Ascariasis

INTRODUCTION — 

Ascaris lumbricoides is the largest intestinal nematode (roundworm) parasitizing the human intestine and is one of the most common helminthic human infections worldwide [1,2]. Ascaris suum is a roundworm intestinal parasite of pigs and can also cause human infection [3,4].

Genetically, A. lumbricoides and A. suum are very closely related [5-9]. While the genus Ascaris has been split into two species, modern genotyping methods suggest that the categories are instead separate genotypes of the same A. lumbricoides species, and that human (A. lumbricoides), pig (A. suum), and hybrid genotypes occur [10,11].

Transmission of ascariasis occurs primarily via ingestion of water or food contaminated with infectious eggs. Most patients with A. lumbricoides or A. suum infection are asymptomatic. When symptoms do occur, they occur most often during the adult worm intestinal stage (as intestinal, hepatobiliary, or pancreatic manifestations) but may also occur during the larval migration stage (as pulmonary manifestations).

The epidemiology, clinical manifestations, diagnosis, treatment, and prevention of ascariasis are reviewed here.

EPIDEMIOLOGY — 

Human acquisition of Ascaris infection can occur via the following mechanisms:

●Ingestion of eggs secreted in the feces of humans (A. lumbricoides) or pigs (A. suum). Eggs must embryonate in soil to become infectious. (See 'Life cycle' below.)

●Ingesting uncooked pig or chicken liver bearing larvae of A. suum [12].

Ascaris infection due to A. lumbricoides occurs worldwide; it is estimated that more than one billion people are infected [2,4]. The majority of individuals with ascariasis live in Asia (73 percent), Africa (12 percent), and South America (8 percent); some populations have infection rates as high as 95 percent [2,13]. In a systematic review and meta-analysis, the global prevalence of human Ascaris infection between 2010 to 2021 was assessed to be 11.01 percent (95% CI, 10.27-11.78 percent), with regional prevalences ranging from 28.77 percent (7.07-57.66 percent) in Melanesia (Oceania) to 1.39 percent (1.07-1.74 percent) in Eastern Asia [14].

Ascariasis is most common among children 2 to 10 years of age, and the prevalence of infection diminishes among individuals >15 years of age. Infections tend to cluster in families. The prevalence of A. lumbricoides infection is highest in tropical countries where warm, wet climates favor year-round transmission. In dry areas, transmission occurs predominantly during the rainy months. Emerging evidence suggests that A. lumbricoides prefers acidic soil [15]. Ascariasis occurs most commonly in areas where suboptimal sanitation practices are associated with fecal contamination of soil, water, and food.

Historically, the highest burden of ascariasis in the United States occurred in the southeast; the prevalence of infection decreased significantly after introduction of modern sanitation and waste treatment in the early 20^th century [16]. However, porcine ascariasis is present in some farmed animals [17].

Infection can occur among travelers to areas with high prevalence of infection.

Ascaris infection due to A. suum has been recognized increasingly in regions where human exposure to pigs enables ingestion of infectious eggs. Pig husbandry and the use of pig feces for fertilizer has been associated with human infection even in temperate regions of resource-abundant countries. Pigs are usually infected from eating eggs shed by other pigs but occasionally become infected after ingestion of livers and lungs from chickens infected with Ascaris of pig origin [9,12]. A. suum infections have been reported in China [6], Japan [9], Thailand, Lao People's Democratic Republic, Myanmar [18], the United States [5], and Europe [7,8].

Infection with human immunodeficiency virus (HIV) has not been associated with increased risk for ascariasis [19].

Life cycle — The life cycle of ascariasis is summarized in the figure (figure 1). Ascaris eggs passed in stool are deposited in soil, where they embryonate and become infective within two to four weeks. After oral ingestion of infective Ascaris eggs (via contaminated food or water), the eggs hatch in the small intestine within four days and release larvae that migrate through the mucosa of the cecum and proximal colon (picture 1).

Subsequently, some larvae penetrate the intestinal wall and migrate hematogenously through the portal system to the liver, then through the hepatic veins to the heart, and then the lungs. Some larvae migrate through the mucosal lymphatics through the thoracic duct to the lungs. Larvae mature within the alveoli over 10 to 14 days, ascend the bronchial tree to the trachea, and are coughed up and swallowed. Occasionally, larvae migrate to other sites such as the brain or kidneys.

Once back in the intestine, larvae mature into adult worms (females 20 to 35 cm; males 15 to 30 cm) in the lumen of the small intestine. The majority of worms are found in the jejunum, though worms may be found anywhere in the gastrointestinal tract and occasionally migrate to other ectopic sites. Adult worms begin to lay eggs approximately 9 to 11 weeks following infection [20]. When both female and male worms are present in the intestine, each female worm produces approximately 200,000 fertilized eggs per day. In the setting of infection with only female worms, infertile eggs are produced that do not develop into the infectious stage. In the setting of infection with only male worms, no eggs are formed.

