Ascaridia galli

Ascaridia galli
Adult worms
Scientific classification
Kingdom: Animalia
Subkingdom: Eumetazoa
Phylum: Nematoda
Class: Secernentea
Order: Ascaridida
Family: Ascaridiidae
Genus: Ascaridia
Species: A. galli
Binomial name
Ascaridia galli
Schrank, 1788

Ascaridia galli is a parasitic roundworm belonging to the phylum Nematoda. Nematodes of the genus Ascaridia are essentially intestinal parasites of birds.[1] A. galli is the most prevalent and pathogenic species, especially in domestic fowl, Gallus domesticus Linnaeus, 1758. It causes ascaridiasis, a disease of poultry due to heavy worm infection, particularly in chicken and turkeys. It inhabits the small intestine, and can be occasionally seen in commercial eggs.[2]

Description

It is the largest nematode in birds. The body is semitransparent, creamy-white and cylindrical. The anterior end is characterized by a prominent mouth, which is surrounded by three large tri-lobed lips. The edges of the lips bear teeth-like denticles.[3] The body is entirely covered with a thick proteinaceous structure called cuticle. The cuticle is striated transversely throughout the length of the body and cuticular alae are poorly developed. Two conspicuous papillae are situated on the dorsal lip and one on each of the subventral lips.[4] These papillae are the sensory organs of the nematode. A. galli is diecious with distinct sexual dimorphism. Females are considerably longer and more robust, with vulva opening at the middle portion (approximately midway from anterior and posterior ends) of the body and anus at the posterior end of the body. The tail end of females is characteristically blunt and straight. Males are relatively shorter and smaller, with a distinct pointed and curved tail..[5] There are also ten pairs of caudal papillae towards the tail region of the body, and they are arranged linearly in well-defined groups such as precloacal (3 pairs), cloacal (1 pair), post-cloacal (1 pair) and subterminal (3 pairs) papillae.[6][7]

Life cycle

The life cycle of A. galli is direct in a single host, involving two principal populations, namely the sexually mature parasite in the gastrointestinal tract and the infective stage (L3). The eggs are oval in shape and have thick, albuminous shells that are highly resistant to desiccation and persist for a long time in the environment.[8] Larvae do not hatch but moult inside the eggs until they reach the L3 stage. This can take about two weeks but the period depends on other factors such as the weather condition. The life cycle is completed when the infective eggs are ingested by new hosts through contaminated water or feed. The eggs containing the L3-larvae are mechanically transported to the duodenum. The infective eggs are ingested by a chicken where it reaches the proventriculus and hatches.[9] Temperature, carbon dioxide levels and pH are thought to be triggering factors that signal the larva to hatch from its egg. The larva then burrows into the mucosal lining of the small intestine where it undergoes two additional moults. It is this phase of their life cycle where these worms causes the most damage to their host. They then re-enter the small intestine and develop into adults where they live their lives out feeding on gut content and making a vast amount of eggs that would then be excreted by a host and free to continue their life cycle. If the animal is able to mount an immune response to the larvae, i.e. from pre-exposure, the larvae do not develop into adults but hide in the mucosa of the small intestine. This is common for infection of older birds. Transport hosts such as earthworms are thought to play a role in transmission of A. galli and hence, free range birds tend to have a higher risk of infection.[6][10]

Pathogenicity

The nematode infects fowl of all ages, but the greatest degree of damage is often found in young birds under 12 weeks of age. Heavy infection is the major cause of weight depression and reduced egg production in poultry husbandry. In severe infections, intestinal blockage can occur. Unthriftiness, drooping of the wings, bleaching of the head and emaciation. It also causes loss of blood, reduced blood sugar content, increased urates, shrunken thymus glands, retarded growth and greatly increased mortality. In heavy infections, adult worms may move up the oviduct and be found in hens' eggs, and sometimes they are also found in the birds' feces.[11]

