Abstract

Neonatal avian pathology has been documented in a variety of avian species.¹ Over the course of a 4-year period (4 breeding seasons), 11 eggs failed to hatch, and 6 neonatal deaths occurred in a captive colony of Magellanic penguins (Spheniscus magellanicus). These eggs came from different parents that were not genetically related, and all parents received anti-malarial prophylaxis during the observed breeding seasons. During the first year, eggs were kept with the parents in nest boxes. All 4 viable eggs from the first year failed to hatch. Common necropsy findings from the first year included evidence of fecal staining on the apex and base of the eggs, cloudy allantoic fluid, and friable yolk membranes. Due to concerns for contamination, humidity and temperature control, all eggs were pulled from parents and maintained in an incubator for subsequent breeding seasons. Environmental factors were closely monitored, and biosecurity protocols were implemented. During the last three breeding seasons 7 eggs failed to hatch. Pathology findings of these eggs included malpositioning, delayed internalization of yolk sac, infection of the yolk membrane (cultured Enterococcus spp. and S. aureus), cervical edema in the region of the musculature associated with pipping behavior, glomerulonephropathy, pneumonia, intestinal hemorrhage, and lymphoid depletion. One chick was assist-hatched due to concerns for an inability to pip given the age of the egg. All 6 chicks that hatched in subsequent breeding seasons had either an open umbilicus or an exterior yolk sac. These chicks lived between 1 and 60 days, and these animals received supportive care including surgical ligation of the yolk sac, daily wound care of an open umbilicus, and antibiotic, fluid, and nutritional support. One chick was confirmed on histopathology to have a developmental anomaly resulting in exteriorized tissue from the umbilicus site, while another chick developed a gastrointestinal obstruction. All chicks showed some evidence of omphalitis, yolk sacculitis, stress, and sepsis on histopathology.

Nutritional deficiencies can play a role in neonatal pathology, including hypovitaminosis E.² All adult breeding pairs were fed a variety of capelin, sardines, and silversides supplemented with Thiamin-E paste (Mazuri®) and Vita-Zu Small Bird Tablets (Mazuri®). Serum levels of vitamin E, vitamin A, cobalt, copper, manganese, molybendum, zinc, selenium, and iron were measured in egg-laying females. Elevations in vitamin A (average 927.7 ng/mL) and selenium (average 545 ng/mL), and decreases in iron (average 58 ng/mL) were noted in breeding females as compared to reported ranges in domestic chickens (Gallus gallus domesticus). Anti-malarial therapy has been noted to decrease folic acid synthesis.³ Areas of further investigation include macronutrient assessment, improving humidity and temperature in nest boxes to allow parent-rearing of eggs, and the effect of malarial prophylaxis on egg development.

Acknowledgements

The authors wish to thank Dr. Susan Fogelson of Fish Head Labs for pathology support, and the animal care staff of the Jacksonville Zoo and Gardens for assistance.

Literature Cited

1.  St. Leger. 2012. Nondomestic Avian Pediatric Pathology. J Vet Clin Exot Anim. 15:233–250.

2.  Dierenfield ES, Sanfort CE, Satterfield WC. 1989. Influence of diet on plasma vitamin E in captive peregrine falcons. J Wildl Manage. 53:160–164.

3.  Waller DG, Sampson AP. 2018. Medical Pharmacology and Therapeutics, 5th ed. Amsterdam: Elsevier. 581–629pp.