Ancylostomiasis pathophysiology: Difference between revisions
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The [[external]] [[surface]] of [[Helminth]] comprises key [[molecules]] [[excretory/secretory]] (ES) products. [[Hookworm]] ES products contain a large range of [[structurally]] and [[functionally]] distinct [[molecules]], mostly [[proteins]], and also [[lipids]], and [[carbohydrates]]. They are [[secreted]] from the [[oral orifice]] or [[outer surfaces]] of the [[parasite]] representing the boundary between the [[helminth]] [[parasites]] and their [[hosts]]. These [[molecules]] react with host [[proteins]] and are essential for the [[penetration]] of the [[host]], [[tissue migration]], [[nourishment]], [[reproduction]], and [[evasion]] of [[host immunity]]. These [[molecules]] also have major functions in the development and survival of [[parasites]]. By inhibiting the [[inflammatory]] [[reaction]], [[encouraging]] [[effector cells]] [[apoptosis]], and [[skewing]] the [[immune reaction]] [[phenotype]], these [[molecules]] help the [[parasite]] to [[survive]] and evade the [[host]] [[immunological]] [[response]].<ref name="pmid32171305">{{cite journal| author=Abuzeid AMI, Zhou X, Huang Y, Li G| title=Twenty-five-year research progress in hookworm excretory/secretory products. | journal=Parasit Vectors | year= 2020 | volume= 13 | issue= 1 | pages= 136 | pmid=32171305 | doi=10.1186/s13071-020-04010-8 | pmc=7071665 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32171305 }} </ref> | The [[external]] [[surface]] of [[Helminth]] comprises key [[molecules]] [[excretory/secretory]] (ES) products. [[Hookworm]] ES products contain a large range of [[structurally]] and [[functionally]] distinct [[molecules]], mostly [[proteins]], and also [[lipids]], and [[carbohydrates]]. They are [[secreted]] from the [[oral orifice]] or [[outer surfaces]] of the [[parasite]] representing the boundary between the [[helminth]] [[parasites]] and their [[hosts]]. These [[molecules]] react with host [[proteins]] and are essential for the [[penetration]] of the [[host]], [[tissue migration]], [[nourishment]], [[reproduction]], and [[evasion]] of [[host immunity]]. These [[molecules]] also have major functions in the development and survival of [[parasites]]. By inhibiting the [[inflammatory]] [[reaction]], [[encouraging]] [[effector cells]] [[apoptosis]], and [[skewing]] the [[immune reaction]] [[phenotype]], these [[molecules]] help the [[parasite]] to [[survive]] and evade the [[host]] [[immunological]] [[response]].<ref name="pmid32171305">{{cite journal| author=Abuzeid AMI, Zhou X, Huang Y, Li G| title=Twenty-five-year research progress in hookworm excretory/secretory products. | journal=Parasit Vectors | year= 2020 | volume= 13 | issue= 1 | pages= 136 | pmid=32171305 | doi=10.1186/s13071-020-04010-8 | pmc=7071665 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32171305 }} </ref> | ||
===Hookworm life cycle=== | ===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 feces 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.<ref name="pmid8939719">{{cite journal| author=Hawdon JM, Hotez PJ| title=Hookworm: developmental biology of the infectious process. | journal=Curr Opin Genet Dev | year= 1996 | volume= 6 | issue= 5 | pages= 618-23 | pmid=8939719 | doi=10.1016/s0959-437x(96)80092-x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8939719 }} </ref> 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. Then they ascend from the bronchial tree to the pharynx, during which the host may develop a cough, sore throat, fever. They coughed up, swallowed, and reach the small intestine where they mount into fourth-stage larvae and mature into blood-feeding adults male or female.