ASCARIASIS

Table of Contents:
1. Introduction
2. Epidemiology
3. Life Cycle
4. Clinical Features
a. Symptoms
b. Fatality
5. Diagnosis
6. Treatment
7. Prevention Adult female Ascaris lumbricoides against a
centimeter ruler. Source: “Ascaris lumbricoides”
8. References page from Universidade Federal do Rio Grande
do Sul, Brazil.

INTRODUCTION — Ascaris lumbricoides, an intestinal roundworm, is one of

the most common helminthic human infections worldwide. Highest prevalence in
tropical and subtropical regions, and areas with inadequate sanitation. Ascariasis
occurs in rural areas of the southeastern United States. In United States, ascariasis
is the third most frequent helminth infection, exceeded only by hookworm and
Trichuris trichiura (whipworm) [1]. A. lumbricoides is the largest intestinal
nematode of man. The female worms are larger than the males and can measure 40
cm in length and 6 mm in diameter. They are white or pink and are tapered at both
ends. The epidemiology, life cycle and clinical features of ascariasis will be
reviewed here.

EPIDEMIOLOGY — It is estimated that more than 1.4 billion people are

infected with A. lumbricoides, representing 25 percent of the world population. A
number of features account for its high prevalence including a ubiquitous
distribution, the durability of eggs under a variety of environmental conditions, the
high number of eggs produced per parasite, and poor socioeconomic conditions
that facilitate its spread. Transmission is enhanced by the fact that individuals can
be asymptomatically infected and can continue to shed eggs for years, yet prior
infection does not confer protective immunity [2].

Although ascariasis occurs at all ages, it is most common in children 2 to 10 years

old, and prevalence decreases over the age of 15 years. Infections tend to cluster in
families, and worm burden correlates with the number of people living in a home
[3]. Infection rates for ascariasis have not been reported to be higher in patients
infected with the human immunodeficiency virus (HIV) [4,5].

The highest prevalence of ascariasis occurs in tropical countries where warm, wet
climates provide environmental conditions that favor year-round transmission of
infection. This contrasts to the situation in dry areas where transmission is
seasonal, occurring predominantly during the rainy months [6]. The prevalence is
also greatest in areas where suboptimal sanitation practices lead to increased
contamination of soil and water. The majority of people with ascariasis live in Asia
(73 percent), Africa (12 percent) and South America (8 percent), where some
populations have infection rates as high as 95 percent [7,8]. In the United States
the prevalence of infection decreased dramatically after the introduction of modern
sanitation and waste treatment in the early 1900s [9]. It is estimated that the current
prevalence of A. lumbricoides in stool samples is approximately two percent in the
United States, but it may be more than 30 percent in children between the ages of
one to five years, particularly in rural areas of the South [10,11]. It is also seen in
travelers from endemic areas [7].

Ova can survive in the environment for prolonged periods and prefer warm, shady,
moist conditions under which they can survive for up to 10 years [1]. The eggs are
resistant to usual methods of chemical water purification but are removed by
filtration or by boiling. Developing larvae will be destroyed by sunlight and
desiccation. There is no significant animal reservoir, but A. suum, which infects
pigs, is morphologically similar to A. lumbricoides, and the larval forms can
occasionally infect humans.

Transmission — Transmission occurs mainly via ingestion of water or food (raw

vegetables or fruit in particular) contaminated with A. lumbricoides eggs and
occasionally via inhalation of contaminated dust. Children playing in contaminated
soil may acquire the parasite from their hands. Transplacental migration of larvae
has also occasionally been reported [12]. Coinfection with other parasitic diseases
occurs with some regularity because of similar predisposing factors for
transmission [10,13].

LIFE CYCLE — Adult worms inhabit the lumen of the small intestine, usually in
the jejunum or ileum. They have a life span of 10 months to 2 years and then are
passed in the stool. When both female and male worms are present in the intestine,
each female worm produces approximately 200,000 fertilized ova per day. When
infections with only female worms occurs, infertile eggs that do not develop into
the infectious stage are produced. With male-only worm infections, no eggs are
formed.

