eMedicine Specialties > Emergency Medicine > Infectious Diseases

Ascaris Lumbricoides

Aaron Dora-Laskey, MD, Emergency Physician, Physician Management Group, Dayton, Ohio
Ugo Anthony Ezenkwele, MD, MPH, Assistant Professor of Emergency Medicine, Department of Emergency Medicine, New York University School of Medicine/Bellevue Hospital Center; Eric L Weiss, MD, DTM&H, Director of Stanford Travel Medicine, Medical Director of Stanford Lifeflight, Assistant Professor, Departments of Emergency Medicine and Infectious Diseases, Stanford University School of Medicine

Updated: Jul 30, 2009

Introduction

Background

Intestinal nematode infections affect one fourth to one third of the world's population. Of these, the intestinal roundworm Ascaris lumbricoides is the most common. While the vast majority of these cases are asymptomatic, infected persons may present with pulmonary or potentially severe gastrointestinal complaints. Ascariasis predominates in areas of poor sanitation and is associated with malnutrition, iron-deficiency anemia, and impairments of growth and cognition.
 

Adult Ascaris lumbricoides.

Pathophysiology

A lumbricoides is the largest of the intestinal nematodes affecting humans, measuring 15-35 cm in length in adulthood. Infection begins with the ingestion of embryonated (infective) eggs in feces-contaminated soil or foodstuffs. Once ingested, eggs hatch, usually in the small intestine, releasing small larvae that penetrate the intestinal wall. Larvae migrate to the pulmonary vascular beds and then to the alveoli via the portal veins usually 1-2 weeks after infection, during which time they may cause pulmonary symptoms (eg, cough, wheezing). During the time frame of pulmonary symptoms, eggs are not being shed, and thus diagnosis via stool ovas and parasites is not possible. Eggs are not shed in stool until roughly 40 days after the development of pulmonary symptoms. 

After migrating up the respiratory tract and being swallowed, they mature, copulate, and lay eggs in the intestines. Adult worms may live in the gut for 6-24 months, where they can cause partial or complete bowel obstruction in large numbers, or they can migrate into the appendix, hepatobiliary system, or pancreatic ducts and rarely other organs such as kidneys or brain. From egg ingestion to new egg passage takes approximately 9 weeks, with an additional 3 weeks needed for egg molting before they are capable of infecting a new host.

Life cycle of Ascaris lumbricoides.

Frequency

United States

In the United States, approximately 4 million people are believed to be infected. High-risk groups include international travelers, recent immigrants (especially from Latin America and Asia), refugees, and international adoptees. Ascariasis is indigenous to the rural southeast, where cross-infection by pigs with the nematode Ascaris suum is thought to occur. (Children aged 2-10 years are thought to be more heavily infected in this and all regions.)

International

Worldwide, 1.4 billion people are infected with A lumbricoides, with prevalence among developing countries as low as 4% in Mafia Island, Zanzibar,¹ to as high as 90% in some areas of Indonesia. Local practices (eg, termite mound–eating in Kenya² ) may predispose to ascariasis in some populations. Other risk factors like dog/cat ownership, presence of pets within the house, and a previous history of geophagia have been noted. In some regions, Ascaris infection is thought to contribute significantly to the burden of abdominal surgical emergencies.

Mortality/Morbidity

The rate of complications secondary to ascariasis ranges from 11-67%, with intestinal and biliary tract obstruction representing the most common serious sequelae. Although infection with A lumbricoides is rarely fatal, it is responsible for an estimated 8,000-100,000 deaths annually, mainly in children, usually from bowel obstruction or perforation in cases of high parasite burden. Due to similarities in the means of infection, many individuals infected with Ascaris are also co-infected with other intestinal parasites.

Race

No racial predilection is known. A genetic predisposition has been described in a study of families from Nepal.³  

Sex

Male children are thought to be infected more frequently, owing to a greater propensity to eat soil.

Age

Children, because of their habits (eg, directly or indirectly consuming soil), are more commonly and more heavily infected than adults. Neonates may be infected by transplacental infection. Frequently, families may be infected and reinfected in group fashion due to shared food and water sources as well as hygiene practices.

