Ascariasis
Ascariasis
Ascariasis
Ascariasis
Classification and external resources
Ascaris lumbricoides
ICD-10 B77.
ICD-9 127.0
DiseasesDB 934
MeSH D001196
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]
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:
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]