Ascaris/Common Roundworm

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Code: p1
Latin name: Ascaris lumbricoides
Source material: Ascaris suum (pig Ascaris), which has a high degree of cross-reactivity with Ascaris lumbricoides.
Common names: Common roundworm
A parasite, which may result in allergy symptoms in sensitised individuals.

Allergen Exposure

Geographical distribution
The nematode Ascaris lumbricoides is one of the most common parasites found in humans, infecting an estimated 25% of the world’s population. It is also one of the largest parasites: the adult females can measure up to 40 cm long (males are generally shorter). The adult worms live in the small intestine, and eggs are passed in the faeces. A single female can produce up to 200,000 eggs each day. About two weeks after passage in the faeces, the eggs contain an infective larval or juvenile stage of the nematode, and humans are infected when they ingest such eggs (primarily in agricultural products and other contaminated foods). The eggs hatch in the small intestine, and the juvenile larvae penetrate the intestine wall and enter the circulatory system, where they are transported to the lungs. In the lungs the larvae enter the alveoli and bronchioles, and then migrate up the tracheobronchial tree into the pharynx, from which the host swallows them; they then develop into adult worms in the intestine.
Human hosts are often surprisingly tolerant of intestinal infestation with adult A. lumbricoides. But the adult worms may physically block the gastrointestinal tract or migrate into the bile or pancreatic duct, resulting in obstruction. Ascaris penetration of the small intestine wall may result in peritonitis. Migration of the larvae through the lungs may cause the blood vessels of the lungs to haemorrhage, triggering an inflammatory response accompanied by oedema. The resulting accumulation of fluids in the lungs causes "ascaris pneumonia," and this can be fatal.
The pulmonary phase can cause potentially lethal hypersensitivity responses in infected individuals, particularly children (1). Bronchial asthma, urticaria, and angioedema occur frequently. Ascaris-specific IgE and non-specific IgE are both produced in large amounts.
A. lumbricoides, A. suum, Toxocara canis and Anisakis simplex belong to the Ascaroidea, the same group of large parasitic nematodes. The A. lumbricoides life cycle is identical to that of A. suum. A. suum is found primarily in pigs, but infections in humans can cause significant pathology. If a human ingests eggs of A. suum, the larvae migrate to the lungs and die. (Adult worms of this species do not develop in the human intestine.) This can cause a particularly serious form of Ascaris pneumonia.
Ascaris infection is very common in rural developing countries with poor sanitation, and especially in regions where pig and human faeces are used as fertiliser. But infections can occur even in industrialised, urban settings whenever raw fruits and vegetables are not washed, peeled or cooked before eating, handwashing is neglected, or there is any other indirect contact with contaminated faeces or soil.
Ascaris allergens were detected over 2 decades ago (2). But isolation and characterisation of Ascaris allergens are difficult. Crude extracts may result in contamination of the soluble protein with non-specific immunomodulatory molecules such as vasoactive amines, arachidonic acid metabolites, non-specific degranulating agents and irrelevant proteins (3-4).
Two allergens have been identified to date:
  • Asc l 1 (common name ABA-1), an allergen of approximately 15 kDa.
  • Asc l Tropomyosin (5-6).
The tissue-invasive and intestinal stages of both A. lumbricoides (of humans) and A. suum (of pigs) contain an antigen of similar molecular weight to ABA-1 (characterised for A. suum and named Asc s 1) in secretions or among somatic antigens. Asc s 1 and Asc l 1 are antigenically indistinguishable (7). The ABA-1 protein of A. lumbricoides and A. suum is abundant in the pseudocoelomic fluid of the parasites and also appears to be released by the tissue-parasitic larvae and the adult stages. Whether its allergenic activity is an intrinsic property of the protein or merely due to generalised IgE potentiation by the infection is questionable (8).
Asc l 1 (ABA-1) is a fatty acid binding protein (FABP). The protein requires unusually high temperatures (89 degrees C) before it denatures, and it can renature upon cooling and recover its allergenicity (9-10).