The ova are oval, have a thick shell, a mamillated outer coat, and measure 45 to 70
µm by 35 to 50 µm. The ova are passed out in the feces, and embryos develop into
infective second-stage larvae in the environment in two to four weeks (depending
upon environmental conditions). When ingested by humans, the ova hatch in the
small intestine and release larvae, which penetrate the intestinal wall and migrate
hematogenously or via lymphatics to the heart and lungs. Occasionally, larvae
migrate to sites other than the lungs, including to the kidney or brain.

Larvae usually reach the lungs by four days after ingestion of eggs. Within the
alveoli of the lungs, the larvae mature over a period of approximately 10 days, then
pass up via bronchi and the trachea, and are subsequently swallowed. Once back in
the intestine, they mature into adult worms. Although the majority of worms are
found in the jejunum, they may be found anywhere from the esophagus to the
rectum. After approximately two to three months, gravid females will begin to
produce ova which, when excreted, complete the cycle.

Adult worms do not multiply in the human host, so the number of adult worms per
infected person relates to the degree of continued exposure to infectious eggs over
time. Worm burdens of several hundred per individual are not uncommon in highly
endemic areas, and case reports of more than 2,000 worms in individual children
exist [8]. However the number of eggs produced per female worm tends to
decrease as the worm burden increases. It has been estimated that 9 x 10(14) eggs
contaminate the soil per day worldwide [14].
Life Cycle Figure – Adult worms (1) live in the lumen of the small intestine. A female may produce
approximately 200,000 eggs per day, which are passed with the feces (2). Unfertilized eggs may be ingested
but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks (3),
depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are
swallowed (4), the larvae hatch (5), invade the intestinal mucosa, and are carried via the portal, then
systemic circulation to the lungs (6). The larvae mature further in the lungs (10 to 14 days), penetrate the
alveolar walls, ascend the bronchial tree to the throat, and are swallowed (7). Upon reaching the small
intestine, they develop into adult worms (1). Between 2 and 3 months are required from ingestion of the
infective eggs to oviposition by the adult female. Adult worms can live 1 to 2 years. Source: CDC’s Parasite
and Health Page about intestinal ascariasis.

CLINICAL FEATURES — The majority of infections with A. lumbricoides are

asymptomatic. However, the burden of symptomatic disease worldwide is still
relatively high because of the high prevalence of disease. Clinical disease is largely
restricted to individuals with a high worm load [1]. When symptoms do occur, they
relate either to the larval migration stage or to the adult worm intestinal stage.
Pathophysiologic mechanisms include

 Direct tissue damage

 The immunologic response of the host to infection with larvae, eggs or adult
worms [2]
 Obstruction of an orifice or the lumen of the gastrointestinal tract by an
aggregation of worms
  Nutritional sequelae of infection [10]

The symptoms and complications of infection can be classified into the following:

1. Pulmonary and hypersensitivity manifestations

2. Intestinal symptoms
3. Intestinal obstruction
4. Hepatobiliary and pancreatic symptoms

1. Pulmonary and hypersensitivity manifestations — Transient

respiratory symptoms can occur in sensitized hosts during the stage of
larval migration through the lungs. (See "Pulmonary manifestations of
ascariasis"). Symptoms associated with the pneumonitis, which are
known as Loffler's syndrome, tend to occur one to two weeks after
ingestion of the eggs. The severity of symptoms tends to correlate
with larval burden, but pulmonary symptoms are also less common in
countries with continuous transmission of A. lumbricoides.

Urticaria and other symptoms related to hypersensitivity usually occur

toward the end of the period of migration through the lungs.

2. Intestinal symptoms — Heavy infections with Ascaris are frequently

believed to result in abdominal discomfort, anorexia, nausea and
diarrhea. However, it has not been confirmed whether or not these
non-specific symptoms can truly be attributed to ascariasis.

