Epidemiology
Earthworm transport hosts are important factors in the transmission of Syngamus trachea when poultry and game birds are reared on soil. The longevity of L3s in earthworms (up to 3 years) is particularly important in perpetuating the infection from year to year. Wild birds may serve as reservoirs of infection and have been implicated as the sources of infections in outbreaks on game-bird farms as well as poultry farms. Wild reservoir hosts may include pheasants, ruffed grouse, partridges, wild turkeys, magpies, meadowlarks, American robins, grackles, jays, jackdaws, rooks, starlings and crows. There is also evidence to suggest that strains of Syngamus trachea from wild bird reservoir hosts may be less effective in domestic birds; if they have an earthworm transport host rather than direct infections via ingestion of L3s, or eggs containing L3s. Clinical signs
Blockage of the bronchi and trachea with worms and mucus will cause infected birds to gasp for air. They stretch out their necks, open their mouths and gasp for air producing a hissing noise as they do so. This "gaping" posture has given rise to the common term "gapeworm" to describe Syngamus trachea. These clinical signs first appear approximately 1–2 weeks after infection. Birds infected with gapeworms show signs of weakness and emaciation, usually spending much of their time with eyes closed and head drawn back against the body. An infected bird may give its head a convulsive shake in an attempt to remove the obstruction from the trachea so that normal breathing may be resumed.
Larvae have been shown to remain viable for more than three years encapsulated in earthworm muscles. Other invertebrates may also serve as paratenic hosts, including terrestrial snails and slugs. The parasitic phase involves substantial migration in the definitive host to reach the predilection site. Young birds are most severely affected with migration of larvae and adults through the lungs causing a severe pneumonia. Lymphoid nodules form at the point of attachment of the worms in the bronchi and trachea. Adult worms also appear to feed on blood. Worms in the bronchi and trachea provoke a hemorrhagic tracheitis and bronchitis, forming large quantities of mucus, plugging the air passages and, in severe cases, causing asphyxiation. Pheasants appear to be particularly susceptible to infections resulting in mortality rates as high as 25% during outbreaks. The rapidly growing worms soon obstruct the lumen of the trachea, causing suffocation. Turkey poults, baby chicks and pheasant chicks are most susceptible to infection. Turkey poults usually develop gapeworm signs earlier and begin to die sooner after infection than young chickens. Lesions are usually found in the trachea of turkeys and pheasants but seldom if ever in the tracheas of young chickens and guinea fowl. The male worm, in the form of lesions, remains permanently attached to the tracheal wall throughout the duration of its life. The female worms apparently detach and reattach from time to time in order to obtain a more abundant supply of food.