An investigation of Leucocytozoon in the endangered yellow-eyed penguin (Megadyptes antipodes) : a thesis presented in partial fulfilment of the requirements for the degree of Master of Veterinary Science at Massey University, Turitea, Palmerston North, New Zealand
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Date
2008
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Massey University
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Abstract
Yellow-eyed penguins have suffered major population declines and periodic mass
mortality without an established cause. On Stewart Island a high incidence of
regional chick mortality was associated with infection by a novel Leucocytozoon sp.
The prevalence, structure and molecular characteristics of this leucocytozoon sp. were
examined in the 2006-07 breeding season. In 2006-07, 100% of chicks (n=32) on the
Anglem coast of Stewart Island died prior to fledging. Neonates showed poor growth
and died acutely at approximately 10 days old. Clinical signs in older chicks up to
108 days included anaemia, loss of body condition, subcutaneous ecchymotic
haemorrhages and sudden death. Infected adults on Stewart Island showed no clinical
signs and were in good body condition, suggesting adequate food availability and a
potential reservoir source of ongoing infections. A polymerase chain reaction (PCR)
survey of blood samples from the South Island, Stewart and Codfish Island found
Leucocytozoon infection exclusively on Stewart Island. The prevalence of
Leucocytozoon infection in yellow-eyed penguin populations from each island ranged
from 0-2.8% (South Island), to 0-21.25% (Codfish Island) and 51.6-97.9% (Stewart
Island). The high prevalence on Stewart Island represented the infection of 100% of
chicks and 83% of adult yellow-eyed penguins when tested by PCR. Sequencing of
Leucocytozoon sp. DNA found similarities between infections in yellow-eyed penguin
adults and chicks, but differences to Leucocytozoon sp. DNA obtained from Fiordland
crested penguins. These findings support the suggestion of cross infection between
adults and chicks, and indicate that endemic infection in yellow-eyed penguins is
unrelated to that in Fiordland crested penguins. Examination by histology and
electron microscopy showed tissue megaloschizonts and circulating round
gametocytes. Megaloschizonts up to 440µm diameter showed an affinity for hepatic
and splenic tissue and were observed releasing occasional intact cytomeres. Round
gametocytes were observed within leucocytes in visceral sections, but not peripheral
blood smears. The morphology of Leucocytozoon sp. in yellow-eyed penguins
showed similarities to the pathogenic species L. simondi and L. sakharoffi but not L.
tawaki. A successful treatment protocol for leucocytozoonosis has not been
established, although treatment in a Fiordland crested penguin was able to suppress
parasitaemia. The role of Leucocytozoon in yellow-eyed penguins as a cause of
morbidity and mortality remains unclear. Further investigation into direct
pathogenicity, and the interaction of concurrent disease and environmental influences
is required. The findings of this thesis provide potential management
recommendations and highlight areas requiring further investigation.
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Keywords
Mass mortality, Endemic infection, Stewart Island, Teucocytozoonosis