Ascariasis - UpToDate

13.03.
2024, 18:06 Ascariasis - UpToDate
Ascariasis
AUTHORS: Karin Leder, MBBS, FRACP, PhD, MPH, DTMH, Peter F Weller, MD, MACP, D Nageshwar Reddy, MD
SECTION EDITOR: Edward T Ryan, MD, DTMH
DEPUTY EDITOR: Elinor L Baron, MD, DTMH
Contributor Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Feb 2024.

This topic last updated: Oct 19, 2022.
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]. A. lumbricoides and A. suum are genetically very closely related [5-9].
Transmission of ascariasis occurs primarily via ingestion of water or food contaminated

with Ascaris 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 [10].
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
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infection rates as high as 95 percent [2,11]. 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 [12]. 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 20th century [13]. 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
developed 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 [9,10]. A. suum infections have been reported in China [6], Japan [9],
Thailand, Lao People's Democratic Republic, Myanmar [14], the United States [5], and
Europe [7,8].
Infection with HIV has not been associated with increased risk for ascariasis [15].
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 about 9 to 11
weeks following infection [16]. 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; there are case reports
of more than 2000 worms in individual children [17]. 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 [18]. 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 [19].
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 [20]. In addition, coinfection with other
parasitic diseases is common given similar predisposing factors for transmission [21].
Transmission of A. suum is associated with pig husbandry and use of pig feces as fertilizer.
ASYMPTOMATIC INFECTION
Most patients with A. lumbricoides or A. suum infection are asymptomatic.
All patients with Ascaris infection warrant anthelminthic treatment, even those with
asymptomatic infection. In endemic areas, mass treatment programs are effective. Outside
endemic areas, screening or administration of presumptive therapy for empiric treatment
is appropriate for adult immigrants and refugees from areas where the prevalence of soil-
transmitted helminths is high.
These issues are discussed further separately. (See "Mass drug administration for control of
parasitic infections" and "Medical care of adult refugees, immigrants, and migrants to the
United States", section on 'Parasitic infections' and "International adoption: Infectious
disease aspects", section on 'Intestinal parasites'.)
SYMPTOMATIC INFECTION
Most patients with A. lumbricoides or A. suum infection are asymptomatic. Nonetheless, the
global burden of symptomatic disease is relatively high because of the high prevalence of
disease. In general, clinical symptoms occur among individuals with relatively high worm
loads [2].
When symptoms do occur, they 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.)
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 [22]. Symptomatic pulmonary involvement is rare among individuals in
highly endemic areas with ongoing exposure, even among young children who can develop
very heavy infections [23,24]. One study in Colombia (where intestinal Ascaris infection
rates range from 25 to 90 percent) noted only four cases of Loeffler syndrome among
about 13,000 patients [23].
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'.)
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

(Loffler 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 about 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 [25]. 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)

[26]. These crystals are also observed in other eosinophilic parasitic lung infections. (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 [9,27,28]. Ground-glass opacities with ill-defined margins may
also be seen. On serial imaging, these nodules are migratory.
Diagnosis — Pulmonary ascariasis should be suspected particularly in individuals with no

prior Ascaris exposure and potential egg ingestion within weeks prior to onset of
respiratory symptoms (dry cough, dyspnea, fever, wheezing), characteristic radiographic
findings (migratory bilateral round infiltrates), peripheral eosinophilia, and relevant
epidemiologic exposure to eggs of A. lumbricoides or A. suum. The diagnosis may be

definitively established via visualization of Ascaris larvae in respiratory secretions or gastric
aspirates ( picture 1), although this is rarely possible. Symptomatic pulmonary
involvement is rare among individuals in highly endemic areas with ongoing exposure. (See
'Epidemiology' above.)
Stool examination is not useful for diagnosis of pulmonary infection, since eggs are
generally detected in the stool at least 40 days following pulmonary symptoms
( figure 1). A positive stool examination for Ascaris eggs at the time of respiratory
symptoms does not establish a causal diagnosis of pulmonary ascariasis, since these eggs
reflect infection acquired 2 to 12 months earlier. (See 'Life cycle' above.)
Treatment — Management of pulmonary manifestations associated with ascariasis

consists of supportive care. Symptomatic alleviation of wheeze and cough may be
managed with inhaled bronchodilators.
In the setting of severe pneumonitis, systemic corticosteroids may be administered, so

