Ascariasis is the most common helminthic infection, with an estimated worldwide prevalence of 804 million cases in 2013.[1, 2, 3] Usually asymptomatic, ascariasis is most prevalent in children of tropical and developing countries,[4] where they are perpetuated by contamination of soil by human feces or use of untreated feces as fertilizer.[5] For more information on ascariasis in children, see the Medscape article Pediatric Ascariasis. Symptomatic ascariasis may manifest as growth retardation, pneumonitis, intestinal obstruction, or hepatobiliary and pancreatic injury. Ascariasis may exist as a zoonotic infection associated with pigs and use of hog manure,[6, 7] but, in most endemic areas, it is most likely transmitted from person to person.[8]

The image below depicts a roundworm that infects humans through soil contaminated by human feces.

View Image

Adult Ascaris lumbricoides.

See Common Intestinal Parasites, a Critical Images slideshow, to help make an accurate diagnosis.


Ascaris lumbricoides is the largest of the common nematodes (roundworms) that infect humans. Adult A lumbricoides are white or yellow and 15-35 cm long (see first image below). They live 10-24 months in the jejunum and middle ileum of the intestine. Each day, female A lumbricoides produce 240,000 eggs (see second image below), which are fertilized by nearby male worms. A Chinese study showed that 45% of infected persons shed only fertilized eggs, 40% shed fertilized and unfertilized eggs, and 20% shed only unfertilized eggs. Unfertilized eggs accounted for only 6-9% of eggs shed. Fertilized eggs released into favorable soil may become infectious within 5-10 days.[9] Eggs may remain viable in soil for up to 17 months. Infection occurs through soil contamination of hands or food, ingestion, and the subsequent hatching of eggs in the small intestine (see third image below).

View Image

Adult Ascaris lumbricoides.

View Image

Ascaris lumbricoides egg.

View Image

Life cycle of Ascaris lumbricoides.

Second-stage larvae pass through the intestinal wall and migrate through the portal system to the liver (4 d) and then the lungs (14 d). A significant exposure may produce subsequent pneumonia and eosinophilia. Symptoms of pneumonitis include wheezing, dyspnea, nonproductive cough, hemoptysis, and fever. Larvae are expectorated and swallowed, eventually reaching the jejunum, where they mature into adults in approximately 65 days.

Adult worms feed on digestion products of the host. Children with a marginal diet may be susceptible to protein, caloric, or vitamin A deficiency, resulting in retarded growth and increased susceptibility to infectious diseases such as malaria.[10] Large and tangled worms may cause intestinal (usually ileal), common duct, pancreatic, or appendiceal obstruction. Mean worm burden varies from more than 16 to 4 and appears related to host factors, particularly age, geophagy,[11] and immunity. Worms do not multiply in the host. For infection to persist beyond the 2-year maximum lifespan of the worms, re-exposure must occur. Some children appear to become very heavily infested, probably from multiple cumulative exposures over time and/or relative immunodeficiency.[12]

Ascaris lumbricoides suum, a swine nematode, has been thought responsible for zoonotic infection. Distinguishing this worm from A lumbricoides is difficult, as it differs by only 6 (1.3%) nucleotides in the first internal transcribed spacer (ITS-1) and by 3%-4% in the mitochondrial genome sequence.[12] A suum appears to responsible for most ascariasis cases in well-developed countries with excellent sanitation (eg, Denmark,[13] United States,[7] UK[14] ). In this setting, infected persons have a low worm burden and may present with only cough, acute eosinophilia, or eosinophilic liver lesions visible on CT scans. However, a molecular genetic study from China casts doubt that infections in pigs are the cause of most human infection.[8]



United States

In 1974, an estimated 4 million people, mainly in the southeast United States, had ascariasis. Recent estimates of ascariasis prevalence are unknown, but probably much lower. Immigrants from countries with a high prevalence of ascariasis comprise most recent cases.


The prevalence of ascariasis is highest in children aged 2-10 years, with the highest intensity of infection occurring in children aged 5-15 years who have simultaneous infections with other soil-transmitted helminths such as Trichuris trichiura and hookworm. A recent Vietnamese study found that adult women living in rural areas, especially those exposed to human night soil and living in households without a latrine, were at surprisingly high risk for ascariasis.[15] In regions with soil-transmitted diseases, ascariasis tends to be more geographically dispersed than Trichuris or hookworm.[16]

The Centers for Disease Control and Prevention (CDC) estimated that worldwide ascariasis rates in 2005 were as follows: 86 million cases in China, 204 million elsewhere in East Asia and the Pacific, 173 million in sub-Saharan Africa, 140 million in India, 97 million elsewhere in South Asia, 84 million in Latin America and the Caribbean, and 23 million in the Middle East and North Africa. Between 1990 and 2013, the disease burden of ascariasis was estimated to have decreased by 75%.[2] Survey data, however, are corrupted by lack of standardized diagnostic methods.[17]