A number of other potential allergens have been isolated from A. suum; they may also be present in A. lumbricoides but have not yet been fully characterised. The following 2 distinct components from A. suum adult worms were shown to have different effects on the immune system: APAS-3, which induces IgE antibody production and a suppressive protein; and PAS-1, which inhibits humoral and cellular immune responses induced by unrelated antigens (11).

Potential Cross-reactivity

Cross-reactive specific IgE against Anisakis simplex, A. lumbricoides and Echinococcus granulosus has been reported (12). However, cross-reactivity is not absolute, as demonstrated in a study of 23 patients with Anisakis simplex allergy, where serum-specific IgE to A. lumbricoides was negative in 13 patients (13).
Cross-reactivity was reported to IgE-binding proteins from Anisakis, Blattella germanica (German cockroach), and chironomids (red mosquito larvae); there was also a strong association among Pandalus borealis (Atlantic shrimp), A. lumbricoides and Daphnia, but this was not confirmed in laboratory studies (14). The common allergen may have been tropomyosin.
It has in fact been postulated that Ascaris and other helminths could share antigens capable of inducing cross-reactive IgE antibody responses after exposure via the inhalation route, such as the antigens in mites and cockroaches; one example is tropomyosin, a protein associated with strong IgE antibody responses, which is highly conserved in invertebrates (6).
Recently, A. lumbricoides tropomyosin was shown to be an IgE-binding protein, and sequencing revealed a high degree of identity of Ascaris tropomyosin to tropomyosins from mites, cockroach, shrimp, and other parasites such as A. simplex and Onchocerca volvulus (69-98%). By contrast, a lower degree of identity was found between Ascaris and Schistosoma tropomyosin (57%) suggesting that Schistosoma tropomyosins may not share extensive IgE cross-reactivity (6).

Clinical Experience

IgE-mediated reactions
Whether infections with intestinal parasites (helminthiases) assist the development of allergy and asthma or whether these result in a protective effect has still not been resolved. Common features of the host’s immune response to parasitic helminthiases are 3 responses typical of immediate hypersensitive reactions: elevated IgE/IgG4 antibody production, eosinophilia, and mastocytosis – but with little sign of clinical hypersensitivity (15). The response is no different than the response of atopic individuals to extrinsic allergens; except that in allergic individuals these antibodies are largely responsible for initiating hypersensitivity reactions such as asthma, whereas in helminth infections, the IgE production is thought to be responsible for a protective immune response to the parasite, as well as for immune-mediated pathology (16-17).
However, an apparent exception to this unexpected gap in hypersensitivity to helminthic infection is A. lumbrioides. The larvae (juvenile form) may induce eosinophilia and high total IgE levels (18-19) that are either of no clinical consequence, or able to elicit severe pulmonary reactions resembling type I hypersensitivity during their migration through the lungs (Löffler’s syndrome) (15).
Ascaris infection induces not only specific but also non-specific IgE antibodies. Parasite-non-specific IgE antibodies begin to elevate a week after infection, and reach a peak about 2 weeks after the elevation of parasite-specific IgE antibodies. It is known that parasite-specific IgE antibodies act to exclude parasites from the host, whereas non-specific IgE antibody production during parasite invasion is involved in the evasion system of those parasites. It is thus important to clarify whether antibody production is as a result of the infection of parasites and in the evasion system of those parasites (20).
Human ascariasis is associated with a polarised Th2-type immune response, with elevated levels across a range of serum immunoglobulins. While some authors propose that parasite-specific antibody responses may confer a degree of protection from re-infection, others suggest that such responses merely reflect infection intensity without involving protective mechanisms. A third opinion suggests that such antibody responses do protect, but only indirectly as a consequence of inflammatory processes (21). A recent study suggested that immune response to Ascaris (Ascaris-sIgE) may be a risk factor of atopic disease in populations exposed to mild Ascaris infection and that Mycobacterium tuberculosis infection may be protective against this risk, probably by stimulation of anti-inflammatory networks (22).
