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.

Helicobasidium purpureum (anamorph Rhizoctonia crocorum) is the causal organism of the carrot disease violet root rot, common in the Ohakune region of New Zealand. Helicobasidium purpureum has proven a difficult organism to isolate and grow in culture, confounding diagnosis of early infections. To enable early diagnosis of the disease, a conventional PCR assay was developed with the primer sequences (HelicoPurp1 and HelicoPurp2, 101bp amplicon) targeting part of the internal transcribed spacer (ITS) region of the organism. The assay detected all 15 H. purpureum isolates collected and maintained by our laboratory in pure culture. The assay was also robust enough to detect the fungi’s full range of inoculum types from the field (sclerotia, hyphae, mycelial mats and ‘black sheaths’), and was also able to detect the fungus when it was in association with plant tissues. Samples required washing, as soil inhibited this assay.

Identifying vectors of soil-borne forest pathogens is crucial in limiting disease spread. Phytophthora agathidicida causes kauri dieback disease, killing kauri (Agathis australis (D. Don) Lindl.), Aotearoa-New Zealand's largest endemic tree. Currently incurable, management focuses on spread prevention. Feral pigs (Sus scrofa) are implicated in spread, through ingestion of infected material; congeneric Phytophthora cinnamomi is known to survive pig gut passage. We investigated P. agathidicida survival of pig gut passage in a captive feeding experiment, and assessed P. agathidicida incidence in feral pig stomachs from DNA. We detected viable P. agathidicida from a kauri root retrieved from captive-fed pig faeces, providing proof of concept that pigs can internally vector P. agathidicida. However, we detected only one positive, despite processing a total of 11.2m of passaged roots and 800 millet (Pennisetum glaucum (L.) R. Br.) seeds, from 12 pigs. We did not detect P. agathidicida in any of 184 wild-caught feral pig stomachs, but did detect five other Phytophthora species including P. multivora and P. cinnamomi. Ingestion of contaminated material by feral pigs is probably a minor pathway for P. agathidicida, and a higher risk pathway for P. cinnamomi. We highlight the need to test Phytophthora species individually, as pathways of spread may be considerably different between related species.

Violet root rot (VRR), caused by the fungus Helicobasidium purpureum (anamorph Rhizoctonia crocorum), is a common problem for carrot growers in the Ohakune region of New Zealand. VRR can still be problematic even after many years of fallow, suggesting that alternative hosts may be maintaining and harbouring the disease. Seeds from a selection of common weed and pasture (ryegrass, clover and plantain) species sourced from the Ohakune area were planted into pots of steam-sterilised Ohakune soil and grown in the glasshouse. Following seedling establishment, pots were inoculated with H. purpureum. Four and a half months post inoculation, all plants were assessed visually, and then well-rinsed root samples were taken for DNA extraction and PCR testing. Of the nine weed species assessed, all tested positive for H. purpureum by PCR, and seven had visual symptoms on plants. For the twelve pasture species assessed, ten tested positive for H. purpureum by PCR, while eight had visual symptoms on plants. Some plants, in particular various clovers, plantain and dock, had numerous sclerotia on the outside of roots. These results indicate that alternate hosts in pasture or fallowed fields are capable of harbouring H. purpureum.

The influence of leaf age on infection of Actinidia species by Pseudomonas syringae pv actinidiae (Psa) was investigated using two approaches (a) inoculation of potted Hayward and Hort16A kiwifruit plants and (b) inoculation of whole leaves in a detached leaf assay Whole plants and detached leaves were spray inoculated with Psa biovar 3 (haplotype NZV; PsaV) and maintained in a saturated environment Flecking was evident on some of the leaves 8 days after inoculation Many of the flecks later became necrotic spots with halos similar to the Psa leaf infections that have been observed in the field With both methods a higher percentage of leaves that were 13 weeks of age at inoculation had flecking and spotting than did leaves of other ages Leaves that were 7 weeks or older did not show any symptoms of infection by Psa Overall leaves of Hort16A showed slightly more flecking and spotting than Hayward

In 2012 trials were established in four kauri forest sites severely affected by kauri dieback (Phytophthora agathidicida P taxon Agathis PTA) to determine the potential of phosphorous acid (phosphite) as a control tool Baseline assessments of 162 trial trees included canopy disease rating trunk lesion dimensions and lesion activity (recent bleeding/ 20cm intervals around the trunk Control trees were left untreated After 1 year half the previously injected trees were reinjected in all cases with 75 phosphite Phytotoxicity symptoms (leaf yellowing browning or leaf/twig abscission) were noted in some phosphiteinjected trees particularly where the 20 concentration was used After 3 years many more trunk lesions remained active (expressing ooze continued expansion) in untreated trees (585) than in phosphitetreated trees (08) Average lesion expansion after 3 years was 127 cm in untreated and 04 cm in phosphitetreated trees