Because the lifespan of adult worms in the intestine is only 1-2 years, persistent infection requires frequent re-exposure and reinfection. The frequency and intensity of infection remain high throughout life in endemic areas and pose a risk to both elderly and young persons. In a recent study in rural southwest Nigeria, the intensity of excreted eggs per gram of feces among infected persons was 2,371 for Ascaris species, 1070 for hookworm, and 500 for Trichuris species, with only slightly lower rates among persons in urban areas.[18]

Estimates of disability-adjusted years of life due to ascariasis have fallen because of development and management programs during the 1990s, especially in Asia, but still constitute a significant burden in some countries. Current ascariasis-associated disability-adjusted life years (DALYs) are approximately 1 million,[2] with nonsurgical morbidity mostly associated with wasting syndrome in children.[2]


Ascariasis is most common and intensive in children, who are more likely than adults to be symptomatic. In children, intestinal obstruction caused by heavy worm burden (≥60) is the most common presenting manifestation of disease. An estimated 2 per 1000 infected children develop intestinal obstruction per year.[19] Among children aged 1-12 years who presented to a Cape Town hospital with abdominal emergencies between 1958-1962, symptomatic A lumbricoides infection was responsible for 12.8% of cases , with 68% of those due to intestinal obstruction, usually at the terminal ileum. The peak incidence was at age 2 years in a series from Colombia and age 4.8 years in a series from Turkey.

The prevalence of infection in Vietnam is estimated at 44.4%, more commonly in the northern peri-urban and rural areas of the country.[20] In Vietnam, vegetable cultivation using night soil fertilizer places adult women at especially high risk. Children with chronic ascariasis may experience decreased growth and development due to decreased food intake.

Adults with ascariasis are more likely to develop biliary complications due to migration of adult worms (see image below), possibly provoked by other illnesses such as malarial fever. In Damascus, of 300 adults referred for complications of ascariasis between 1988 and 1993, 98% had abdominal pain, 4.3% had acute pancreatitis, 1.3% had obstructive jaundice, and 25% had worm emesis. Twenty-one to 80% of patients had undergone previous cholecystectomy or endoscopic sphincterotomy.

View Image

Adult Ascaris lumbricoides in biliary system.

Because of improved access to care and availability of ultrasonography, biliary ascariasis has been increasingly recognized and reported from endemic areas.[21] In Kashmir, it may account for up to 36% of patients presenting with biliary or pancreatic disorders and is reported to cause 20% of biliary disease in the Philippines.[21]

A review of biliary ascariasis suggests that this association may be causative as a result of dilatation of the common bile duct and elevation of cholecystokinin levels with resultant relaxation of the sphincter of Oddi.[22]

A report from India indicated that, of consecutive patients diagnosed with biliary ascariasis, 80% presented with recurrent abdominal pain, 30% with acute cholecystitis, 25% with obstructive jaundice, 25% with cholangitis, only 5% with pancreatitis, 5% with perforated viscus, and 5% with hepatolithiasis. Only 25% of the Indian patients required surgery, and conservative medical therapy with oral anthelminthics has recently been recommended.[21]

A postcholecystectomy syndrome of pain and jaundice is frequently due to ascariasis in endemic areas, presumably owing to enhanced patency of the biliary system after surgical or endoscopic sphincterotomy.[23]

Intestinal obstruction, usually of the terminal ileum in children, is the most commonly attributed fatal complication, resulting in 60,000 deaths per year.[3] Besides direct obstruction of the bowel lumen, toxins released by live or degenerating worms may result in bowel inflammation, ischemia, and fibrosis.


See International and Mortality/Morbidity.


Immediate cure rates after single-dose albendazole in South Africa were 95%, with egg reduction rates of more than 99%.[24]

Most treated patients become reinfected within months unless they are relocated to an area of significantly improved sanitation.

Patient Education

Because of the limited (two-year) lifespan of the disease, education on hand hygiene, fecal waste disposal, and general public health could be instrumental in breaking the cycle of infection in households and communities.[3]


Early symptoms of ascariasis, during the initial lung migration (first 10-14 days after ingestion) include cough, dyspnea, wheezing, urticaria, hemoptysis, and chest pain.[2] This may be seasonal after rains in some countries, such as Saudi Arabia. Returning travelers could also present with Loeffler syndrome of eosinophilic pneumonia if exposed in a high-risk environment.

Abdominal pain, distension, colic, nausea, anorexia, and intermittent diarrhea may be manifestations of partial or complete intestinal obstruction by adult worms.

Jaundice, nausea, vomiting, fever, and severe or radiating abdominal pain may suggest cholangitis, pancreatitis, hepatic abscess, or appendicitis.


