Ascaridia - Poultry

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Scientific Classification
Kingdom Metazoa
Phylum Nematoda
Class Secernentea
Sub-class Rhabditia
Order Ascaridida
Family Ascaridiidae
Genus Ascaridia

Also known as: AscaridosisAscarids


A. galli, A. compar, A. dissimilis and A. columbae are nematodes that occur in the small intestine of poultry. They can cause haemorrhagic enteritis. Heavy infections cause partial or total obstruction of the duodenum/jejunum.

Adult A. galli are semi-transparent, have three prominent lips in their oral openings and are the biggest nematodes found in poultry. Females range from 72 to 116 mm in length and their reproductive organ opens in the middle of the body. Their eggs are oval, with smooth shells and measure 73-92 by 45-57 µm. Even if the eggs of H. gallinarum have slightly smaller and parallel sides[1], they can almost not be distinguished from A. galli eggs. Males vary from 51 to 76 mm in length and they have pre-anal suckers and two equal spicules of 1-2.4 mm long.

Compared to A. galli, A. dissimilis is slightly bigger and A. columbae is slightly smaller.


The usual host for A. galli and A. compar is the chicken, but it can also infect turkeys, geese, guinea fowl and wild birds. A. dissimilis can infect turkeys and A. columbae is found in pigeons.

Clinical Signs

Ascarids cause anorexia, diarrhoea, dehydration, stunted growth, unthriftiness, drooping wings, ruffled feathers, weight loss, reduced feed consumption rates, changes in behaviour, dullness, lethargy and misshapened and soft thin shelled eggs in poultry.

Clinical signs are more pronounced in chickens up to 3 months of age, after which the worm burden normally decreases but can still be very high.[2] Birds will suffer from blood loss, reduced blood sugar and distended ureters with urates.




Infected chickens pass A. galli eggs in their faeces. The larvae develop inside the egg until they reach their infective stage (L3) within 10-20 days or more, depending on environmental temperature and humidity. The embryonated egg can survive a winter with moderate frost and remain infective in deep litter systems for years depending on the temperature, humidity, pH and ammonium concentration.

Ascaridia galli has a direct lifecycle and it is complete when a new host (another chicken) ingests the infective embryonated eggs (L3) from contaminated water or feed. Three layers around the egg protect the larvae until it reaches the duodenum/ jejunum, where they hatch within 24hrs and enter the histotropic phase. They embed themselves into the mucosal layer of the intestine. The more eggs are present the longer the histotropic phase may last. The length of this stage before the final maturation has been reported to be between 3 to 54 days [3]. The prepatent period varies from 5 to 8 weeks.

Adult A. galli worms may migrate through the lumina of the large intestine and cloaca and end up in the oviduct, where they can be incorporated into the hen’s egg. Occasionally, earthworms can ingest A. galli eggs and ascarids are transmitted when the chicken ingests the worm.

The life cycles of A. dissimilis and A. columbae are also direct and A. dissimilis may migrate through the liver [4].


Ascaridia can be diagnosed by the above clinical signs, faecal examination or by post-mortem (PM). Evidence of enteritis/haemorrhagic enteritis can be seen on PM; as large numbers of larvae in the histotropic phase can cause extensive damage to the glandular epithelium. Adhesion of the mucosal villi can also be noted as a result of the proliferation of mucous-secretory cells.

Adult worms can also cause damage to the epithelia as a result of pressure atrophy of the villi, causing occasional necrosis of the mucosal layer. In chronic infections the intestinal wall can become distended as muscle tone is lost.


In feed treatment with piperazine salts, levamisole or a benzimidazole.[5]


In free range systems, young birds can be isolated and put onto ground previously unused by poultry. Rotation of poultry runs is recommended. In houses, raised feeding and watering stations will reduce the transmission of the pathogen via the faecal oral route. The use of genetically based resistance is intensively discussed.[6][7]

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  1. Soulsby EJL (1982) Helminths, arthropods and protozoa of domesticated animals. Helminths, arthropods and protozoa of domesticated animals., Ed. 7:xi + 809 pp.44; [many fig., 260 x 195 mm]; many ref.
  2. Kaufmann F, Das G, Sohnrey B, Gauly M (2011) Helminth infections in laying hens kept in organic free range systems in Germany. Livestock Science. 10.1016/j.livsci.2011.05.015.
  3. Herd RP, McNaught DJ (1975) Arrested development and the histotropic phase of Ascaridia galli in the chicken ,International Journal for Parasitology , 5: 401-406
  4. Norton RA, Clark FD, Beasley JN (1999) An outbreak of histomoniasis in turkeys infected with a moderate level of Ascaridia dissimilis but no Heterakis gallinarum. Avian Diseases, 43(2):342-8
  5. Taylor, M.A., Coop, R.L., Wall, R.L., (2007) Parasites of poultry and gamebirds in: Veterinary Parasitology (third edition), 467-468.
  6. Gauly M, Bauer C, Preisinger R, Erhardt G (2002) Genetic differences of Ascaridia galli egg output in laying hens following a single dose infection. Vet. Parasitol., 103, 99-107.
  7. Kaufmann F, Daş G; Preisinger R, Schmutz M, König S, Gauly M (2011) Genetic resistance to natural helminth infections in two chicken layer lines. Vet. Parasitol., 176, 250 – 257.


This article was originally sourced from The Animal Health & Production Compendium (AHPC) published online by CABI during the OVAL Project.

The datasheet was accessed on August 08, 2011.

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