NECATOR AMERICANUS & ANCHYLOSTOMA DUODENALE (Hookworms)

GEOGRAPHICAL DISTRIBUTION

The parasite is widely distributed in the tropics and sub-tropics. In cold climates with suitable microclimates (such as in coal mines) the parasite may be found. Two species infect humans. Necator americanus is the species found in South Asia, Africa, pacific and in North and South America whereas Ancylostoma duodenale is the main hookworm of Eastern Europe, North Africa, India, Northern China and Japan. Both species can be found together in South East Asia, the pacific and West Africa.

MORPHOLOGY

The worms measure 1-2cm in length. The head ends of the worm are sharply bent backwards like a hook. In the case of N. americanus the buccal cavity bears a pair of ventral cutting plates used in biting the mucosa for feeding. A. duodenale is larger with the head end bending backwards smoothly. The buccal cavity has two pairs of curved teeth. In both species, the tail end of the male is flattened and expanded to form the copulatory bursa.

LOCATION IN THE HOST

The hookworms inhabit the small intestine of humans. Unlike Ascariasis it is attached to the mucosa of the intestine of the intestine with the buccal capsule.

LIFE CYCLE

Each female N.americanus lays about 3000-6000 eggs per day (A. duodenale lays about 10,000-20,000 per day). The eggs are oval in shape and have thin, glass-like egg-shells. The embryo is usually divided when the eggs are passed in faeces. On reaching soil and under optimum conditions the eggs hatch into L₁ larva within 24 hours. The optimum conditions are; shade, warmth’ moisture and sandy type soil.

L₁ is an actively feeding rhabditiform larva (esophagus with a posterior bulb, like in the Rhabtid species).These larvae grow rapidly and moult on about the 3^rd day into L₂ rhabditiform larvae. On or about the 5^th day the second moult transform them into long, non-feeding L₃ infective or filariform larvae. These larvae have long, narrow esophagi and retain the cuticle of L₂ as a sheath. The infective larvae move on to the topsoil and on to low vegetation seeking hosts. Under favorable conditions they remain alive for 3-6 weeks. When they come into contact with human skin, the activated larvae shed the sheath and penetrate the skin (usually between toes).

The larvae are carried in the blood or lymphatics and finally reach the lungs. They penetrate the alveoli and start ascending along small bronchioles to bronchi and then to trachea (unlike Ascariasis there are no moults in the lungs). At the pharynx they are swallowed. On reaching the small intestine the final moult transform them in to young males and females. The time taken between larval penetration and the formation of mature worms is 4-7 to weeks. Infective A.duodenale larvae ingested with contaminated food can establish in the intestine without undergoing lung migration. Ancylostoma is a unique parasite as it can go into a phase of ‘arrested development’ when the external conditions are not favorable and restart the life cycle when the conditions are good.

PATHOGENESIS AND CLINICAL FEATURES

In the acute infection the initial sings and symptoms are due to the penetration and migration of larvae in the skin. At the site of entry, a transient dermatitis with intense pruritus can result. This condition is called ‘ground itch’. The lesions may get secondarily infected. The lung migratory phase of hookworms is short and the pulmonary symptoms are either assent or minimum.

The pathogenesis of hookworm disease is directly related to the attachment of the worms to the mucosa. They attach to the mucosa by biting in plugs of mucosa (including 7-9 villi), which are stripped off the lamina propria. The pool of blood thus created is sucked in using the muscular pharynx. Only part of the sucked blood is used for food and oxygen, a large part being excreted continuously. This leads to blood loss and results in hypochromic, microcytic (iron deficiency) anemia. Each N.americanus sucks about 0.03 ml of blood per day while A.duodenale sucks about 0.26 ml per day.

The degree of anemia is related to the worm load and the nutritional status of the host. Hypoproteinemia seen in severe hookworm disease may be related to poor food intake (poverty, anorexia), impaired absorption, increased loss and a combination of all. Impairment of nutrient absorption, intestinal protein loss and lowered food intake collectively result in stunting (growth retardation). The pathogenesis of impaired mental and physical development in hookworm disease is not clear.

DIAGNOSIS

This is done by demonstrating characteristic eggs in the faeces. The eggs can be cultured into infective larval stage to distinguish between Necator and Ancylostoma.

PREVENTION AND CONTROL

Avoidance of indiscriminate defaecation and use of footwear help in prevention. Provision of hygienic latrines, chemotherapy of infected people and health education are important in control of the infection.

TREATMENT

Hookworm infection can be eradicated with several safe and highly effective antihelmintic drugs, including albendazole (400 mg once), mebandazole (500 mg once), and pyrantel pamoate (11 mg/kg for 3 days). Mild iron-deficiency anemia can often be treated with oral iron alone. Severe hookworm disease with protein loss and malabsorption necessitates nutritional support and oral iron replacement along with deworming.