Adult worms do not multiply in the human host; the number of adult worms in an infected individual depends on the degree of exposure to infectious eggs over time. Adult worms have a lifespan of 10 to 24 months and are passed in the stool. In highly endemic areas, worm burdens of several hundred per individual may be observed [21]. The number of eggs produced per female worm tends to decrease as the worm burden increases.

The eggs are passed in stool; they are oval, have a thick shell and mamillated outer coat, and measure 45 to 70 microns by 35 to 50 microns (picture 2). Unfertilized eggs are not infective; fertile eggs embryonate and become infective after 18 days to several weeks. In favorable environmental conditions (moist, warm, shaded soil), eggs can survive for up to 10 years [22]. The eggs are resistant to chemical water purification but may be eliminated by filtration or boiling.

Transmission — Transmission of ascariasis occurs primarily via ingestion of water or food contaminated with infectious A. lumbricoides or A. suum eggs. Children playing in contaminated soil may acquire the parasite from their hands, and poor hygiene facilitates spread of infection. Uncommonly, transmission occurs via airborne ingestion of contaminated dust. Maternal-fetal transmission via transplacental migration of larvae has been described [23].

Transmission of infection is enhanced by asymptomatically infected individuals who can continue to shed eggs for years. Reinfection occurring in endemic areas is common. Prior infection does not confer protective immunity [24]. In addition, coinfection with other parasitic diseases is common given similar predisposing factors for transmission [25].

Transmission of A. suum is associated with pig husbandry and use of pig feces as fertilizer.

SPECTRUM OF PRESENTATION — 

Most patients with A. lumbricoides or A. suum infection are asymptomatic; however, the global burden of symptomatic disease is relatively high because of the high disease prevalence.

In general, symptoms occur among individuals with relatively high worm loads [2]. Symptoms occur most often during the late-phase adult worm intestinal stage (as intestinal, hepatobiliary, or pancreatic manifestations) but may also occur during the early-phase larval migration stage (as pulmonary manifestations). (See 'Life cycle' above.)

Regardless of the presence or type of symptoms, all patients with Ascaris infection warrant anthelminthic treatment, although timing varies by presentation. (See 'Management of complications' below.)

EARLY PHASE PULMONARY MANIFESTATIONS — 

Pulmonary ascariasis generally occurs in individuals with no prior Ascaris exposure and potential egg ingestion within weeks prior to onset of symptoms [26]. Symptomatic pulmonary involvement is rare among individuals in highly endemic areas with ongoing exposure, even among young children who can develop very heavy infections [27,28]. One study in Colombia (where intestinal Ascaris infection rates range from 25 to 90 percent) noted only four cases of Loeffler syndrome among approximately 13,000 patients [27].

The eosinophil-enriched pulmonary inflammation associated with pulmonary Ascaris infection in previously unexposed individuals may be analogous to the eosinophilic inflammatory response that characterizes the immune response of individuals with no prior exposure to Loa loa or schistosomiasis (Katayama fever). (See "Loiasis (Loa loa infection)" and "Schistosomiasis: Epidemiology and clinical manifestations", section on 'Acute schistosomiasis syndrome' and "Overview of pulmonary eosinophilia".)

Clinical manifestations

Symptoms and signs — During the early phase of infection (4 to 16 days following egg ingestion), migration of Ascaris larvae through the lungs may be associated with transient respiratory symptoms and eosinophilic pneumonitis. In general, respiratory manifestations occur primarily in the larval stage of infection; they rarely complicate the intestinal phase.

Pulmonary involvement associated with parasitic infection is known as Loeffler syndrome (Löffler syndrome); the initial description of the syndrome consisted of eosinophilic pneumonitis later attributed by Loeffler to A. lumbricoides infection. Other parasitic infections associated with pulmonary syndromes include Strongyloides, hookworm (Ancylostoma duodenale, Necator americanus, and Toxocara), schistosomiasis, and lymphatic filariasis associated with tropical pulmonary eosinophilia. (See "Overview of pulmonary eosinophilia".)

Pulmonary manifestations associated with migration of Ascaris larvae include dry cough, dyspnea, fever, wheezing, substernal discomfort, and blood-tinged sputum. Over half of patients have crackles and wheezing in the absence of focal consolidation. Urticaria occurs during the first five days of illness in approximately 15 percent of cases. Hepatomegaly may develop. Lymphadenopathy is generally not observed. Symptoms generally subside within 5 to 10 days; the syndrome is usually self-limited and very rarely fatal.

Laboratory findings — Peripheral eosinophilia may be observed in association with pulmonary manifestations [29]. Eosinophilia may be absent in the early symptomatic period but increase in magnitude after several days of symptoms; it resolves over many weeks. Eosinophil levels are usually 5 to 12 percent but can be as high as 30 to 50 percent. Eosinophilia is masked by administration of steroids.

Sputum analysis may demonstrate eosinophils and Charcot-Leyden crystals (picture 3) [30]. These crystals are also observed in other eosinophilic lung diseases. (See "Overview of pulmonary eosinophilia".)

