Haemolytic fungi isolated from sago starch in Papua New Guinea.

Sago haemolytic disease (SHD) is a rare but often fatal illness linked to consumption of stale sago starch in Papua New Guinea. Although the aetiology of SHD remains unknown, mycotoxins are suspected. This study investigated whether fungi isolated from Papua New Guinean sago starch were haemolytic. Filamentous fungi and yeasts from sago starch were grown on sheep blood agar and some on human blood agar. Clear haemolytic activity was demonstrated by 55% of filamentous fungal isolates, but not by yeasts. A semi-quantitative bioassay was developed involving incubation of human erythrocytes with fungal extracts. Extracts of cultures of Penicillium, Aspergillus and Fusarium all caused rapid haemolysis in the bioassay. Partial fractionation of extracts suggested that both polar and non-polar haemolytic components had haemolytic activity in vitro. Further work is warranted to identify these metabolites and determine if they play a role in SHD.

Is Penicillium citrinum implicated in sago hemolytic disease?

Sago hemolytic disease (SHD) is an acute hemolytic syndrome affecting rural Papua New Guineans who depend on the starch of Metroxylon sagu as a staple carbohydrate. It is a suspected mycotoxicosis associated with fungal succession in stored and perhaps poorly fermented sago. Despite a mortality rate of approximately 25%, little is know about the disease. Recent studies have identified Penicillium citrinum as a possible candidate in the etiology of SHD. This is based on the frequency of isolation from sago starch and the hemolytic nature of the organism as demonstrated when cultured on sheep and human blood agar. A highly non-polar lipophilic P. citrinum fraction from C18 solid phase extraction demonstrated high hemolytic activity in a semi-quantitative assay using both mouse and human erythrocytes. When the red cell membrane proteins were subjected to sodium dodecyl-sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) separation, cleavage of protein band 3 and spectrin was demonstrated. This breach of major structural red cell proteins is consistent with the severe hemolysis found in vivo. Our findings warrant further investigation into the hemolytic activity of P. citrinum and its role as the etiological agent of SHD.