It is possible that the relationship of asthma and allergy to parasitic infection could vary according to the particular kinds of parasites; however, the molecular basis of these effects is largely unknown. As the biological cycle of A. lumbricoides results in pulmonary passage of larvae, and other nematodes, including hookworms and Strongyloides stercoralis, also undergo pulmonary passage of larvae, it may be that Ascaris allergen, on the evidence of the reactions it causes is the most potent of all allergens of parasitic origin (6).6 It may be that exposure to cross-reactive allergens such as tropomyosin at the initial Ascaris infection could facilitate subsequent development of cross-reactive IgE antibody responses upon exposure to mite or cockroach, and that this could lead to airway inflammation and asthma. It may be that infection with Ascaris would have an adjuvant effect on the development of asthma in a subset of Ascaris-infected children who become sensitised to the tropomyosin allergen. Experimental work has demonstrated a dramatic alteration in the parasite’s antigens, which occurs during its development: A. suum larvae have been shown to change the composition of both their secreted and surface antigens during the tissue-invasive stage of infection, thus expressing quite different antigens than those provoking pulmonary hypersensitivity responses (15). This may be similar for A. lumbricoides, and certainly direct inflammatory responses in the lungs caused by parasite antigens can account for wheezing and other respiratory symptoms.
Humans respond heterogeneously to A. simplex allergens, and experience with other nematodes would indicate that this is due to genetic control of the immune repertoire by the major histocompatibility complex (15).
It has also been argued that the response of the induction of large quantities of IgE antibody is in part directed against the helminths’ own antigens, but that a polyclonal stimulation also occurs that may increase the allergic reactivity toward environmental allergens. A study demonstrated that regular anthelminthic treatment resulted in significant improvement in all clinical indicators of asthma, not only during the period of anthelminth administration, but also for the year following. However, after 2 years without treatment, the severity of asthma reverted to its initial level. The authors concluded that intestinal helminthic infections can contribute to the clinical symptoms of asthma in an endemic situation (23). However, a more recent study found that anthelminthic treatment of chronically infected children resulted in increased atopic reactivity, arguing that helminths directly suppress allergic reactions (24).
Previous studies also have confirmed the protective effect of helminthic infections. A study of slum children concluded that the polyclonal production of IgE stimulated by helminthic infection could suppress the allergic response to environmental and parasite allergens via both mast cell saturation and inhibition of specific IgE production (25). Similarly, it was shown that adult worm extracts from Ascaris suum suppress IgE antibody production against unrelated antigens (26).
Similarly, epidemiological studies in developing countries suggest that intestinal parasite infection may reduce the risk of asthma (27). In a survey of 7,155 children aged 1 to 4 years living in urban and rural areas of Jimma, Ethiopia, the conclusion was reached that Ascaris and possibly hookworm infection protected against wheeze in young children, and that this effect was not mediated by inhibition of allergen sensitisation (28).
Children putatively immune to A. lumbricoides were identified in an area of Nigeria where infection is hyperendemic. Among those individuals who produced IgG antibody to recombinant ABA-1 allergen of Ascaris, the naturally immune group had significantly more IgE antibody to the allergen than did those susceptible to the infection. IgE antibody responses in conjunction with innate inflammatory processes therefore appear to associate with natural immunity to ascariasis in this community (1).
In contrast, a number of studies have reported sensitisation and subsequent allergic symptoms to Ascaris, including a report of 41 patients with eosinophilic asthma-associated Ascaris infection (18). Ascaris material is known to provoke allergic reactions in laboratory workers (29). A. lumbrioides has been associated with an increased risk of wheezing, asthma and allergic sensitisation in certain populations (30-31). In a cross-sectional sample of 2,164 children between the ages of 8 and 18 years from Anqing Province, China, infection with A. lumbricoides was associated with a significantly increased risk of asthma and skin-specific IgE to aeroallergens. This suggested a complex relationship between ascariasis and susceptibility to childhood asthma that may involve an interaction with the immune response to inhaled aeroallergens (30).
