Open Access Articles- Top Results for Ascariasis


This article is about the infection. For the organism, see Ascaris.
File:Ascaris infection in X-ray image- Duedenal worms - in the first portion of the bowel after the stomach (South Africa) (16238958958).jpg
High number of ascaris worms - visible as black tangled mass - are filling the duodenum, the first portion of the bowel after the stomach, of this South African patient (X-ray image with barium as contrast medium)
Classification and external resources
Specialty Infectious disease
ICD-10 B77
ICD-9 127.0
OMIM 604291
DiseasesDB 934
MedlinePlus 000628
eMedicine article/212510
NCI Ascariasis
Patient UK Ascariasis
MeSH D001196

Ascariasis is a disease caused by the parasitic roundworm Ascaris lumbricoides.[1] Infections have no symptoms in more than 85% of cases, especially if the number of worms is small.[1] Symptoms increase with the number of worms present and may include shortness of breath and fever in the beginning of the disease.[1] These may be followed by symptoms of abdominal swelling, abdominal pain and diarrhea.[1] Children are most commonly affected, and in this age group the infection may also cause poor weight gain, malnutrition and learning problems.[1][2][3]

Infection occurs by eating food or drink contaminated with Ascaris eggs from feces.[2] The eggs hatch in the intestines, burrow through the gut wall, and migrate to the lungs via the blood.[2] There they break into the alveoli and pass up the trachea, where they are coughed up and swallowed.[2] The larvae then pass through the stomach for a second time into the intestine where they become adult worms.[2] Ascariasis is classified as a neglected tropical disease as it is a type of soil-transmitted helminthiasis. These diseases are in turn part of a group of diseases called helminthiasis.[4]

Prevention is by improved sanitation, which includes improving access to toilets and proper disposal of feces.[1][5] Handwashing with soap appears protective.[6] In areas where more than 20% of the population is affected, treating everyone at regular intervals is recommended.[1] Reoccurring infections are common.[2][7] There is no vaccine.[2] Treatments recommended by the World Health Organization are the medications albendazole, mebendazole, levamisole or pyrantel pamoate.[2] Other effective agents include tribendimidine and nitazoxanide.[2]

About 0.8 to 1.2 billion people globally have ascariasis with the most heavily affected populations being in sub-Saharan Africa, Latin America, and Asia.[1][8][9] This makes ascariasis the most common form of soil-transmitted helminthiasis.[8] As of 2010 it caused about 2,700 deaths down from 3,400 in 1990.[10] Another type of Ascaris infects pigs.[1]

Signs and symptoms

Most people who are infected with only a small number of worms have no symptoms. It is common to find that most people are infected by a small number of worms, while a small number of people are heavily infected, something that is characteristic of many worm infections.[1][11] Clinical features depend on the affected body site.

Migrating larvae

As larval stages travel through the body, they may cause visceral damage, peritonitis and inflammation, enlargement of the liver or spleen, and an inflammation of the lungs. Pulmonary manifestations take place during larval migration and may present as Loeffler's syndrome, a transient respiratory illness associated with blood eosinophilia and pulmonary infiltrates with radiographic shadowing.[12]

Intestinal blockage

File:Piece of intestine, blocked by worms (16424898321).jpg
Piece of intestine, blocked by worms, surgically removed from a 3-year-old boy in South Africa.[13]

The worms can occasionally cause intestinal blockage when large numbers get tangled into a bolus or they may migrate from the small intestine, which may require surgery. 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.[14]

Bowel obstruction

Bowel obstruction may occur in up to 0.2 per 1000 per year.[1] Sometimes the worm blocks the Ampulla of Vater or goes into the main pancreatic duct resulting in acute pancreatitis with raised serum levels of Amylase and Lipase. Occasionally they can travel through the billiary tree and even into the gallbladder causing acute cholangitis or acute cholecystitis.