Pseudomonas syringae pv. actinidiae (Psa) causes leaf spotting, cane and leader cankers, or death of kiwifruit vines. Growers require management strategies that minimise the spread of cankers or systemic infection, whilst also minimising canopy loss. This project investigated whether cauterising cankers or pruning beyond the visible canker had any long-term effect in containing progression of the pathogen within the vine. The study included 72 'Zesy002' (commonly known as Gold3) (Actinidia chinensis) vines on one orchard and 87 'Hayward' (A. deliciosa) vines on two orchards, in Te Puke, New Zealand. From one to 30 cane or leader cankers per vine were monitored. Cankers were either left untreated, cauterised using a gas blowtorch, or pruned 40 cm below the lowest symptom. Cankers were delineated initially and canker advance was measured after 1, 3, 7 and 12 months. In 'Hayward', pruning proved to be the most effective, and most pruning wounds callused and healed. Cankers spread only where pruning wounds had not callused and healed. Only 11% and 3% of pruned canes on the two orchards, respectively, showed canker advance after 7 months. In comparison, in cauterised and untreated vines the majority (over 80%) of cankers continued to expand, with no obvious difference between these two treatments, and many instances where cankers expanded beyond the 40-cm mark. In Gold3, canker expansion was greater than in 'Hayward'. Pruning 40 cm below the visible canker margin did not remove the infection from the cane, and cankers continued to expand, in 18.4% of cases. This compares with 27.6 and 27.8% of cankers that expanded beyond the 40-cm mark in the untreated and cauterised vines, respectively, with more than 80% of cankers expanded beyond the original canker margin. The experiments showed that pruning beyond the visible canker reduced the systemic spread of Psa more effectively than cauterising cankers or leaving them untreated.

The causal agent of kauri dieback Phytophthora taxon Agathis (PTA) poses a significant threat to kauri (Agathis australis) in northern New Zealand Groundbased field surveys have previously confirmed PTA presence at several locations across Auckland and Northland However ground surveys are limited to areas adjacent to tracks because of difficulty and cost associated with offtrack access in steep terrain along with concern about furthering spread of PTA A methodology for aerial photographic surveillance of kauri dieback was developed and implemented in Wait257;kere Ranges Hunua Ranges and adjacent forest areas Using recently developed GPS technology photographs were embedded with position data so unhealthy trees were easily located later for groundtruthing Aerial survey was found to be a time and costeffective method for surveying large inaccessible areas of forest for kauri dieback The methodology would also be applicable for detection of visible disease or damage symptoms in other canopy tree species

In kauri forest soils surveys Phytophthora taxon Agathis (PTA) P cinnamomi P multivora and P cryptogea were detected frequently In vitro and glasshouse studies determined that all four Phytophthora species produced lesions on excised kauri leaves and stems Lesion advance was significantly slower with P cinnamomi P multivora and P cryptogea than with PTA When 2yearold kauri seedlings were trunkinoculated lesion spread was rapid with PTA trunks were girdled and all trees died within 46 weeks Phytophthora cinnamomi P multivora and P cryptogea produced substantially smaller lesions than PTA no trees died and plant growth was only slightly suppressed Following soil inoculation with PTA all kauri seedlings died within 10 weeks There were no deaths following soil inoculation with P cinnamomi P multivora or P cryptogea although feeder root damage was observed and the respective pathogens were reisolated Results suggest that PTA is an aggressive pathogen and the other three species are weaker pathogens of kauri

Kauri dieback is a pest issue that is increasingly affecting kauri forests A water and soilborne pathogen Phytophthora taxon Agathis (PTA) has been identified as a causal agent of kauri dieback at multiple locations particularly within Auckland and Northland In 2008 a passive surveillance and adaptive management programme was initiated to manage the disease across the natural range of kauri Surveys were initially undertaken to determine the distribution and rate of spread of kauri dieback on private land in the Auckland region Methods to evaluate and monitor overall tree health disease symptoms and other potential contributing factors were developed Diagnostic sampling was undertaken to isolate and identify pathogens associated with kauri dieback Along with PTA other Phytophthora species and environmental stress were frequently associated with symptoms at over 400 properties inspected Further management is now required to develop control tools and mitigate further spread

Trials have been established in three Bay of Plenty kiwifruit orchards to determine the impact of blockscale breathableplastic covers on the progression of PsaV (Pseudomonas syringae pv actinidiae) in preinfected established vines and in newly grafted uninfected plants On each orchard there were three replicated covered areas each spanning four rows and five bays with the uncovered control areas adjacent Two sites with established previously infected vines showed little or no reduction in the expression of disease relative to that observed in vines in uncovered control areas No major progression of disease was observed in one of these orchards In the second there was widespread expression of PsaV symptoms postgirdling irrespective of whether they were covered or not In the third orchard uninfected grafted vines planted under the canopies of mature infected vines remained relatively disease free compared with similar vines not under cover where numerous leaf spots and secondary symptoms were observed The trials will continue to be monitored