Rales, wheezes, and tachypnea may develop during pulmonary migration, particularly in persons with a high worm burden. Urticaria and fever may also develop late in the migratory phase.

Abdominal distension is nonspecific but is common in children with ascariasis.

Abdominal tenderness, especially in the right upper quadrant, hypogastrium, or right lower quadrant, may suggest complications of ascariasis.

Evidence for nutritional deficiency due to ascariasis is strongest for vitamins A and C, as well as for protein, as indicated by albumin and growth studies in children observed prospectively. Some studies have not confirmed nutritional or developmental delay due to ascariasis.


Complications of ascariasis are related to worm burden and location of the relatively large nematode. They include acute abdomen, upper GI bleeding, small-bowel obstruction, volvulus and intussusception, peritonitis, biliary colic, acute cholecystitis, acute pancreatitis, acute cholangitis, and hepatic abscess. As such, ascariasis could be considered a potential cause of surgical emergency in endemic areas.[2]

Laboratory Studies

Stool examination for ova and parasites almost always discloses large, brown 60 µm X 50 µm trilayered eggs in persons with ascariasis. However, stool examination may be negative for ova for up to 40 days after infection because of the time needed for migration and maturation of the worm. The outer surfaces of fertilized eggs have an uneven mucopolysaccharide coat.

Ascaris larvae may be observed in microscopic wet preparations of sputum during the pulmonary migration phase.

CBC counts show eosinophilia during the tissue migration phase of the infection.

Serological tests are not clinically useful for ascariasis.

Imaging Studies

Radiologists practicing in Europe and North America should be familiar with unexpected but specific abnormalities associated with parasitic disease, especially in this age of increasing migration and tourism.[25]

Chest radiographs may show fleeting opacities during pulmonary migration.

Abdominal radiographs may show a whirlpool pattern of intraluminal worms. Narrow-based air fluid levels without distended loops of bowel on upright plain films suggest partial obstruction. Wide-based air fluid levels with distended loops suggest complete obstruction.

Worms have been increasingly identified in the biliary duct or gallbladder with ultrasonography and CT scanning.[26] Liver granulomata due to A suum infection have been described as ill-defined, 3- to 35-mm, nodular- or wedge-shaped lesions in the periportal or subcapsular regions.

Other Tests

Endoscopic retrograde cholangiopancreatography (ERCP) has become a commonly used procedure for both diagnosis of ascariasis and removal of worms from the biliary tract. The ease of diagnosis and therapy in the same setting makes ERCP particularly valuable when used with real-time ultrasonography. The combined procedures yield a sensitivity of nearly 100%.[22]

Approach Considerations

Specific patient and community-wide public health approaches to ascariasis should be coordinated. Individual patient deworming can prevent surgical and nutritional complications and can serve as an opportunity to investigate, educate, and treat other family members and neighbors. Community- and school-based epidemiological deworming programs should be administered under WHO guidelines and would be subject to diagnostic methods used to determine pretherapy and posttherapy prevalence. Newer highly sensitive diagnostic methods instead of classic stool sampling would be most useful for communities with moderate (30%-70%) prevalence, rather than very high or low prevalence,[27] while they may be more useful for screening in adults, who have lower worm burden and lower prevalence than children.[4]

Medical Care

Because of the risk of complications, patients with ascariasis who have other concomitant helminthic infections should always undergo treatment for ascariasis first. Medical therapy is usually not indicated during active pulmonary infection because dying larvae are considered a higher risk for significant pneumonitis. Pulmonary symptoms may be ameliorated with inhaled bronchodilator therapy or corticosteroids, if necessary.

Albendazole 400 mg one dose orally is the drug of choice for ascariasis in stable patients older than 12 months with uncomplicated infection.[2] A 2012 study from Indonesia showed that albendazole provided statistically significant better sterilization of Ascaris eggs than mebendazole but equivalent cure rates and egg reduction rates.[28] A 2017 systemic review and meta-analysis of 34 studies demonstrated a 95.7% cure rate with single-dose albendazole.[29] Ascariasis commonly coexists with whipworm infection, which appears to be most susceptible to triple-dose mebendazole.[30] Albendazole is not recommended during pregnancy; pyrantel pamoate is the drug of choice in these cases.

Alternative therapy is mebendazole (100 mg bid for 3 days). Mebendazole is not recommended during pregnancy; pyrantel pamoate is the drug of choice in these cases.

As an alternative to albendazole and mebendazole, ivermectin can be given in a dose of 150-200 micrograms/kg bodyweight.[2]

Paralyzing vermifuges (eg, pyrantel pamoate, piperazine, ivermectin) should be avoided in patients with complete or partial intestinal obstruction since the paralyzed worms may necessitate or further complicate surgery.

