Despite significant conservation intervention, the kiwi (Apteryx spp.) is in serious population decline. To increase survival in the wild, conservation management includes rearing of young birds in captivity, safe from introduced mammalian predators. However, an increase in density
of immunologically naïve kiwi increases the risk of exposure to disease, including coccidia. Intestinal coccidiosis has recently been described in the kiwi, and although extra-intestinal coccidiosis was first recognized in kiwi in 1978, very little is known about this disease entity.
This study used archived histological tissues and reports from routine necropsies to describe the pathology of naturally occurring extra-intestinal coccidiosis. At least 4.5% of all kiwi necropsied during 1991 to 2011 (n=558) were affected by extra-intestinal coccidiosis, and it is
estimated that it caused death in 0.9 to 1.2% of kiwi in the study group. Four forms were recognized: renal, hepatic, and, less commonly, splenic and pulmonary. At necropsy, renal coccidiosis was associated with miliary white streaks and foci through the kidneys, renomegaly, and renal pallor
or congestion. Renal meronts and gametocytes were confined to the distal convoluted tubules and collecting ducts, and were associated with renal tubular necrosis and tubular obstruction. Hepatic miliary pinpoint foci were present throughout the hepatic parenchyma associated microscopically
with macromeronts measuring 304×227 µm. In two cases, clusters of splenic meronts were identified, and a similar lesion was identified in the pulmonary interstitium of another case. Juvenile, captive kiwi were most often affected with extra-intestinal coccidiosis, illustrating
an increased expression of disease with population manipulation for conservation purposes.
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Document Type: Research Article
Institute of Veterinary, Animal and Biomedical Sciences,Massey University, Palmerston North,4442, New Zealand
Institute of Natural Resources,Massey University, Palmerston North,4442, New Zealand
Publication date: April 1, 2013
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