<ref name="pmid28882382">{{cite journal| author=Jourdan PM, Lamberton PHL, Fenwick A, Addiss DG| title=Soil-transmitted helminth infections. | journal=Lancet | year= 2018 | volume= 391 | issue= 10117 | pages= 252-265 | pmid=28882382 | doi=10.1016/S0140-6736(17)31930-X | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28882382 }} </ref> The adult worms attached to the mucosal layer of the small intestine, using their buccal capsule leads to arterioles and venules ruptures along with the luminal surface of the intestine. These adult worms release hyaluronidase and other hydrolytic enzymes result in blood extravasation by degrading the intestinal mucosa and erosion of blood vessels.<ref name="pmid27929101">{{cite journal| author=Loukas A, Hotez PJ, Diemert D, Yazdanbakhsh M, McCarthy JS, Correa-Oliveira R | display-authors=etal| title=Hookworm infection. | journal=Nat Rev Dis Primers | year= 2016 | volume= 2 | issue= | pages= 16088 | pmid=27929101 | doi=10.1038/nrdp.2016.88 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27929101 }} </ref> Hookworms also secrete Ancylostoma ceylanicum anticoagulant peptide-1, which inhibits the blood coagulation in the attachment site and leads to blood loss from the intestine.<ref name="pmid18171264">{{cite journal| author=Diemert DJ, Bethony JM, Hotez PJ| title=Hookworm vaccines. | journal=Clin Infect Dis | year= 2008 | volume= 46 | issue= 2 | pages= 282-8 | pmid=18171264 | doi=10.1086/524070 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18171264 }} </ref> The adult worms colonize the intestinal tract and in 3-5 weeks the adults becomes sexually mature and female worms begin to lay eggs in the intestine that pass in the stool.<ref name="pmid28882382">{{cite journal| author=Jourdan PM, Lamberton PHL, Fenwick A, Addiss DG| title=Soil-transmitted helminth infections. | journal=Lancet | year= 2018 | volume= 391 | issue= 10117 | pages= 252-265 | pmid=28882382 | doi=10.1016/S0140-6736(17)31930-X | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28882382 }} </ref> | 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 feces 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]].<ref name="pmid8939719">{{cite journal| author=Hawdon JM, Hotez PJ| title=Hookworm: developmental biology of the infectious process. | journal=Curr Opin Genet Dev | year= 1996 | volume= 6 | issue= 5 | pages= 618-23 | pmid=8939719 | doi=10.1016/s0959-437x(96)80092-x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8939719 }} </ref> 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]]. Then they [[ascend]] from the [[bronchial tree]] to the [[pharynx]], during which the [[host]] may develop a [[cough]], [[sore throat]], [[fever]]. They [[coughed up]], [[swallowed]], and reach the [[small intestine]] where they [[mount]] into [[fourth-stage]] [[larvae]] and [[mature]] into [[blood-feeding]] [[adults]] [[male]] or [[female]].<ref name="pmid28882382">{{cite journal| author=Jourdan PM, Lamberton PHL, Fenwick A, Addiss DG| title=Soil-transmitted helminth infections. | journal=Lancet | year= 2018 | volume= 391 | issue= 10117 | pages= 252-265 | pmid=28882382 | doi=10.1016/S0140-6736(17)31930-X | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28882382 }} </ref> The [[adult]] [[worms]] attached to the [[mucosal]] layer of the [[small intestine]], using their [[buccal]] [[capsule]] leads to [[arterioles]] and [[venules]] [[ruptures]] along with the [[luminal]] [[surface]] of the [[intestine]]. These [[adult worms]] release [[hyaluronidase]] and other [[hydrolytic enzymes]] result in [[blood]] [[extravasation]] by degrading the [[intestinal mucosa]] and [[erosion]] of [[blood vessels]].<ref name="pmid27929101">{{cite journal| author=Loukas A, Hotez PJ, Diemert D, Yazdanbakhsh M, McCarthy JS, Correa-Oliveira R | display-authors=etal| title=Hookworm infection. | journal=Nat Rev Dis Primers | year= 2016 | volume= 2 | issue= | pages= 16088 | pmid=27929101 | doi=10.1038/nrdp.2016.88 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27929101 }} </ref> [[Hookworms]] also [[secrete]] [[Ancylostoma ceylanicum]] [[anticoagulant]] [[peptide-1]], which inhibits the [[blood]] [[coagulation]] in the [[attachment site]] and leads to [[blood loss]] from the [[intestine]].