Vitamin A supplementation improved growth development of children in Zaire; deworming did not improve growth development in this study.[31]

Drug therapy affects only adult worms. If the patient lives in an endemic area or has recently relocated, he or she may still be carrying larvae that are not yet susceptible. Such patients should be re-evaluated in 3 months and retreated if stool ova persist. In endemic areas, reinfection rates approach 80% within 6 months.

Nitazoxanide, a drug used primarily for protozoal infection, was shown to have 89% clinical efficacy for the treatment of ascariasis in rural Mexico and may offer a future alternative to other medications.[32]

Compliance with antiparasitic drugs, especially at the community level, has recently emerged as a concern, particularly for the effectiveness of community-wide therapy.[17, 33]

Newer agents are being developed because of concern for emergence of resistance potentially associated with mass deworming campaigns.[34]

Surgical Care

Conservative (nothing by mouth) management of partial intestinal obstruction and biliary ascariasis is usually effective but might be more quickly accomplished with orally administered contrast medium.[2] A controlled trial from Pakistan found that, in patients without peritonitis, hypertonic saline enemas relieved obstruction more quickly (1.6 d vs 3.4 d) and resulted in shorter hospital stays (4 d vs 6 d) than intravenous fluids alone. A recent study from India demonstrated that conservative therapy was successful in 19 of 22 (89%) children with intestinal obstruction. The regimen used consisted of no oral intake, intravenous fluids, antibiotics, piperazine salt per nasogastric tube, and glycerine plus liquid paraffin emulsion enemas.[19]

Recommended criteria for surgical exploration include the following:

Most (49-90%) worms eventually migrate from the biliary system spontaneously. Drug therapy should be delayed in patients with right upper quadrant or pancreatic pain, as no evidence has shown that drugs are active against worms located in the biliary tree. Regardless, death of the worm in the duct may provoke both inflammation and obstruction. Patients with ascariasis who have only minor symptoms can undergo observation for 3 days. If the minor symptoms persist after 3 days or the patient develops frank cholangitis or pancreatitis, removal of the worms with ERCP should be attempted, if available. Although technically challenging at times, ERCP extraction rates have exceeded 90%.[22]

Intestinal or biliary surgery may be necessary for complications of ascariasis.

Intestinal gangrene usually occurs at the terminal ileum, more often after the use of pyrantel pamoate, which tetanically paralyzes worms and thereby enhances the risk of obstruction. Recently, 2 cases of delayed distal intestinal disease have been reported, which were thought to be secondary to toxins from the worms. Therefore, patients should probably be monitored for some time after the surgical removal of worms.

Milking of worms to the large bowel, resection of gangrenous bowel, ileostomy, and enterotomy are the most common surgical procedures used to manage bowel obstruction.

Invasion of the gall bladder necessitates cholecystectomy, common duct exploration, and T-tube drainage until the patient is stabilized and dewormed.

Any patients from highly endemic areas should be screened, and if positive, treated for ascariasis and malnutrion prior to elective surgery because of possible provocation of worm migration with anesthesia agents.[35] In particular, patients who live in endemic areas should be dewormed before and after elective cholecystectomy.


Community control of ascariasis has been difficult to achieve. The most successful control programs, such as those in Japan, have consisted of combined approaches, including improved sanitation, night soil disposal, and mass community treatment. Concern has increased for the emergence of drug resistance among heavily retreated populations.

The prevalence of ascariasis in Japan in 1949 was 63%; the disease was essentially eliminated by 1973. Hand washing may be a neglected means of prevention, even in endemic areas, as shown by a recent study from Sri Lanka.

A program of latrine construction, health education, and twice-annual anthelmintics decreased the prevalence of ascariasis in Korea from 80% in 1949 to 55% by 1971. After a 4-year educational campaign and latrine construction program in northern Bangladesh, 36% of children aged 5-13 remained infected. Rates of infection were lower among children who used latrines and who had been educated concerning the risks of ascariasis.[36]  As rates of ascariasis lessen, specific infected families should be targeted. A recent systematic review and meta-analysis of preventive water and sanitation measures concluded that the risk of ascariasis was lowered 60% by piped water, 38% by access to sanitarian latrines, and 62% by handwashing before eating and 55% after defecating.[37]  Each, in combination with the use of soap, has the potential for significant control, especially if applied in schools together with thrice yearly deworming.[38]

Current ascariasis treatment strategies recommend repeated mass treatment of communities to reduce intensity of worm burden until socioeconomic progress allows improved sanitation. Although such targeted therapy programs may control the morbidity of ascariasis by decreasing the number of worms per patient, they do not seem to decrease transmission rates. The ascariasis reinfection rate after a single community campaign in South Africa was 40% at 29 weeks. Children have been targeted in school campaigns, but continued worm burden and shedding by adults have blunted impact, especially if campaigns are less than thrice yearly. A 6-month educational program directed at behavioral remediation of school children and their parents in Java has shown promise when combined with a deworming campaign.

