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Amphistomiasis

From Wikipedia, the free encyclopedia
Medical condition
Amphistomiasis
Other namesParamphistomiasis, amphistomosis, paramphistomosis
SpecialtyInfectious disease

Amphistomiasis is aparasiticdisease oflivestockanimals, more commonly ofcattle andsheep, andhumans caused byimmaturehelminthic flatworms belonging to the orderEchinostomida. The term amphistomiasis is used for broader connotation implying the disease inflicted by members of Echinostomida including thefamily Paramphistomidae/Gastrodiscidae (to be precise, the speciesGastrodiscoides hominis); whereas paramphistomiasis is restricted to that of the members of the familyParamphistomidae only.G. discoides andWatsonius watsoni are responsible for the disease in humans, while mostparamphistomes are responsible in livestock animals, and some wildmammals.[1][2][3][4][5] In livestock industry the disease causes heavy economic backlashes due to poor production ofmilk,meat andwool.[6][7]

Signs and symptoms

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Symptoms include:

Cause

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Amphistomiasis in farm and wild mammals is due to infection of paramphistomes, such as the species ofParamphistomum,Calicophoron,Cotylophoron,Pseudophisthodiscus, etc. These are essentially rumenflukes, of whichParamphistomum cervi is the most notorious in terms of prevalence andpathogenicity. Infection occurs throughingestion of contaminated vegetables and raw meat, in which the viable infectivemetacercaria are deposited fromsnails, which are theintermediate hosts.[13][14] Theimmature flukes are responsible for destroying themucosal walls of thealimentary tract on their way to growing into adults. It is by this fervent tissue obliteration that the clinical symptoms are manifested. The adult flukes, on the other hand, are quite harmless, as they merely prepare for reproduction.[15]

Thezoonotic infection in human is caused byG. discoides andW. watsoni which are essentially intestinal flukes. The disease due toG. discoides is more specifically termed gastrodiscoidiasis.[16] In their natural hosts such aspigs andmonkeys, their infection inasymptomatic, but human infection is prevalent, by which they cause serious health problems, characterised bydiarrhoea,fever, abdominal pain,colic, and an increasedmucous production. In extreme situations such as inAssam,India, a number of mortality among children is attributed to this disease.[17]

Pathogenesis

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Adult flukes are known to be quite harmless, as they do not attack on thehost tissue. It is the immature flukes which are most damaging as they get attached to the intestinal wall, literally and actively sloughing off of the tissue. Thisnecrosis is indicated byhaemorrhage infaeces, which in turn is a sign of severe enteritis. Under such condition the animals becomeanorexic and lethargic. It is often accompanied by pronounced diarrhoea,dehydration,oedema,polydipsia,anaemia, listlessness and weight loss. In sheep profuse diarrhoea usually develops two to four weeks after initial infection. If infection is not properly attended death can ensue within 20 days, and in a farm mortality can be very high. In fact there are intermittent reports of mortality as high as 80% among sheep and cattle.[3][4][18][19] Sometimes chronic form is also seen with severeemaciation, anaemia, rough coat, mucosal oedema, thickenedduodenum and oedema in the sub maxillary space.[5][20][21] The terminally sick animals lie prostrate on the ground, completely emaciated until they die. Inbuffalos, severe haemorrhage was found to be associated withliver cirrhosis and nodularhepatitis.[22]

Diagnosis

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Under most situations, infection is hard to recognize because the symptoms are mild or even absent. In humans and wild animals, infection is not easily identified. Especially the adult flukes, even if in large number, generally do not cause complications. There is not yet a standard diagnostic test. Therefore, manual diagnosis is done at many levels. Diagnosis basically relies on a combination ofpostmortem analyses, clinical signs displayed by the animals, and response todrenching. In heavy infection, symptoms are easily observed in sheep and cattle as they become severelyanorexic or inefficiently digest food, and become unthrifty. Copious fetid diarrhea is an obvious indication, as the soiling of hind legs and tails with fluid feces are readily noticeable.[3][16]

Even though it not always the case, immature flukes can be identified from the fluid excrement. On rare occasions, eggs can be identified from stools of suspected animals.[1] In developing countries diagnosis andprognosis is often hindered by multiple infections with other trematodes, such asFasciola hepatica andschistosomes, because these flukes are given primary importance due to their pervasive nature.[5]

