Abstract

Little penguins (Eudyptula minor) dying on Phillip Island, near Melbourne, Australia, between 1992 and 1995 were necropsied to examine the relationship between the nematode parasite Contracaecum eudyptulae, Johnston and Mawson, 1942, and this host. Sixty-four percent (227 of 353) of penguins examined were killed by foxes or road traffic. Factors, including starvation, fungal pneumonia, parasitic cholangiohepatitis, coccidial nephritis, enteritis, septicemia, neoplasia, and possibly hyperthermia contributed to the deaths of the remaining 36% (126 of 353). Ages of penguins examined ranged from a few days post-hatching to mature adults, with 118 unfledged chicks (i.e., chicks that had not yet gone to sea) and 228 adults and post-fledging juveniles. Archived fixed stomachs from adult penguins collected in 1979 and 1980 were also examined for lesions.

Unfledged chicks were initially infected with C. eudyptulae when fed by regurgitation by parents. Lesions associated with C. eudyptulae infection varied in number, size, and severity. The smallest lesions were superficial foci of epithelial erosion or coagulative necrosis associated with a single nematode attached by its mouthparts to the gastric mucosa, or occasionally the esophageal mucosa. Nematodes penetrated the compound tubular glands of the proventriculus and initiated proventricular gland abscesses. Proventricular or ventricular ulceration resulted from nematodes invading the lamina propria and submucosa. Chronic infection resulted in obliteration of compound tubular proventricular glands, with fibrosis and granulomas at the sites where nematodes were embedded in the tissue. Rarely, nematodes reached the muscularis or serosa. Healed lesions with scarring and distortion of the mucosa were sometimes observed in mature penguins. Nematodes could be expelled by regurgitation, and gastric lesions were sometimes found without any worms being present, particularly in fledged birds.

Prevalence of infection with C. eudyptulae was 68% (mean intensity: 46; range: 1–374; S.D. 63.5; n=228) and the prevalence of lesions was 66%.

The prevalence of infection amongst penguins which died due to disease or starvation was 76% (mean intensity 79.1; range: 1–374; S.D. 83.0; n=89) and the prevalence of lesions was 78%. The prevalence of infection amongst penguins which were killed by foxes or road traffic was 64% (mean intensity 24.7; range: 1–186; S.D. 32.7; n=139) and the prevalence of lesions in this group was 60%.

The prevalence of infection amongst unfledged penguins was 98% (mean intensity 56.5; range: 1–244; S.D. 55.1; n=112) and the prevalence of lesions was 77%. The prevalence of infection amongst fledged penguins was 52% (mean intensity 35.8; range: 1–374; S.D. 69.9; n=114) and the prevalence of lesions was 61%. Fledged penguins which were killed by foxes or road traffic had a prevalence of infection of 49% (mean intensity 10.5; range: 1–68; S.D. 13.9; n=77) and the prevalence of lesions was 56%. Adult penguins killed in 1979 and 1980 had a prevalence of gastric lesions of 68% (72 of 106).

Other pathogenic helminths found included the tapeworm, Tetrabothrius lutzi, the liver fluke, Mawsonotrema eudyptulae, and a new schistosome.