A 2012 Cochrane review[39]  was rather discouraging in its assessment of the benefit of community deworming programs, suggesting only the possibility of slight benefit in weight gain and hemoglobin, but not cognitive improvement as measured by school attendance and performance.

Avoiding pigs and pig manure prevents A suum infection in developed countries.

Work continues on a vaccine. A recombinant, nasally administered 16-kd secretory protein, As16, was shown to result in a 56% decrease in worm burden in mice challenged with A suum larvae.[40]  The Sabin Vaccine Institute is developing a "Pan-anthelmintic" vaccine against hookworm, trichuriasis, and ascariasis using at least 2 of 6 candidate A suum antigens. It appears that at least 5 years will be required to field such a candidate vaccine.[41]


Patients with ascariasis who have partial or complete obstruction should be treated at facilities with surgical support.

Guidelines Summary

In 2017, WHO published an extensive guideline on community-based deworming programs. They recommended that areas with greater than 20% prevalence undergo mass periodic administration of benzimidazoles.[42]

Medication Summary

The goals of pharmacotherapy are to eradicate infestation, to prevent complications, and to reduce morbidity.

Albendazole (Albenza)

Clinical Context:  First DOC. A benzimidazole carbamate drug that inhibits tubulin polymerization, resulting in degeneration of cytoplasmic microtubules. Decreases ATP production in worms, causing energy depletion, immobilization, and, finally, death. Converted in the liver to its primary metabolite, albendazole sulfoxide. Less than 1% of the primary metabolite is excreted in the urine. Plasma level is noted to rise significantly (as much as 5-fold) when ingested after high-fat meal. Experience with patients < 6 y is limited.

To avoid inflammatory response in CNS, patient must also be started on anticonvulsants and high-dose glucocorticoids.

Well tolerated and does not appear to increase risk of worm obstruction.

Mebendazole (Emverm)

Clinical Context:  Well tolerated and does not appear to increase risk of worm obstruction. Causes worm death by selectively and irreversibly blocking uptake of glucose and other nutrients in susceptible adult intestine where helminths dwell. Available as a 100-mg chewable tablet that can be swallowed whole, chewed, or crushed and mixed with food.

Pyrantel pamoate (Pin-Rid, Reese's Pinworm Medicine)

Clinical Context:  Neuromuscular blocking agent used to slowly paralyze worm to be eliminated from GI tract. May be DOC during pregnancy.

Class Summary

Parasite biochemical pathways are sufficiently different from the human host to allow selective interference by chemotherapeutic agents in relatively small doses.


David R Haburchak, MD, FACP, Professor Emeritus of Medicine, Department of Medicine, Division of Infectious Diseases, Medical College of Georgia at Augusta University

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Richard B Brown, MD, FACP, Chief, Division of Infectious Diseases, Baystate Medical Center; Professor, Department of Internal Medicine, Tufts University School of Medicine

Disclosure: Nothing to disclose.

Chief Editor

Pranatharthi Haran Chandrasekar, MBBS, MD, Professor, Chief of Infectious Disease, Department of Internal Medicine, Wayne State University School of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Jeffrey D Band, MD, FACP, FIDSA, Professor of Medicine, Oakland University William Beaumont School of Medicine; Health System Chair, Healthcare Epidemiology and International Medicine, Beaumont Health System; Former Chief of Infectious Diseases, Beaumont Hospital; Clinical Professor of Medicine, Wayne State University School of Medicine

Disclosure: Nothing to disclose.


