Ascaris lumbricoides
 

 

 

 

 


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Introduction

          Ascariasis is a disease caused by a parasite, which is an organism that

depends on another organism for its survival.  The specific parasite involved in

Ascariasis is known as Ascaris lumbricoides.  A. lumbricoides is a type of

nematode or roundworm.  It has also been referred to more commonly as the giant,

intestinal roundworm.  A. lumbricoides is actually the largest intestinal roundworm

found in humans.  It is also one of the most common parasites found in humans. 

It currently affects more than 1-1.5 billion people worldwide. 

Most people harboring A. lumbricoides show no signs of infection with

the roundworm.  Some people may show early pulmonary symptoms and

eosinophilia during the larval migration of the parasite.  Later on, some patients may

also have abdominal symptoms.  Occasionally, A. lumbricoides can cause life-

threatening disease from the worm bolus or ectopic migration of the worms.  The worm

lives in the upper part of the small intestine, and there are no reservoirs for the parasite. 

Some effective drugs exist to treat the Ascaris.

 

A picture of a female A. lumbricoides. 

This roundworm was passed by a young girl living in Florida. 

 

Image taken from DPDx (Identification and diagnosis of Parasites

Of Public Health Concern.    http://www.cdc.gov/ncidod/dpd/parasites/ascaris

 
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Agent

          The disease known as ascariasis is caused specifically by the parasitic agent

Ascaris lumbricoides.  Occasionally, the swine ascarid, Ascaris suum, can infect

humans as well.  It is still debated whether or not A. lumbricoides and A. suum are

different species.  

A. lumbricoides is a type of organism grouped with other helminthes or

worms.  Three different phyla comprise the group known as Helminths.  There are

Cestodes, which include blood parasites or flukes, Trematodes, which consist of

segmented worms like tape worms, and Nematodes, which are roundworms like

Ascaris.  Nematodes or roundworms are a type of invertebrate, animals without

backbones.  Specifically, nematodes are characterized by their long, round bodies. 

Common parasitic roundworms apart from A. lumbricoides include: the pinworm,

the hookworm, and the whipworm.    

A.    lumbricoides gets its name from the earthworm Lumbricus terrestrias. 

When it was first discovered, this roundworm was called Lumbricus teres.    

 

Here is the specific classification of Ascaris lumbricoides:

Domain  Eukarya

Phylum   Nematoda

Order     Asaridida

Family    Ascaridoidea

Genus     Ascaris

Species   lumbricoides

 

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Synonyms

          Ascaris is also known as a large, intestinal roundworm. 

 

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History of Discovery

          The anatomy of A. lumbricoides was first described by Edward Tyson in

1683.  However, at that time it was known as Lumbricus teres not A. lumbricoides.  

It was actually Linnaeus, who renamed Ascaris and gave it its current name.

Linnaeus named the roundworm Ascaris lumbricoides because it showed very

similar morphology as that of the earthworm, Lumbricus terrestrias. 

Then in 1917, Brayton Ransom and Winthrop Foster were able to document

the actual life cycle of Ascaris.  Afterwards in 1922, Shimesu Koino experimented

on himself and his younger brother in order to describe the clinical disease produced

by Ascaris.  Koino worked with both A. lumbricoides  and A. suum.  He swallowed

2000 A. lumbricoides eggs, and he made his younger brother swallow 500 A. suum  

larvae.  Koino became very ill for the experiment but luckily no lasting damage

occurred, and his brother did not suffer from as severe a disease.  Specifically, in

this daring self-experiment, Koino showed that a pneumonia-like syndrome can

develop during early infection with Ascaris.  He also discovered that this syndrome

was caused by migration of larvae through the lungs to the stomach.   

 

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Clinical Presentation in Humans

 

 Clinical Case Study

Taken from an article by C. Randall Clinch and LCDR March B. Stephens. 

“Case description of Ascaris,” Arch Fam Med.  2000, 9; 1193-1194.

 

A 37-year-old man comes to your office after passing something in his stool

that he thought was a rubberband.  He became worried when he saw the object

moving in the toilet.  Apart from this occurrence, he is a healthy man and is not

taking any medications.  He has had no recent change in bowel habits or stool

appearance.  He has not had fever, abdominal pain, cough or rash.  He does not

smoke, drink alcohol, or use recreational drugs.  He has been physically active

and recently completed a weeklong backcountry hiking expedition in the

Southeastern U.S.  Other than this expedition, he has not been traveling recently.