Treatment

Piperazine is the drug of choice. Continuous medication in feed with hygromycin B is also widely employed. Piperazine may be administered to chickens in the feed (0.2-0.4%) or water (0.1-0.2%), or as a single treatment (50–100 mg/bird). However, piperazine is quite ineffective for young chickens, while tetramisole is 89-100% effective for chicken of different ages.[12] More recent drugs such as albendazole and levamisole are also highly effective.[13] Fenbendazole is also very effective, 99.2-100% and 69.0-89.6% effective at administration doses of 60.6 ppm and 30.3 ppm.[14] Ivermectin was also demonstrated to be 90 and 95% effective against immature and adult worms, respectively.[15]

References

  1. ↑ Yamaguti, S.(1961). Systema Helminthum. 3. The nematodes of vertebrates. Interscience Publishers, New York and London, pp. 1261.
  2. ↑ Griffiths HJ (1978). A Handbook of Veterinary Parasitology: Domestic Animals of North America. University of Minnesota Press, Minneapolis, Minnesota, USA, pp. 46-47.
  3. ↑ Ashour, AA (1994). "Scanning electron microscopy of Ascaridia galli (Schrank, 1788), Freeborn, 1923 and A. columbae (Linstow, 1903)". J Egypt Soc Parasitol 24 (2): 349–55. PMID 8077754.
  4. ↑ Lalchhandama K; Roy, Bishnupada; Dutta, Biman Kumar (2009). "Anthelmintic activity of Acacia oxyphylla stem bark against Ascaridia galli". Pharmaceutical Biology 47 (7): 578–583. doi:10.1080/13880200902902463.
  5. ↑ Ackert, JE (1940). "The large roundworm of chickens". Vet. Med. 35: 106–108.
  6. 1 2 Ramadan, HH; Znada, NYA (1992). "Morphology and life history of Ascaridia galli in the domestic fowl that are raised in Jeddah" (PDF). J.K.A.U. Sci. 4: 87–99. doi:10.4197/sci.4-1.9.
  7. ↑ Lalchhandama K (2010). "On the structure of Ascaridia galli, the roundworm of domestic fowl" (PDF). Science Vision 10 (1): 20–30.
  8. ↑ Ackert, JE (1931). "The morphology and life history of the fowl nematode Ascaridia lineata (Schneider)". Parasitology 23: 360–379. doi:10.1017/s0031182000013731.
  9. ↑ "Helminthiasis: Introduction". The Merck Veterinary Manual. 2006. Archived from the original on 22 June 2007. Retrieved 2007-07-01.
  10. ↑ Anderson RC (2000). Nematode Parasites of Vertebrates. Their Development and Transmission, 2nd ed. CAB International, Wallingford, Oxon, UK, pp. 265,290-299. ISBN 0-85199-421-0
  11. ↑ Jacobs RD, Hogsette JA, Butcher JD (2003). Nematode parasites of poultry (and where to find them). The Institute of Food and Agricultural Sciences (IFAS) series PS18, University of Florida, USA, pp. 1-3.
  12. ↑ Pavlícek J, Dyková I. (1976). "Tetramisol, piperazine, and metrifonate treatment of experimental invasion by Ascaridia galli in chickens of differents ages". Vet Med (Praha) 21 (6): 353–358. PMID 826003.
  13. ↑ Sharma RK, Singh K, Saxena KK (1989). "The effect of levamisole and albendazole on some enzymes of Ascaridia galli and Heterakis gallinae". Vet Parasitol 30 (3): 213–222. doi:10.1016/0304-4017(89)90017-4. PMID 2705287.
  14. ↑ Sander JE, Schwartz RD (1994). "Evaluation of three water-suspensible formulations of fenbendazole against Ascaridia galli infection in broiler chickens". Avian Dis 38 (2): 350–353. doi:10.2307/1591961. PMID 7980286.
  15. ↑ Sharma RL, Bhat TK, Hemaprasanth (1990). "Anthelmintic activity of ivermectin against experimental Ascaridia galli infection in chickens". Vet Parasitol 37 (3–4): 307–314. doi:10.1016/0304-4017(90)90014-3. PMID 2267731.

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