  1. Bethony J, Brooker S, Albonico M, Geiger SM, Loukas A, Diemert D, et al. Soil-transmitted helminth infections: ascariasis, trichuriasis, and hookworm. Lancet. 2006 May 6. 367(9521):1521-32. [View Abstract]
  2. Jourdan PM, Lamberton PHL, Fenwick A, Addiss DG. Soil-transmitted helminth infections. Lancet. 2017 Sep 4. [View Abstract]
  3. de Lima Corvino DF, Bhimji SS. Ascariasis. 2018 Jan. [View Abstract]
  4. Wright JE, Werkman M, Dunn JC, Anderson RM. Current epidemiological evidence for predisposition to high or low intensity human helminth infection: a systematic review. Parasit Vectors. 2018 Jan 31. 11 (1):65. [View Abstract]
  5. Walker M, Hall A, Basáñez MG. Individual predisposition, household clustering and risk factors for human infection with Ascaris lumbricoides: new epidemiological insights. PLoS Negl Trop Dis. 2011 Apr 26. 5(4):e1047. [View Abstract]
  6. Hoenigl M, Seeber K, Valentin T, Zollner-Schwetz I, Krause R. Pulmonary ascariasis in patients from wealthy countries: shift in epidemiology?. Int J Infect Dis. 2012 Dec. 16(12):e888. [View Abstract]
  7. Notes from the field: ascariasis associated with pig farming - Maine, 2010-2013. MMWR Morb Mortal Wkly Rep. 2013 May 24. 62(20):413. [View Abstract]
  8. Peng W, Yuan K, Hu M, et al. Recent insights into the epidemiology and genetics of Ascaris in China using molecular tools. Parasitology. 2007 Mar. 134:325-30. [View Abstract]
  9. Peng W, Zhou X, Gasser RB. Ascaris egg profiles in human faeces: biological and epidemiological implications. Parasitology. 2003 Sep. 127:283-90. [View Abstract]
  10. Le Hesran JY, Akiana J, Ndiaye el HM, et al. Severe malaria attack is associated with high prevalence of Ascaris lumbricoides infection among children in rural Senegal. Trans R Soc Trop Med Hyg. 2004 Jul. 98(7):397-9. [View Abstract]
  11. Geissler PW, Mwaniki D, Thiong F, et al. Geophagy as a risk factor for geohelminth infections: a longitudinal study of Kenyan primary schoolchildren. Trans R Soc Trop Med Hyg. 1998 Jan-Feb. 92(1):7-11. [View Abstract]
  12. Dold C, Holland CV. Ascaris and ascariasis. Microbes Infect. 2011 Jul. 13(7):632-7. [View Abstract]
  13. Nejsum P, Parker ED, Frydenberg J, et al. Ascariasis is a zoonosis in denmark. J Clin Microbiol. 2005 Mar. 43(3):1142-8. [View Abstract]
  14. Bendall RP, Barlow M, Betson M, Stothard JR, Nejsum P. Zoonotic ascariasis, United kingdom. Emerg Infect Dis. 2011 Oct. 17(10):1964-6. [View Abstract]
  15. Do TT, Molbak K, Phung DC, et al. Helminth infections among people using wastewater and human excreta in peri-urban agriculture and aquaculture in Hanoi, Vietnam. Trop Med Int Health. 2007 Dec. 12 Suppl 2:82-90. [View Abstract]
  16. Halpenny CM, Paller C, Koski KG, Valdés VE, Scott ME. Regional, household and individual factors that influence soil transmitted helminth reinfection dynamics in preschool children from rural indigenous Panamá. PLoS Negl Trop Dis. 2013. 7(2):e2070. [View Abstract]
  17. Dunn JC, Turner HC, Tun A, Anderson RM. Epidemiological surveys of, and research on, soil-transmitted helminths in Southeast Asia: a systematic review. Parasit Vectors. 2016 Jan 27. 9:31. [View Abstract]
  18. Oninla SO, Owa JA, Onayade AA, et al. Intestinal helminthiases among rural and urban schoolchildren in south-western Nigeria. Ann Trop Med Parasitol. 2007 Dec. 101(8):705-13. [View Abstract]
  19. Gangopadhyay AN, Upadhyaya VD, Gupta DK, et al. Conservative treatment for round worm intestinal obstruction. Indian J Pediatr. 2007 Dec. 74(12):1085-7. [View Abstract]
  20. van der Hoek W, De NV, Konradsen F, et al. Current status of soil-transmitted helminths in Vietnam. Southeast Asian J Trop Med Public Health. 2003. 34 Suppl 1:1-11. [View Abstract]
  21. Das AK. Hepatic and biliary ascariasis. J Glob Infect Dis. 2014 Apr. 6(2):65-72. [View Abstract]
  22. Sanai Fm, Al-Karawi MA. Biliary Ascariasis: Report of a Complicated Case and Literature Review. Saudi Journal of Gastroenterology. 2007/01. 13:25-32.
  23. Shah OJ, Dar MA, Wani NA, et al. Biliary ascariasis as a cause of post-cholecystectomy syndrome in an endemic area. Dig Surg. 2004. 21(2):108-13; discussion 113. [View Abstract]