Treatment

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Amphistomiasis is considered a neglectedtropical disease, with no prescription drug for treatment and control. Therefore, management of infestation is based mainly on control of the snail population, which transmit the infective larvae of the flukes. However, there are now drugs shown to be effective including resorantel,oxyclozanide, clorsulon,ivermectin,niclosamide, bithional andlevamisole.[13][23][24][25] An in vitro demonstration shows thatplumbagin exhibits high efficacy on adult flukes.[26][27]

Since the juvenile flukes are the causative individuals of the disease, effective treatment means control of the immature fluke population.Prophylaxis is therefore based on disruption of the environment (such as proper drainage) where the carrier snails inhabit, or more drastic action of usingmolluscicides to eradicate the entire population. For treatment of the infection, drugs effective against the immature flukes are recommended for drenching. For this reason oxyclozanide is advocated as the drug of choice. It effectivelykills the flukes within a few hours and it effective against the flukesresistant to other drugs. The commercially prescribed dosage is 5 mg/kg body weight or 18.7 mg/kg body weight in two divided dose within 72 hours.[2][28] Niclosamide is also extensively used in mass drenching of sheep. Successfully treated sheep regain appetite within a week, diarrhoea stops in about three days, and physiological indicators (such as plasma protein and albumin levels) return to normal in a month.[3]