With relatively heavy infections, impaired absorption of dietary

proteins, lactose and vitamin A has been noted, and steatorrhea may
occur. One review concluded that Ascaris-free or treated children
showed better nutritional status in terms of growth, lactose tolerance,
vitamins A and C, and albumin levels than Ascaris-infected children
based upon almost 20 years of published cross-sectional and
intervention studies from Africa, Asia and South America [15]. This
review also found significant improvement in weight or height
following therapy for ascariasis. However, other studies have not
confirmed these conclusions, and the true effect of ascariasis on
nutrition is still widely debated, especially as additional nutritional
 deficiencies commonly co-exist in infected children [16-23]. It has
also been proposed that heavy infections may be associated with
impaired cognitive development in school children [24,25].

3. Intestinal obstruction — A mass of worms can obstruct the bowel

lumen in heavy Ascaris infection, leading to acute intestinal
obstruction. The obstruction occurs most commonly at the ileocecal
valve. Symptoms include colicky abdominal pain, vomiting and
constipation. Vomitus may contain worms. Approximately 85 percent
of obstructions occur in children between the ages of one and five
years. Sometimes an abdominal mass that changes in size and location
on serial examinations may be appreciated [10]. Complications
including volvulus, ileocecal intussusception, gangrene, and intestinal
perforation occasionally result.

The overall incidence of obstruction is approximately 1 in 500

children. In endemic areas, it has been shown that between five and 35
percent of all cases of bowel obstruction are due to ascariasis [1]. One
review estimated the worm burden with intestinal obstruction to be
>60 (and ten times higher in fatal cases) [26]. Ascariasis is said to be
the most common cause of acute abdominal surgical emergencies in
certain countries including South Africa and Myanmar [8]. In a recent
meta-analysis of morbidity and mortality related to ascariasis,
intestinal obstruction accounted for a mean of 72 percent of
complications of the infection [27].

4. Hepatobiliary and pancreatic symptoms — Symptoms related to the

migration of adult worms into the biliary tree can cause abdominal
pain, biliary colic, acalculous cholecystitis, ascending cholangitis,
obstructive jaundice, or bile duct perforation with peritonitis.
Strictures of the biliary tree may occur [28]. Hepatic abscesses can
also result [29]. Retained worm fragments can serve as a nidus for
recurrent pyogenic cholangitis. The pancreatic duct may also be
obstructed, leading to pancreatitis, and the appendix resulting in
appendicitis. Occasionally, migrating adult worms emerge from the
mouth, nose, lacrimal ducts, umbilicus or inguinal canal. High fever,
diarrhea, spicy foods, anesthesia and other stresses have all been
associated with an increased likelihood of worm migration [10].
 In endemic countries such as India, ascariasis has been found to cause
up to one-third of biliary and pancreatic disease [30,31]. In one study
performed in Syria, 300 patients with biliary or pancreatic ascariasis
were diagnosed by endoscopic retrograde cholangiopancreatography
(ERCP) over a five-year period [32]. Of these 300 patients, 98 percent
presented with abdominal pain, 16 percent developed ascending
cholangitis, 4 percent developed acute pancreatitis, and 1 percent
developed obstructive jaundice. A previous cholecystectomy or
endoscopic sphincterotomy had been performed in 80 percent.
Endoscopic extraction of the worms, successful in all but two cases,
led to rapid resolution of symptoms.

Complications associated with A. lumbricoides infections are fatal in up to five

percent of cases. It is estimated that 20,000 deaths from ascariasis occur annually,
primarily as a consequence of intestinal obstruction [33].

Ascaris lumbricoides in small intestine – Intestinal

obstruction occurs when large masses of Ascaris
accumulate. Source: Dr. Scott Smith’s lecture on GI
Nematodes for “Parasites and Pestilence,” Stanford
University.

DIAGNOSIS — The diagnosis of ascariasis is usually made via stool microscopy.

Other forms of diagnosis are through eosinophilia, imaging, ultrasound,
or serologyexamination.