Ascariasis may result in allergies to shrimp and dustmites due to the shared antigen, tropomyosin; this has not been confirmed in the laboratory.[15][16]


The worms in the intestine may cause malabsorption and anorexia which contribute to malnutrition.[17] The malabsorption may be due to a loss of brush border enzymes, erosion and flattening of the villi, and inflammation of the lamina propria.[18]


Ascaris have an aversion to some general anesthetics and may exit the body, sometimes through the mouth.[19]


File:Ascaris Larva.png
The larva of Ascaris lumbricoides developing in the egg
File:Ascaris lumbricoides.jpeg
Ascaris lumbricoides adult worms (with measuring tape for scale)
File:Ascaris lumbricoides adult worms.png
Ascaris lumbricoides adult worms
File:Ascaris egg, incubation process.png
Ascaris egg, incubation process: The ascaris egg incubation process consists in placing the egg in a controlled environment, at 26°C during 28 days, in acidic conditions. This process allows to evaluate if an egg is viable or not, by watching the bipartition of the nucleus, and the growth of the larva.
File:Ascariasis LifeCycle - CDC Division of Parasitic Diseases.gif
Ascaris 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.


The source of infection is from objects which fecal matter containing eggs have contaminated.[2] Ingestion of infective eggs from soil contaminated with human feces or contaminated vegetables and water is the primary route of infection. Infectious eggs may occur on other objects such as hands, money and furniture.[2] Transmission from human to human by direct contact is impossible.[20]

Transmission comes through municipal recycling of wastewater into crop fields. This is quite common in emerging industrial economies, and poses serious risks for local crop sales and exports of contaminated vegetables. A 1986 outbreak of ascariasis in Italy was traced to irresponsible wastewater recycling used to grow Balkan vegetable exports.[21]

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[22] and in Czechoslovakia was as high as 240–1050 eggs per litre.[23]

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.[24] 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.

Life cycle

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. There are generally few or no symptoms. A bolus of worms may obstruct the intestine; migrating larvae may cause pneumonitis and eosinophilia. Adult worms have a life-span of 1–2 years which means that individuals may be infected all their lives as worms die and new worms are acquired.[11]

Eggs can survive potentially for 15 years and a single worm may produce 200 thousand eggs a day.[2] They maintain their position by swimming against the intestinal flow.[25]


The diagnosis is usually incidental when the host passes a worm in the stool or vomit. The eggs can be seen in smear of fresh feces examined on a glass slide under a microscope and there are various techniques to concentrate them first or increase their visibility, such as the ether sedimentation method or the Kato technique. The eggs have a characteristic shape: they are oval with a thick, mamillated shell (covered with rounded mounds or lumps), measuring 35-50 micrometer in diameter and 40-70 in length. During pulmonary disease larvae may be found in fluids aspirated from the lungs. White blood cells counts may demonstrate peripheral eosinophilia; this is common in many parasitic infections and is not specific to ascariasis. On X-ray, 15–35 cm long filling defects, sometimes with whirled appearance (bolus of worms).


Ascaris takes most of its nutrients from the partially digested host food in the intestine. There is some evidence that it can secrete anti-enzymes, presumably to protect itself from digestion by the hosts' enzymes. Children are often more severely affected.[1]


Prevention is by improved access to sanitation which includes the use of properly functioning and clean toilets by all community members as one important aspect.[1] Handwashing with soap may be protective; however, there is no evidence it affects the severity of disease.[6] Eliminating the use of untreated human faeces as fertilizer is also important.

In areas where more than 20% of the population is affected treating everyone is recommended.[1] This has a cost of about 2 to 3 cents per person per treatment.[1] This is known as mass drug administration and is often carried out among school-age children.[26] For this purpose, broad-spectrum benzimidazoles such as mebendazole and albendazole are the drugs of choice recommended by WHO.[27]


Further information: Helminthiasis § Treatment


Medications that are used to kill roundworms are called ascaricides. Those recommended by the World Health Organization for ascariasis are: albendazole, mebendazole, levamisole and pyrantel pamoate.[2] Other effective agents include tribendimidine and nitazoxanide.[2]

  • Piperazine 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.
  • Pyrantel pamoate may induce intestinal obstruction in a heavy worm load. Albendazole is 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.

Corticosteroids can treat some of the symptoms, such as inflammation.

Surgical intervention

In some cases with severe infestation the worms may cause bowel obstruction, requiring emergency surgery.[28] The bowel obstruction may be due to all the worms or twisting of the bowel.[28] During the surgery the worms may be manually removed.[28]

Alternative medicine

Santonin is often only partly effective.[30]


It is rare for the infections to be life-threatening.[1]


File:Ascariasis world map - DALY - WHO2002.svg
Disability-adjusted life year for ascariasis per 100,000 inhabitants in 2002.
  no data
  less than 10
  more than 150


Ascariasis is common in Africa and in Southeast Asia. It also occurs in the United States including Gulf Coast.