Similarly, among African children with bronchial asthma who were evaluated for Ascaris-skin-specific IgE, 27% of 270 children were shown to have detectable specific IgE to the Ascaris antigen, compared to 8% of controls (32). In a study of about 2300 East German children, those who were Ascaris-IgE seropositive had 10-fold higher levels of total IgE and higher prevalence rates of allergen-specific IgE seropositivity, allergic rhinitis and asthma. The study concluded that contact with low doses of helminthic antigen is associated with an increase of total and specific IgE production and that helminthic infections in East German children are not the cause for a low prevalence of allergies in the former East Germany (33). In an early South African study utilising skin-specific IgE determination to evaluate the incidence of allergic asthma in Ascaris-infested patients, 17% of the non-allergic controls and 51% of the allergic asthmatics had a clinically detectable immunogenic response to the parasite. The predicted incidence of asthma was significantly higher than the observed incidence in the subjects in whom skin-specific IgE had been found. Inhalation of Ascaris antigen induced asthmatic reactions in 7 of 8 patients who were Ascaris-positive on skin testing, but not in the negative controls (19).
Ascaris may also result in chronic urticaria as a result of its close association with the parasite larva Anisakis simplex, which has been proposed as the cause of acute urticaria and anaphylaxis. In 101 patients with chronic urticaria, 35% were found to have skin-specific IgE to A. simplex, and serum-specific IgE to A. simplex was positive in 55%. A total of 22% of all the patients had detectable serum-specific IgE to A. lumbricoides, and of these 91% had serum-specific IgE to A. simplex. The authors concluded that sensitisation to A. simplex is higher among patients with chronic urticaria and that sensitisation to other parasites occurs because of cross-reactivity, but that a causal relationship between the presence of specific IgE to A. simplex and chronic urticaria had not been fully established (34).
Although serological responsiveness (e.g., serum-specific IgE) to Ascaris may indicate serum antibody responses to the parasite, serology has a relatively poor specificity and specificity as a marker of infection (35).
IgG4 has been proposed to act as a 'blocking antibody' due to its ability to compete for the same epitopes as IgE thus preventing IgE-dependent allergic responses. IgG4 and IgE are both elevated in helminth infections. In a study aimed at determining the relationship between anti-parasite IgG4 and IgE antibodies and Ascaris lumbricoides infection status, anti-parasite responses, including antibody levels to recombinant Ascaris allergen-1A (rABA-1A), a target of serum IgE antibodies in endemic populations were examined. Individuals who had detectable levels of IgE but not IgG4 antibodiesto rABA-1A (11%) had lower average levels of infection compared with individuals who produced anti-rABA-1A IgG4 (40%) and sero-negative individuals (49%). The ratio of IgG4/IgE in rABA-1A responders positively correlated with intensity of infection. IgG4 levels positively correlated with infection level in younger children (age 4-11) where average levels of infection were increasing, whereas allergen specific IgE emerged as a correlate of immunity in older children and adults (age 12-36) where infection levels were decreasing. The study demonstrated that in a gastrointestinal helminth infection, differential regulation of anti-allergen antibody isotypes relate to infection level, and concluded that the results were consistent with the concept that IgG4 antibody can block IgE-mediated immunity and therefore allergic processes in humans (36).

Compiled by Dr Harris Steinman,


  1. McSharry C, Xia Y, Holland CV, Kennedy MW. Natural immunity to Ascaris lumbricoides associated with immunoglobulin E antibody to ABA-1 allergen and inflammation indicators in children. Infect Immun 1999;67(2):484-9.
  2. O'Donnell IJ, Mitchell GF. An investigation of the allergens of Ascaris lumbricoides using a radioallergosorbent test (RAST) and sera of naturally infected humans: comparison with an allergen for mice identified by a passive cutaneous anaphylaxis test. Aust J Biol Sci 1978;31(5):459-87.
  3. Hussain R, Bradbury SM, Strejan G. Hypersensitivity to Ascaris antigens. 8. Characterization of a highly purified allergen. J Immunol 1973;111(1):260-8.
  4. McGibbon AM, Christie JF, Kennedy MW, Lee TD. Identification of the major Ascaris allergen and its purification to homogeneity by high-performance liquid chromatography. Mol Biochem Parasitol 1990;39(2):163-71.
