• There is diffuse loss of coelomic detail.
• The ventriculus is moderately distended with mineral opaque material of variable size and at least two metal opaque coiled foreign bodies.
• Segments of small bowel are moderately gas filled and at least one segment of small bowel contains punctate granular mineral material.
• In the VD view, there is loss of the cardiohepatic silhouette with increased soft tissue opacity caudally at the level of the liver

• Moderate volume coelomic effusion. Differentials include egg yolk coelomitis, ascites from cardiac disease or less likely hepatic disease. Neoplastic effusion cannot be excluded. The volume of effusion is likely contributing to the respiratory signs due to air sac compression.
• Mineral debris in the ventriculus is routine grit and expected in this species
• Metal foreign material (springs/wire) in the ventriculus could result in zinc or lead toxicosis but does not account for the ascites.
• Small intestinal gas distension is moderate and may represent functional ileus secondary to the intra-coelomic effusion (particularly if inflammatory effusion)
• Although widening of the cardiohepatic silhouette may be due to hepatomegaly, the primary consideration in this patient is that it is largely due to the mass effect from ascites and overall coelomic distension with cranial displacement of the liver. In other cases, widening of the silhouette could be secondary to reproductive tract enlargement or other intra-coelomic organomegaly.

Based on the coelomic appearance, centesis was performed yielding 68mL of yellow-tinged effusion (looked like yolk). The patient was initially treated with antibiotics for suspected coelomitis with secondary bacterial infection, but re-presented several days later due to lack of clinical improvement. At that time, cytology of coelomic effusion and a CBC were performed. CBC showed a heterophillic leukocytosis with atypical large round cells in circulation thought to represent circulating neoplastic lymphocytes. Cytology of the coelomic effusion was also consistent with lymphoid neoplasia. Granules in some of the cells within the effusion suggested the neoplasia may have been of T-cell origin. The patient was subsequently euthanized. Gross findings at necropsy included diffuse yellow, thick fluid filling the coelom, splenomegaly, and several ruptured ovarian follicles. Histology confirmed infiltration of multiple organs (ovary, lung, liver, kidney, heart, gastrointestinal tract, omentum) by round cell neoplasia with marked histiocytic infiltrates. Primary differentials based on clinical and anatomic pathology findings included Marek’s disease, avian leukemia, and reticuloendotheliosis. 

Marek’s disease is caused by a herpes virus that results in T-cell lymphomas and peripheral nerve enlargement.  It may present in a variety of ways including progressive limb paralysis due to sciatic nerve involvement, coelomic tumors (liver, spleen, kidney, ovary), or generalized hepatosplenomegaly, enlargement of feather follicles and reddening, and discoloration of the iris due to lymphoid infiltration. Aside from asymmetric paralysis when involving the sciatic nerve, clinical signs are often nonspecific (lethargy/dehydration/weight loss) or birds may die without showing clinical signs at all. Marek’s disease typically affects younger birds (6-30weeks) and is highly infectious. Although commercial flocks are commonly vaccinated, there is no treatment for Marek’s disease.  

Avian leukosis/sarcoma group are caused by retroviruses with lymphoid leukosis being the most commonly encountered resulting in neoplasia of the bursa of Fabricius and other organ metastasis. Clinical signs are nonspecific and although widely distributed, the incidence is considered low.

Finally, reticuloendotheliosis encompasses a variety of syndromes caused by retroviruses including a chronic lymphoma in turkeys and rarely, other fowl species. 

In this patient, PCR testing of the spleen for Marek’s disease was negative. Ultimately differentiating between avian round cell neoplasia is challenging, as highlighted in this case, and the prognosis of individual patients is poor.

And in this case, the ingested springs were a red herring (get it? Not the spring, chicken!)

1. Ojkic D, et al. 2013. Viral diseases. In Boulianne M (Ed). Avian Disease Manual, 7th ed. American Association of Avian Pathologists. https://aaap.memberclicks.net/avian-disease-manual-past-edition-#calibre_link-1
2. Marek’s disease in chickens. (2018, August 27). PennState Extension. Retrieved March 10, 2022, from https://extension.psu.edu/mareks-disease-in-chickens
3. Dunn, J. (2019, October). Marek’s disease in poultry. Merck Manual. https://www.merckvetmanual.com/poultry/neoplasms/marek-s-disease-in-poultry