  24. Saathoff E, Olsen A, Kvalsvig JD, et al. Patterns of geohelminth infection, impact of albendazole treatment and re-infection after treatment in schoolchildren from rural KwaZulu-Natal/South-Africa. BMC Infect Dis. 2004 Aug 13. 4:27. [View Abstract]
  25. Rodríguez Carnero P, Hernández Mateo P, Martín-Garre S, García Pérez Á, Del Campo L. Unexpected hosts: imaging parasitic diseases. Insights Imaging. 2017 Feb. 8 (1):101-125. [View Abstract]
  26. Wani I. Gallbladder ascariasis. Turk J Gastroenterol. 2011. 22(2):178-82. [View Abstract]
  27. Medley GF, Turner HC, Baggaley RF, Holland C, Hollingsworth TD. The Role of More Sensitive Helminth Diagnostics in Mass Drug Administration Campaigns: Elimination and Health Impacts. Adv Parasitol. 2016. 94:343-392. [View Abstract]
  28. Lubis IN, Pasaribu S, Lubis CP. Current status of the efficacy and effectiveness of albendazole and mebendazole for the treatment of Ascaris lumbricoides in North-Western Indonesia. Asian Pac J Trop Med. 2012 Aug. 5 (8):605-9. [View Abstract]
  29. Moser W, Schindler C, Keiser J. Efficacy of recommended drugs against soil transmitted helminths: systematic review and network meta-analysis. BMJ. 2017 Sep 25. 358:j4307. [View Abstract]
  30. Steinmann P, Utzinger J, Du ZW, Jiang JY, Chen JX, Hattendorf J, et al. Efficacy of single-dose and triple-dose albendazole and mebendazole against soil-transmitted helminths and Taenia spp.: a randomized controlled trial. PLoS One. 2011. 6 (9):e25003. [View Abstract]
  31. Donnen P, Brasseur D, Dramaix M, et al. Vitamin A supplementation but not deworming improves growth of malnourished preschool children in eastern Zaire. J Nutr. 1998 Aug. 128(8):1320-7. [View Abstract]
  32. Galvan-Ramirez ML, Rivera N, Loeza ME, et al. Nitazoxanide in the treatment of Ascaris lumbricoides in a rural zone of Colima, Mexico. J Helminthol. 2007 Sep. 81(3):255-9. [View Abstract]
  33. Shuford KV, Turner HC, Anderson RM. Compliance with anthelmintic treatment in the neglected tropical diseases control programmes: a systematic review. Parasit Vectors. 2016 Jan 27. 9:29. [View Abstract]
  34. Tyagi R, Maddirala AR, Elfawal M, Fischer C, Bulman CA, Rosa BA, et al. Small Molecule Inhibitors of Metabolic Enzymes Repurposed as a New Class of Anthelmintics. ACS Infect Dis. 2018 Jul 13. 4 (7):1130-1145. [View Abstract]
  35. Finsnes KD. Laryngeal spasm after general anaesthesia due to Ascaris lumbricoides. Acta Anaesthesiol Scand. 2013 Aug. 57(7):944-5. [View Abstract]
  36. Hosain GM, Saha S, Begum A. Impact of sanitation and health education on intestinal parasite infection among primary school aged children of Sherpur, Bangladesh. Trop Doct. 2003 Jul. 33(3):139-43. [View Abstract]
  37. Strunz EC, Addiss DG, Stocks ME, Ogden S, Utzinger J, Freeman MC. Water, sanitation, hygiene, and soil-transmitted helminth infection: a systematic review and meta-analysis. PLoS Med. 2014 Mar. 11(3):e1001620. [View Abstract]
  38. Gabrie JA, Rueda MM, Canales M, Gyorkos TW, Sanchez AL. School hygiene and deworming are key protective factors for reduced transmission of soil-transmitted helminths among schoolchildren in Honduras. Parasit Vectors. 2014 Aug 4. 7(1):354. [View Abstract]
  39. Taylor-Robinson DC, Maayan N, Soares-Weiser K, Donegan S, Garner P. Deworming drugs for soil-transmitted intestinal worms in children: effects on nutritional indicators, haemoglobin and school performance. Cochrane Database Syst Rev. 2012 Nov 14. 11:CD000371. [View Abstract]
  40. Tsuji N, Suzuki K, Kasuga-Aoki H, et al. Mice intranasally immunized with a recombinant 16-kilodalton antigen from roundworm Ascaris parasites are protected against larval migration of Ascaris suum. Infect Immun. 2003 Sep. 71(9):5314-23. [View Abstract]
  41. Zhan B, Beaumier CM, Briggs N, Jones KM, Keegan BP, Bottazzi ME, et al. Advancing a multivalent 'Pan-anthelmintic' vaccine against soil-transmitted nematode infections. Expert Rev Vaccines. 2014 Mar. 13(3):321-31. [View Abstract]
  42. [Guideline] World Health Organization. Preventive chemotherapy to control soil-transmitted helminth infections in at-risk population groups. WHO. Available at 2017; Accessed: July 28, 2018.