  5. Arruda LK, Santos AB. Immunologic responses to common antigens in helminthic infections and allergic disease. Curr Opin Allergy Clin Immunol 2005;5(5):5-402
  6. Arruda LK. Tropomyosin in parasites - A crossreactive IgE-binding protein? ACI International 2005;17(6):243-245.
  7. Christie JF, Dunbar B, Davidson I, Kennedy MW. N-terminal amino acid sequence identity between a major allergen of Ascaris lumbricoides and Ascaris suum, and MHC-restricted IgE responses to it. Immunology 1990;69(4):596-602.
  8. Xia Y, Spence HJ, Moore J, Heaney N, McDermott L, Cooper A, Watson DG, Mei B, Komuniecki R, Kennedy MW. The ABA-1 allergen of Ascaris lumbricoides: sequence polymorphism, stage and tissue-specific expression, lipid binding function, and protein biophysical properties. Parasitology 2000;120 (Pt 2):211-24.
  9. Timanova AM, Marti T, Walter RD, Bankov IY. Isolation and partial characterization of a fatty-acid-binding protein from Ascaris suum reproductive tissue. Parasitol Res 1997;83(5):518-21.
  10. Kennedy MW, Brass A, McCruden AB, Price NC, Kelly SM, Cooper A. The ABA-1 allergen of the parasitic nematode Ascaris suum: fatty acid and retinoid binding function and structural characterization. Biochemistry 1995;34(20):6700-10.
  11. Itami DM, Oshiro TM, Araujo CA, Perini A, Martins MA, Macedo MS, Macedo-Soares MF. Modulation of murine experimental asthma by Ascaris suum components. Clin Exp Allergy 2005;35(7):873-9.
  12. Daschner A, Alonso-Gomez A, Lopez Serrano C. What does Anisakis simplex parasitism in gastro-allergic anisakiasis teach us about interpreting specific and total IgE values? Allergol Immunopathol (Madr). 2000;28(2):67-70
  13. Moreno-Ancillo A, Caballero MT, Cabanas R, Contreras J, Martin-Barroso JA, Barranco P, Lopez-Serrano MC. Allergic reactions to anisakis simplex parasitizing seafood. Ann Allergy Asthma Immunol. 1997;79(3):246-50
  14. Pascual CY, Crespo JF, San Martin S, Ornia N, Ortega N, et al. Cross-reactivity between IgE-binding proteins from Anisakis, German cockroach, and chironomids. Allergy 1997;52(5):514-20.
  15. Kennedy MW. Immune response to Anisakis simplex and other ascarid nematodes. Allergy 2000;55(Suppl. 59):7-13.
  16. Weiss ST. Parasites and asthma/allergy: what is the relationship? J Allergy Clin Immunol 2000;105:205-210.
  17. Ortona E, Margutti P, Vaccari S, Rigano R, Profumo E, Buttari B, Chersi A, Teggi A, Siracusano A. Elongation factor 1 beta/delta of Echinococcus granulosus and allergic manifestations in human cystic echinococcosis. Clin Exp Immunol. 2001;125(1):110-6
  18. Li CY, Li F, Qiu HL. Clinical analysis of 41 cases with eosinophil asthma associated Ascaris infection. [Chinese] Zhongguo Ji Sheng Chong Xue Yu Ji Sheng Chong Bing Za Zhi. 2000;18(4):223.
  19. Joubert JR, de Klerk HC, Malan C. Ascaris lumbricoides and allergic asthma: A new perspective. S Afr Med J. 1979;56(15):599-602.
  20. Muto R, Imai S, Tezuka H, Furuhashi Y, Fujita K. The biological activity of ABA-1-like protein from Ascaris lumbricoides. J Med Dent Sci 2001;48(3):95-104.
  21. King EM, Kim HT, Dang NT, Michael E, Drake L, Needham C, Haque R, Bundy DA, Webster JP. Immuno-epidemiology of Ascaris lumbricoides infection in a high transmission community: antibody responses and their impact on current and future infection intensity. Parasite Immunol. 2005;27(3):89-96.
