Hookworms represent a widespread and clinically important human nematode infection.

Prevalence figures indicate that the roundworms Ancylostoma duodenale and Necator americanus. Hookworm infection is acquired through skin exposure to larvae in soil contaminated by human feces. Adults, especially agricultural workers, Soil becomes infectious about 9 days after contamination and remains so for about 2 weeks. Cutaneous larva migrans (CLM) is the most common tropically. Cutaneous larva migrans manifests as an erythematous, serpiginous, pruritic, cutaneous eruption caused by accidental percutaneous penetration and subsequent migration of larvae of various nematode parasites. Cutaneous larva migrans (CLM) is a serpiginous eruption usually confined to the skin of the feet, buttocks, or abdomen caused by dog and cat hookworms, which are types of nematodes (roundworms).[1] Skin findings are due to a hypersensitivity reaction to the worms and their byproducts. Pathophysiology Larvae from animal nematodes that infect humans usually cause CLM. The normal hosts for these hookworms are cats and dogs, in which the roundworm eggs pass through the feces. Humans are infected with the larvae by walking barefoot on the sand. In cutaneous larva migrans (CLM), the life cycle of the parasites begins when eggs are passed from animal feces into warm, moist, sandy soil, where the larvae hatch. They initially feed on soil bacteria and molt twice before the infective third stage. By using their proteases, larvae penetrate through follicles, fissures, or intact skin of the new host. After penetrating the stratum corneum, the larvae shed their natural cuticle. Usually, they begin migration within a few days. the larvae can burrow into your skin. They cause an intense inflammatory response that leads to a rash and severe itching. In their natural animal hosts, the larvae of cutaneous larva migrans are able to penetrate into the dermis and are transported via the lymphatic and venous systems to the lungs. They break through into the alveoli and migrate to the trachea, where they are swallowed. In the intestine they mature sexually, and the cycle begins again as their eggs are excreted. Humans are accidental hosts, and the larvae are believed to lack the collagenase enzymes required to penetrate the basement membrane to invade the dermis. Therefore, cutaneous larva migrans remains limited to the skin when humans are infected. The production of interleukin (IL)5 during primary hookworm infection appears to enhance eosinophil function in limiting second-episode infection by invading larvae. Worms, however, also seem to provoke IL-10, IL-4, IL-5, and IL-13, which shift the cytokine response toward T helper 2 cells rather than toward T helper 1 cells. Hookworms also appear to secrete an inhibitor or natural killer cells, thereby suppressing production of gammainterferon and the T helper 2 response that would be expected to clear the parasite. In the search for possible vaccine targets, investigators have ascertained the existence of hookworm molecular inhibitors of coagulation factors Xa and VIIa-tissue factor and metalloproteases that degrade hemoglobin and intestinal mucosal cells. ASP-2, a protein isolated from larval N americanus, appears necessary for chemokine receptor binding and invasion and has shown some promise in animal vaccine trials.

Intestinal blood loss secondary to infection is the major clinical manifestation of hookworm infection.[7] In fact, hookworm disease historically refers to the clinically significant hypochromic, microcytic anemia and the depletion of iron stores resulting from chronic intestinal blood loss secondary to hookworm infection. Attaching to the mucosal layer and using their mouth parts, hookworms rupture the arterioles and venules along the luminal surface of the intestine. The worms ingested and digested some of the blood from the injured mucosa by means of a multienzyme cascade of metallohemoglobinases. Inhibited host coagulation due to a series of anticoagulants directed against factor Xa and the factor VIIa tissue factor complex, as well as again platelet aggregation, further exacerbate blood loss. As part of recent public health efforts to reduce rates of hookworm infection, the evoked immune response has been extensively investigated in both human and animal models.[8, 9, 10] Although hookworm infection stimulates a helper T-cell type-2 response, the role of this response in maintaining or deterring ongoing infection is debated. levels of immunoglobulin G (IgG) increase in the 2-8 weeks after the primary infection. In addition, in naturally infected populations, levels of all 5 subtypes of immunoglobulins appear elevated, with substantial upregulation of polyclonal immunoglobulin E (IgE). Eosinophilia is commonly observed, peaking at 35-65 days after infection. Hookworm infection also appears to cause upregulation of the cytokine interleukin (IL)-10 and is a proposed mechanism of proinflammatory cytokine suppression.[11] The hookworm digests the tissue within its buccal capsule, using its teeth or cutting plates, powerful esophageal muscles, and hydrolytic enzymes. At the same time, the worm releases a potent anticoagulant, which causes profound bleeding from eroded capillaries in the lamina propria. Masuknya larva ke dalam kulit, tambah Qimi, biasanya disertai dengan rasa gatal dan panas pada tempat masuknya. Kemudian akan muncul tonjolan pada permukaan kulit, beberapa saat akan muncul bentuk yang khas yaitu tonjolan di atas permukaan kulit yang berkelok-kelok berwarna kemerahan. Untuk selanjutnya, tonjolan kemerahan ini akan makin berkelok-kelok membentuk terowongan sesuai dengan pergerakan larva. Rasanya sangat gatal terutama pada malam hari. penyakit kulit yang disebabkan oleh larva cacing ini biasanya sembuh spontan. Karena pada dasarnya manusia bukan tempat hidupnya larva ini. Penyembuhan spontan ini tergantung pada jenis larva yang dikandung. Biasanya luka akan sembuh dalam beberapa minggu atau beberapa bulan. There is intense itching, particularly at night when the larvae become most active. As the larvae most often enter the skin of the feet, legs, buttocks and the back it is there where the itch is most intense. As the patient scratches the skin open, bacterial superinfection can occur.