  43. Olds GR. Deworming the world. Trans Am Clin Climatol Assoc. 2013. 124:265-74. [View Abstract]
  44. Albright JW, Basaric-Keys J. Instruction in behavior modification can significantly alter soil-transmitted helminth (STH) re-infection following therapeutic de-worming. Southeast Asian J Trop Med Public Health. 2006 Jan. 37(1):48-57. [View Abstract]
  45. Bradley JE, Jackson JA. Immunity, immunoregulation and the ecology of trichuriasis and ascariasis. Parasite Immunol. 2004 Nov-Dec. 26(11-12):429-41. [View Abstract]
  46. Choudhury SY, Kaiser MS. Varied presentation of biliary ascariasis and its consequences. Mymensingh Med J. 2006 Jul. 15(2):150-2. [View Abstract]
  47. Cleary JD, Graham D, Lushbaugh WB, et al. Single low-dose mebendazole administered quarterly for ascaris treatment. Am J Med Sci. 2007 Jun. 333(6):340-5. [View Abstract]
  48. Crompton DWT. Gastrointestinal Nematodes-Ascaris, Hookworm, Trichuris, and Enterobius. Topley and Wilson's Microbiology and Microbial Infections. 1998. Volume 5-Parasitology:561-580.
  49. Cunha BA. Antibiotic Essentials. Royal Oak, Mich: Physicians Press; 2005.
  50. de Silva NR, Guyatt HL, Bundy DA. Worm burden in intestinal obstruction caused by Ascaris lumbricoides. Trop Med Int Health. 1997 Feb. 2(2):189-90. [View Abstract]
  51. Holland CV, O'Shea E, Asaolu SO, et al. A cost-effectiveness analysis of anthelminthic intervention for community control of soil-transmitted helminth infection: levamisole and Ascaris lumbricoides. J Parasitol. 1996 Aug. 82(4):527-30. [View Abstract]
  52. Hotez PJ, Zheng F, Long-qi X, et al. Emerging and reemerging helminthiases and the public health of China. Emerg Infect Dis. 1997 Jul-Sep. 3(3):303-10. [View Abstract]
  53. Kakihara D, Yoshimitsu K, Ishigami K, et al. Liver lesions of visceral larva migrans due to Ascaris suum infection: CT findings. Abdom Imaging. 2004 Sep-Oct. 29(5):598-602. [View Abstract]
  54. Khuroo MS. Ascariasis. Gastroenterol Clin North Am. 1996 Sep. 25(3):553-77. [View Abstract]
  55. Legesse M, Erko B, Medhin G. Comparative efficacy of albendazole and three brands of mebendazole in the treatment of ascariasis and trichuriasis. East Afr Med J. 2004 Mar. 81(3):134-8. [View Abstract]
  56. Maruyama H, Nawa Y, Noda S, et al. An outbreak of ascariasis with marked eosinophilia in the southern part of Kyushu District, Japan, caused by infection with swine ascaris. Southeast Asian J Trop Med Public Health. 1997. 28 Suppl 1:194-6. [View Abstract]
  57. Misra SP, Dwivedi M. Endoscopy-assisted emergency treatment of gastroduodenal and pancreatobiliary ascariasis. Endoscopy. 1996 Sep. 28(7):629-32. [View Abstract]
  58. Salman AB. Management of intestinal obstruction caused by ascariasis. J Pediatr Surg. 1997 Apr. 32(4):585-7. [View Abstract]
  59. Sandouk F, Haffar S, Zada MM, et al. Pancreatic-biliary ascariasis: experience of 300 cases. Am J Gastroenterol. 1997 Dec. 92(12):2264-7. [View Abstract]
  60. Schuster DI, Belin RP, Parker JC Jr, Burke JA, Jona JZ. Ascariasis--its complications, unusual presentations and surgical approaches. South Med J. 1977 Feb. 70(2):176-8. [View Abstract]
  61. Soomro MA, Akhtar J. Non-operative management of intestinal obstruction due to ascaris lumbricoides. J Coll Physicians Surg Pak. 2003 Feb. 13(2):86-9. [View Abstract]
  62. Steinberg R, Davies J, Millar AJ, et al. Unusual intestinal sequelae after operations for Ascaris lumbricoides infestation. Pediatr Surg Int. 2003 Apr. 19(1-2):85-7. [View Abstract]
  63. Villamizar E, Mendez M, Bonilla E, et al. Ascaris lumbricoides infestation as a cause of intestinal obstruction in children: experience with 87 cases. J Pediatr Surg. 1996 Jan. 31(1):201-4; discussion 204-5. [View Abstract]
  64. Zargar SA, Khan BA, Javid G, et al. Endoscopic management of early postoperative biliary ascariasis in patients with biliary tract surgery. World J Surg. 2004 Jul. 28(7):712-5. [View Abstract]

Adult Ascaris lumbricoides.

Adult Ascaris lumbricoides.

Ascaris lumbricoides egg.

Life cycle of Ascaris lumbricoides.

Adult Ascaris lumbricoides in biliary system.

Adult Ascaris lumbricoides.

Life cycle of Ascaris lumbricoides.

Ascaris lumbricoides egg.

Adult Ascaris lumbricoides in biliary system.