  22. Obihara CC, Beyers N, Gie RP, Hoekstra MO, Fincham JE, Marais BJ, Lombard CJ, Dini LA, Kimpen JL. Respiratory atopic disease, Ascaris-immunoglobulin E and tuberculin testing in urban South African children. Clin Exp Allergy 2006;36(5):640-8.
  23. Lynch NR, Palenque M, Hagel I, DiPrisco MC. Clinical improvement of asthma after anthelminthic treatment in a tropical situation. Am J Respir Crit Care Med. 1997;156(1):50-4.
  24. van den Biggelaar AH, Rodrigues LC, van Ree R, van der Zee JS, Hoeksma-Kruize YC, Souverijn JH, Missinou MA, Borrmann S, Kremsner PG, Yazdanbakhsh M. Long-term treatment of intestinal helminths increases mite skin-test reactivity in Gabonese schoolchildren. J Infect Dis. 2004;189(5):892-900.
  25. Hagel I, Lynch NR, Perez M, Di Prisco MC, Lopez R, Rojas E. Modulation of the allergic reactivity of slum children by helminthic infection. Parasite Immunol. 1993;15(6):311-5.
  26. Lima C, Perini A, Garcia ML, Martins MA, Teixeira MM, Macedo MS. Eosinophilic inflammation and airway hyper-responsiveness are profoundly inhibited by a helminth (Ascaris suum) extract in a murine model of asthma. Clin Exp Allergy. 2002;32(11):1659-66.
  27. Cooper PJ, Chico ME, Bland M, Griffin GE, Nutman TB. Allergic symptoms, atopy, and geohelminth infections in a rural area of Ecuador. Am J Respir Crit Care Med. 2003;168(3):313-7.
  28. Dagoye D, Bekele Z, Woldemichael K, Nida H, Yimam M, Hall A, Venn AJ, Britton JR, Hubbard R, Lewis SA. Wheezing, allergy, and parasite infection in children in urban and rural Ethiopia. Am J Respir Crit Care Med. 2003 15;167(10):1369-73.
  29. Ogilvie BM, de Savigny D. Immune response to nematodes, in Immunology of parasitic infections. Eds. Cohen S, Warren KS. Blackwell Scientific Publications, Oxford, England 1982:715-757.
  30. Palmer LJ, Celedon JC, Weiss ST, Wang B, Fang Z, Xu X. Ascaris lumbricoides infection is associated with increased risk of childhood asthma and atopy in rural China. Am J Respir Crit Care Med. 2002;165(11):1489-93.
  31. Sales VS, Rodrigues CE, Trombone APF, Lima RC, Santos ABR, Oliver C, Ferriani VPL, Chapman MD, Arruda LK. Infection with Ascaris lumbricoides in preschool children: Role in wheezing and IgE responses to inhalant allergens. [Abstract] J Allergy Clin Immunol 2002;109:S27.
  32. Aderele WI, Oduwole O. Ascaris and bronchial asthma in children. Afr J Med Med Sci 1982;11(4):161-6.
  33. Dold S, Heinrich J, Wichmann HE, Wjst M. Ascaris-specific IgE and allergic sensitization in a cohort of school children in the former East Germany. J Allergy Clin Immunol. 1998;102(3):414-20.
  34. Lopez-Saez MP, Zubeldia JM, Caloto M, Olalde S, Pelta R, Rubio M, Baeza ML. Is Anisakis simplex responsible for chronic urticaria? Allergy Asthma Proc 2003;24(5):339-45.
  35. Yazdanbakhsh M, Wahyuni S. The role of helminth infections in protection from atopic disorders. Curr Opin Allergy Clin Immunol 2005;5(5):5-391.
  36. Turner JD, Faulkner H, Kamgno J, Kennedy MW, Behnke J, Boussinesq M, Bradley JE. Allergen-specific IgE and IgG4 are markers of resistance and susceptibility in a human intestinal nematode infection. Microbes Infect 2005;7(7-8):990-6.


As in all diagnostic testing, the diagnosis is made by the physican based on both test results and the patient history.