Serum levels of total immunoglobulin (Ig)G and total IgE are often elevated during early infection.

Imaging findings — Chest radiography may demonstrate round or oval infiltrates ranging in size from several millimeters to several centimeters in both lung fields. These findings are more likely to be present when blood eosinophilia exceeds 10 percent. The infiltrates are migratory and may become confluent in perihilar areas; they usually clear after several weeks (image 1).

Computed tomography imaging generally demonstrates multiple nodules (generally up to 3 cm diameter); these are most commonly peripherally based and often have a halo of ground-glass attenuation [9,31,32]. Ground-glass opacities with ill-defined margins may also be seen. On serial imaging, these nodules are migratory.

Evaluation and diagnosis — Definitive diagnosis of pulmonary ascariasis rarely occurs contemporaneously during early phase respiratory manifestations because eggs are not yet detectable in stool. Diagnosis during the pulmonary phase is typically presumptive.

Among patients with respiratory symptoms, the possibility of pulmonary ascariasis should be considered in those from nonendemic areas who have had recent epidemiologic exposure within the prior weeks. The presence of characteristic respiratory symptoms (dry cough, dyspnea, fever, wheezing) or radiographic findings (migratory bilateral round infiltrates) and peripheral eosinophilia should further increase suspicion for the diagnosis. In contrast, symptomatic pulmonary infection is rare among individuals who live in endemic areas and have ongoing exposure. (See 'Epidemiology' above.)

When the diagnosis of early phase ascariasis is suspected, detection of Ascaris larvae in respiratory secretions or gastric aspirates (picture 1) confirms the diagnosis, although such tests are rarely positive or performed for this indication. Transpulmonary passage of other helminths (eg, Strongyloides, hookworm) can cause similar respiratory symptoms and radiographic findings; the approach to patients with pulmonary symptoms and eosinophilia (Löffler syndrome) is discussed elsewhere. (See "Overview of pulmonary eosinophilia", section on 'Infectious causes' and 'Differential diagnosis' below.)

Otherwise, in patients who had suspected pulmonary ascariasis, stool examination for Ascaris eggs could be performed approximately two or more months after the resolution of pulmonary symptoms to try to retrospectively establish the diagnosis. Eggs are generally not detectable in stool until at least 40 days following acute pulmonary symptoms (figure 1). Ascaris eggs in stool reflect infection acquired 2 to 12 months earlier. (See 'Microbiologic testing' below.)

Differential diagnosis — Parasitic infections associated with pulmonary syndromes include Ascaris, Strongyloides, hookworm (A. duodenale, N. americanus, and Toxocara), schistosomiasis, and lymphatic filariasis associated with tropical pulmonary eosinophilia. Migrating hookworm and Strongyloides larvae rarely elicit pulmonary eosinophilia. These entities may be distinguished via exposure and epidemiologic histories and stool examinations approximately two months after resolution of pulmonary symptoms (for diagnosis of Ascaris). (See related topics.)

A number of noninfectious entities may present with symptoms similar to pulmonary ascariasis; these include asthma, hypersensitivity pneumonitis, and eosinophilic pneumonia due to other causes (medications, vasculitis, idiopathic, and others). The diagnosis of these entities is established via clinical history, laboratory studies, and radiographic imaging. (See "Asthma in adolescents and adults: Evaluation and diagnosis" and "Hypersensitivity pneumonitis (extrinsic allergic alveolitis): Clinical manifestations and diagnosis" and "Overview of pulmonary eosinophilia".)

LATE PHASE INTESTINAL MANIFESTATIONS

Clinical manifestations

Symptoms and signs — During the late phase of infection (six to eight weeks after egg ingestion), symptoms of ascariasis may consist of nonspecific symptoms such as abdominal discomfort, anorexia, nausea, vomiting, and diarrhea. Macroscopic adult worms are passed in the stool.

Complications — Complications of ascariasis include intestinal obstruction, malnutrition, hepatobiliary involvement, pancreatitis, and other manifestations.

●Intestinal obstruction – In the setting of heavy Ascaris infection, adult worms can obstruct the bowel lumen, leading to acute intestinal obstruction [33]. In one meta-analysis, intestinal obstruction accounted for 38 to 87 percent of all complications of ascariasis [34]. Another report noted that individuals presenting with intestinal obstruction associated with ascariasis had an estimated burden of >60 intestinal worms [35,36].

In some regions, ascariasis is the most common cause of acute abdominal surgical emergencies [21], and, in endemic areas, 5 to 35 percent of all bowel obstructions are due to ascariasis [22]. Approximately 85 percent of obstructions due to ascariasis occur in children between one and five years of age. The overall incidence of obstruction associated with ascariasis in children is approximately 1 in 500.

