Abstract

A 22-day-old, captive born rockhopper penguin chick (Eudyptes chrysocome) housed in an indoor closed population presented with a two-day history of breathing hard. The chick was noted to be smaller in size than a conspecific that hatched the same day. Both animals were assist fed three times daily in addition to parent feeds. Animals were assist-fed a vitamin supplemented penguin formula in addition to pieces of krill, capelin, and herring. This animal was noted to have much smaller weight gains than its cohort despite a consistently positive feed response.

On physical examination the bird was active and vocal. The plumage was stained with food debris and feces. The chick exhibited a moderate inspiratory effort with a respiratory rate of 32 breaths/min. On auscultation a grade IV/VI holosystolic murmur was noted. It radiated throughout the thorax and obscured respiratory sounds, HR was > 200 bpm. The cohort animal was examined for comparison. It exhibited a similar inspiratory effort, respiratory rate, and heart rate but no murmur was ausculted. It was significantly larger in size (826 grams compared to 535 grams), with only a mild difference in body condition scores (4.5/9 vs. 3.75/9).

Blood was submitted from both animals for CBC, plasma biochemistries, and DNA sexing. CBC revealed a leukocytosis, mature heterophilia, and anemia. Plasma biochemistries were within normal limits. Blood sexing determined both animals to be females. The healthy female's bloodwork was within ISIS reference ranges for this species. Radiographs and ECG were attempted on the conspecific animal to be used as a basis for comparison. Both were unrewarding diagnostically based on manual restraint, positioning, and equipment. It was determined that rather than anesthetizing a compromised patient a cardiac ultrasonography consult should be pursued. Treatment with trimethoprim-sulfa was initiated.

An echocardiogram was performed in an attempt to determine etiology of the murmur and clinical signs. The healthy juvenile was done first to determine comparable measurements and approach. Evaluation showed significant differences in chamber size, velocity, and valve thickness. A ventricular septal defect, left to right shunt measuring 0.25 cm was diagnosed in the affected animal. She also had mitral valve thickening (dysplasia) with mitral insufficiency and secondary left atrial enlargement as well as mild tricuspid insufficiency and mild aortic insufficiency. There was also evidence of mild-moderate pulmonary arterial hypertension leading to an increase in right ventricular pressure and a decrease in the left ventricular to right ventricular shunt. Etiologies for this include secondary to increased flow through the pulmonary vasculature (Eisenmenger's physiology), pulmonary vascular disease, respiratory disease, or a clot in the pulmonary artery.

Over the following 4 weeks the animal's condition remained the same aside from increased reports of exercise intolerance at the end of assist feeds. She had a fluctuating growth curve of losing and gaining weight from feed to feed. Follow-up bloodwork indicated a persistent leukocytosis as well as an inverse calcium phosphorous ratio and mildly elevated uric acid. Differential diagnosis for the elevated uric acid included renal toxicosis from the trimethoprim sulfa or possible nutritional factors. A fungal etiology was considered for the persistent leukocytosis, SMZ-TMP was discontinued and itraconazole started. Calcium supplementation in the formula was also discontinued. Over the following 6 weeks the animal began steadily gaining weight and catching up to her healthy conspecific female. Repeat bloodwork showed uric acid and Ca levels back within normal limits and a decrease in the WBC count to near normal. The bird clinically looked much better though the murmur could still be ausculted (slightly muted, grade III/VI). 3 months after the initial onset of clinical signs the animal was difficult to differentiate from other conspecifics. A recheck echo was scheduled but could not be performed as the animal had molted and had its full adult feather coat. Various formations of ultrasound gel, dishwashing soap, and water were mixed to try to penetrate the feather/air barrier to allow ultrasonographic visualization, all were unsuccessful.

Cardiovascular disease has been under-diagnosed in the avian patient for a number of years. With advanced diagnostic techniques becoming more readily available. Electrocardiograms (ECGs), radiography, and ultrasonography have advanced the understanding of cardiovascular disease, but there is still a paucity of information especially in the non-domestic avian species¹. The most common heart defect reported in caged birds is the interventricular septal defect². Aside from the pet bird industry and research involving poultry, little information has been gathered towards determining normal ECG and echocardiogram values. Diagnosis of cardiac disease in avian patients is more challenging than in mammals due to their rapid heart rates, and the difficulty of imaging with the location of the air sacs in relation to the heart. However, it can be a valuable tool in directing the course of treatment.

References

1.  Harcourt-Brown N, Chitty J. In BSAVA Manual of Psittacine Birds, 2nd Edition, Harcourt-Brown, Nigel and Chitty, John (eds), BSAVA Press, pp 252-253, 2005

2.  Phalen, D. Respiratory Medicine of Caged and Aviary Birds. Vet Clin Exot Anim 3:2 pp 423-452