          With the clinical history and presentation in mind the following are some

possible diagnoses: 1) Ascaris lumbricoides (round worm) infection 2) Toxocara

(visceral larva migrans) infection 3) Trichuris (whipworm) infection 4) rubberband

ingestion. It turned out that this patient had Ascaris lumbricoides.   

 

Clinical Correlation (Signs and Symptoms)

          Ascariasis is the disease caused by the parasite Ascaris lumbricoides. 

Typically, Ascaris infection does not cause visible disease.  Most cases of Ascaris

infection tend to be asymptomatic.  Clinically inapparent disease occurs with low

infection of Ascaris, meaning that not many eggs are ingested.  However, if hundreds

of eggs are ingested, as seen in the early experiments by Shimesu Koino, the patient

can develop pneumonitis.  Pneumonitis occurs when the larvae migrate to the lungs. 

This pneumonitis also known as Loeffler’s syndrome, can appear four days to two

weeks after infection occurs. 

Some patients may also develop asthma, and the asthma attacks can persist

until worms are removed.  Often times the development of asthma in a nonsasthmatic

person can be a clue of ascariasis.  In addition, liver enlargement and general toxicity

can also occur during this period and persist for up to two weeks.  Other health

problems include fever, urticaria, malaise, nausea, vomiting, diarrhea, central nervous

system disorders, and colic.  Nutritional problems that may develop can then lead to

abnormal development in children. 

             While the worms are in the intestine, they can sometimes cause a life-

threatening disease.  If many worms are present, they can become entangled and

form a bolus, which blocks the lumen.  Each year two cases out of one thousand

have been reported noting this severe intestinal obstruction.  Another fatal condition

has been reported where the worms have penetrated the small intestine leading to

acute peritonitis.   

          In addition, adult worms can migrate ectopically to the appendix, common

bile duct, and pancreatic duct.  This is another life-threatening condition that is most

often seen in small children with high parasite loads.  As a result of the worm in the

biliary duct, cholecystitis, cholangitis, hepatic abscess, and pancreatitis can occur. 

Suppuration can follow from deterioration of the trapped worm and secondary

bacterial infection.

 

General Summary of Symptom Timeline

 

Early phase (The early phase coincides with larval tissue-migration.  Typically,

4-16 days after egg ingestion.)  The main symptoms include the following:

-fever

-cough

-wheeze

 

Late Phase (The late phase coincides with the mechanical effects of the worms.

These include GI symptoms from mechanical irritation.  Typically, 6-8 weeks

after egg ingestion)  The main symptoms include the following:

 

-vague abdominal complaints (cramping, nausea, vomiting)

-small bowel obstruction (mainly in children)

-pancreatitis (2ndary to worm migration)

-cholecystitis (2ndary to worm migration)

-appendicitis (less common, 2ndary to worm migration)

 

Multiple Nematode infections. Four year old Puerto Rican patient

with multiple parasites including Strongyloides stercoralis,, hookworm,

Ascaris lumbricoides and Trichuris trichiura. He was small of stature

(equivalent to 1 3/4 year old) and his weight was that of a 2 year old.

 

http://parasitepics.biosci.uga.edu

 

       

Ascaris in the small intestine.                                         A. lumbricoides penetrating the

http://parasitepics.biosci.uga.edu                                   small intestine causing an acute

condition known as peritonitis. 

 

Dr. Scott Smith’s lecture on ascariasis

              

Child passing A. lumbricoides.  

       Bolus of A. lumbricoides passed from intestinal tract. 

From Dr. Scott Smith’s                               The large mass was about 1.5 inches in length.

Lecture on Ascariasis.                                                              

 

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Transmission

A.    lumbricoides  is transmitted primarily through fecal-oral contamination. 

The transmission can occur by ingesting contaminated soil, water, or food.  Usually,

ascariasis is caused by directly or indirectly eating soil contaminated with feces

carrying these eggs.  These eggs mature in the body, and adult female worms can

then lay eggs that come out in the feces.  Note, however, that in order for the eggs

to be infective or embryonated, the feces must have been infected 2-4 weeks before it

is ingested.  Infection with Ascaris eggs is so common because the eggs are frequently

found in the environment due to poor sanitation practices and the use of night fertilizer.    