Obstruction occurs most commonly at the ileocecal valve. Migrating adult worms can also obstruct the appendix, resulting in appendicitis. Symptoms of intestinal obstruction associated with ascariasis include colicky abdominal pain, vomiting, and constipation. Emesis may contain worms. In some cases, an abdominal mass that changes in size and location may be appreciated on serial physical examinations [25].

Other complications associated with A. lumbricoides intestinal obstruction include volvulus, ileocecal intussusception, gangrene, and intestinal perforation.

●Hepatobiliary and pancreatic involvement – Migration of adult Ascaris worms into the biliary tree can cause biliary colic, biliary strictures, acalculous cholecystitis, ascending cholangitis, obstructive jaundice, liver abscesses, and bile duct perforation with peritonitis [37-39]. The bile duct is involved most commonly [40]. Retained worm fragments can serve as a nidus for biliary stones. Recurrent pyogenic cholangitis, caused by stone formation around dead A. lumbricoides in the bile duct, also occurs. Adult Ascaris worms may also obstruct the pancreatic duct, leading to pancreatitis.

Ascariasis has been associated with up to one-third of biliary and pancreatic disease in India [39,41-43]. In one study, hepatobiliary and pancreatic ascariasis was the etiologic factor for biliary disease, acute pancreatitis, liver abscess, and biliary lithiasis in 37, 23, 15, and 13 percent of cases, respectively [44]. Another study including 300 Syrian patients with biliary or pancreatic ascariasis noted ascending cholangitis, acute pancreatitis, and obstructive jaundice in 16, 4, and 1 percent of cases, respectively [45].

●Malnutrition – Ascariasis has been associated with malnutrition, growth retardation, and impaired cognitive development in school children [46]. A high burden of infection can lead to impaired absorption of dietary proteins, lactose, and vitamins A and C; steatorrhea may occur. Children treated for ascariasis reportedly have better nutritional status in terms of growth, lactose tolerance, vitamins A and C, and albumin levels than children with untreated ascariasis [47]. However, it is difficult to discern the true effect of ascariasis on nutritional status given other coexisting nutritional deficiencies in infected children [48,49].

●Other manifestations – Occasionally, adult worms migrate outside the gastrointestinal tract to ectopic sites [50]. Migrating adult worms may emerge from the mouth, nose, lacrimal ducts, umbilicus, or inguinal canal. Rarely, aspiration pneumonia can occur in association with migration of adult worms up the esophagus and into the trachea in association with vomiting. Adult worm migration may be stimulated by stresses including fever, anthelmintic drugs, fasting, and anesthesia [25].

Laboratory findings — Peripheral eosinophilia may be observed during the late phase of infection but is more likely to be observed during the early phase [29]. (See 'Laboratory findings' above.)

Stool microscopy is discussed below. (See 'Microbiologic testing' below.)

Imaging findings — Imaging tools include plain radiography, barium swallow, ultrasonography, computed tomography (CT), and magnetic resonance imaging (MRI):

●Plain radiography – Plain radiography of the abdomen may demonstrate large collections of adult Ascaris worms in heavily infected individuals (particularly in children). The mass of worms contrasts against the gas in the bowel, producing a "whirlpool" effect (image 2) [21]. Plain radiography can also demonstrate intestinal obstruction. (See 'Late phase intestinal manifestations' above.)

●Barium swallow – Barium swallow may also demonstrate adult Ascaris worms, which manifest as elongated filling defects of the small bowel. The worms may ingest barium; in such cases, the worm's alimentary canal appears as a white thread bisecting the length of the worm's body (image 3) [21].

●Ultrasonography – Ultrasonography may demonstrate intestinal echogenic tubular structures, curved strips, or a "target" sign [51]. In some cases, the worms demonstrate curling movements [52,53]. Ultrasonography can also be useful for demonstration of hepatobiliary or pancreatic ascariasis; single worms, bundles of worms, or a pseudotumor-like appearance may be seen [51-53].

●CT or MRI – CT or MRI may demonstrate worms in the bowel [54]. Imaging the worm in cross-section demonstrates a "bull's eye" appearance (image 4). In the setting of hepatobiliary involvement, CT or MRI may demonstrate adult Ascaris worms in the liver or bile ducts [36].

Magnetic resonance cholangiopancreatography (MRCP) may demonstrate adult worms in bile or pancreatic ducts, as linear low intensity filling defect with a characteristic three parallel lines appearance [55,56].

Diagnosis

Clinical approach — Intestinal ascariasis should be suspected in patients with nonspecific abdominal symptoms (discomfort, anorexia, nausea, or vomiting) and/or associated complications (biliary or pancreatic involvement) in association with relevant epidemiologic exposure in an area with high prevalence of soil-transmitted helminths.

The diagnosis is usually established via stool microscopy for eggs (or polymerase chain reaction [PCR]) and less commonly by reliable identification of passed adult worms(See 'Epidemiology' above and 'Microbiologic testing' below.)