References

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  1. ^abOlsen OW (1974).Animal Parasites: Their Life Cycles and Ecology (3 ed.). Dover Publications, Inc., New York/University Park Press, Baltimore, US. pp. 273–274.ISBN 978-0486651262.
  2. ^abHugh-Jones ME, Hubbert WT, Hagstad HV (2008).Zoonoses: Recognition, Control, and Prevention (1 ed.). Iowa State University Press/John Wiley & Sons, Inc. pp. 243–244.ISBN 978-0470390313.
  3. ^abcdKumar V (1998).Trematode Infections and Diseases of Man and Animals (1 ed.). Springer, Netherlands. pp. 275–321.ISBN 978-0792355090.
  4. ^abWhitten LK (1955). "Paramphistomiasis in sheep".New Zealand Veterinary Journal.3 (4): 144.doi:10.1080/00480169.1955.33203.
  5. ^abcPhiri AM, Phiri IK, Monrad J (2006). "Prevalence of amphistomiasis and its association withFasciola gigantica infections in Zambian cattle from communal grazing areas".Journal of Helminthology.80 (1):65–68.doi:10.1079/joh2005313.PMID 16469175.S2CID 30224614.
  6. ^Spence SA, Fraser GC, Chang S (1996). "Responses in milk production to control of gastrointestinal nematode and paramphistome parasites in dairy cattle".Australian Veterinary Journal.74 (6):456–459.doi:10.1111/j.1751-0813.1996.tb07569.x.PMID 9006864.
  7. ^Gupta A, Mahajan C, Sharma M, Tiwari S, Majeed U, Rajput DS (2011)."Studies on incidence and transmission of amphistomiasis in domestic and wild ruminants of Udaipur region".Advances in Parasitology.12 (1):88–89. Archived fromthe original on 2014-05-05. Retrieved2013-03-19.
  8. ^abcdeHuson, Kathryn M.; Oliver, Nicola A. M.; Robinson, Mark W. (2017). "Paramphistomosis of Ruminants: An Emerging Parasitic Disease in Europe".Trends in Parasitology.33 (11):836–844.doi:10.1016/j.pt.2017.07.002.ISSN 1471-5007.PMID 28754416.S2CID 3512476.
  9. ^abcdChai, Jong-Yil (2019),"Amphistomes",Human Intestinal Flukes, Dordrecht: Springer Netherlands, pp. 345–368,doi:10.1007/978-94-024-1704-3_3,ISBN 978-94-024-1702-9, retrieved2023-03-21{{citation}}: CS1 maint: work parameter with ISBN (link)
  10. ^abAhluwalia, J. S.; Singh, A. N. (1975)."Treatment of Amphistomiasis in Sheep".Current Science.44 (24):907–908.ISSN 0011-3891.JSTOR 24081963.
  11. ^abcRajkumari, Nonika (2022), Parija, Subhash Chandra; Chaudhury, Abhijit (eds.),"Amphistomiasis",Textbook of Parasitic Zoonoses, Microbial Zoonoses, Singapore: Springer Nature Singapore, pp. 293–300,doi:10.1007/978-981-16-7204-0_27,ISBN 978-981-16-7203-3, retrieved2023-03-21{{citation}}: CS1 maint: work parameter with ISBN (link)
  12. ^Mas-Coma S, Bargues MD, Valero MA (2006)."Gastrodiscoidiasis, a plant-borne zoonotic disease caused by the intestinal amphistome flukeGastrodiscoides hominis (Trematoda: Gastrodiscidae)".Revista Ibérica de Parasitología.66 (1–4):75–81.ISSN 0034-9623. Archived fromthe original on 2014-05-03.
  13. ^abBowman DD, Georgi JR (2009).Georgis' Parasitology for Veterinarians (9 ed.). W.B. Saunders Company. p. 124.ISBN 978-1-4160-4412-3.
  14. ^Chai JY, Shin EH, Lee SH, Rim HJ (2009)."Foodborne intestinal flukes in Southeast Asia".The Korean Journal of Parasitology.47 (Suppl):69–102.doi:10.3347/kjp.2009.47.S.S69.PMC 2769220.PMID 19885337.
  15. ^Brown DS (2005).Freshwater Snails Of Africa And Their Medical Importance (2 ed.). Taylor & Francis Ltd. pp. 366–370.ISBN 978-0-203-48144-8.
  16. ^abLiu D (2012).Molecular Detection of Human Parasitic Pathogens. Crc Press, Boca Raton, FL. pp. 365–368.ISBN 978-1-4398-1242-6.
  17. ^Mas-Coma S, Bargues MD, Valero MA (2006)."Gastrodiscoidiasis, a plant-borne zoonotic disease caused by the intestinal amphistome flukeGastrodiscoides hominis (Trematoda:Gastrodiscidae)".Revista Ibérica de Parasitología.66 (1–4):75–81.ISSN 0034-9623. Archived fromthe original on 2014-05-03.
  18. ^Vasilev I, Denev I, Savova S, Kostov R, Georgiev B (1985). "Pathogenesis of paramphistomiasis in sheep".Veterinarno-Meditsinski Nauki.22 (2):67–73.PMID 3992928.
  19. ^Rolfe PF, Boray JC, Collins GH (1994). "Pathology of infection with Paramphistomum ichikawai in sheep".International Journal for Parasitology.24 (7):995–1004.doi:10.1016/0020-7519(94)90165-1.PMID 7883450.
  20. ^Singh RP, Sahai BN, Jha GJ (1984). "Histopathology of the duodenum and rumen of goats during experimental infections withParamphistomum cervi".Veterinary Parasitology.15 (1):39–46.doi:10.1016/0304-4017(84)90108-0.PMID 6541393.
  21. ^Mavenyengwa M, Mukaratirwa S, Obwolo M, Monrad J (2005)."A macro- and light microscopical study of the pathology ofCalicophoron microbothrium infection in experimentally infected cattle".The Onderstepoort Journal of Veterinary Research.72 (4):321–32.doi:10.4102/ojvr.v72i4.189.PMID 16562736.
  22. ^Ahmedullah F, Akbor M, Haider MG, Hossain MM, Khan M, Hossain MI, Shanta IS (2007)."Pathological investigation of liver of the slaughtered buffaloes in Barisal district".Bangladesh Journal of Veterinary Medicine.5 (1–2):81–85.doi:10.3329/bjvm.v5i1.1321.
  23. ^Georgiev B, Gruev A (1979). "Effectiveness of levamisole and oxyclozanide in paramphistomiasis in sheep and cattle".Vet Med Nauki.16 (3):45–51.PMID 524749.
  24. ^Rolfe PF, Boray JC (1987). "Chemotherapy of paramphistomosis in cattle".Australian Veterinary Journal.64 (11):328–332.doi:10.1111/j.1751-0813.1987.tb06060.x.PMID 3447575.
  25. ^Rolfe PF, Boray JC (1988). "Chemotherapy of paramphistomosis in sheep".Australian Veterinary Journal.65 (5):148–150.doi:10.1111/j.1751-0813.1988.tb14443.x.PMID 3401161.
  26. ^Saowakon N, Lorsuwannarat N, Changklungmoa N, Wanichanon C, Sobhon P (2013). "Paramphistomum cervi: the in vitro effect of plumbagin on motility, survival and tegument structure".Experimental Parasitology.133 (2):179–186.doi:10.1016/j.exppara.2012.11.018.PMID 23206952.
  27. ^Katiyar RD, Garg RK (1965). "Comparative efficacy of various chemotherapeutic agents in amphistomiasis".Advances in Parasitology.42 (10):761–768.PMID 5892245.
  28. ^Mereminskiĭ AI, Gluzman IIa (1979). "Prognosis and prevention of fascioliasis and paramphistomiasis".Veterinariia.7 (1):43–45.PMID 543077.

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