Ascaridia galli infection

Occurrence: Worldwide.
Species affected: All.
Age affected: All.
Causes: Parasitic nematode worm- Ascaridia galli.
Effects: Weight depression. In severe infections, intestinal blockage can occur. At high levels of infection, there is loss of blood, reduced blood sugar content, retarded growth and greatly increased mortality. Parasite can occasionally be seen in commercial eggs.

Detailed causes:
This parasitic nematode worm exists in the lumen of the intestine, occasionally in the oesophagus, crop, gizzard, oviduct, and body cavity.

The life history is simple and direct. Infective eggs hatch in either the proventriculus or the duodenum of the susceptible host. The young larvae, after hatching, live free in the lumen of the posterior protion of the duodenum for the first 9 days, then penetrate the mucosa and cause haemorrhages. The young worms enter the lumen of the duodenum by 17 or 18 days and remain there until maturity, at approximately 28-30 days after ingestion of embryonated eggs. Larvae may enter the tissues as early as the 1st day and remain there as long as 26 days after infection. The majority spend from 8-17 days in the intestinal mucosa. A few of the larvae penetrate deep into the tissue, while the majority undergo only a brief and shallow association with the intestinal mucosa during the “tissue phase”. A. galli eggs ingested by grasshoppers or earthworms hatch and are infective to chickens, although no development of the larvae occurs.

Under optimum temperature and moisture conditions, eggs in the droppings become infective in 10-12 days; under less favourable conditions a longer time is necessary. Eggs are quite resistant to lower temperatures.

Clinical signs:
A. galli infection causes weight depression in the host, which correlates with increasing worm burden. In severe infections, intestinal blockage can occur. The nutritional state of the host is also important, since weight depression is greater with high dietary levels of protein (15%) than with low levels (12.5%). Chickens infected with a large number of ascarides suffer from loss of blood, reduced blood sugar content, increased urates, shrunken thymus glands, retarded growth and greatly increased mortality. However, no effects of infection on blood protein level, packed-cell volume, or haemoglobin levels were found. A. galli can also have detrimental effedts through interaction (synergism) with other disease conditions such as coccidiosis and infectious bronchitis. A. galli has also been shown to contain and transmit aian reoviruses.

One of the most striking effects of infection, at least from an aesthetic standpoint, is the occasional finding of this parasite in commercial eggs. Presumably the worms migrate up the oviduct via the cloaca, with subsequent inclusion in the egg. Infected eggs can be detected by candling, thus eliminating a potential consumer complaint.

The age of the host and severity of exposure play a role in A. galli infections. Chickens 3-months or older manifest considerable resistance to infection with A. galli. In older fowl, larvae are recovered that have undergone little or no development since emerging from the egg. Larval development is arrested in the third stage at high dose rates as a result of resistance rather than a dessity-dependent phenomenon. Heavier broiler breeds are more resistant to ascarid infections than are the lighter White Leghorns.

Worms have a large, thick, yellowish white head with 3 large lips. The male is 50-76 mm long, 490-1.21 mm wide. It has a preanal sucker oval or circular, with strong chitinous wall with a papilliform interruption on its posterior rim; tail with narrow caudal alae or membranes and 10 pairs of papillae. The first pair of ventral caudal papillae are anterior to the preanal sucker, the fourth pair are widely separated (compare with A. dissimillis); spicules nearly equal and narrow and end blunt with a slight indentation. The female is 60-116 mm long, 900-1.8 mm wide; the vulva is in the anterior part of the body, eggs are elliptical, thick-shelled and not embryonated at time of deposition.

Treatment and control:

Modern poultry practices, especially confinement-rearing of broilers and pullets and caging of laying hens, have significantly influenced the quantity and variety of nematode infections in poultry. Many that caused extensive problems in backyard flocks are seldom seen in commercial operations. Others such as Ascaridia are still commonly found in commercial birds.

For most nematodes, control measures consist of sanitation and breaking the life cycle rather than chemotherapy. Confinement-rearing on litter largely prevents infections with nematodes using outdoor intermediate hosts such as earthworms or grasshoppers. Conversely, nematodes with direct life cycles or those that utilise indoor intermediate hosts such as beetles may prosper. Treatment of the soil or litter to kill intermediate hosts may be beneficial. Insecticides suitable for litter treatment include carbaryl, tetrachlorvinphos (stirofos), or Ronnel®, Safecide®. Treatment is carried out usually only between grow-outs. Extreme care should be taken to ensure that feed and water are not contaminated.

Treatment of range soil to kill ova is only partially successful. Changing litter can reduce infections, but treating floors with oil is not very effective. After the old litter has been removed, spraying with permethrin or a mixture of Rabon and Vapona has proved effective for beetle control.

Raising different species or different ages of birds together or in close proximity is bad practice with regards to parasites. Adult turkeys, which are carriers or gapeworms, can transmit the disease to young chicks or pheasants, although older chickens are almost resistant to infection.
None of the products mentioned are allowed in NL, nor to the best of my knowledge in western Europe.

Currently used in chickens are Hygromycin B (at a level of 0.00088-0.00132%) or coumaphos in feed for replacements (0.004%) or layers (0.003%), Piperazine compounds in feed or water have been widely adopted as a method of treatment for ascaridia, since they are practically non-toxic. 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). A high concentration of piperazine in contact with worms at a given time is very important for maximum elimination, therefore, to be most effective it should be consumed by birds in a period of a few hours. Piperazine in drinking water is the most practical method of application for commercial flocks. Since piperazines are available as a wide variety of salts, the level should be calculated on the basis of milligrams of active piperazine. A combination of piperazine (0.11%) and phenothiazine (0.50-0.56%) as a 1-day treatment is only used for removal of both Heterakis and ascarids.
None of these products are registered in the US, where only Flubenol â is used as a treatment.