Patients with suspected intestinal obstruction or other intestinal complication in association with ascariasis should undergo radiographic imaging with plain radiography and/or computed tomography. (See 'Imaging findings' above and "Etiologies, clinical manifestations, and diagnosis of mechanical small bowel obstruction in adults", section on 'Diagnosis'.)

Patients with suspected involvement of the biliary tree or pancreatic duct in association with ascariasis should have endoscopic retrograde cholangiopancreatography (ERCP), if possible, to establish the diagnosis and facilitate removal of the worm. (See 'Endoscopy' below.)

Microbiologic testing — The diagnosis of ascariasis is generally established via stool microscopy for evaluation of Ascaris ova (ie ova and parasite examination). When available, PCR testing has higher sensitivity and specificity compared with microscopy. Occasionally, the diagnosis is made by reliable identification of passed adult worms.

●Stool microscopy – The diagnosis of ascariasis is generally established via stool microscopy for evaluation of Ascaris ova, although the eggs of A. lumbricoides and A. suum are morphologically indistinguishable by this method. Characteristic eggs may be seen on direct examination of stool or following concentration techniques (picture 2). Eggs of other parasites may also be detected since coinfection with other parasitic diseases is common. Eggs do not appear in the stool until at least 40 days after infection; thus, an early diagnosis cannot be made via stool microscopy, including during the phase of respiratory symptoms. Stool concentration methods for detection of Ascaris eggs include Kato-Katz and FLOTAC techniques [57-61] (see "Approach to stool microscopy"):

•The Kato-Katz method is the most common technique for stool preparation; it involves filtering a stool sample followed by staining using materials provided in a kit. It is the method recommended by the World Health Organization (WHO) and is the most widely used technique due to its simplicity, low cost, and capacity to facilitate detection of multiple parasite species. However, the sensitivity of the Kato-Katz method is limited for low-intensity infection. In general, examination of two Kato-Katz slides on each of three stool samples collected on consecutive days is considered sufficient for a false-negative rate of ≤1 percent in a moderate prevalence setting [62].

•The FLOTAC method is generally considered the most sensitive stool preparation technique but requires a centrifuge, which limits its utility in some settings.

●Adult worm identification – The diagnosis of Ascaris infection can be made in the rare case that a patient expels an adult worm (per rectum or regurgitated/expectorated) or when a worm is extracted from the gastrointestinal tract during endoscopy, as long as it can be reliably confirmed as Ascaris by an experienced microbiologist. For patients with biliary involvement (such as biliary duct stones and/or cholangitis), the diagnosis may be made by identifying eggs or adult worms in bile. An infection may become evident when an infected host is placed under general anesthesia, which causes aberrant migration of worms up the esophagus to be passed from the mouth or nose or into the lung, causing tracheal obstruction.

Adult A. lumbricoides worms mature to become up to 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 (picture 4).

●PCR – PCR is increasingly becoming available in resource-abundant settings and is a useful adjunctive diagnostic tool as it has superior sensitivity and specificity compared with microscopy [63-68]. However, it is not routinely available as a diagnostic tool in most endemic areas [69]. In contrast to stool microscopy, PCR testing can distinguish between the eggs of A. lumbricoides and A. suum [70].

Endoscopy — Endoscopy is warranted for evaluation of patients with suspected involvement of the biliary tree or pancreatic duct due to ascariasis. In addition to allowing visualization of Ascaris, it also is important for management and worm removal. (See 'Biliary ascariasis' below.)

On endoscopic ultrasonography, worms appear as long, linear hyperechoic structures without acoustic shadowing ("single-tube sign") or with a central hypoechoic tube ("double-tube sign") (image 5).

ERCP is useful for demonstrating worms in the biliary and pancreatic ducts; worms may be visualized endoscopically in the duodenum and protruding from the ampulla of Vater (picture 5) [71,72]. Characteristic cholangiogram findings include filling defects (long, smooth, linear filling defects with tapering ends (image 6)), curves and loops crossing the hepatic ducts transversely, and bile duct dilatation.

Cholangioscopy allows direct visualization of worm(s) within the bile duct (picture 6). (See "Cholangioscopy and pancreatoscopy".)

Other tests — Serology is generally reserved for epidemiologic studies rather than clinical diagnosis [24]. Individuals with ascariasis produce detectable antibodies to A. lumbricoides, but IgG antibodies do not appear to have protective function against infection, and antibody cross-reactivity with antigens from other helminths is common [73].

Differential diagnosis — The differential diagnosis of intestinal manifestations associated with ascariasis includes:

●Intestinal nematode infection – Apart from Ascaris, intestinal nematodes (roundworms) that are usually human parasites include hookworm (A. duodenale and N. americanus), Trichuris (whipworm), Enterobius (pinworm), and Strongyloides.

•Enterobius infection is generally asymptomatic or associated with perianal itching. Trichuris infection is generally asymptomatic or associated with loose stool. Hookworm and Strongyloides are associated with epigastric pain, nausea, and diarrhea as well as nutritional impairment. (See "Enterobiasis (pinworm) and trichuriasis (whipworm)" and "Hookworm infection" and "Strongyloidiasis".)

