Ascariasis

Ascariasis
Classification and external resources

Ascaris lumbricoides
ICD-10 B77.
ICD-9 127.0
DiseasesDB 934
MeSH D001196

Ascariasis is a human disease caused by the parasitic roundworm Ascaris lumbricoides.

Perhaps as many as one quarter of the world's people are infected[1], and ascariasis is particularly
prevalent in tropical regions and in areas of poor hygiene. Other species of the genus Ascaris are
parasitic and can cause disease in domestic animals.

Infection occurs through ingestion of food contaminated with feces containing Ascaris
eggs. The larvae hatch, burrow through the intestine, reach the lungs, and finally migrate up the
respiratory tract. From there they are then reswallowed and mature in the intestine, growing up to
30 cm (12 in.) in length and anchoring themselves to the intestinal wall.

Infections are usually asymptomatic, especially if the number of worms is small. They
may however be accompanied by inflammation, fever, and diarrhea, and serious problems may
develop if the worms migrate to other parts of the body.
Signs and symptoms
Patients can remain asymptomatic for very long periods of time. As larval stages travel
through the body, they may cause visceral damage, peritonitis and inflammation, enlargement of
the liver or spleen, toxicity, and pneumonia. A heavy worm infestation may cause nutritional
deficiency; other complications, sometimes fatal, include obstruction of the bowel by a bolus of
worms (observed particularly in children) and obstruction of the bile or pancreatic duct. More
than 796 Ascaris lumbricoides worms weighing up to 550 g [19 ounces] were recovered at
autopsy from a 2-year-old South African girl. The worms had caused torsion and gangrene of the
ileum, which was interpreted as the cause of death.[2]

Ascaris takes most of its nutrients from the partially digested host food in the intestine.
There is limited evidence that it can also pierce the intestinal mucous membrane and feed on
blood, but this is not its usual source of nutrition.[3] As a result, Ascaris infection does not
produce the anemia associated with some other roundworm infections.[citation needed]

In Canada in 1970, a postgraduate student tainted his roommates' food with Ascaris
lumbricoides. Four of the victims became seriously ill; two of these suffered acute respiratory
failure.[4][5]

Mechanism
Life cycle

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 and/or lymphatics to the lungs . The
larvae mature further in the lungs (6) (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 (8). 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.

First appearance of eggs in stools is 60–70 days. In larval ascariasis, symptoms occur 4–
16 days after infection. The final symptoms are gastrointestinal discomfort, colic and vomiting,
fever, and observation of live worms in stools. Some patients may have pulmonary symptoms or
neurological disorders during migration of the larvae. However there are generally few or no
symptoms. A bolus of worms may obstruct the intestine; migrating larvae may cause
pneumonitis and eosinophilia.

Source

The source of transmission is from soil and vegetation on which fecal matter containing
eggs has been deposited. Ingestion of infective eggs from soil contaminated with human feces or
transmission and contaminated vegetables and water is the primary route of infection. Intimate
contact with pets which have been in contact with contaminated soil may result in infection,
while pets which are infested themselves by a different type of roundworm can cause infection
with that type of worm (Toxocara canis, etc.) as occasionally occurs with groomers.

Transmission also comes through municipal recycling of wastewater into crop fields.
This is quite common in emerging industrial economies, and poses serious risks for not only
local crop sales but also exports of contaminated vegetables. A 1986 outbreak of ascariasis in
Italy was traced to irresponsible wastewater recycling used to grow Balkan vegetable exports.[6]

Transmission from human to human by direct contact is impossible.[7]

Diagnosis
The diagnosis is usually incidental when the host passes a worm in the stool or vomit.
Stool samples for ova and parasites will demonstrate Ascaris eggs. Larvae may be found in
gastric or respiratory secretions in pulmonary disease. Blood counts may demonstrate peripheral
eosinophilia. On X-ray, 15–35 cm long filling defects, sometimes with whirled appearance
(bolus of worms).

Prevention
Prevention includes: use of toilet facilities; safe excreta disposal; protection of food from
dirt and soil; thorough washing of produce; and hand washing.