Infection estimates

Roughly 0.8-1.3 billion individuals are infected with this intestinal worm, primarily in Africa and Asia.[1][2][9] About 120 to 220 million of these cases are symptomatic.[1] One study indicated that the prevalence of ascariasis in the United States at about 4 million (2%).[citation needed]


As of 2010 Ascariasis caused about 2,700 directly attributable deaths, down from 3,400 in 1990.[10] The indirectly attributable deaths due to the malnutrition link may be much higher.


There are two animal models, the mouse and pig, used in studying Ascaris infection.[31][32]

Other animals

Infections in pigs leads to poor weight gain and thus financial losses for the farmer.[1] In pigs the infection is due to Ascaris suum.[1] In horses and other equines, the equine roundworm is Parascaris equorum and the parasites are colloquially called Ascarids. A problem for young animals more than for mature ones, clinical signs include unthriftiness, potbelly, rough hair coat, and slow growth.[33]


  1. ^ a b c d e f g h i j k l m n o p q r s t Dold, C; Holland, CV (Jul 2011). "Ascaris and ascariasis.". Microbes and infection / Institut Pasteur 13 (7): 632–7. PMID 20934531. doi:10.1016/j.micinf.2010.09.012. 
  2. ^ a b c d e f g h i j k l m n o Hagel, I; Giusti, T (Oct 2010). "Ascaris lumbricoides: an overview of therapeutic targets.". Infectious disorders drug targets 10 (5): 349–67. PMID 20701574. doi:10.2174/187152610793180876. 
  3. ^ "Soil-transmitted helminth infections Fact sheet N°366". World Health Organization. June 2013. 
  4. ^ "Neglected Tropical Diseases". June 6, 2011. Retrieved 28 November 2014. 
  5. ^ Ziegelbauer, K; Speich, B; Mäusezahl, D; Bos, R; Keiser, J; Utzinger, J (Jan 2012). "Effect of sanitation on soil-transmitted helminth infection: systematic review and meta-analysis.". PLoS medicine 9 (1): e1001162. PMC 3265535. PMID 22291577. doi:10.1371/journal.pmed.1001162. 
  6. ^ a b Fung, IC; Cairncross, S (Mar 2009). "Ascariasis and handwashing.". Transactions of the Royal Society of Tropical Medicine and Hygiene 103 (3): 215–22. PMID 18789465. doi:10.1016/j.trstmh.2008.08.003. 
  7. ^ Jia, TW; Melville, S; Utzinger, J; King, CH; Zhou, XN (2012). "Soil-transmitted helminth reinfection after drug treatment: a systematic review and meta-analysis.". PLoS neglected tropical diseases 6 (5): e1621. PMC 3348161. PMID 22590656. doi:10.1371/journal.pntd.0001621. 
  8. ^ a b Keiser, J; Utzinger, J (2010). "The drugs we have and the drugs we need against major helminth infections.". Advances in parasitology 73: 197–230. PMID 20627144. doi:10.1016/s0065-308x(10)73008-6. 
  9. ^ a b Fenwick, A (Mar 2012). "The global burden of neglected tropical diseases.". Public health 126 (3): 233–6. PMID 22325616. doi:10.1016/j.puhe.2011.11.015. 
  10. ^ a b Lozano, R (Dec 15, 2012). "Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010.". Lancet 380 (9859): 2095–128. PMID 23245604. doi:10.1016/S0140-6736(12)61728-0. 
  11. ^ a b Anderson, R.M. & May, R.M. (1991). Infectious diseases of humans. Dynamics and control. Oxford: Oxford Scientific Publications
  12. ^ Torok E. Oxford Handbook Infect Dis and Microbiol, 2009
  13. ^ Fincham, J., Dhansay, A. (2006). Worms in SA's children - MRC Policy Brief. Nutritional Intervention Research Unit of the South African Medical Research Council, South Africa
  14. ^ Baird JK, Mistrey M, Pimsler M, Connor DH (March 1986). "Fatal human ascariasis following secondary massive infection". Am. J. Trop. Med. Hyg. 35 (2): 314–8. PMID 3953945. 