In addition to fecal-oral transmission of A. lumbricoides, it is also believed

that ascariasis can occur by way of trasnplacental transmission, since many

neonatal cases have been documented.

          It should be noted that Ascaris eggs are some of the most resistant

existing microorganisms.  Their hearty egg shells consist of four layers: ascaroside,

chitinous, vitelline and uterine.  The eggs are not responsive to chlorine, high pH, low

pH, and UV irradiation.  They are resistant to high and low temperatures.  Alcohol,

ether, and surfactants can inactivate the eggs.  In fact, Ascaris eggs can survive for

many years in the soil.

 

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Life Cycle

 

Adult worms reside in the upper part of the small intestine, where they

survive on predigested food.  The worms make themselves into an S-shape

and press against the epithelium of the intestine while moving against the peristalsis

to keep themselves in the small intestine.  The female worm lays eggs, and she can

produce up to 200,000 eggs per day.  These eggs are fertilized but

nonembryonated, and the eggs are passed out with feces.

          The fertilized eggs develop through embryonation in feces deposited

in the soil.  The process of embryonation takes 2-4 weeks.  The eggs can survive

many months before embryonation starts, but they need a moist aerobic

environment to develop.  The eggs are only infective once they are embryonated

and have larvae in them. 

          Once embryonated, the infective egg must be swallowed to complete

the life cycle of A. lumbricoides.  Bile salts and alkaline enteric juice of the small

intestine stimulate the release of the larvae from the eggs.  These second-stage larvae

then travel from the small intestine to the liver.   Then the larvae migrate to the heart

via pulmonary circulation.  The larvae are now third-stage larvae in the alveolar

capillaries, and they enter the alveolar spaces.  Afterwards they migrate to the bronchi

into the tranchea and then to the epiglottis. 

The larvae are then swallowed, and they pass once again to the small

intestine.  There they molt twice and mature into adult worms.  The adult worms

can live up to one year, and the females can lay eggs in the small intestine.  However,

A. lumbricoides cannot reproduce in the intestine, and it can only lay eggs that are

not yet infective.

 

 

Found in Feachem et al, 1983

From webpage by Kara Nelson.

 

 

Adult worms  live in the lumen of the small intestine.  A female may produce up

to 240,000 eggs per day, which are passed with the feces  .  Fertile eggs

embryonate and become infective after 18 days to several weeks  , depending

on the environmental conditions (optimum: moist, warm, shaded soil).  After

infective eggs are swallowed  , the larvae hatch  , invade the intestinal mucosa,

and are carried via the portal, then systemic circulation to the lungs  .  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  .  Upon reaching the

small intestine, they develop into adult worms  .  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.

 

Taken from http://www.cdc.gov/ncidod/dpd/parasites/ascaris

 

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Reservoir

          No reservoir for this type of Ascaris exists outside of humans.  Pigs

have their own type of Ascaris, which was mentioned previously.

 

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Vector

          No vector exists for Ascaris.

 

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Incubation Period

          The appearance of early symptoms of clinical disease can occur

anywhere between 4-16 days after ingestion of the eggs.  Loeffler’s syndrome

and other symptoms.  Such as fever, coughing, and wheezing take this long to

develop.  However, GI symptoms take 6-8 weeks after ingestion of the eggs to

 develop.

 

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Morphology

          Ascaris is a large intestinal roundworm.  It superficially resembles the

common earthworms found in the soil.  Female worms can be as long as 20-35

cms, and males tend to be smaller, no larger than 30 cms.  They can be anywhere

from 2-6 mm wide.  Mature worms are cylindrical, creamy white or light brown.

They tend to have tapered ends.

The worms have a thick cuticle, 3 lips at its head, small teeth, and its own

digestive tract.  The fertilized eggs are oval shaped, and they are about 65 to 40

um in size.   The eggs are brown or yellow brown, and they have a thick shell. 

 

      

An adult male (coiled posterior end) and a female A. lumbricoides. 