<ref name="pmid18171264">{{cite journal| author=Diemert DJ, Bethony JM, Hotez PJ| title=Hookworm vaccines. | journal=Clin Infect Dis | year= 2008 | volume= 46 | issue= 2 | pages= 282-8 | pmid=18171264 | doi=10.1086/524070 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18171264 }} </ref> The [[adult worms]] [[colonize]] the [[intestinal tract]] and in 3-5 weeks the [[adults]] becomes [[sexually]] [[mature]] and [[female worms]] begin to [[lay eggs]] in the [[intestine]] that pass in the [[stool]].<ref name="pmid28882382">{{cite journal| author=Jourdan PM, Lamberton PHL, Fenwick A, Addiss DG| title=Soil-transmitted helminth infections. | journal=Lancet | year= 2018 | volume= 391 | issue= 10117 | pages= 252-265 | pmid=28882382 | doi=10.1016/S0140-6736(17)31930-X | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28882382 }} </ref> | ||
==References== | ==References== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
Pathophysiology
The external surface of Helminth comprises key molecules excretory/secretory (ES) products. Hookworm ES products contain a large range of structurally and functionally distinct molecules, mostly proteins, and also lipids, and carbohydrates. They are secreted from the oral orifice or outer surfaces of the parasite representing the boundary between the helminth parasites and their hosts. These molecules react with host proteins and are essential for the penetration of the host, tissue migration, nourishment, reproduction, and evasion of host immunity. These molecules also have major functions in the development and survival of parasites. By inhibiting the inflammatory reaction, encouraging effector cells apoptosis, and skewing the immune reaction phenotype, these molecules help the parasite to survive and evade the host immunological response.[1]
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 feces 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.[2] 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. Then they ascend from the bronchial tree to the pharynx, during which the host may develop a cough, sore throat, fever. They coughed up, swallowed, and reach the small intestine where they mount into fourth-stage larvae and mature into blood-feeding adults male or female.[3] The adult worms attached to the mucosal layer of the small intestine, using their buccal capsule leads to arterioles and venules ruptures along with the luminal surface of the intestine. These adult worms release hyaluronidase and other hydrolytic enzymes result in blood extravasation by degrading the intestinal mucosa and erosion of blood vessels.[4] Hookworms also secrete Ancylostoma ceylanicum anticoagulant peptide-1, which inhibits the blood coagulation in the attachment site and leads to blood loss from the intestine.[5] The adult worms colonize the intestinal tract and in 3-5 weeks the adults becomes sexually mature and female worms begin to lay eggs in the intestine that pass in the stool.[3]
References
- ↑ Abuzeid AMI, Zhou X, Huang Y, Li G (2020). "Twenty-five-year research progress in hookworm excretory/secretory products". Parasit Vectors. 13 (1): 136. doi:10.1186/s13071-020-04010-8. PMC 7071665 Check
|pmc=value (help). PMID 32171305 Check|pmid=value (help). - ↑ 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.
- ↑ 3.0 3.1 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.
- ↑ Loukas A, Hotez PJ, Diemert D, Yazdanbakhsh M, McCarthy JS, Correa-Oliveira R; et al. (2016). "Hookworm infection". Nat Rev Dis Primers. 2: 16088. doi:10.1038/nrdp.2016.88. PMID 27929101.
- ↑ Diemert DJ, Bethony JM, Hotez PJ (2008). "Hookworm vaccines". Clin Infect Dis. 46 (2): 282–8. doi:10.1086/524070. PMID 18171264.