Food dropped on the floor should never be eaten without washing or cooking, particularly
in endemic areas. Fruits and vegetables should always be washed thoroughly before
consumption.
Treatment
Pharmaceutical drugs that are used to kill roundworms are called ascaricides and include:

• Mebendazole (Vermox) (C16H13N3O2). Causes slow immobilization and death of the

worms by selectively and irreversibly blocking uptake of glucose and other nutrients in
susceptible adult intestine where helminths dwell. Oral dosage is 100 mg 12 hourly for 3
days.
• Piperazine (C4H10N2.C6H10O4). A flaccid paralyzing agent that causes a blocking response
of ascaris muscle to acetylcholine. The narcotizing effect immobilizes the worm, which
prevents migration when treatment is accomplished with weak drugs such as
thiabendazole. If used by itself it causes the worm to be passed out in the feces. Dosage is
75 mg/kg (max 3.5 g) as a single oral dose.
• Pyrantel pamoate (Antiminth, Pin-Rid, Pin-X) (C11H14N2S.C23H16O6) Depolarizes
ganglionic block of nicotinic neuromuscular transmission, resulting in spastic paralysis of
the worm. Spastic (tetanic) paralyzing agents, in particular pyrantel pamoate, may induce
complete intestinal obstruction in a heavy worm load. Dosage is 11 mg/kg not to exceed
1 g as a single dose.
• Albendazole (C12H15N3O2S) A broad-spectrum antihelminthic agent that decreases ATP
production in the worm, causing energy depletion, immobilization, and finally death.
Dosage is 400 mg given as single oral dose (contraindicated during pregnancy and
children under 2 years).
• Thiabendazole. This may cause migration of the worm into the esophagus, so it is usually
combined with piperazine.
• Hexylresorcinol effective in single dose, mentioned in : Holt, Jr Emmett L, McIntosh
Rustin: Holt's Diseases of Infancy and Childhood: A Textbook for the Use of Students
and Practitioners. Appleton and Co, New York,11th edition
• Santonin, more toxic than hexylresorcinol, mentioned in : Holt, Jr Emmett L, McIntosh
Rustin: Holt's Diseases of Infancy and Childhood: A Textbook for the Use of Students
and Practitioners. Appleton and Co, New York,, 11th edition
• Oil of chenopodium, more toxic than hexylresorcinol, mentioned in : Holt, Jr Emmett L,
McIntosh Rustin: Holt's Diseases of Infancy and Childhood: A Textbook for the Use of
Students and Practitioners. Appleton and Co, New York, 11th edition

Also, corticosteroids can treat some of the symptoms, such as inflammation.

Native Americans have traditionally used epazote (Chenopodium ambrisioides) for treatment,
which was not as powerful as pharmaceutical compounds, but spontaneous passage of Ascarids
provided some proof of efficacy.[citation needed]
Society and culture
Trivia

• Ascariasis may result in allergies to shrimp and dustmites due to the shared antigen,
tropomyosin.
• Ascaris have an aversion to some general anesthetics and may exit the body, sometimes
through the mouth.[13]

Genus and Species Ascaris lumbricoides

Common Name Giant Intestinal Roundworm
Etiologic Agent of: Ascariasis
Infective stage Embryonated Egg
Definitive Host Human
Portal of Entry Mouth
Mode of
Ingestion of Embryonated egg through contaminated food or water
Transmission
Habitat Small Intestine
Pathogenic Stage Adult, Larva
Mode of Attachment Retention in the mucosal folds using pressure
Mode of Nutrition Feeding of Chyme
Larva – pneumonitis, Loeffler’s Syndrome;
Pathogenesis
Adult – Obstruction, Liver abscess, Appendicitis. With Blood-Lung Phase
along with Hookworms and Strongyloides stercoralis.
Laboratory
Concentration methods and Direct Fecal Smear: Kato-Katz
diagnosis
Treatment Albendazole, Mebendazole, or Pyrantel pamoate
Diagnostic Feature –
Female – prominent genital girdle
Adult
Diagnostic Feature – Coarse mammilated albuminous coating
Egg