Phytophthora taxon Agathis (PTA) threatens the health and survival of New Zealand kauri trees Longterm trials testing phosphite (phosphorous acid) for control of PTA in infected kauri were established in four Auckland and Northland forest sites in January 2012 All 160 trial trees (girths from 40 to 120 cm) showed symptoms of PTA infection At the start of the trial tree canopy health was assessed basal trunk lesions were measured and marked and reference photographs were taken Trees were injected with either high (20) or low (75) concentrations of phosphite (20 ml/20cm trunk circumference) or left untreated Treatment with the higher concentration resulted in moderate phytotoxicity symptoms with leaf yellowing browning and some premature twig drop These symptoms were no longer apparent in most trees after a few months Reassessments of canopy health and trunk lesion activity or spread are being made 6monthly One year after initial treatment application canopy health was generally similar to or slightly worse than at the start of the trial (using baseline photographs) regardless of treatment On average more lesions were active (expressing fresh ooze) in untreated controls than in phosphitetreated trees Lesion advance was greater in untreated trees than in phosphiteinjected trees Phosphite applications will continue either annually or at longer intervals in various treatment regimes

The influence of leaf age on infection by Pseudomonas syringae pv actinidiae (Psa) was investigated using potted Hayward and Hort16A kiwifruit plants Leaves were spray inoculated with an isolate of Psa (haplotype NZV) at a rate of 69 108 cfu/ml Plants were maintained in a saturated environment in a plastic hot house within the confines of a containment laboratory at Plant Food Research Mt Albert Research Centre Auckland All leaves were assessed for symptoms 8 days after inoculation and thereafter at approximately weekly intervals for 4 weeks At each assessment changes in symptom expression on the leaves were recorded Flecking was evident on some of the leaves 8 days after inoculation Many of these flecks later became necrotic spots with halos similar to Psa infections that have been observed in the field A higher percentage of leaves that were 23 weeks of age at inoculation had flecking and spotting than leaves of other ages Leaves that were 7 weeks or older did not show any symptoms of infection by Psa Overall leaves on Hort16A showed slightly more flecking and spotting than Hayward

Violet root rot (VRR) caused by Rhizoctonia crocorum causes substantial economic losses and threatens the longterm viability of the carrot industry in the Ohakune region New Zealand Previous attempts at control have been largely unsuccessful Pre planting soil fumigation trials were carried out in two heavily infested Ohakune carrot fields In 2007/08 chloropicrindichloropropene (TriForm 60) and metam sodium (Fumasol) failed to provide a commercially useful level of VRR control Deficiencies in fumigant placement and distribution and inadequate sealing of the soil for gas retention were identified as likely reasons for the failure Modified application techniques improved soil sealing and different combinations of fumigants in the 2008/09 season provided excellent control in some treatments At Site A VRR incidence was 06 and 667 in the chloropicrinmetam sodium and chloropicrin treatments respectively compared with 986 incidence in untreated control plots At Site B VRR incidence was 23 and 38 in the chloropicrindichloropropene and combined chloropicrindichloropropene metam sodium treatments with and without plastic covering respectively compared with 415 in untreated control plots

Specific apple replant disease (SARD) is a problem in replanted apple orchards worldwide. The causative agents in New Zealand are thought to be biotic in nature. The effect of commercial Trichoderma bio-inoculants on SARD symptoms was investigated in two independent experiments in two SARD soils and one non-SARD soil treated with chloropicrin, commercial Trichoderma pellet and powder formulations, and a nitrogen, phosphorus and potassium (NPK) supplement. Rooted stool-bed cuttings of ungrafted ‘M.26’ apple rootstocks grown in the SARD soils treated with chloropicrin fumigation produced significantly more biomass over the growing season with reduced root disease symptoms compared with untreated controls. The plants grown in the SARD soils treated with the Trichoderma pellet formulations or the NPK supplement also exhibited a significant improvement in growth, with no reduction in root disease symptoms. Similar responses were noted when dead (autoclaved) Trichoderma pellet formulations or unformulated pellets were applied. No disease reduction or growth improvement was observed in the plants grown in soil treated with a Trichoderma spore powder (without the standard carrier included in the pellet formulations). Thus, the improved growth response associated with the Trichoderma treatments correlated with an additive associated with the pellet formulation, and not to the presence of ‘live’ Trichoderma inoculum.