  15. ^ Berman, Jules J. (2012), Taxonomic Guide to Infectious Diseases: Understanding the Biologic Classes of Pathogenic Organisms, Academic Press, p. 151, ISBN 9780124158955 
  16. ^ Rollinson, D.; Hay, S.I. (2011), Advances in Parasitology, Volume 66, Academic Press, p. 165, ISBN 9780080879000 
  17. ^ Hall A., Hewitt G., Tuffrey V. (2008). "A review and meta-analysis of the impact of intestinal worms on child growth and nutrition". Maternal and Child Nutrition 4 (Suppl 1): 118–236. doi:10.1111/j.1740-8709.2007.00127.x. 
  18. ^ Stephenson, L.S. (1987). The Impact of Helminth Infections on Human Nutrition. London: Taylor & Francis.
  19. ^ Wu ML, Jones VA (January 2000). "Ascaris lumbricoides". Arch. Pathol. Lab. Med. 124 (1): 174–5. PMID 10629158. doi:10.1043/0003-9985(2000)124<0174:AL>2.0.CO;2. 
  20. ^ "AscarisInfection Fact Sheet". 
  21. ^ Pawlowski, ZS; Schultzberg K (1986). "Ascariasis and sewage in Europe". In Block JC. Epidemiological Studies of Risks Associated With the Agricultural Use of Sewage Sludge: Knowledge and Needs (EUR). Elsevier Science Pub Co. pp. 83–93. ISBN 1-85166-035-6. 
  22. ^ Bolbol AS (1992). "Risk of contamination of human and agricultural environment with parasites through reuse of treated municipal wastewater in Riyadh, Saudi Arabia". J Hyg Epidemiol Microbiol Immunol 36 (4): 330–7. PMID 1300348. 
  23. ^ Horák P (1992). "Helminth eggs in the sludge from three sewage treatment plants in Czechoslovakia". Folia Parasitol. 39 (2): 153–7. PMID 1644362. 
  24. ^ Habbari K, Tifnouti A, Bitton G, Mandil A (September 1999). "Helminthic infections associated with the use of raw wastewater for agricultural purposes in Beni Mellal, Morocco". East. Mediterr. Health J. 5 (5): 912–21. PMID 10983530. 
  25. ^ Crompton, D.W. and Pawlowski, Z. (1985). Life history and development of Ascaris lumbricoides and the persistence of human ascariasis. In: Ascariasis and its public health significance. Eds Crompton, D.W. Nesheim, M.C. and Pawlowski, Z.S. London: Taylor & Francis
  26. ^ Mascarini-Serra L (2011). "Prevention of soil-transmitted helminth infection". Journal of Global Infectious Diseases 3 (2): 175–182. PMC 3125032. PMID 21731306. doi:10.4103/0974-777X.81696. 
  27. ^ WHO (2006). Preventive Chemotherapy in Human Helminthiasis : Coordinated Use of Anthelminthic Drugs in Control Interventions : a Manual for Health Professionals and Programme Managers (PDF). WHO Press, World Health Organization, Geneva, Switzerland. pp. 1–61. ISBN 9241547103. 
  28. ^ a b c Hefny, AF; Saadeldin, YA; Abu-Zidan, FM (May 2009). "Management algorithm for intestinal obstruction due to ascariasis: a case report and review of the literature.". Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES 15 (3): 301–5. PMID 19562557. 
  29. ^ a b c 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
  30. ^ Ravina, Enrique (2011). The evolution of drug discovery : from traditional medicines to modern drugs (1. Aufl. ed.). Weinheim: Wiley-VCH. p. 91. ISBN 9783527326693. 
  31. ^ Howes HL (June 1971). "Anthelmintic studies with pyrantel. II. Prophylactic activity in a mouse-ascaris suum test model". J. Parasitol. (The Journal of Parasitology, Vol. 57, No. 3) 57 (3): 487–93. JSTOR 3277899. PMID 5090955. doi:10.2307/3277899. 
  32. ^ 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. PMID 10348103. doi:10.1016/S0304-4017(99)00018-7. 
  33. ^ "Parasites:Ascarids". eXtension. September 27, 2011. Retrieved 9 November 2014. 

External links