Note that the anterior ends are more slender than the posterior ends.

 

image taken from “A pictorial Presentation of Parasites”

http://parasitepics.biosci.uga.edu/CumulusCGI/Cumulus.acgi$KLS2672,105

 

This picture shows the male and female worms.  The female shown is approximately

16 inches long.

 

Taken from P. Darben.

 

A scanning electron micrograph picture taken of the

anterior end of Ascaris.  The three lips of the worm are shown.

 

Taken from “Wormland” site. 

 

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Diagnostic Test

          Diagnosis is usually not made clinically based on signs and symptoms. 

Sometimes it can be diagnosed using ultrasonography and endoscopic

retrograde cholangiopancreatography (ERCP). 

Instead, diagnosis is made primarily by examining a stool specimen.

Infection with A. lumbricoides is determined by microscopic identification of

eggs in the stool.  Typically, the procedure used involves the following:

1)    collecting stool specimen  2) fixing specimen in 10% formalin

3)    concentrate using formalin-ethyl acetate sedimentation technique

4) examine wet mount of sediment

Occasionally, emergence of a worm in the stool or coughed up can be used

to diagnosis the patient.

 

  

Comparative egg morphology for different Nematodes and Cestodes using in diagnostics.

 

           

 

A picture of a fertilized egg. 

Note the rounded shape,                             Another picture of a fertilized egg. 

the thick shape, external mammilated           Taken from “Atlas of Medical Parasitology.”

layer.    (brown from bile).

http://www.cdc.gov/ncidod/dpd/parasites/ascaris

 

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Management and Therapy      

 Image taken from Brian E. Keas

  webpage on Ascaris lumbricoides.

 

          People with Ascaris should be treated regardless of the presence of

high worm load, for ectopic migration of worms can cause life-threatening health

problems.  The choice drugs for the treatment of Ascaris infection are albendazole,

mebendazole, and pyrantel pamoate.  These drugs are effective with few side-effects.

          Mebendazole (Vermox) and Albedazole are one class of drugs used to treat

Ascaris infection.  Mebendazole has often times been considered the choice drug to

treat intestinal roundworm infections.  The adult dose is 100 mg PO BID on 3

consecutive days or 500 mg once.  A second course is administered if the patient is

not cured in 3-4 weeks.  Side-effects are mild, but migratory activity has been reported

in response to the drug.  The dosage for Albendazole is 400 mg once.   

          Pyrantel pamoate is also effective in treating Ascaris.  It can treat

other nematodes, and it works by paralyzing the worms.  The dosage is 11mg/kg once

(max. 1 gram). 

Apart from the 3 drugs listed above, a few other treatments exist.  Yet, these are

choice drug treatments listed by the CDC.  Levamisole hydrochloride is another type

of drug used to treat Ascaris.  This drug has more side-effects than Mebendazole and

Pyrantel, and it works by paralyzing the worm.  In addition, piperazine salts can also be

used to treat Ascaris.  Not many side-effects have been noted, but they tend to be more

common than other drugs available.  They are often times used because they are

cheap and effective.

 

 

 Courtesy Dr. Tom Nutman at the NIH

 

From Dr. Scott Smith’s lecture.

 

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Epidemiology

          Ascariasis plagues more people in the world than any other parasitic

infection.  Some estimate that as many as 1-1.5 billion people or approximately 1

out of 4 people are infected with Ascaris.  In some tropical areas, 100% of the

population have Ascaris. 

Ascariasis tends to occur more commonly in places where sanitation is

minimal and human feces is used to fertilize crops.  As a result, the majority of

Ascaris infections are concentrated in the developing world. 

Approximately, 59 million people are at risk of morbidity or clinical illness from

Ascaris.  Children are more likely to be infected and have higher levels of worms. 

1.5 million children with Ascaris infections will suffer from irreversible growth

retardation.  While death from Ascaris is rare, approximately 10,000 people die from

Ascaris each year. 

          Males tend to be more infected then females, due to behavioral habits that

make it more likely for them to ingest soil.  Some evidence of genetic predisposition

has also been noted in a study of families in Nepal. 

   

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Country InformationImage taken from Brian E. Keas webpage

                     on A. lumbricoides.