•The diagnosis of Trichuris, Enterobius, and hookworm may be established via visualization of eggs on stool microscopy. The diagnosis of hookworm and Strongyloides may be established via visualization of larvae on stool microscopy. (See "Approach to stool microscopy".)

●Bowel obstruction – Bowel obstruction can occur in a number of clinical circumstances apart from Ascaris infection; these include adhesions, herniation, neoplasm, irradiation, and foreign body ingestion. The diagnosis is usually established radiographically. (See "Etiologies, clinical manifestations, and diagnosis of mechanical small bowel obstruction in adults".)

●Malabsorption – Malabsorption can occur in a number of clinical circumstances apart from Ascaris infection; these include other parasitic infections (such as hookworm and Strongyloides), cirrhosis, intestinal resection, enzyme deficiency, and other causes. The diagnosis is established based on a several invasive and noninvasive tests. (See "Approach to the adult patient with suspected malabsorption".)

●Biliary obstruction – Biliary obstruction can occur in a number of clinical circumstances apart from Ascaris infection; these include intestinal fluke infections (such as Clonorchis and Fasciola), gallstones (associated with cholangitis and/or cholecystitis in some cases), stricture, tumor, and other causes. The diagnosis is established via radiographic imaging, laboratory studies, and endoscopic retrograde cholangiopancreatography in some cases. (See "Diagnostic approach to the adult with jaundice or asymptomatic hyperbilirubinemia".)

●Pancreatitis – Pancreatitis can occur in a number of clinical circumstances apart from Ascaris infection; these include mechanical obstruction, alcohol, infection, and other causes. The diagnosis is established via clinical history, laboratory studies, and radiographic imaging. (See "Clinical manifestations, diagnosis, and natural history of acute pancreatitis".)

TREATMENT

Management of complications

Severe pneumonitis — Supportive care and inhaled bronchodilators for alleviation of wheeze and cough are used for management of early phase pulmonary manifestations. Although we do not routinely recommend glucocorticoids, some clinicians use glucocorticoids for severe symptoms of pneumonitis. (See "Overview of pulmonary eosinophilia", section on 'Infectious causes'.)

Anthelminthic therapy is generally not administered during the pulmonary phase since the efficacy of drugs against larvae in the lungs is uncertain. If the diagnosis of ascariasis is confirmed retrospectively by detection of eggs in the stool after respiratory symptoms have resolved, anthelminthic treatment should then be administered accordingly for intestinal infection. (See 'Anthelminthic therapy for all patients' below.)

Intestinal obstruction — Patients with intestinal obstruction are managed conservatively with nasogastric suction and repletion of fluids and electrolytes. Indications for surgery include complete obstruction with inadequate decompression, lack of clinical response within 24 to 48 hours, volvulus, intussusception, appendicitis, or perforation. (See "Management of small bowel obstruction in adults".)

We defer anthelminthic therapy until bowel motility is restored. (See 'Anthelminthic therapy for all patients' below.)

Biliary ascariasis — Management includes treatment of biliary sepsis and removal of worms in the biliary tree in addition to anthelminthic therapy. (See 'Anthelminthic therapy for all patients' below.)

●Supportive care – Initial management of biliary ascariasis includes supportive measures such as nasogastric suction and repletion of fluids and electrolytes.

●Antibiotics for biliary sepsis – Patients with cholangitis warrant antibiotic therapy; regimens are discussed elsewhere. (See "Acute cholangitis: Clinical manifestations, diagnosis, and management", section on 'Antibiotics'.)

Anthelminthic therapy should be administered once acute symptoms subside. (See 'Anthelminthic therapy for all patients' below.)

●Endoscopic removal of biliary worms – Patients with one or more worms in the biliary tree warrant ERCP for removal [74-76]. The worm(s) should be extracted completely since remnants can lead to stone formation.

•Approach – Worms protruding from the papilla may be grasped with a forceps and withdrawn (picture 5). For worms within the bile duct, in some cases, contrast injection or occlusion balloon stimulates migration out of the papilla. Alternatively, the worm can be grasped gently in a basket within the biliary tree, pulled into the duodenum, and removed with a forceps [77]. A polypectomy snare should not be used since it tends to cut the worm.

•Adjunctive techniques – For patients with worms that are not amenable to removal with the technique described above, we use papillary balloon dilatation to facilitate extraction. (See "Endoscopic balloon dilation for removal of bile duct stones".)

The utility of endoscopic sphincterotomy for worm removal is uncertain; the widened opening may facilitate further entry of worms into the biliary tree (figure 2). Some studies have observed pancreatic-biliary ascariasis more frequently among patients with prior sphincterotomy or cholecystectomy [45,78]; however, others have observed no recurrence of biliary ascariasis following sphincterotomy [79,80].

Patients with persistent biliary involvement despite ERCP warrant surgical intervention.