long as Strongyloides infection has been ruled out via examination of sputum and stool for
Strongyloides larvae. This is because administration of corticosteroids in the setting of
Strongyloides infection can induce Strongyloides hyperinfection syndrome (which can be
associated multiorgan system dysfunction and septic shock). Detection of Strongyloides
larvae should prompt management as discussed separately. (See "Strongyloidiasis".)
Anthelminthic therapy is generally not administered during the pulmonary phase since the
efficacy of drugs against larvae in the lungs is uncertain. Rather, follow-up should be
performed approximately two months after symptoms have resolved; at this time,
evaluation should include a stool examination for helminth eggs as well as Strongyloides
serologic testing. Treatment should then be administered accordingly for intestinal
infection(s) identified. (See 'Treatment' below.)
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 [29]. In one meta-
analysis, intestinal obstruction accounted for 38 to 87 percent of all complications of
ascariasis [30]. Another report noted that individuals presenting with intestinal
obstruction associated with ascariasis had an estimated burden of >60 intestinal
worms [31].
In some regions, ascariasis is the most common cause of acute abdominal surgical
emergencies [17], and, in endemic areas, 5 to 35 percent of all bowel obstructions are
due to ascariasis [18]. 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 [21].
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 [32-34]. 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 [34-37]. In one study, hepatobiliary and pancreatic ascariasis was the
etiological factor for biliary disease, acute pancreatitis, liver abscess, and biliary
lithiasis in 37, 23, 15, and 13 percent of cases, respectively [38]. 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 [39].
● Malnutrition – Ascariasis has been associated with malnutrition, growth retardation,

and impaired cognitive development in school children [40]. 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 [41]. However, it is difficult to discern the
true effect of ascariasis on nutritional status given other coexisting nutritional
deficiencies in infected children [42,43].
● Other manifestations – Occasionally, adult worms migrate outside the gastrointestinal

tract to ectopic sites. Migrating adult worms may emerge from the mouth, nose,
lacrimal ducts, umbilicus, or inguinal canal. Fever, anthelmintic drugs, fasting,
anesthesia, and other stresses have all been associated with stimulation of adult
worm migration [21]. Rarely, aspiration pneumonia can occur in association with
migration of adult worms up the esophagus and into the trachea in association with
vomiting.
Laboratory findings — Peripheral eosinophilia may be observed during the late

phase of infection but is more likely to be observed during the early phase [25]. (See
'Laboratory findings' above.)
Stool microscopy is discussed below. (See 'Ova and parasite examination' 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) [17]. 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) [17].
● Ultrasonography - Ultrasonography may demonstrate intestinal echogenic tubular

structures, curved strips, or a "target" sign [44]. In some cases, the worms
demonstrate curling movements [45,46]. 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 [44-46].
● CT or MRI – CT or MRI may demonstrate worms in the bowel. 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.
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 [47].
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 established via stool microscopy for eggs or via examination of adult
worms, which may be passed per rectum, coughed up, or passed in urine. 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. (See 'Epidemiology' above and 'Ova and
parasite examination' 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.)
Ova and parasite examination — The diagnosis of ascariasis is generally established

via stool microscopy for evaluation of Ascaris ova (the eggs of A. lumbricoides and A. suum
are indistinguishable). 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. In addition, no eggs will be present in stool if the infection is due to male
worms only.
Stool concentration methods for detection of Ascaris eggs include Kato-Katz and FLOTAC
techniques [48-52] (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. Examination of two stool samples
collected over consecutive days (compared with a single sample) increases hookworm
prevalence estimates by 20 to 25 percent [53]. 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 [54].
● The FLOTAC method is generally considered the most sensitive stool preparation
technique but requires a centrifuge, which limits its utility in some settings. In settings
with high prevalence of ascariasis, the sensitivity of Kato-Katz and FLOTAC are
comparable [55].
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).
Endoscopy — Endoscopy is warranted for evaluation of patients with suspected

involvement of the biliary tree or pancreatic duct due to ascariasis.
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) [56,57]. 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 — Polymerase chain reaction has superior sensitivity and specificity
compared with microscopy but is not yet a routine diagnostic tool [58-63].
Serology is generally reserved for epidemiologic studies rather than clinical diagnosis [20].
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 [64].
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Treatment
Clinical approach — Management of intestinal ascariasis consists of anthelminthic

therapy. (See 'Anthelminthic therapy' below.)
The approach to management of complications is as follows:
● Intestinal obstruction - Patients with intestinal obstruction should be managed

