Table 19c.1 Summary of non-human migrating helminths


Natural host

Principal syndrome

Diagnostic method


Ancylostoma caninum


Cutaneous larva migrans Eosinophilic enteritis

Clinical features

Antibody capture EIA Tissue biopsy

10% thiabendazole paste with occlusive dressing 200 mg mebendazole

Ancylostoma braziliense


Cutaneous larva migrans

Clinical features

10% thiabendazole paste with occlusive dressing

Gnathostoma spinigerum

Dog, cat, mink, racoon, others

Migrating space-occupying inflammatory lesions Visceral disease: pulmonary, myelitis-encephalitis, ocular

Clinical features, biopsy, antibody capture EIA

Surgical removal if accessible

Angiostrongylus cantonensis


Eosinophilic meningitis

CSF eosinophilic antibody capture EIA

Naturally self-limiting

Angiostrongylus costaricensis


Acute abdominal mass

Antibody capture EIA

See text

Sparganum mansoni

Dogs, cats, other carnivores

Subcutaneous mass

Clinical features, CT scan, excision biopsy Antibody capture EIA

Excision, praziquantel

Dirofilaria immitis


Granulomatous lung lesions

Chest X-ray, eosinophilia and antibody capture EIA

Conservative, alternatively DEC

Baylisascaris procyonis


Visceral larva migrans

History of exposure, clinical features and eosinophilia

Insufficient experience Benzimidazoles may be beneficial

Alaria spp.

Small game, frogs

Ocular lesions, respiratory symptoms, rare fatal infections

History of exposure, eosinophilia, biopsy

Insufficient experience Praziquantel may be beneficial

DEC, diethylcarbamazine; EIA, enzyme immunoassay.

DEC, diethylcarbamazine; EIA, enzyme immunoassay.

Fig. 19c.1 Mouth parts of Ancylostoma caninum

Fig. 19c.2 Characteristic hookworm egg longer at 10mm x 0.3 mm. The buccal capsule possesses a pair of small inconspicuous median teeth and a pair of larger outer teeth (Beaver et al., 1984) (Figure 19c.3). The eggs are not readily distinguishable from those of A. duodenale.


Hookworm eggs are passed in dog faeces and L1 larvae hatch within 24-48 hours at optimal

Fig. 19c.3 Mouth parts of Ancylostoma braziliense temperatures and humidity, rapidly developing through the L2 to the filariform stage (L3) from day 5. Survival in the L3 form is for probably less than 1 week in the environment. The larvae stand up on their tails and undulate in response to vibrations, warmth and carbon dioxide and adhere to the host on contact (Granzer and Haas, 1991). Invasion occurs via hair follicles, which provides the necessary traction for penetration in dogs. Additionally, L3 larvae, when swallowed, can cause infection in dogs. L3 larvae undergo somatic migration, puncturing the alveolae to reach the gut via the tracheal or oesophageal migration route. For A. caninum a similar path may be followed in humans. In the intestine L4 larvae attach to the mucosa by the buccal capsule and moult again to become an adult within a week. In their definitive hosts, hookworms survive for approximately 6 months and adult females can produce up to 28 000 eggs/ day at their peak, usually within the first to second month (Anderson, 1991). In humans both adult females and males have been found, although they have never been fertile and probably do not survive long.

L3 larvae may undergo larval arrest in the canine host and there is some evidence that this may also occur in humans. Larval arrest allows the larvae to reactivate at a later date and complete their development to adults. There have been many theories about the environmental cues which control this process by changes in humidity, host factors or a parasite 'clock' (Schad and Page, 1982; Gibbs 1986). Larval arrest may explain the seasonality of eosinophilic enteritis and relapse of infections after cure.

PATHOGENESIS Cutaneous Larva Migrans

Cutaneous larva migrans does not occur after the first exposure to A. caninum and A. braziliense L3 but follows re-infection only after several weeks, and this suggests that the disease is due to hypersensitivity to larval secretions (Provic and Croese, 1996b). The larva produces a number of enzymes which may assist in dermal invasion. These include a metaloprotease of 68 kDa and a minor protease of 38 kDa (Hotez et al., 1990). Both organisms produce a hyaluronidase of 87 kDa (Hotez, Hawdon and Capello, 1995).

Eosinophilic Enteritis

Adult hookworms secrete a wide range of molecules that are essential for the attachment to the intestine and all of these may result in allergy. The organisms produce potent anticoagulant activity, expressing a 37 kDa elastinolytic metaloprotease that demonstrates fibrinolytic anticoagulant properties (Capello et al., 1995). A. caninum also expresses a peptide inhibitor of the clotting factor 1Xa (Capello et al., 1995). A. caninum expresses two proteases, a 41 kDa cysteine protease (Dowd et al., 1994) and another 68 kDa protease with uncertain function. Hyaluronidases have been associated with tissue invasion for a number of hookworms and A. caninum produces one such (Hotez et al., 1994). It also expresses a 41 kDa glycoprotein which is a potent inhibitor of neutrophil function (Moyle et al., 1994).


Intense inflammation is found in the small bowel and occasionally in the colon, caecum and appendix area. It is inflamed and oedematous and heavily infiltrated with eosinophils (Croese et al., 1996). Worms can be seen surrounded by an eosinophilic infiltration. In some patients the disease may be much more mild, limited to asymptomatic aphthous ulceration of the gut. The immunological mechanisms in eosinophilic enteritis are unknown but probably reflect common mechanisms of helminth inflammation, described elsewhere (see p. 563).

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