• Multiple air fluid levels on abdominal radiographs

• An ill child with abdominal distension and rebound tenderness

• Unsatisfactory response to conservative therapy

• Appendicitis and primary peritonitis

• Hepatobiliary disease

• Pancreatic pseudocyst

Patients with biliary ascariasis usually respond with conservative management. Antibiotics may be needed for cholangitis or bacterial peritonitis. Indications for endoscopic or surgical worm removal include presence of worm(s) trapped in the biliary tree or invasion of the liver by one or more worms.[40, 58]

Biliary tract obstruction:

Most (49-90%) worms eventually migrate from the biliary system spontaneously. Drug therapy should be delayed in patients with right upper quadrant or pancreatic pain, as no evidence has shown that drugs are active against worms located in the biliary tree. Regardless, death of the worm in the duct may provoke both inflammation and obstruction. Patients with ascariasis who have only minor symptoms can undergo observation for 3 days. If the minor symptoms persist after 3 days or the patient develops frank cholangitis or pancreatitis, removal of the worms with ERCP should be attempted, if available. Although technically challenging at times, ERCP extraction rates have exceeded 90%.[41]

Invasion of the gall bladder necessitates cholecystectomy, common duct exploration, and T-tube drainage until the patient is stabilized and dewormed.

Intestinal gangrene usually occurs at the terminal ileum, more often after the use of pyrantel pamoate, which tetanically paralyzes worms and thereby enhances the risk for obstruction. Recently, two cases of delayed distal intestinal disease have been reported, which were thought to be secondary to toxins from the worms. Therefore, patients should probably be monitored for some time after the surgical removal of worms.

Milking of worms to the large bowel, resection of gangrenous bowel, ileostomy, and enterotomy are the most common surgical procedures used to manage bowel obstruction. Intestinal or biliary surgery may be necessary for complications of ascariasis.

Any patients from highly endemic areas should be screened, and if positive, treated for ascariasis and malnutrion prior to elective surgery because of possible provocation of worm migration with anesthesia agents.[59] In particular, patients who live in endemic areas should be dewormed before and after elective cholecystectomy.

Community control of ascariasis has been difficult to achieve. The most successful control programs, such as those in Japan, have consisted of combined approaches, including improved sanitation, night soil disposal, and mass community treatment. Concern has increased for the emergence of drug resistance among heavily retreated populations.

The prevalence of ascariasis in Japan in 1949 was 63%; the disease was essentially eliminated by 1973. Hand washing may be a neglected means of prevention, even in endemic areas, as shown by a recent study from Sri Lanka.

A program of latrine construction, health education, and twice-annual anthelmintics decreased the prevalence of ascariasis in Korea from 80% in 1949 to 55% by 1971. After a 4-year educational campaign and latrine construction program in northern Bangladesh, 36% of children aged 5 to 13 remained infected. Rates of infection were lower among children who used latrines and who had been educated concerning the risks of ascariasis.[60]  As rates of ascariasis lessen, specific infected families should be targeted. A recent systematic review and meta-analysis of preventive water and sanitation measures concluded that the risk of ascariasis was lowered 60% by piped water, 38% by access to sanitarian latrines, and 62% by handwashing before eating and 55% after defecating.[61]  Each, in combination with the use of soap, has the potential for significant control, especially if applied in schools together with thrice yearly deworming.[62]

Current ascariasis treatment strategies recommend repeated mass treatment of communities to reduce intensity of worm burden until socioeconomic progress allows improved sanitation. Although such targeted therapy programs may control the morbidity of ascariasis by decreasing the number of worms per patient, they do not seem to decrease transmission rates. The ascariasis reinfection rate after a single community campaign in South Africa was 40% at 29 weeks. Children have been targeted in school campaigns, but continued worm burden and shedding by adults have blunted impact, especially if campaigns are less than thrice yearly. A 6-month educational program directed at behavioral remediation of school children and their parents in Java has shown promise when combined with a deworming campaign.

A 2012 Cochrane review[63]  was rather discouraging in its assessment of the benefit of community deworming programs, suggesting only the possibility of slight benefit in weight gain and hemoglobin, but not cognitive improvement as measured by school attendance and performance.

Avoiding pigs and pig manure prevents A suum infection in developed countries.

Work continues on a vaccine. A recombinant, nasally administered 16-kd secretory protein, As16, was shown to result in a 56% decrease in worm burden in mice challenged with A suum larvae.[64]  The Sabin Vaccine Institute is developing a "Pan-anthelminthic" vaccine against hookworm, trichuriasis, and ascariasis using at least two of six candidate A suum antigens. It appears that at least 5 years will be required to field such a candidate vaccine.[65]

Follow-up 

 Routine repeat stool testing is not essential due to the high cure rate with anthelminthic therapy, however, in endemic areas, repeat stool testing may be done 2 to 3 months after treatment to ensure resolution of infection. Detection of eggs at follow-up stool examination suggests inadequate elimination of adult worms or reinfection. In such cases, retreatment with the same regimen is warranted. It takes about 10 days for the complete expulsion of adult Ascaris worms after albendazole treatment; therefore, it is pertinent to  wait at least 2 weeks after treatment before performing follow-up egg count or stool testing. In endemic areas or case clusters with persistent or repeated infections despite prior therapy it is important to test all family members and concurrent treatment  with albendazole or mebendazole. Reinfection occurs frequently in these cases, sometimes more than 80 percent of individuals become reinfected within 6 months. Intermittent mass drug therapy for such circumstances is discussed separately.[66]

Patients with ascariasis who have partial or complete obstruction should be treated at facilities with surgical support.

In 2017, WHO published an extensive guideline on community-based deworming programs. They recommended that areas with greater than 20% prevalence undergo mass periodic administration of benzimidazoles.[67]

CDC has good information about management and diagnosis of ascariasis.[14, 52]

The goals of pharmacotherapy are to eradicate infestation, to prevent complications, and to reduce morbidity.

Class Summary

Parasite biochemical pathways are sufficiently different from the human host to allow selective interference by chemotherapeutic agents in relatively small doses.

Albendazole (Albenza)

First DOC. A benzimidazole carbamate drug that inhibits tubulin polymerization, resulting in degeneration of cytoplasmic microtubules. Decreases ATP production in worms, causing energy depletion, immobilization, and, finally, death. Converted in the liver to its primary metabolite, albendazole sulfoxide. Less than 1% of the primary metabolite is excreted in the urine. Plasma level is noted to rise significantly (as much as 5-fold) when ingested after high-fat meal. Experience with patients < 6 y is limited.

To avoid inflammatory response in CNS, patient must also be started on anticonvulsants and high-dose glucocorticoids.

Well tolerated and does not appear to increase risk of worm obstruction.

Mebendazole (Emverm)

Well tolerated and does not appear to increase risk of worm obstruction. Causes worm death by selectively and irreversibly blocking uptake of glucose and other nutrients in susceptible adult intestine where helminths dwell. Available as a 100-mg chewable tablet that can be swallowed whole, chewed, or crushed and mixed with food.

Pyrantel pamoate (Pin-Rid, Reese's Pinworm Medicine)

Neuromuscular blocking agent used to slowly paralyze worm to be eliminated from GI tract. May be DOC during pregnancy.