conservatively, with nasogastric suction and repletion of fluids and electrolytes; once
bowel motility is restored, anthelminthic therapy should be administered. 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".)
● Biliary ascariasis - Patients with biliary ascariasis usually respond with conservative
management including nasogastric suction and repletion of fluids and electrolytes. In
the setting of concomitant cholangitis, administration of antibiotics is warranted.
Anthelminthic therapy should be administered once acute symptoms subside. (See
"Acute cholangitis: Clinical manifestations, diagnosis, and management", section on
'Antibiotics'.)
Patients with one or more worms in the biliary tree warrant endoscopy for removal
[65-67]. (See 'Endoscopy' below.)
Anthelminthic therapy — Anthelminthic therapy helps reduce morbidity associated

with Ascaris infection but does not prevent reinfection [68]. Several agents have activity
against A. lumbricoides as discussed in the following sections. These agents are active
against adult worms but not against larvae.
Issues related to mass drug administration for control of ascariasis are discussed
separately. (See "Mass drug administration for control of parasitic infections".)
Nonpregnant individuals — The mainstays of treatment for ascariasis (caused by

A. suum or A. lumbricoides) in nonpregnant adults and children are the benzimidazoles:
albendazole (400 mg orally single dose) or mebendazole (500 mg orally single dose or 100
mg orally twice daily for three days) [69]. Adverse effects of the benzimidazoles include
transient gastrointestinal discomfort, headache, and, rarely, leukopenia. (See
"Anthelminthic therapies".)
A single dose of albendazole is effective in achieving cure in almost 100 percent of

ascariasis cases [70,71]. Both mebendazole regimens (three day and single dose) are
approximately 95 percent effective. A meta-analysis including 20 randomized trials
demonstrated high cure rates with single doses of albendazole and mebendazole [72].
However, single-dose therapy is not sufficient for treatment of concomitant hookworm or

Trichuris infection [73].
In a systematic review and network meta-analysis, average cure rates for treatment of A.
lumbricoides with albendazole, mebendazole, and pyrantel pamoate were 96, 96, and 93
percent, respectively [74]. The highest estimated egg reduction rate was highest for
albendazole (99 percent), followed by mebendazole and pyrantel pamoate (98 and 94
percent, respectively). There were no significant differences among the treatments.
Pregnant women — Pregnant women should be treated with pyrantel pamoate,

given potential teratogenic effects associated with benzimidazoles in animals [72]. Pyrantel
pamoate (11 mg/kg up to a maximum of 1 g) is administered as a single dose. The efficacy
varies with worm load; single-dose therapy is approximately 90 percent effective in
eradicating adult worms [75]. Adverse effects of pyrantel pamoate 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 [76]. (See "Mass drug administration for control of
parasitic infections".)
Alternative agents — Alternative agents for treatment of ascariasis include

ivermectin, nitazoxanide, piperazine citrate, and levamisole. (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)
[77]. Other studies of ivermectin at a range of doses (50 to 200 mcg/kg) [78] showed
cure rates and egg reduction rates comparable with those of albendazole and
mebendazole [69].
● Nitazoxanide – The efficacy of nitazoxanide varies according to egg burden [79-81]. 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 [81]. 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) [82].
● 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.
Endoscopy — Patients with one or more worms in the biliary tree warrant ERCP for
removal. 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 [83]. 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 [39,84]; however, others have observed
no recurrence of biliary ascariasis following sphincterotomy [85,86].
Worm extraction is usually associated with rapid symptomatic relief and is successful in
more than 80 percent of patients [39,83,87]. Patients with persistent biliary involvement
despite ERCP warrant surgical intervention.
Follow-up — Given the high cure rate with anthelminthic therapy, routine repeat
stool testing is not essential. However, it may be pursued two to three months following
treatment for patients in nonendemic areas to ensure infection has resolved. 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. (See 'Clinical
approach' above.)
Complete expulsion of adult Ascaris worms takes up to 10 days following albendazole

treatment, suggesting that follow-up at seven days is too early. Based on these findings,
the authors recommended waiting at least 14 days after treatment before performing
follow-up egg count [88].
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 these individuals, all may be treated simultaneously with a
benzimidazole (albendazole or mebendazole). (See 'Clinical approach' above.)
In endemic areas, reinfection occurs frequently; in some areas, more than 80 percent of
individuals become reinfected within six months. Intermittent mass drug therapy for such
circumstances is discussed separately. (See "Mass drug administration for control of
parasitic infections".)
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 and diagnosis of acute
pancreatitis".)
● Eosinophilic pneumonitis – 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".)
PREVENTION
In regions where Ascaris worms are abundant in soil, prevention of reinfection is extremely
difficult. Strategies for control include improvements in sanitation, health education, and
mass anthelminthic treatment [11]. Sanitation measures associated with lower rates of
helminth infection include use of treated water, availability of soap, and handwashing after
defecation [89,90]. In areas where human feces are used as fertilizer, educational programs
are needed to change this practice.
Issues related to mass drug administration for control of parasitic infections are discussed
separately. (See "Mass drug administration for control of parasitic infections".)
SUMMARY AND RECOMMENDATIONS
● Epidemiology – Ascaris lumbricoides is an intestinal nematode (roundworm); it is