 

          Ascaris is found all over the world.  However, it is most prevalent in warm,

tropical climates, where eggs can survive the longest in the soil.  It is less common

in places that are arid and seasonal.  Concentration of Ascaris seems to fall most

heavily in South-EastAsia with less cases in Africa and Latin America.  In South-East

Asia approximately 73% of the people are infected.  India, Bangladesh, Burma,

Indonesia, Malaysia, Philippines, Vietnam, China, Kenya, Tanzania, West Africa,

Turkey, Iran, Afghanistan, Brazil, Columbia, Mexico, and Peru have all reported areas

where Ascaris occurs in more than 50% of the local population living in these places.

          Even in the U.S., many cases of Ascaris occur.  Approximately 4 million

people in the U.S. are infected with Ascaris, and the majority of these cases are

concentrated in the rural southeast part of the country.  

 

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Public Health and Prevention Strategies (Vaccines)

          Prevention and control of Ascaris can occur on two fronts: drug treatment

and sanitation improvement.  Mass chemotherapy programs given every 6 months

can help break the cycle of constant Ascaris infection.  It is also important to educate

people about adopting healthier living habits.  For instance, people can avoid eating

noncooked vegetables and fruits in places lacking proper sanitation and areas that

use human fertilizer.  No vaccines are currently in use to prevent the spread of this

parasite.

 

Listed below are some of the World Health Organization’s listed combined

strategies to control soil-transmitted helminthes such as A. lumbricoides:

 

1) ensuring the wide availability of  single dose antihelminthic drugs

in all health services in endemic areas

2) ensuring good passive and active case management

3) regularly treating at least 75% of all school-age children at

risk of morbidity by 2010

4)regularly treating children at risk of morbidity through the IMCI strategy

5)improving access to safe water and sanitation through intersectoral

             collaboration

6) improving hygiene behavior by scaling up sanitation education, targeted at

             high-risk groups such as school-age children, women, and special

             occupation groups

 

 

Collection of passed Ascaris from treatment project in school children. 

Courtesy Dr. Tom Nutman at the NIH

Dr. Scott Smith’s lecture on Ascariasis

 

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Useful Web Links

http://www.cdc.gov/ncidod/dpd/parasites/ascaris

http://parasitepics.biosci.uga.edu

http://www.biosci.ohio-state.edu/~parasite/ascaris.html

http://vm.cfsan.fda.gov/~mow/chap30.html

http://www.path.cam.ac.uk/~schisto/Nematodes/Ascaris.html

http://www.nematode.net/Species.Summaries/Ascaris.lumbricoides/

http://www.medinfo.ufl.edu/year2/mmid/bms5300/bugs/asclum.html

http://www.ce.berkeley.edu/~nelson/ce210a/Ascaris/ascaris.htm

http://www.life.sci.qut.edu.au/LIFESCI/darben/nematode.htm

http://radiology.uchc.edu/eAtlas/GI/1208.htm

http://www.niaid.nih.gov/factsheets/roundwor.htm

 

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References

Ascariasis and its Public Health Significance.  Edited by DWT Crompton et al.

Medical Parasitology.  Markell, Voge, John 7th and 8th edition (WB Saunders 1992)

http://www.cdc.gov/ncidod/dpd/parasites/ascaris

Handbook of Medical Parasitology.  Viqar Zaman and Loh Ah Keong.  2nd edition 1991 (Churchill Livingstone)

Parasitic diseases.  Dickson D. Despommier and Robert W. Gwadz etc.  3rd edition.  (Springer-Werlag NY 1995) 

http://www.dpd.cdc.gov/dpdx/HTML/Ascariasis.htm

http://parasitepics.biosci.uga.edu/CumulusCGI/Cumulus.acgi$KLS2672,105

http://www.biosci.ohio-state.edu/~parasite/ascaris.html

http://www.who.int/ctd/intpara/burdens.htm

http://www.who.int/infectious-disease-news/CDS2000/PDF/cd2000-e.pdf

 

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Website compiled by Kristina Adachi

For Dr. Scott Smith’s Human Biology Class 103: Parasites and Pestilence

At Stanford University, Spring Quarter 2002

Questions?  Email adachik@stanford.edu