Anthelminthic therapy for all patients — All patients with Ascaris infection warrant anthelminthic treatment, even those with asymptomatic infection. Anthelminthic therapy reduces morbidity associated with Ascaris infection but does not prevent reinfection [81]. Several agents have activity against A. lumbricoides as discussed in the following sections.

Nonpregnant individuals

Benzimidazoles as preferred therapy — The mainstays of treatment for ascariasis (caused by A. suum or A. lumbricoides) in nonpregnant adults and children are the benzimidazoles. Albendazole is given as 400 mg orally as a single dose on an empty stomach; mebendazole is given at 500 mg orally as a single dose or 100 mg orally twice daily for three days. If follow-up testing is performed and does not demonstrate cure, the same regimen can be repeated. (See 'Follow-up' below.)

Coinfection with hookworm and Trichuris is common; if hookworm coinfection is known or possible, we use albendazole 400 mg orally for three days if resources are not limited (see "Hookworm infection", section on 'Treatment'). Treatment of trichuriasis is discussed elsewhere. (See "Enterobiasis (pinworm) and trichuriasis (whipworm)", section on 'Treatment'.)

Meta-analyses of trials evaluating benzimidazoles have demonstrated high microbiologic cure rates (93 versus 16 percent with placebo; risk ratio 6.3, 95% CI 3.9-10.1) [82]. Although the high cure rates in these trials were with single-dose albendazole, some subsequent reports of reduced efficacy have emerged, with studies in Rwanda (2017) and in Peru [83] and Ethiopia (2024) reporting cure rates of approximately 70 to 80 percent with single-dose albendazole [84,85]. These observations may reflect benzimidazole resistance due to mutations in beta-tubulin proteins [86], increasing sensitivity of newer testing methods [85] or reinfection.

A study from Uganda showed higher cure rates for Ascaris infection following combination therapy with single dose albendazole plus ivermectin compared with albendazole monotherapy (100 versus 83.9 percent) [83,87]. However, other studies have reported no benefit from the combination [88].

Adverse effects of the benzimidazoles include transient gastrointestinal discomfort, headache, and, rarely, leukopenia. (See "Anthelminthic therapies".)

Alternative agents — Alternative agents for treatment of ascariasis include ivermectin, nitazoxanide, and piperazine citrate. (See "Anthelminthic therapies".)

●Ivermectin – Ivermectin (200 mcg/kg, rounded to the nearest 3 mg dose) causes paralysis of adult worms. In one study comparing ivermectin (200 mcg/kg single dose) and albendazole (400 mg single dose), cure rates were similar (78 versus 70 percent) [89]. Other studies of ivermectin at a range of doses (50 to 200 mcg/kg) [90] showed cure rates and egg reduction rates comparable with those of albendazole and mebendazole [82].

●Nitazoxanide – The efficacy of nitazoxanide varies according to egg burden [91-93]. In patients with light infection, cure rates of 100 percent have been observed; in patients with heavy egg burdens (>10,000 eggs/g stool), cure rates of 50 to 80 percent can be achieved [93]. In a randomized trial among Peruvian children, comparable cure rates with nitazoxanide (three-day course) and albendazole (single dose) were observed (89 percent versus 91 percent) [94].

●Piperazine citrate – Piperazine citrate (50 to 75 mg/kg once daily up to a maximum of 3.5 g for two days) was a frequently used treatment regimen; it has been withdrawn from the market in many regions because other available alternatives are less toxic and more efficacious. However, it may still be useful for cases in which intestinal or biliary obstruction is suspected since the drug paralyzes worms, aiding expulsion.

Pregnant individuals — Our preferred regimen for pregnant individuals is pyrantel pamoate 11 mg/kg (up to a maximum of 1 g) administered as a single dose. The efficacy varies with worm load; single-dose therapy is approximately 90 percent effective in eradicating adult worms [95,96]. Adverse effects of pyrantel pamoate include gastrointestinal disturbances, headaches, rash, and fever.

Pyrantel pamoate is considered safe in pregnancy because it has limited systemic absorption. Other anthelminthic agents that are active against ascaris (eg, benzimidazoles, ivermectin) are generally avoided during pregnancy given their potential for teratogenicity in animals. However, in the setting of mass treatment, the WHO allows use of albendazole for pregnant individuals in the second and third trimesters [97]. (See "Mass drug administration for control of parasitic infections".)

FOLLOW-UP

Endemic areas — Routine repeat stool testing is not essential in endemic areas. Reinfection is common in endemic areas; in some areas, more than 80 percent of individuals become reinfected within six months. In such settings, mass drug administration is likely a more effective strategy for infection control than identifying individual infections. (See "Mass drug administration for control of parasitic infections".)

Nonendemic areas — In nonendemic areas, we perform follow-up stool testing for eggs at least 14 days after treatment or at least four weeks if testing by polymerase chain reaction (PCR).

