Treatment of the soil or litter to kill intermediate hosts may be beneficial. Insecticides suitable for litter treatment include carbaryl, tetrachlorvinphos (stirofos). However, treatment is usually done 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. Raising different species or different ages of birds together or in close proximity is a dangerous procedure as regards parasitism. Adult turkeys, which are carriers of gapeworms, can transmit the disease to young chicks or pheasants, although older chickens are almost resistant to infection. Treatment
Flubendazole (Flubenvet) is the only licensed anthelmintic for use in poultry and game birds. Continuous medication of pen-reared birds has been recommended, but is not economical and increases the possibility of drug resistance. Several other compounds have been shown effective against S. trachea under experimental conditions. Methyl 5-benzoyl-2-benzimidazole was 100% efficacious when fed prophylactically to turkey poults. 5-Isopropoxycarbonylamino-2-(4-thizolyl)-benzimidazole was found to be more efficacious than thiabendazole or disophenol. The level of control with three treatments of cambendazole on days 3–4, 6–7, and 16-17 post-infection was 94.9% in chickens and 99.1% in turkeys. Levamisole (Ergamisol), fed at a level of 0.04% for 2 days or 2 g/gal drinking water for 1 day each month, has proven effective in game birds. Fenbendazole (Panacur) at 20 mg/kg for 3–4 days is also effective. Ivermectin injections may be effective in treating resistant strains. Sources

https://web.archive.org/web/20100703145151/http://cal.vet.upenn.edu/projects/merial/Strongls/strong_4.htm
https://web.archive.org/web/20110717194656/http://www.vetsweb.com/diseases/syngamus-trachea-d75.html#effects
Identifying characteristics on the sonogram include: an echogenic (bright) mass appearing in the chest of the fetus, displacement of the heart from its normal position, a flat or everted (pushed downward) diaphragm, or the absence of visible lung tissue.CPAMs are classified into three different types based largely on their gross appearance. Type I has a large (>2 cm) multiloculated cysts. Type II has smaller uniform cysts. Type III is not grossly cystic, referred to as the "adenomatoid" type. Microscopically, the lesions are not true cysts, but communicate with the surrounding parenchyma. Some lesions have an abnormal connection to a blood vessel from an aorta and are referred to as "hybrid lesions." Imaging
The earliest point at which a CPAM can be detected is by prenatal ultrasound. The classic description is of an echogenic lung mass that gradually disappears over subsequent ultrasounds. The disappearance is due to the malformation becoming filled with fluid over the course of the gestation, allowing the ultrasound waves to penetrate it more easily and rendering it invisible on sonographic imaging. When a CPAM is rapidly growing, either solid or with a dominant cyst, they have a higher incidence of developing venous outflow obstruction, cardiac failure and ultimately hydrops fetalis. If hydrops is not present, the fetus has a 95% chance of survival. When hydrops is present, risk of fetal demise is much greater without in utero surgery to correct the pathophysiology.