estimated that more than one billion people are infected with A. lumbricoides
worldwide. The prevalence of infection is highest in tropical countries where warm,

wet climates favor year-round transmission of infection. In addition, the prevalence is
high in areas where suboptimal sanitation practices lead to increased contamination
of soil, water, and food. Ascaris suum is an intestinal parasite of pigs that is closely
related to A. lumbricoides. (See 'Epidemiology' above.)
● Life cycle – The life cycle of ascariasis is summarized in the Figure ( figure 1). 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. 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
(females 20 to 35 cm; males 15 to 30 cm) that inhabit the lumen of the small intestine,
usually in the jejunum or ileum. When both female and male worms are present in the
intestine, female worms produce fertilized eggs that pass into the stool. The eggs
prefer warm, shady, moist conditions under which they can survive for up to 10 years.
(See 'Life cycle' above.)
● Asymptomatic infection – Most patients with A. lumbricoides or A. suum infection are

asymptomatic. All patients with Ascaris infection warrant anthelminthic treatment,
even those with asymptomatic infection. (See 'Asymptomatic infection' above.)
● Symptomatic infection – When symptoms do occur, they occur most often during
the late-phase adult worm intestinal stage (as intestinal obstruction [most common]
or hepatobiliary or pancreatic manifestations) but may also occur during the early-
phase larval migration stage (as pulmonary manifestations).
• Early phase – 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. (See 'Early phase:
Pulmonary manifestations' above.)
• Late phase – During the late phase of infection (6 to 8 weeks after egg ingestion),
symptoms of ascariasis may consist of nonspecific symptoms such as abdominal
discomfort, anorexia, nausea, vomiting, and diarrhea. Complications of ascariasis
may include obstruction of the intestine, biliary, and/or pancreatic duct. (See 'Late
phase: Intestinal manifestations' above.)
● Pulmonary ascariasis
• Diagnosis – Pulmonary ascariasis should be suspected in individuals with no prior

Ascaris exposure and potential egg ingestion within weeks prior to onset of
respiratory symptoms (dry cough, dyspnea, fever, wheezing), characteristic
radiographic findings (migratory bilateral round infiltrates), and peripheral
eosinophilia. Symptomatic pulmonary involvement is rare among individuals in

highly endemic areas with ongoing exposure. The diagnosis may be definitively
established via visualization of Ascaris larvae in respiratory secretions or gastric
aspirates ( picture 1), although this is rarely possible. Stool examination is not
useful for diagnosis of pulmonary infection, since eggs are generally detected in
the stool at least 40 days following pulmonary symptoms. (See 'Diagnosis' above.)
• Management – Management of pulmonary ascariasis consists of supportive care.

Symptomatic alleviation of wheeze and cough may be managed with inhaled
bronchodilators. Anthelminthic therapy is generally not administered at the time
of pulmonary symptoms since the efficacy of drugs against larvae in the lungs is
uncertain. Rather, anthelminthic for intestinal ascariasis should be administered
following resolution of pulmonary manifestations, once adult worms have
developed to maturity in the small intestine. (See 'Treatment' above.)
● Intestinal ascariasis
• Diagnosis – 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 established via stool microscopy for ova
( picture 2) or via examination of adult worms. (See 'Clinical approach' above and
'Ova and parasite examination' above.)
• Management – Management of intestinal ascariasis and associated complications

consists of anthelminthic therapy. We recommend albendazole (400 mg orally
once) or mebendazole (500 mg orally single dose or 100 mg orally twice daily for
three days) for treatment of ascariasis (Grade 1A). For treatment of pregnant
women, pyrantel pamoate (11 mg/kg as a single dose up to a maximum of 1 g)
should be used. In some cases, surgical or endoscopic intervention is also
warranted. (See 'Clinical approach' above and 'Anthelminthic therapy' above.)
● Prevention – In regions where Ascaris worms are abundant in soil, prevention of

reinfection is extremely difficult. Strategies for the control include improvements in
sanitation, health education, and mass anthelminthic treatment. Sanitation measures
associated with lower rates of helminth infection include use of treated water,
availability of soap, and handwashing after defecation. Issues related to mass drug
administration for control of parasitic infections are discussed separately. (See
'Prevention' above and "Mass drug administration for control of parasitic infections".)
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13.03.