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. Given the propensity of ascariasis to cluster in households, detection of persistent or repeat infection should prompt stool evaluation of other household members. If infection is detected among multiple household members, all may be treated simultaneously with a benzimidazole (albendazole or mebendazole). Household clustering is not common in areas with adequate sanitation and hygiene because eggs require a period of extraintestinal maturation before they become infectious. (See 'Anthelminthic therapy for all patients' above.)

PREVENTION AND CONTROL — 

In regions where Ascaris worms are abundant in soil, prevention of reinfection is extremely difficult. Strategies for control include [13]:

●Improvements in sanitation – Sanitation measures associated with lower rates of helminth infection include use of treated water, increasing the availability of soap, and handwashing after defecation [98,99].

●Health education – As an example, in areas where human feces are used as fertilizer, educational programs are needed to change this practice.

●Mass anthelminthic treatment – This is discussed in detail elsewhere. (See "Mass drug administration for control of parasitic infections".)

Efforts to develop a vaccine are underway but remain exploratory [100,101]. Outside endemic areas, screening or administration of presumptive therapy may be appropriate for adult immigrants and refugees from areas where the prevalence of soil-transmitted helminths is high. This is also discussed in detail elsewhere. (See "Medical care of adult refugees, immigrants, and migrants to the United States", section on 'Parasitic infections'.)

SUMMARY AND RECOMMENDATIONS

●Epidemiology – More than one billion people worldwide are infected with the intestinal nematode (roundworm) Ascaris lumbricoides. The prevalence of infection is highest in warm wet (tropical) climates and in areas where suboptimal sanitation practices lead to contamination of soil, water, and food. Ascaris suum is a related parasite of pigs that can cause infections in humans. (See 'Epidemiology' above.)

●Life cycle – After oral ingestion of eggs (via contaminated food or water), the eggs hatch in the small intestine and release larvae that migrate hematogenously to the lungs (figure 1). In the alveoli, the larvae mature over a period of approximately 10 days, then ascend the bronchial tree and are swallowed. Once back in the intestine, they mature into adult worms that inhabit the lumen of the small intestine. Female worms produce eggs that pass into the stool and can survive for up to 10 years. (See 'Life cycle' above.)

●Asymptomatic infection – Most patients with A. lumbricoides or A. suum infection are asymptomatic. (See 'Spectrum of presentation' above.)

●Early phase pulmonary ascariasis – During early infection (4 to 16 days following egg ingestion), migration of Ascaris larvae through the lungs can cause transient respiratory symptoms. Clinical features include dry cough, dyspnea, fever, or wheezing, migratory bilateral round infiltrates on chest imaging, and peripheral eosinophilia; these mainly occur in individuals from nonendemic areas without ongoing exposure.

The diagnosis is usually presumptive; it can rarely be definitively established via visualization of Ascaris larvae in respiratory secretions or gastric aspirates at the time of symptoms (picture 1). Stool examination is not useful for diagnosis during the pulmonary phase, as eggs are not present until later. (See 'Early phase pulmonary manifestations' above.)

●Late phase intestinal ascariasis – During late infection (six to eight weeks after egg ingestion), intestinal Ascaris can cause gastrointestinal symptoms (discomfort, anorexia, nausea, or vomiting) and obstructive complications (intestinal, biliary, or pancreatic duct obstruction). (See 'Clinical manifestations' above.)

The diagnosis is established via identification of Ascaris ova on stool microscopy (picture 2), polymerase chain reaction (PCR; if available),or by reliable identification of passed adult worms. For patients with biliary involvement, identifying eggs or adult worms in bile establishes the diagnosis. (See 'Diagnosis' above.)

●Anthelminthic therapy – All patients with documented Ascaris infection warrant anthelminthic treatment, even those with asymptomatic infection; for those who present with pulmonary symptoms, anthelminthic therapy is generally deferred until intestinal infection has been subsequently confirmed. For anthelminthic therapy in nonpregnant individuals, we recommend albendazole (400 mg orally once) or mebendazole (500 mg orally once or 100 mg orally twice daily for three days) (Grade 1A). In nonendemic areas, we perform follow-up stool testing for eggs at least 14 days after treatment (or at least four weeks if diagnosis was by PCR). For patients with persistent infection, the initial regimen can be repeated. (See 'Anthelminthic therapy for all patients' above.)

●Management of complications – Pulmonary symptoms can generally be managed with inhaled bronchodilators and supportive care. Surgical or endoscopic intervention may be warranted for obstructive complications of intestinal ascariasis. Management of biliary ascariasis includes treatment of biliary sepsis and removal of worms from the biliary tree. (See 'Management of complications' above.)

●Prevention – In regions where Ascaris worms are abundant in soil, prevention of reinfection is extremely difficult. Strategies include health education, mass anthelminthic treatment, and sanitation improvements (eg, treated water, availability of soap, and handwashing). Issues related to mass drug administration for control of parasitic infections are discussed separately. (See 'Prevention and control' above and "Mass drug administration for control of parasitic infections".)