The Superfamily Ancylostomatoidea

Hookworms occur in the small intestine of mammals. Like species of the Strongyloidea, they have large, highly cuticularized buccal capsules provided with teeth or cutting plates (Chabaud, 1974) which they use to attach themselves to the intestinal mucosa of the host. However, unlike species of strongyles, the buccal region is never hexagonal in transverse section and a corona radiata is absent. Also many hookworms, unlike strongyles, infect the host mainly through skin penetration. The Ancylostomatoidea has a single family, the Ancylostomatidae, divided into the Ancylostomatinae and the Bunostominae based on the position of the duct of the dorsal oesophageal gland and other characters described by Lichtenfels (1980c). Fourth-stage and adult hookworms suck blood, and infection by the three species that are well-known pathogens in humans results in anaemia caused by blood loss, particularly in malnourished individuals. For excellent reviews on hookworms in humans, refer to Chandler (1929), Komiya and Yasuraoha (1966), Miller (1979) and Schad and Warren (1990).

Female worms deposit oval, thin-shelled eggs into the gut lumen (Fig. 3.1A). Eggs are generally in the four- to six-cell stage when passed in faeces of the host. Under suitable conditions of moisture and temperature (e.g. 23—33°C) the egg embryonates in about 24 h to a first-stage larva about 250-300 mm in length with a pointed tapered tail, an elongate buccal cavity and an oesophagus usually with a valved bulb (Fig. 3.1B-F). This larva is generally referred to as rhabditiform, mainly because the oesophagus resembles that of the free-living rhabditids. Larvae feed on bacteria and within 2 days moult to the second stage (Fig. 3.1H), which is about 400-430 mm in length but otherwise similar to the first stage. Within 4-5 days after eggs are passed from the host, the second-stage larvae become lethargic and development proceeds to the third and infective stage (Fig. 3.1H). The oesophagus loses its valved bulb and the tail becomes relatively short and blunt. The larva retains the cuticle of the second stage with its attenuated tail. Such larvae are often referred to as strongyliform. Unlike the first two larval stages, the third stage does not feed and its survival depends on stored nutrients in its tissues. Strongyliform larvae are active, 500-700 mm in length, long-lived and often resistant to adverse environmental conditions. Some tend to be thermotactic, thigmotactic, phototactic and negatively geotactic. They readily contaminate the food and environment of the host (see for example Harada, 1954a).

Many hookworms (unlike strongyles) infect the host by penetrating the skin after shedding their sheaths, an important discovery made by Looss (1898) when he accidentally spilt water containing larvae on his hand. Enzymes released by the larvae aid their passage through the skin (Bruni and Passalacqua, 1954; Lewert and Lee, 1954). In

Stages Hookworm
Fig. 3.1. Stages in the development of Uncinaria stenocephala: stages in the development of the egg; (F) first-stage larva; (G) second-stage larva; (H) sheathed infective third-stage larva; (I) male fourth-stage larva. (After H.C. Gibbs, 1961 -courtesy Canadian Journal of Zoology.)
Uncinaria Lucasi

Fig. 3.2. Development of the provisional and adult buccal capsule in Uncinaria stenocephala: (A) parasitic third stage showing beginning of provisional buccal capsule; (B) later stage of A; (C) parasitic third stage with fully developed provisional buccal capsule; (D) early third stage moulting; (E) early fourth stage; (F) fourth stage with fully developed provisional buccal capsule; (G) late fourth stage, beginning of adult buccal capsule (ventral); (H) lateral view of G; (I) completion of development of adult buccal capsule; (J) adult buccal capsule (lateral). (After H.C. Gibbs, 1961 -courtesy Canadian Journal of Zoology.)

Fig. 3.2. Development of the provisional and adult buccal capsule in Uncinaria stenocephala: (A) parasitic third stage showing beginning of provisional buccal capsule; (B) later stage of A; (C) parasitic third stage with fully developed provisional buccal capsule; (D) early third stage moulting; (E) early fourth stage; (F) fourth stage with fully developed provisional buccal capsule; (G) late fourth stage, beginning of adult buccal capsule (ventral); (H) lateral view of G; (I) completion of development of adult buccal capsule; (J) adult buccal capsule (lateral). (After H.C. Gibbs, 1961 -courtesy Canadian Journal of Zoology.)

a few hours larvae enter subcutaneous tissues, invade lymphatic capillaries and are carried to regional lymph nodes, the larger lymph channels leading to the thoracic duct, and the general circulation, which carries them to the heart and lungs. In lungs, larvae enter alveoli and begin to develop to the fourth stage (Fig. 3.1I). Development continues as larvae migrate from the lungs to the trachea and intestine. Arriving as fourth-stage larvae in the intestine, they have acquired a spherical provisional or temporary buccal capsule which enables them to attach to the gut wall (Fig. 3.2A—F). During development of the fourth stage (Fig. 3.2G—J) the buccal capsule of the adult parasite forms posterior and lateral to the provisional buccal capsule, the cuticular lining of which is shed at the final moult. Worms reach the adult stage in 2—7 weeks, depending on the species.

Although skin penetration appears to be the main route for some hookworms to infect the host, third-stage larvae reaching the intestine by the oral route nevertheless will grow to adulthood, although they may undergo a brief sojourn in the mucosa before maturing in the lumen of the intestine (Leichtenstern, 1886; Fulleborn, 1926, 1927; Foster and Cross, 1934).

The phenomenon of arrest, widely known and studied in trichostrongyles of herbivores, is also reported in hookworms such as Ancylostoma caninum of canids, Uncinaria lucasi of fur seals and Ancylostoma duodenale of humans. In the resistant host, unsheathed infective third-stage larvae invade and persist in the tissues and can eventually be mobilized in the female host for transmammary and prenatal infection of the young. There is evidence that environmental factors such as temperature, acting on the free-living stages of hookworms, may also induce arrest among worms in the host (Schad et al, 1982; Gibbs, 1986; Prociv and Luke, 1995).

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