2024, 18:06 Ascariasis - UpToDate

Literature review current through: Feb 2024.

Transmission of ascariasis occurs primarily via ingestion of water or food contaminated

The epidemiology, clinical manifestations, diagnosis, treatment, and prevention of

● Ingesting uncooked pig or chicken liver bearing larvae of A. suum [10].

Transmission — Transmission of ascariasis occurs primarily via ingestion of water or food

Transmission of infection is enhanced by asymptomatically infected individuals who can

Most patients with A. lumbricoides or A. suum infection are asymptomatic.

Early phase: Pulmonary manifestations — Pulmonary ascariasis generally occurs in

The eosinophil-enriched pulmonary inflammation associated with pulmonary Ascaris

Pulmonary involvement associated with parasitic infection is known as Loeffler syndrome

Laboratory findings — Peripheral eosinophilia may be observed in association with

Sputum analysis may demonstrate eosinophils and Charcot-Leyden crystals ( picture 3)

Imaging findings — Chest radiography may demonstrate round or oval infiltrates

Computed tomography imaging generally demonstrates multiple nodules (generally up to

Diagnosis — Pulmonary ascariasis should be suspected particularly in individuals with no

epidemiologic exposure to eggs of A. lumbricoides or A. suum. The diagnosis may be

Treatment — Management of pulmonary manifestations associated with ascariasis

In the setting of severe pneumonitis, systemic corticosteroids may be administered, so

Late phase: Intestinal manifestations

Complications — Complications of ascariasis include intestinal obstruction,

Other complications associated with A. lumbricoides intestinal obstruction include

● Malnutrition – Ascariasis has been associated with malnutrition, growth retardation,

● Other manifestations – Occasionally, adult worms migrate outside the gastrointestinal

Laboratory findings — Peripheral eosinophilia may be observed during the late

Imaging findings — Imaging tools include plain radiography, barium swallow,

● Plain radiography - Plain radiography of the abdomen may demonstrate large

● Ultrasonography - Ultrasonography may demonstrate intestinal echogenic tubular

Magnetic resonance cholangiopancreatography (MRCP) may demonstrate adult

Clinical approach — Intestinal ascariasis should be suspected in patients with

Patients with suspected intestinal obstruction or other intestinal complication in

Ova and parasite examination — The diagnosis of ascariasis is generally established

Adult A. lumbricoides worms mature to become up to 35 cm long (females 20 to 35 cm;

Endoscopy — Endoscopy is warranted for evaluation of patients with suspected

On endoscopic ultrasonography, worms appear as long, linear hyperechoic structures

Clinical approach — Management of intestinal ascariasis consists of anthelminthic

The approach to management of complications is as follows:

● Intestinal obstruction - Patients with intestinal obstruction should be managed

Anthelminthic therapy — Anthelminthic therapy helps reduce morbidity associated

Nonpregnant individuals — The mainstays of treatment for ascariasis (caused by

A single dose of albendazole is effective in achieving cure in almost 100 percent of

However, single-dose therapy is not sufficient for treatment of concomitant hookworm or

Pregnant women — Pregnant women should be treated with pyrantel pamoate,

Alternative agents — Alternative agents for treatment of ascariasis include

● Ivermectin – Ivermectin (200 mcg/kg, rounded to the nearest 3 mg dose) causes

● Nitazoxanide – The efficacy of nitazoxanide varies according to egg burden [79-81]. In

● Piperazine citrate – Piperazine citrate (50 to 75 mg/kg once daily up to a maximum of

Complete expulsion of adult Ascaris worms takes up to 10 days following albendazole

Given the propensity of ascariasis to cluster in households, detection of persistent or

The differential diagnosis of intestinal manifestations associated with ascariasis includes:

● Intestinal nematode infection – Apart from Ascaris, intestinal nematodes

• Enterobius infection is generally asymptomatic or associated with perianal itching.

• The diagnosis of Trichuris, Enterobius, and hookworm may be established via

● Bowel obstruction – Bowel obstruction can occur in a number of clinical circumstances

● Malabsorption – Malabsorption can occur in a number of clinical circumstances apart

● Biliary obstruction – Biliary obstruction can occur in a number of clinical

cholangiopancreatography in some cases. (See "Diagnostic approach to the adult with

● Pancreatitis – Pancreatitis can occur in a number of clinical circumstances apart from