 Microscopy — Characteristic eggs may be seen on direct examination of

feces or following concentration techniques. However, eggs do not appear in
the stool for at least 40 days after infection; thus, the main drawback of
relying upon eggs in feces as the sole diagnostic marker for Ascaris infection
 is that an early diagnosis cannot be made, 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. Sometimes an adult worm is passed,
usually per rectum. If an Ascaris worm is found in the feces, a stool
specimen can be checked for eggs to document whether or not additional
worms are present prior to instituting therapy [10].

Ascaris lumbricoides in stool – Wet mount of stool (x400) showing the ovum of ascaris
lumbricoides. Source: UpToDate’s Ascariasis Graphics.

 Eosinophilia — Peripheral eosinophilia can be found, particularly during

the phase of larval migration through the lungs but also sometimes at other
stages of Ascaris infection [34]. Eosinophil levels are usually in the range of
5 to 12 percent but can be as high as 30 to 50 percent. Serum levels of IgG
and IgE are also often elevated during early infection.

 Imaging — In heavily infested individuals, particularly children, large

collections of worms may be detectable on plain film of the abdomen. The
mass of worms contrasts against the gas in the bowel, typically producing a
"whirlpool" effect [8]. Radiologic detection of adult worms is sometimes
made by detecting elongated filling defects following barium meal
examinations of the small bowel. The worms also sometimes ingest barium,
in which case the alimentary canal appears as a white thread bisecting the
length of the worm's body [8]. Radiographs will also show when there is
associated intestinal obstruction.
 Biliary ascariasis – Cholangiogram obtained during
endoscopic retrograde cholangiopancreatography
shows a linear filling defect (arrow) that was later
identified as an adult Ascaris lumbricoides worm.
Source: UpToDate’s Ascariasis Graphics page.

 Ultrasound — Ultrasound examinations can help to diagnose hepatobiliary

or pancreatic ascariasis. Single worms, bundles of worms, or a pseudotumor-
like appearance may be seen [35]. Individual body segments of worms may
be visible, and on prolonged scanning, the worms will show curling
movements [36]. Computed tomographic (CT) scanning or magnetic
resonance imaging (MRI) may also be used to identify worm(s) in the liver
or bile ducts, but this is not usually necessary. Imaging the worm in cross-
section gives a "bull's eye" appearance. When ascariasis involving the biliary
tree or pancreatic duct is suspected, an ERCP will not only establish the
diagnosis but also allows for the direct removal of the worm [32,37].

 Serology — Infected individuals make antibodies to A. lumbricoides which

can be detected. However, serology is generally reserved for epidemiologic
studies rather than in the diagnosis in a particular individual [2]. IgG
antibodies are not protective against infection [38]. Antibodies to Ascaris
also often cross react with antigens from other helminths.

TREATMENT — Treatment consists of choosing the

right drugs, therapy, follow-up, and supportive care for each patient.
Choice of Drugs — A number of drugs can be used in the treatment of
ascariasis. These include: pyrantel
pamoate, mebendazole, albendazole, ivermectin,piperazine citrate,
and levamizole.

Ascaris lumbricoides expelled following effective drug treatment. Source:

Courtesy of Dr. Tom Nutman, NIH.

* Pyrantel pamoate — Pyrantel pamoate (11 mg/kg up to a

maximum of 1 g) is administered as a single dose. Adverse
effects include gastrointestinal (GI) disturbances, headaches,
rash, and fever. Parasite immobilization and death occur,
although this happens slowly and complete clearance of the
worm from the GI tract may take up to three days. Efficacy
varies with worm load, but single dose therapy is approximately
90 percent effective in eradicating adult worms [6].

* Mebendazole — Mebendazole (100 mg BID for 3 days or 500

mg as a single dose) is an alternative. Adverse effects include
transient GI discomfort, headache, and rarely leukopenia. The
three-day regimen is approximately 95 percent effective, and
the single dose seems to have similar results.

* Albendazole — A single dose of albendazole (400 mg) is

effective in almost 100 percent of cases, although reinfection
commonly occurs [39]. Albendazole causes the same adverse
effects as mebendazole.
 * Ivermectin — Ivermectin causes paralysis of adult worms and is
approximately as effective as other available therapies but is not
generally used.

