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 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]}

Epidemiology

Disability-adjusted life year for ascariasis per 100,000 inhabitants in 2002.

     no data      less than 10      10-20      20-30      30-40      40-50      50-60      60-80      80-100      100-120      120-140      140-150      more than 150

Roughly 1.5 billion individuals are infected with this worm, primarily in Africa and Asia.^[8][1] 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%) [8]. 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^[9]. 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^{[citation needed]}. In Frankfort, Indiana, 87.5% of the sludge samples were positive with Ascaris, Toxocara, Trichuris, and hookworm^{[citation needed]}. In Macon, Georgia, one of the 13 soil samples tested positive for Ascaris^{[citation needed]}. Municipal wastewater in Riyadh, Saudi Arabia detected over 100 eggs per litre of wastewater ^[10] and in Czechoslovakia was as high as 240–1050 eggs per litre ^[11].

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^[12]. 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.

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]

Research

There are two animal models for studying Ascaris infection:

• Howes HL (June 1971). "Anthelmintic studies with pyrantel. II. Prophylactic activity in a mouse-ascaris suum test model". J. Parasitol. 57 (3): 487–93. doi:10.2307/3277899. PMID 5090955. 

• Lichtensteiger CA, DiPietro JA, Paul AJ, Neumann EJ, Thompson L (April 1999). "Persistent activity of doramectin and ivermectin against Ascaris suum in experimentally infected pigs". Vet. Parasitol. 82 (3): 235–41. doi:10.1016/S0304-4017(99)00018-7. PMID 10348103. http://linkinghub.elsevier.com/retrieve/pii/S0304-4017(99)00018-7. 

See also

• Tapeworm infection
• Toxocariasis
• 1970 ascariasis poisoning incident

References

External links

• Video of removal of Ascari lumbricoides with an endoscope
• Images (warning, very graphic): [2], [3]
• CDC DPDx Parasitology Diagnostic Web Site

• Ascariasis: Radiology and color pathology pictures from MedPix