Neuronal Storage Disease in a Group of Captive Humboldt Penguins (Spheniscus humboldti)

Abstract

A neuronal storage disease affecting 5 captive Humboldt penguins is described. One bird died after 3 days of lethargy and anorexia. The 4 remaining birds died after a slowly progressing course of disease with signs that included lethargy, weakness, and neurologic dysfunction. Neurologic signs included dysphagia and ataxia. Gross lesions in the first animal to die consisted of hepatosplenomegaly indicative of avian malaria, which was confirmed histologically. The 4 remaining animals were mildly to moderately emaciated. Moderate to marked vacuolation of the neuronal perikarya was observed in Purkinje cells, neurons of the brainstem nuclei, and motorneurons of the spinal cord in all birds. By electron microscopy the vacuoles represented multilayered concentric lamellar structures. These findings were indicative of sphingolipidosis. All animals had been prophylactically treated for avian malaria, aspergillosis, and possible bacterial infections with chloroquine, itraconazole, and enrofloxacin. Circumstantial evidence implicates chloroquine therapy as the possible cause of the storage disease.

Malaria in penguins – current perceptions

“…Regurgitation has been noticed in African penguins when treated for several consecutive days on a mefloquine prophylactic treatment (Gyimesi, 9 August, personal communication, 2015). Wünschmann et al (2006) described a neuronal storage disease in Humboldt penguins treated prophylactically with chloroquine during the mosquito season (June until end of October or death). Chloroquine has been shown to cause the same effects in rats and miniature pigs in experimental conditions (Klinghardt et al, 1981;Dietzmann et al, 1985), hence caution is advised when employing high and long-term treatment with this drug.…”

Giant axonal neuropathy–like disease in an Alexandrine parrot (Psittacula eupatria)

“…14 Axonopathies in birds most commonly result from exposure to toxins such as organophosphates and heavy metals, although a hereditary axonopathy characterized by reduced axonal size has been documented in neurofilament-deficient quail. 22 Giant axonal neuropathy is a rare condition caused by a heterogeneous range of recessive defects in the gigaxonin (GAN) gene. 3 Gigaxonin regulates neurofilament degradation by the ubiquitin-proteasome pathway, and defects in gigaxonin expression lead to accumulation of neurofilaments within axons.…”

“…Lysosomal storage disease with neurological involvement has also been diagnosed in emus 15 and Humboldt penguins. 22 A number of nutritional deficiencies may induce neurological degeneration in birds, in particular encephalomalacia associated with vitamin E deficiency, 5 and peripheral neuropathy and myelinopathy caused by riboflavin deficiency. 14 Axonopathies in birds most commonly result from exposure to toxins such as organophosphates and heavy metals, although a hereditary axonopathy characterized by reduced axonal size has been documented in neurofilament-deficient quail.…”

“…14 Axonopathies in birds most commonly result from exposure to toxins such as organophosphates and heavy metals, although a hereditary axonopathy characterized by reduced axonal size has been documented in neurofilament-deficient quail. 22…”

A novel gyrovirus associated with a fatal respiratory disease in yellow-eyed penguin (Megadyptes antipodes) chicks

“…During the 2020 and 2021 seasons, 15% and 23% of the chicks that were monitored on the mainland died as a result of RDS, respectively. Although clinical symptoms are highly suggestive, there are a number of potential causes of respiratory disease in young penguins (2, 28–31). At present, RDS is highly suspected on post-mortem with grossly visible dark pink to purple lungs with extensive haemorrhage identifiable on cut surface and histological examination provides further confirmation.…”