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Fig. 12.7A,B. Life cycle of the hookworm.

Humans are infected when larvae penetrate the skin, usually of the foot (Fig. 12.7), or rarely the buccal mucosa. Larvae enter the skin through the hair follicles; from the subcutaneous tissues they eventually enter venules or lymphatics. By either route they reach the pulmonary capillaries and break into alveoli, from where they migrate up the bronchioles and trachea and pass over the epiglottis and down the esophagus to mature in the small intestine, usually the jejunum. Here they molt again to become fourth-stage larvae possessing a buccal capsule by which they attach themselves to the intestinal mucosa. Within a week, a fourth and final molt results in development of the adult parasite. The reproductive systems develop rapidly; the worms copulate and the female begins laying eggs within 2 months after the larvae penetrate the skin. Although 75% of the worms that reach the intestine die within a year, the others remain viable for up to 6-years, and occasionally up to 15 years, in untreated individuals.

Another rarer method of infection is by direct ingestion of dirt (pica) or fresh vegetables containing filariform larvae. Infected mothers can likely pass developmentally arrested third-stage larvae to their suckling infants through colostrum and milk. There is also some evidence that infective larvae may take an alternative shortcut from the pulmonary artery to the pulmonary veins and via the systemic circulation to the jejunum, where they pierce the mucosa to reach the bowel lumen.

The pathological changes induced by hookworms have been poorly studied in tissues other than the intestines. In the lungs, there may be localized intra-alveolar and interstitial hemorrhage, mononuclear infiltrate, and vascular congestion produced by the migrating larvae, but these changes are very transient and usually seen only in heavy infections. The primary pathological manifestations of hookworm infection are seen in the duodenum with Necator and in the proximal jejunum with Ancylostoma, although the worms can be found anywhere from the stomach to the proximal colon. The parasites attach to the intestinal mucosa and graze from one site to another, with each worm damaging several villi per day. Their attachment and subsequent detachment can cause bleeding as well as leaking plasma, with a protein and electrolyte loss that can be significant in severe infections. Most infections, however, cause only minor mucosal changes in the intestine which disappear with therapy. Biopsy specimens of the jejunum may show eosinophilia of the mucosa and submucosa. Sprue-like changes have been described by several investigators, consisting of flattening and fusion of villi, fibrosis of the lamina propria, and chronic inflammatory cells, although these findings are disputed by others because of the difficulty in assessing villous architecture in biopsy specimens that lack proper orientation and because estimation of the intensity of inflammatory infiltrates is very subjective. Also, several controlled studies have shown no difference in morphological and absorption defects in hookworm patients in endemic countries when compared with the uninfected local populace.

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Copyright: Palmer and Reeder by Springer


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