Kauri (Agathis australis), which is one of the world's largest and longest‐living conifer species, is under threat from a root and collar dieback disease caused by the oomycete pathogen Phytophthora agathidicida. The noted incidence of kauri dieback has increased in the past decade, and even trees >1000 years old are not immune. This disease has profound effects on both forest ecosystems and human society, particularly indigenous Māori, for whom kauri is a taonga or treasure of immense significance. This review brings together existing scientific knowledge about the pathogen and the devastating disease it causes, as well as highlighting important knowledge gaps and potential approaches for disease management. The life cycle of P. agathidicida is similar to those of other soilborne Phytophthora pathogens, with roles for vegetative hyphae, zoospores and oospores in the disease. However, there is comparatively little known about many aspects of the biology of P. agathidicida, such as its host range and disease latency, or about the impact on the disease of abiotic and biotic factors such as soil health and co‐occurring Phytophthora species. This review discusses current and emerging tools and strategies for surveillance, diagnostics and management, including a consideration of genomic resources, and the role these play in understanding the pathogen and how it causes this deadly disease. Key aspects of indigenous Māori knowledge, which include rich ecological and historical knowledge of kauri forests and a holistic approach to forest health, are highlighted.

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Parenchymal necrosis has recently been recognized as the principal determinant of the incidence of secondary infection in acute pancreatitis. Because secondary infection of pancreatic necrosis accounts for more than 80% of all deaths from acute pancreatitis, a method for determining the presence or absence of parenchymal necrosis would offer considerable prognostic and therapeutic information. Thirty seven patients with unequivocal acute pancreatitis and five normal controls were prospectively studied with intravenous bolus, contrast-enhanced computed tomography (dynamic pancreatography). In the absence of pancreatic necrosis, there were no significant differences in parenchymal enhancement between any of the following patient groups: controls (5), uncomplicated pancreatitis (20), pancreatic abscess (7), or peripancreatic necrosis (4)(p less than 0.05). On the other hand, pancreatic parenchymal enhancement was significantly reduced or absent in all six patients with segmental or diffuse pancreatic necrosis (p less than 0.05). Postcontrast pancreatic parenchymal enhancement was also found to be inversely correlated with the number of Ranson signs (p less than 0.001). Dynamic pancreatography offers prognostic information and is a safe and reliable technique for predicting the presence or absence of pancreatic parenchymal necrosis.

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