* Piperazine citrate — Piperazine citrate (50 to 75 mg/kg QD up

to a maximum of 3.5 g for 2 days) was a frequent treatment
regimen, but it is now being withdrawn from the market in
many developed countries because the other alternatives are
less toxic and more efficacious. However, it may still be
recommended when there is suspected intestinal or biliary
obstruction since this drug paralyzes worms to aid expulsion.

* Levamisole — Levamisole (150 mg for adults and 5 mg/kg for

children) is safe and is effective in 77 to 96 percent of cases of
ascariasis.

Choice of therapy — The mainstays of treatment currently are the

benzimidazoles, mebendazole and albendazole. However, they should
not be given during pregnancy because of possible teratogenic effects.
Thus, pyrantel pamoate should be used in pregnancy. In a randomized
study conducted among 2,294 children aged 6 to 12 years in Zanzibar,
single dose mebendazole and albendazole were both found to have
efficacies greater than 97 percent [40]. Similar results with both drugs
and good tolerability have also been observed in other studies [41-43].

Follow-up — All of these therapies act against the adult worm but not
the larvae. Following therapy, patients should be reevaluated at two to
three months to ensure that no eggs are detectable, either because of
inadequate elimination of adult worms or because of reinfection.
Reinfection occurs frequently; more than 80 percent of individuals in
some endemic areas become reinfected within six months [1].
Evaluation of other family members should be entertained whenever
the diagnosis is made because of the propensity of the infection to
cluster in families [10,12].

Supportive care — In addition to specific anthelminthic therapy,

supportive therapy for complications of ascariasis may be required,
including potential surgical intervention for intraabdominal
complications. In biliary infections, conservative therapy with
anthelminthics, often combined with antispasmodics, is often
 successful. However, surgical or endoscopic interventions may be
required.

Since pulmonary ascariasis is a self-limited disease, symptomatic

alleviation of wheeze and cough with inhaled bronchodilators can be
instituted. Occasionally, systemic corticosteroids may be required for
symptoms. Following symptomatic therapy, standard therapy for
intestinal ascariasis can be given after the worms have developed to
maturity in the small intestine [6]. Anthelminth therapy is not usually
given at the time of pulmonary symptoms because dying larvae may
do more harm than migrating ones.

Biliary ascariasis – An adult Ascaris lumbricoides worm protruding

from the major papilla is grasped with forceps during endoscopic
retrograde cholangiopancreatography. Source:
UpToDate’s Ascariasis Graphics page.

PREVENTION — Prevention of reinfection poses a substantial problem since

Ascaris parasites are abundant in soil. Good sanitation to prevent fecal
contamination of soil is required. An education program advising against the use of
human feces as a fertilizer is also needed in some areas. Soil treatments have been
attempted but are generally not practical.

Mass treatments with single dose mebendazole or albendazole for all school-age
children every three to four months has been used in some communities. This
serves the dual function of treating the children and reducing the overall worm
burden in the community. Indeed, mass community therapy has been shown to
reduce Ascaris burden and transmission, although it has a greater effect on the
intensity of infection than on the overall prevalence [44-47]. This approach has
been shown to be cost-effective [48]. Because reinfections occur so frequently,
shorter intervals between treatments have been found to be preferable. Targeted
treatment helps control the morbidity of infection but does not have a substantial
effect on transmission [44,49,50]. In a large randomized trial of school-based
deworming performed in Zanzibar, for example, single dose mebendazole, given
either twice or three times a year, decreased intensity of A. lumbricoides infection
by 63 and 97 percent, respectively, compared to control children who received no
mebendazole [51].

CREDITS — This website has been adapted by Jessika Lora from Karin Leder
and Peter F. Weller’s UpToDate review of ascariasis.

“UpToDate performs a continuous review of over 330 journals and

other resources. Updates are added as important new information is
published. The literature review for version 13.1 is current through
December 2004. The next version of UpToDate (13.2) will be released
in June 2005.”

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