Ancylostomiasis pathophysiology
|
Ancylostomiasis Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Ancylostomiasis pathophysiology On the Web |
|
American Roentgen Ray Society Images of Ancylostomiasis pathophysiology |
|
Risk calculators and risk factors for Ancylostomiasis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
Pathophysiology
Hookworm life cycle
All species of hookworm have no intermediate host, they have a direct life cycle. Mature females released eggs in the host’s small intestine and these eggs are passed in the feces, where they hatch first stage rhabditiform larva (L1) within several days. The L1 feeds on soil microbes and molts to the L2 stage, and under appropriate conditions, each eggs hatch in warm, moist, sandy soil, or in faeces and develops into an infective filariform (L3) stage larva. The infective-stage larvae (L3) enter the body either through a cutaneous route or by direct oral ingestion. Some species of human hookworm such as Ancylostoma and Necator Americanus enter the body by skin penetration which may cause a local pruritic dermatitis, also called ground itch at the site of penetration whereas the ancylostoma species can also enter the body orally.[1] The infective larvae (L3) migrate through the dermis, enters the bloodstream, and reach the lungs within 10 days. Once they reach the lungs, they migrate across the alveoli and breaks into alveoli leads to mild and usually asymptomatic alveolitis with eosinophilia.[2]
References
- ↑ Hawdon JM, Hotez PJ (1996). "Hookworm: developmental biology of the infectious process". Curr Opin Genet Dev. 6 (5): 618–23. doi:10.1016/s0959-437x(96)80092-x. PMID 8939719.
- ↑ Jourdan PM, Lamberton PHL, Fenwick A, Addiss DG (2018). "Soil-transmitted helminth infections". Lancet. 391 (10117): 252–265. doi:10.1016/S0140-6736(17)31930-X. PMID 28882382.