Clinical

History

Most patients are asymptomatic. When symptoms occur, they are divided into 2 categories: early (larval migration) and late (mechanical effects).

• In the early phase (4-16 d after egg ingestion), respiratory symptoms result from the migration of larvae through the lungs. Classically, these symptoms occur in the setting of eosinophilic pneumonia (Löffler syndrome).
  • Fever
  • Nonproductive cough
  • Dyspnea
  • Wheezing
• In the late phase (6-8 wk after egg ingestion), gastrointestinal symptoms may occur and are more typically related to the mechanical effects of high parasite loads.
  • Passage of worms (from mouth, nares, anus)
  • Diffuse or epigastric abdominal pain
  • Nausea, vomiting
  • Pharyngeal globus, "tingling throat"
  • Frequent throat clearing, dry cough
  • Complications - Biliary and intestinal obstruction, appendicitis, pancreatitis

Physical

• General
  • Fever
  • Jaundice (in biliary obstruction)
  • Cachexia (due to malnutrition)  
  • Pallor (anemia)
  • Urticaria (early infection)
• Pulmonary
  • Wheezing
  • Rales
  • Diminished breath sounds
• Abdominal
  • Abdominal tenderness, which may be diffuse (in obstructive infections), or localized to the right lower (appendicitis) or right upper quadrant (hepatobiliary infections)
  • Peritoneal signs in cases of bowel perforation
  • Obstructive symptoms (nausea/vomiting/constipation/distention)
• Migrating larvae may transmit other organisms, causing bacterial pneumonia or cholangitis. Rare cases of airway obstruction have also been reported. Other much less common presentations include lacrimal drainage obstruction,⁴ small bowel intussusception,⁵ acute interstitial nephritis,⁶ and encephalopathy.⁷

Causes

Symptoms are typically associated with early larval migration, heavy intestinal burdens of adult worms, or aberrant worm migration. Worm migration may be stimulated by anesthetic agents, fever, or subtherapeutic anthelmintic treatment, or by use of certain anthelmintics (eg, pyrantel pamoate).

Differential Diagnoses

Other Problems to Be Considered

Hepatic abscess
Tropical pulmonary eosinophilia
Visceral larva migrans

Workup

Laboratory Studies

• Early infection (larval migration)
  • Complete blood count (CBC) may show eosinophilia.
  • Sputum analysis may reveal larvae or Charcot-Leyden crystals.
  • Stool examination findings are typically normal in absence of previous infection (during the first 40 d).
  • Ascaris specific antibodies (not useful in acute infection and not protective)
  • Increases in IgE and later IgG 
• Established infection (adult phase): Stool examination findings include characteristic eggs. Adult females lay about 200,000 eggs per day, aiding microscopic identification of characteristic eggs.

Ascaris lumbricoides egg.

Adult Ascaris lumbricoides in biliary system.

Ascaris lumbricoides egg in feces (formalin-ethyl acetate sedimentation method).

Imaging Studies

• Early infection (larval migration): Chest radiography may reveal patchy infiltrates of eosinophilic pneumonia.
• Established infection (adult phase)
  • Abdominal radiography may reveal adult worms (especially with contrast). 
  • Obstructing Ascaris lesions cause cylindrical filling defects on contrast computed tomography (CT) scans.
  • Cholangiopancreatography by endoscopy (ERCP) or magnetic resonance imaging (MRCP, or magnetic resonance cholangiopancreatography) may detect adult worms in bile or pancreatic ducts.⁸
  • Ultrasonography may detect worms in the gallbladder.

Treatment

Emergency Department Care

• Early infection (larval migration)
  • Inhaled beta-agonists may be indicated.
  • Steroids for pulmonary symptoms are controversial.
  • Whether anthelmintic therapy is effective against larval stages is unclear. (Stool ova microscopy will likely be negative at this phase). Because infection in the early phase is rarely serious, generally treatment is delayed until definitive diagnosis can be made.
• Established infection (adult phase)
  • Benzimidazoles are the mainstay of treatment of symptomatic and asymptomatic infections. They are poorly systemically absorbed and thus have low human toxicity and exert their action directly on worms. The most common members of this family are albendazole and mebendazole.  
  • Treatment of bowel obstruction includes intravenous hydration, nasogastric suctioning, electrolyte monitoring, and laparotomy if conservative measures fail. Colonoscopy and esophagogastroduodenoscopy (EGD) may be useful in removing obstructing masses of worms.
  • Piperazine citrate, a helminth paralytic, has been suggested in cases of obstruction; however, it is no longer commercially available in the United States.
  • Hepatobiliary ascariasis typically responds to similarly conservative therapy, but it may require invasive intervention (eg, ERCP).

Consultations

Bowel or hepatobiliary obstruction may require surgical or gastroenterologic consultation.

Medication

Anthelmintics

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

Albendazole (Albenza)

Decreases ATP production in worm, causing energy depletion, immobilization, and finally death.

Dosing

Adult

400 mg/d PO single dose; repeat in 3 wk if not cured

Pediatric

<2 years: 200 mg/d PO single dose; repeat in 3 wk if not cured
>2 years: Administer as in adults

Interactions

Coadministration with carbamazepine may decrease efficacy; dexamethasone and praziquantel may increase toxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Discontinue use if LFT values increase significantly (resume when levels decrease to pretest values); GI symptoms (nausea, vomiting, diarrhea) or CNS symptoms (dizziness, headache, meningeal signs) may occur; granulocytopenia, thrombocytopenia, and pancytopenia have been reported

Mebendazole (Vermox)

Causes worm death by selectively and irreversibly blocking uptake of glucose and other nutrients in susceptible adult intestine where helminths dwell.

Dosing

Adult

100 mg PO bid on 3 consecutive days
Administer second course if not cured within 3-4 wk

Pediatric

<2 years: Not established
>2 years: Administer as in adults

Interactions

Carbamazepine and phenytoin may decrease effects

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adjust dose in hepatic impairment; GI symptoms (nausea, vomiting, abdominal pain, diarrhea) and CNS symptoms (headache, dizziness) are common; alopecia may be associated with high doses; rare reactions include angioedema, seizures, and agranulocytosis

Piperazine citrate

Recommend for GI or biliary obstruction secondary to ascariasis; causes flaccid paralysis of the helminth by blocking response to worm muscle to acetylcholine.

Dosing

Adult

3.5 g PO qd for 2 d

Pediatric

75 mg/kg PO qd for 2 d; not to exceed 3.5 g/dose

Interactions

Coadministration with chlorpromazine may increase toxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Most commonly reported reactions include GI and CNS effects; discontinue therapy if effects become significant; prolonged, repeated, or excessive therapy should be avoided because of potential neurotoxicity

Pyrantel pamoate (Antiminth)

Depolarizing neuromuscular blocking agent; inhibits cholinesterases, resulting in spastic paralysis of worm.

Dosing

Adult

11 mg/kg/dose PO as single dose; not to exceed 1 g

Pediatric

Administer as in adults

Interactions

Pyrantel and piperazine are mutually antagonistic and should not be used concomitantly

Contraindications

Documented hypersensitivity; hepatic disease

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in liver impairment, anemia, and malnutrition; GI effects, headache, insomnia, rash, tenesmus, and elevated LFT values may occur

Ivermectin (Stromectol)

Binds selectively with glutamate-gated chloride ion channels in invertebrate nerve and muscle cells, causing cell death.

Dosing

Adult

150-200 mcg/kg PO once

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Serious reactions include Stevens-Johnson syndrome, asthma exacerbation, and vision loss (rare); common reactions include pruritus, rash, headache, myalgias, and elevated LFT values

Levamisole (Ergamisol)

May inhibit worm copulation via agonism of L-subtype nicotinic acetylcholine receptors in male nematode muscles.

Dosing

Adult

2.5 mg/kg PO once

Pediatric

Administer as in adults

Interactions

Increases toxicity and serum levels of phenytoin; causes disulfiram reactions when taken with alcohol

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Agranulocytosis can occur asymptomatically

Follow-up

Further Inpatient Care

• Further inpatient care is warranted for patients with complications due to worm migration.

Further Outpatient Care

• Primary care follow up is suggested to confirm cure.
• Presumptive administration of albendazole to all immigrants at risk for parasitosis has been suggested and shown to save lives and money. However, current recommendations do not include its implementation.
• Follow-up stool ova and parasite microscopic testing is warranted post treatment to ensure clearance of parasite infection and as well to monitor for re-infection, which can be common.

Deterrence/Prevention

• Screening programs for the carrier state may assist in eradication in endemic areas.
• Given the association with poverty and malnutrition, long-term control will require sustained economic growth in developing countries and the creation of sanitation and education systems including those to reduce the use of human feces for fertilizer.
• Many nations have such high rates of Ascaris infection that they empirically treat some age groups without testing. Medication choices and the frequency of testing vary from country to country, but data are favorable for reducing the load of parasites in the community and as well for reducing individual morbidity and mortality associated with infection.

Complications

• Complications may be attributed to larval migration typically involving the lungs, and intestinal tract producing vague symptoms but may as well involve the kidneys, brain, and heart.
• Severe complications later in disease are usually attributable to mechanical obstruction of intestines or biliary tree secondary to high worm burden.
• Complications may arise early in disease due to allergic reaction to Ascaris infection (urticaria).
• Malnutrition, anemia, growth, and developmental retardation (subject to some debate)

Prognosis

• The prognosis for ascariasis is excellent. However, in higher worm burden infections, serious complications such as obstruction are more common.

Patient Education

• Recommend good personal hygiene and food handling techniques: discriminate defecation, hand-washing, cleaning fruits and vegetables, and avoiding soil consumption. Educational programs should also address the use of human feces as fertilizer, a practice that persists in many communities internationally.

Multimedia

Media file 1: Adult Ascaris lumbricoides.

Media file 2: Life cycle of Ascaris lumbricoides.

Media file 3: Ascaris lumbricoides egg.

Media file 4: Adult Ascaris lumbricoides in biliary system.

Media file 5: The roundworm Ascaris lumbricoides causes ascariasis. Worms can reach 10-30 cm in length. Clinical disease results from effects of pulmonary larval migration, intestinal obstruction, or migration through the biliary tree.

Media file 6: Ascaris lumbricoides egg in feces (formalin-ethyl acetate sedimentation method).

References

1. Albonico M, Ramsan M, Wright V, et al. Soil-transmitted nematode infections and mebendazole treatment in Mafia Island schoolchildren. Ann Trop Med Parasitol. Oct 2002;96(7):717-26. [Medline].

2. Luoba AI, Wenzel Geissler P, Estambale B, et al. Earth-eating and reinfection with intestinal helminths among pregnant and lactating women in western Kenya. Trop Med Int Health. Mar 2005;10(3):220-7. [Medline].

3. Williams-Blangero S, Subedi J, Upadhayay RP, et al. Genetic analysis of susceptibility to infection with Ascaris lumbricoides. Am J Trop Med Hyg. Jun 1999;60(6):921-6. [Medline].

4. Mwanza JC. Lacrimal drainage obstruction by Ascaris lumbricoides. Bull Soc Belge Ophtalmol. 2004;71-3. [Medline].

5. Karatepe O, Tukenmez M, Salmashogul A, et al. Ascaris as a leading point for small-bowel intussusception in an adult: a rare cause of intussusception. Am J Emerg Med. Mar 1 2008;26(3):381.e3-381.e4.

6. Jung O, Ditting T, Grone HJ, Geiger H, Hauser IA. Acute interstitial nephritis in a case of Ascaris lumbricoides infection. Nephrol Dial Transplant. Jun 2004;19(6):1625-8. [Medline].

7. Selimoglu MA, Ozturk CF, Ertekin V. A rare manifestation of ascariasis: encephalopathy. J Emerg Med. Jan 2005;28(1):87-8. [Medline].

8. Arya PK, Kukreti R, Arya M, Gupta SN. Magnetic resonace appearance of gall bladder ascariasis. Indian J Med Sci. May 2005;59(5):208-10. [Medline].

9. Xiao SH, Hui-Ming W, Tanner M, Utzinger J, Chong W. Tribendimidine: a promising, safe and broad-spectrum anthelmintic agent from China. Acta Trop. Apr 2005;94(1):1-14. [Medline].

10. Steinmann P, Zhou XN, Du ZW, Jiang JY, Xiao SH, Wu ZX, et al. Tribendimidine and Albendazole for Treating Soil-Transmitted Helminths, Strongyloides stercoralis and Taenia spp.: Open-Label Randomized Trial. PLoS Negl Trop Dis. 2008;2(10):e322. [Medline].

11. Bell DR. Soil transmitted helminths. In: Lecture Notes on Tropical Medicine. Boston: Blackwell Science; 1985:167-192.

12. Cappello M, Hotez PJ. Intestinal Nematodes. Philadelphia: Churchill-Livingstone; 2003:1331-1333.

13. Freedman DO. Intestinal nematodes. In: Gorbach, ed. Infectious Diseases. Philadelphia: WB Saunders; 1992:2003-2008.

14. Gilles HM. Intestinal nematode infections. In: GT Strickland, ed. Hunter's Tropical Medicine. Philadelphia: WB Saunders; 1984:620-644.

15. Liu LX, Weller PF. Antiparasitic drugs. N Engl J Med. May 2 1996;334(18):1178-84. [Medline].

16. Muennig P, Pallin D, Sell RL, Chan MS. The cost effectiveness of strategies for the treatment of intestinal parasites in immigrants. N Engl J Med. Mar 11 1999;340(10):773-9. [Medline].

17. Talaat KR, Nutman TB. Parasitic Diseases. In: Mason, ed. Murray & Nadel's Textbook of Respiratory Medicine. Philadelphia: Saunders; 2003:1090-1092.

18. Urbani C, Albonico M. Anthelminthic drug safety and drug administration in the control of soil-transmitted helminthiasis in community campaigns. Acta Trop. May 2003;86(2-3):215-21. [Medline].

Keywords

Ascaris lumbricoides, A lumbricoides, ascariasis, roundworm, intestinal parasite, roundworm treatment, roundworm symptoms, intestinal roundworm, human parasite, nematode infection, malnutrition, iron-deficiency anemia, bowel obstruction, Ascaris suum, eosinophilic pneumonia, Löffler syndrome

Contributor Information and Disclosures

Author

Aaron Dora-Laskey, MD, Emergency Physician, Physician Management Group, Dayton, Ohio
Aaron Dora-Laskey, MD is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Ugo Anthony Ezenkwele, MD, MPH, Assistant Professor of Emergency Medicine, Department of Emergency Medicine, New York University School of Medicine/Bellevue Hospital Center
Ugo Anthony Ezenkwele, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, National Medical Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Eric L Weiss, MD, DTM&H, Director of Stanford Travel Medicine, Medical Director of Stanford Lifeflight, Assistant Professor, Departments of Emergency Medicine and Infectious Diseases, Stanford University School of Medicine
Eric L Weiss, MD, DTM&H is a member of the following medical societies: American College of Emergency Physicians, American College of Occupational and Environmental Medicine, American Medical Association, American Society of Tropical Medicine and Hygiene, Physicians for Social Responsibility, Southeastern Surgical Congress, Southern Association for Oncology, Southern Clinical Neurological Society, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Mark Louden, MD, FACEP, Assistant Medical Director, Emergency Department, Duke Raleigh Hospital
Mark Louden, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Jon Mark Hirshon, MD, MPH, Associate Professor, Department of Emergency Medicine, University of Maryland School of Medicine
Jon Mark Hirshon, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Public Health Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD, Medical Director, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: WebMD Salary Employment

The authors and editors of eMedicine gratefully acknowledge the medical review of this article by Joseph U Becker, MD.

© 1994- by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)