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Atherosclerosis refers to the accumulation of plaque (fatty deposits) in the chicken's arteries. These deposits are made up of cholesterol, fatty substances, cellular waste products, calcium and fibrin. As the plaque builds up, the wall of the blood vessel thickens and narrow the channel within the artery. This obstructs blood flow and reduces the supply of oxygen-rich blood to tissues of vital organs in the chicken's body.

The most frequently affected site in birds is the aorta at the heart’s base. Other sites of importance include the brachiocephalic trunk, pulmonary artery, dorsal aorta, heart valves, and mural arteries. In all cases, atherosclerotic lesions are more pronounced at the level of, or just before, the branching of smaller arteries. Clinical conditions associated with atherosclerosis in chickens include vascular occlusion, rupture, and thrombosis.

Risk factors for the development of atherosclerosis in chickens include:
  • Poor Diet: Consumption of a high-cholesterol diet, a diet low in polyunsaturated fatty acids (PUFA) and high in saturated fatty acids, or a high-fat diet enriched in linoleic acid.
  • Viral induced: Infection with the Marek's disease virus, which is known to cause atherosclerotic-like lesions in the arteries.

Clinical Signs of Atherosclerosis in Chickens

Signs of atherosclerosis don't appear until the arteries are severely narrowed which leads to a poor oxygen-rich blood supply. They also depend on which arteries are affected and how much blood flow is blocked.

Signs of atherosclerosis may initially appear intermittently, such as when the chicken is experiencing physical or emotional stress where the body requires more oxygen. Signs may include:
  • Exercise intolerance: The chicken tires easily and demonstrates heavy panting and darkening of face and comb color. It returns to a normal color after the chicken rests or calms down.
  • Behavioral changes: Chickens may act out of character--suddenly becoming more 'aggressive' towards humans (roosters) or more shy and anti-social.
  • Reduced activity: The chicken may become less interested in normal activities and appear more lethargic or subdued.
  • Weight loss: Affected chickens may lose their appetite and interest in certain foods or feed altogether.
  • Ascites: The chicken's abdomen may become enlarged due to accumulation of fluid.
Unless you are observant of each individual flock member, the first indication of the disease will likely be a mysterious sudden death.

Clinical Signs

Behavioral changes
Exercise intolerance
Difficulty breathing
Darkening of the comb
Falling off perch
Decreased appetite
One leg lameness to paralysis
Sudden death


  • History
  • Radiographs - may identify cardiomegaly associated with atherosclerosis and severe vascular mineralization.
  • changes in serum cholesterol and lipoprotein levels
  • CBC
  • ECG
  • CT
  • Necropsy

Reported Cases

  • Case 1: Arteriosclerosis in a Parrot A 40-year-old female African grey parrot exhibited weakness due to anorexia for several days. Physical examination revealed that the bird was weak, cachectic and had abdominal effusion. There was 15 ml of clear fluid in the thoracic cavity and 25 ml of clear fluid in the abdominal cavity. The aorta and left and right pulmonary arteries were firm, gritty, and had a nodular appearance. The right thyroid was enlarged, 6 mm in diameter. The left thyroid was 3 mm in diameter. Hypoalbuminemia (total protein 1.2 gm/dl, albumin 0.5 gm/dl, and globulin 0.7 gm/dl) was observed in blood chemistry profile. The lesions of the aorta and pulmonary arteries consisted of fragmentation of elastic and collagen fibers with cholesterol deposition and proliferation of spindle cells in the media. There was chondroid metaplasia, mineralization and proliferation of smooth muscle cells in the subintimal tissue and intima, which caused narrowing of the lumen. Ref

  • Case 2: Presumed atherosclerosis in a Eagle A 19-year-old male golden eagle presented for an abnormal heart rhythm on auscultation. An electrocardiogram was performed on the patient and demonstrated frequent supraventricular premature complexes. While an echocardiogram on the same patient revealed marked systolic dysfunction of the severely enlarged left ventricle as well as severely enlarged left atrium. No clinical evidence of left-sided congestive heart failure was noted. Treatment with isoxsuprine and atenolol was initiated. After 2 weeks, no significant changes were appreciable on repeat examination. The medical therapy was modified to isoxsuprine, sotalol, and pimobendan. Following 4 weeks of the new treatment plan, chamber sizes of the left ventricle and atrium were reduced, and the cardiac rhythm had converted to a normal rhythm. A computed tomography angiography (CTA) was conducted and identified substantial narrowing of the internal diameter of the right brachiocephalic artery. Fifteen months after initial diagnosis, the patient continued to maintain a normal sinus rhythm, normal cardiac size, and appropriate systolic function of the left ventricle despite no changes observed in the right brachiocephalic arterial diameter on repeat CTA. This case report demonstrates the therapeutic potential of sotalol at 1 mg/kg PO BID for the treatment of supraventricular premature complexes and a diagnostic utility of CTA for the case of suspected atherosclerosis. Ref

