|Classification and external resources|
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, 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.
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.
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. As a result, Ascaris infection does not produce the anemia associated with some other roundworm infections.
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.
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 .
Transmission from human to human by direct contact is impossible.
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 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.
Pharmaceutical drugs that are used to kill roundworms are called ascaricides and include:
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.
Roughly 1.5 billion individuals are infected with this worm, primarily in Africa and Asia. Ascariasis is endemic in the United States including Gulf Coast; in Nigeria and in Southeast Asia. One study indicated that the prevalence of ascariasis in the United States at about 4 million (2%) . In a survey of a rural Nova Scotia community, 28.1% of 431 individuals tested were positive for Ascaris, all of them being under age 20, while all 276 tested in metropolitan Halifax were negative. Deposition of ova (eggs) in sewage hints at the degree of ascariasis incidence. A 1978 study showed about 75% of all sewage sludge samples sampled in United States urban catchments contained Ascaris ova, with rates as high as 5 to 100 eggs per litre. In Frankfort, Indiana, 87.5% of the sludge samples were positive with Ascaris, Toxocara, Trichuris, and hookworm. In Macon, Georgia, one of the 13 soil samples tested positive for Ascaris. Municipal wastewater in Riyadh, Saudi Arabia detected over 100 eggs per litre of wastewater  and in Czechoslovakia was as high as 240–1050 eggs per litre .
Ascariasis can often be measured by examining food for ova. In one field study in Marrakech, Morocco, where raw sewage is used to fertilize crop fields, Ascaris eggs were detected at the rate of 0.18 eggs/kg in potatoes, 0.27 eggs/kg in turnip, 4.63 eggs/kg in mint, 0.7 eggs/kg in carrots, and 1.64 eggs/kg in radish. A similar study in the same area showed that 73% of children working on these farms were infected with helminths, particularly Ascaris, probably as a result of exposure to the raw sewage.
|Genus and Species||Ascaris lumbricoides|
|Common Name||Giant Intestinal Roundworm|
|Etiologic Agent of:||Ascariasis|
|Infective stage||Embryonated Egg|
|Portal of Entry||Mouth|
|Mode of Transmission||Ingestion of Embryonated egg through contaminated food or water|
|Pathogenic Stage||Adult, Larva|
|Mode of Attachment||Retention in the mucosal folds using pressure|
|Mode of Nutrition||Feeding of Chyme|
|Pathogenesis||Larva – pneumonitis, Loeffler’s
Adult – Obstruction, Liver abscess, Appendicitis. With Blood-Lung Phase along with Hookworms and Strongyloides stercoralis.
|Laboratory diagnosis||Concentration methods and Direct Fecal Smear: Kato-Katz|
|Treatment||Albendazole, Mebendazole, or Pyrantel pamoate|
|Diagnostic Feature – Adult||Female – prominent genital girdle|
|Diagnostic Feature – Egg||Coarse mammilated albuminous coating|
There are two animal models for studying Ascaris infection: