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This article is for Medical Professionals

Professional Reference articles are designed for health professionals to use. They are written by UK doctors and based on research evidence, UK and European Guidelines. You may find the Roundworms article more useful, or one of our other health articles.

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The nematode (roundworm) Angiostrongylus cantonensis (the rat lungworm) is the most common cause of human eosinophilic meningitis. Angiostrongylus costaricensis causes abdominal (or intestinal) angiostrongyliasis. Angiostrongylus spp. belong to the order Strongyloidea subfamily Metastrongyloidea (lungworms).[1]

  • The normal life cycle of the lungworm A. cantonensis involves rats (definitive host) and snails or slugs (intermediate hosts), and also transport hosts such as crabs, freshwater shrimps, fish, reptiles and amphibians who feed on them.
  • Humans are incidental hosts and acquire the infection by eating raw or undercooked infected snails, slugs, crabs or freshwater shrimps, or by eating raw vegetables contaminated by a small snail or slug.[2] Humans do not transmit either eggs or larvae.

A. cantonensis

  • Adult worms of A. cantonensis live in the pulmonary arteries of rats. The females lay eggs that hatch in the terminal branches of the pulmonary arteries.
  • Larvae migrate to the pharynx, and are then swallowed and passed in the faeces. The larvae penetrate or are ingested by an intermediate host (snail or slug). Third-stage larvae are produced, which are infective to mammals.
  • When the mollusc is ingested by the definitive host, the third-stage larvae migrate to the brain where they develop into young adults. The young adults return to the venous system and then the pulmonary arteries where they become sexually mature.
  • In humans, juvenile worms migrate to the brain (or, rarely, the lungs), where the worms ultimately die.

A. costaricensis

  • The life cycle is similar except that the adult worms live in the arterioles of the ileocaecal area of the definitive host.
  • In humans, A. costaricensis often reaches sexual maturity and releases eggs into the intestinal tissues. The eggs and larvae degenerate causing severe local inflammation and do not appear to be shed in the stool.
  • Most cases of eosinophilic meningitis have been reported from Southeast Asia and the Pacific Basin, although the infection is spreading to many other areas of the world, including Africa and the Caribbean.
  • Abdominal angiostrongyliasis has been reported from Central and South America, and occurs most commonly in young children.

Eosinophilic meningitis

  • Symptoms are caused by the presence of larvae and local host reactions in the brain.
  • Symptoms include severe headaches, nausea, vomiting, neck stiffness, seizures, and paraesthesiae.
  • Eye involvement can occur but ocular angiostrongyliasis is very rare.[3]
  • Eosinophilia is present in most cases.

Abdominal angiostrongyliasis
This presents with acute abdominal pain in the right lower quadrant, associated with prolonged fever, anorexia and eosinophilia. Infection usually involves the terminal ileum, appendix or ascending colon.

  • A. cantonensis is the most common cause of human eosinophilic meningitis. Other causes include gnathostomiasis, cysticercosis, and non-infectious causes - eg, haematological malignancies and antibiotics (eg, ciprofloxacin).
  • A. costaricensis presents with acute abdominal pain and can mimic acute appendicitis. Other differential diagnoses to consider include hydatid disease, cysticercosis, strongyloidiasis and visceral larva migrans.
  • FBC: eosinophilia.
  • Eosinophilic meningitis: cerebrospinal fluid (CSF) is abnormal with elevated pressure, proteins, and eosinophilia. On rare occasions, larvae have been found in the CSF.
  • Abdominal angiostrongyliasis: eggs and larvae can be identified in the tissues removed at surgery.
  • Tests for parasite-specific immunoglobulin G (IgG) antibodies are reliable.[4]

Eosinophilic meningitis

  • There is no effective curative treatment.[5] Treatment is supportive, including adequate analgesia, therapeutic CSF aspiration and the use of corticosteroids.
  • Repeated CSF drainage may give symptomatic relief.
  • Steroid treatment appears to be beneficial with reported regimens of 40-60 mg per day of prednisolone for up to two weeks.
  • Avoidance of anthelmintic agents has been recommended because of their potential for harm from the inflammatory response provoked by antigen release after the death of the parasite.[6]

Abdominal angiostrongyliasis
There is no effective treatment for abdominal angiostrongyliasis.[5]

  • Meningitis is usually mild and resolves spontaneously over six weeks. Occasionally, cases are severe and may lead to long-term neurological complications.
  • Abdominal angiostrongyliasis is usually benign but it may cause intestinal obstruction or perforation requiring surgery.[7]
  • Theoretically, control of rodents and molluscs should limit disease.
  • Scrupulous attention to personal hygiene and handwashing after outdoor work.
  • Washing vegetables thoroughly.
  • Avoiding raw or undercooked molluscs, crustaceans, and fish, etc.
  • Provision of clean drinking water.

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Further reading and references

  1. Angiostrongyliasis; DPDx, Centers for Disease Control and Prevention

  2. New D, Little MD, Cross J; Angiostrongylus cantonensis infection from eating raw snails. N Engl J Med. 1995 Apr 20332(16):1105-6.

  3. Sawanyawisuth K, Sawanyawisuth K; Treatment of angiostrongyliasis. Trans R Soc Trop Med Hyg. 2008 May 23.

  4. Intapan PM, Maleewong W, Sawanyawisuth K, et al; Evaluation of human IgG subclass antibodies in the serodiagnosis of angiostrongyliasis. Parasitol Res. 2003 Apr89(6):425-9. Epub 2002 Nov 26.

  5. Mentz MB, Graeff-Teixeira C; Drug trials for treatment of human angiostrongyliasis. Rev Inst Med Trop Sao Paulo. 2003 Jul-Aug45(4):179-84. Epub 2003 Sep 17.

  6. Senanayake SN, Pryor DS, Walker J, et al; First report of human angiostrongyliasis acquired in Sydney. Med J Aust. 2003 Oct 20179(8):430-1.

  7. Waisberg J, Corsi CE, Rebelo MV, et al; Jejunal perforation caused by abdominal angiostrongyliasis. Rev Inst Med Trop Sao Paulo. 1999 Sep-Oct41(5):325-8.