Amphistomiasis

Amphistomiasis is a parasitic disease of livestock animals, more commonly of cattle and sheep, and humans caused by immature helminthic flatworms belonging to the order Echinostomida. The term amphistomiasis is used for broader connotation implying the disease inflicted by members of Echinostomida including the family Paramphistomidae/Gastrodiscidae (to be precise, the species Gastrodiscoides hominis); whereas paramphistomiasis is restricted to that of the members of the family Paramphistomatidae only. G. discoides and Watsonius watsoni are responsible for the disease in humans, while most paramphistomes are responsible in livestock animals, and some wild mammals.[1][2][3][4][5] In livestock industry the disease causes heavy economic backlashes due to poor production of milk, meat and wool.[6][7]

Amphistomiasis
Other namesParamphistomiasis, amphistomosis, paramphistomosis
SpecialtyInfectious disease

Cause

Amphistomiasis in farm and wild mammals is due to infection of paramphistomes, such as the species of Paramphistomum, Calicophoron, Cotylophoron, Pseudophisthodiscus, etc. These are essentially rumen flukes, of which Paramphistomum cervi is the most notorious in terms of prevalence and pathogenicity. Infection occurs through ingestion of contaminated vegetables and raw meat, in which the viable infective metacercaria are deposited from snails, which are the intermediate hosts.[8][9] The immature flukes are responsible for destroying the mucosal walls of the alimentary 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.[10] The zoonotic infection in human is caused by G. discoides and W. watsoni which are essentially intestinal flukes. The disease due to G. discoides is more specifically termed gastrodiscoidiasis.[11] In their natural hosts such as pigs and monkeys, their infection in asymptomatic, but human infection is prevalent, by which they cause serious health problems, characterised by diarrhoea, fever, abdominal pain, colic, and an increased mucous production. In extreme situations such as in Assam, India, a number of mortality among children is attributed to this disease.[12]

Pathogenesis and symptoms

Adult flukes are known to be quite harmless, as they do not attack on the host 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. This necrosis is indicated by haemorrhage in faeces, which in turn is a sign of severe enteritis. Under such condition the animals become anorexic 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][13][14] Sometimes chronic form is also seen with severe emaciation, anaemia, rough coat, mucosal oedema, thickened duodenum and oedema in the sub maxillary space.[5][15][16] The terminally sick animals lie prostrate on the ground, completely emaciated until they die. In buffalos, severe haemorrhage was found to be associated with liver cirrhosis and nodular hepatitis.[17]

Diagnosis

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 of postmortem analyses, clinical signs displayed by the animals, and response to drenching. In heavy infection, symptoms are easily observed in sheep and cattle as they become severely anorexic 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][11] 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 and prognosis is often hindered by multiple infections with other trematodes, such as Fasciola hepatica and schistosomes, because these flukes are given primary importance due to their pervasive nature.[5]

Treatment

Amphistomiasis is considered a neglected tropical 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 and levamisole.[8][18][19][20] An in vitro demonstration shows that plumbagin exhibits high efficacy on adult flukes.[21][22] 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 using molluscicides 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 effectively kills the flukes within a few hours and it effective against the flukes resistant 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][23] 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]

gollark: Even better, apply this to 1 in 100 people, because random means fair!
gollark: What *could* go wrong?!
gollark: But mostly rares.
gollark: Then at 5000 dragons allow access to an ultracave containing only uncommons and up.
gollark: Constantly empty the cave and force everyone to buy bred ones? Seems fair.

References
  1. Olsen 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. Hugh-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. Kumar V (1998). Trematode Infections and Diseases of Man and Animals (1 ed.). Springer, Netherlands. pp. 275–321. ISBN 978-0792355090.
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  5. Phiri AM, Phiri IK, Monrad J (2006). "Prevalence of amphistomiasis and its association with Fasciola gigantica infections in Zambian cattle from communal grazing areas". Journal of Helminthology. 80 (1): 65–68. doi:10.1079/joh2005313. PMID 16469175.
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  10. 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.
  11. Liu D (2012). Molecular Detection of Human Parasitic Pathogens. Crc Press, Boca Raton, FL. pp. 365–368. ISBN 978-1-4398-1242-6.
  12. Mas-Coma S, Bargues MD, Valero MA (2006). "Gastrodiscoidiasis, a plant-borne zoonotic disease caused by the intestinal amphistome fluke Gastrodiscoides hominis (Trematoda:Gastrodiscidae)". Revista Ibérica de Parasitología. 66 (1–4): 75–81. ISSN 0034-9623. Archived from the original on 2014-05-03.
  13. 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.
  14. 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.
  15. Singh RP, Sahai BN, Jha GJ (1984). "Histopathology of the duodenum and rumen of goats during experimental infections with Paramphistomum cervi". Veterinary Parasitology. 15 (1): 39–46. doi:10.1016/0304-4017(84)90108-0. PMID 6541393.
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  18. 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.
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  21. 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.
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Classification
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