  • Case 3: Atherosclerosis in a Budgie A 16-year-old male grey-cheeked parakeet was presented for dyspnea and decreased activity. The bird's diet was primarily table food, with a large proportion of animal products. Radiographs revealed a linear mineralized structure in the plane of the aorta and an enlarged hepatocardiac silhouette. Left atrial and left ventricular enlargement and a left ventricular systolic dysfunction were diagnosed by echocardiography. The bird's condition progressively declined, and it died 5 days after presentation. A postmortem examination revealed marked atherosclerosis of the aorta, great vessels of the heart, and coronary arteries with myocardial degeneration, pulmonary congestion, and ascites. Ref

  • Case 4: Atherosclerosis in a Parrot A 20-year-old female African Grey parrot was evaluated to determine the cause of lethargy, hyporexia, weight loss, and persistent ascites of 21 days' duration. Physical examination revealed a markedly distended abdomen and systolic heart murmur. Thoracic radiography revealed cardiomegaly and hepatomegaly. Doppler echocardiography revealed severe eccentric and concentric hypertrophy of the right ventricle with systolic dysfunction, moderate regurgitation through the right atrioventricular valve, a substantial increase in estimated systolic pulmonary arterial pressure, hepatic venous congestion, and coelomic effusion. A clinical diagnosis of chronic cor pulmonale was established. The parrot was initially stabilized by use of coelomocentesis. During the next month, the parrot was treated by administration of furosemide, hydrochlorothiazide, spironolactone, benazepril, and pimobendan. The parrot appeared to be responding well to treatment but was found dead in its cage 35 days following initial examination. Postmortem examination revealed substantial atherosclerosis of the large pulmonary arteries, with lesions extending into the medium-size arteries. Pulmonary atherosclerosis was suspected as a cause of the severe pulmonary hypertension. Ref

  • Case 5: Atherosclerosis in a Parrot A 35-year-old yellow-naped Amazon parrot was presented for gradually increasing inappetence, ataxia, weakness, and lethargy. Radiographic and ultrasonographic findings were strongly suggestive of atherosclerosis. Isoxsuprine, a peripheral vasodilator demonstrated to be of benefit in humans with intermittent limb pain, weakness, and lameness secondary to occlusive vascular disease, was selected for treatment. The bird's clinical signs resolved during treatment but recurred after varying periods of time when the medication was stopped intermittently. Nearly 3 years after the initial examination, the parrot was doing well on isoxsuprine therapy, with normal prehension of food with its feet and no recurrence of clinical signs. Ref


Supportive careIsolate the bird from the flock and place in a safe, comfortable, warm location (your own chicken "intensive care unit") with easy access to water and food. Limit stress. Call your veterinarian.
Modification of dietStop feeding table scraps and choose a lower protein feed.
Omega-3 fatty acidsAdded to the diet at 0.22 ml/kg. Concurrently add 160 mg/kg of Vitamin E (since the bird's requirements for dietary vitamin E will increaseO Cojean et al., 2020; A Sekikawa et al., 2019
NiacinUsed to help lower total cholesterolN Ruperelia et al., 2011; D Meyers et al., 2004;
Isoxsuprine5-10 mg/kg POFitzgerald, Brenna Colleen et al., 2018; Simone-Freilicher, Elisabeth., 2007
Propolis0.25 g/kgI Klaric et al., 2018; Nader et al., 2010
Sotalol1 mg/kg PO BIDS Oster et al., 2019



  • Feed a low fat, low cholesterol diet with plenty of omega-3 fatty acids, particularly long chain EPA and DHA sources.
  • Vaccinate chicks for Marek's disease



Scientific References

Age Range

Usually seen in adult chickens.

Risk Factors

  • Unhealthy diet. Foods that are high in saturated and trans fats, cholesterol, sodium (salt), and sugar.
  • Feeding chickens a steady diet of table food.
  • Infection with Marek's Disease virus (MDV)
  • Heavier breeds and/or obesity
  • Age

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