Recent Administration of Iodinated Contrast Renders Core Infarct Estimation Inaccurate Using RAPID Software.

BACKGROUND AND PURPOSE: Automated CTP software is increasingly used for extended window emergent large-vessel occlusion to quantify core infarct. We aimed to assess whether RAPID software underestimates core infarct in patients with an extended window recently receiving IV iodinated contrast. MATERIALS AND METHODS: We reviewed a prospective, single-center data base of 271 consecutive patients who underwent CTA ± CTP for acute ischemic stroke from May 2018 through January 2019. Patients with emergent large-vessel occlusion confirmed by CTA in the extended window (>6 hours since last known well) and CTP with RAPID postprocessing were included. Two blinded raters independently assessed CT ASPECTS on NCCT performed at the time of CTP. RAPID software used relative cerebral blood flow of <30% as a surrogate for irreversible core infarct. Patients were dichotomized on the basis of receiving recent IV iodinated contrast (<8 hours before CTP) for a separate imaging study. RESULTS: The recent IV contrast and contrast-naïve cohorts comprised 23 and 15 patients, respectively. Multivariate linear regression analysis demonstrated that recent IV contrast administration was independently associated with a decrease in the RAPID core infarct estimate (proportional increase = 0.34; 95% CI, 0.12-0.96; P = .04). CONCLUSIONS: Patients who received IV iodinated contrast in proximity (<8 hours) to CTA/CTP as part of a separate imaging study had a much higher likelihood of core infarct underestimation with RAPID compared with contrast-naïve patients. Over-reliance on RAPID postprocessing for treatment disposition of patients with extended window emergent large-vessel occlusion should be avoided, particularly with recent IV contrast administration.

Reduced Jet Velocity in Venous Flow after CSF Drainage: Assessing Hemodynamic Causes of Pulsatile Tinnitus.

BACKGROUND AND PURPOSE: Idiopathic intracranial hypertension is commonly associated with transverse sinus stenosis, a venous cause of pulsatile tinnitus. In patients with idiopathic intracranial hypertension, CSF drainage via lumbar puncture decreases intracranial pressure, which relieves the stenosis, and may provide at least temporary cessation of pulsatile tinnitus. The objective of this study was to evaluate changes in venous blood flow caused by lowered intracranial pressure in patients with pulsatile tinnitus to help identify the cause of pulsatile tinnitus. MATERIALS AND METHODS: Ten patients with suspected transverse sinus stenosis as a venous etiology for pulsatile tinnitus symptoms underwent MR imaging before and after lumbar puncture in the same session. The protocol included flow assessment and rating of pulsatile tinnitus intensity before and after lumbar puncture and MR venography before lumbar puncture. Post-lumbar puncture MR venography was performed in 1 subject. RESULTS: There was a lumbar puncture-induced reduction in venous peak velocity that correlated with the opening pressure (r = -0.72, P = .019) without a concomitant reduction in flow rate. Patients with flow jets had their peak velocity reduced by 0.30 ± 0.18 m/s (P = .002), correlating with a reduction in CSF pressure (r = 0.82, P = .024) and the reduction in subjectively scored pulsatile tinnitus intensity (r = 0.78, P = .023). The post-lumbar puncture MR venography demonstrated alleviation of the stenosis. CONCLUSIONS: Our results show a lumbar puncture-induced reduction in venous peak velocity without a concomitant reduction in flow rate. We hypothesize that the reduction is caused by the expansion of the stenosis after lumbar puncture. Our results further show a correlation between the peak velocity and pulsatile tinnitus intensity, suggesting the flow jet to be instrumental in the development of sound.

MR Venous Flow in Sigmoid Sinus Diverticulum.

BACKGROUND AND PURPOSE: Case reports demonstrate that coiling of a sigmoid sinus diverticulum can treat pulsatile tinnitus. We hypothesized that MR imaging 4D flow and computational fluid dynamics would reveal distinct blood flow patterns in the venous outflow tract in these patients. MATERIALS AND METHODS: Patients with pulsatile tinnitus of suspected venous etiology underwent MR imaging at 3T, using venous phase contrast-enhanced MR angiography, 4D flow, and 2D phase contrast. The contrast-enhanced MRA contours were evaluated to determine the presence and extent of a sigmoid sinus diverticulum. Computational fluid dynamics analysis was performed using the 4D flow inlet flow and the luminal contours from contrast-enhanced MRA as boundary conditions. In addition, computational fluid dynamics was performed for the expected post treatment conditions by smoothing the venous geometry to exclude the sigmoid sinus diverticulum from the anatomic boundary conditions. Streamlines were generated from the 4D flow and computational fluid dynamics velocity maps, and flow patterns were examined for the presence of rotational components. RESULTS: Twenty-five patients with pulsatile tinnitus of suspected venous etiology and 10 control subjects were enrolled. Five (20%) of the symptomatic subjects had sigmoid sinus diverticula, all associated with an upstream stenosis. In each of these patients, but none of the controls, a stenosis-related flow jet was directed toward the opening of the sigmoid sinus diverticulum with rotational flow patterns in the sigmoid sinus diverticulum and parent sigmoid sinus on both 4D flow and computational fluid dynamics. CONCLUSIONS: Consistent patterns of blood flow can be visualized in a sigmoid sinus diverticulum and the parent sinus using 4D flow and computational fluid dynamics. Strong components of rotational blood flow were seen in subjects with sigmoid sinus diverticula that were absent in controls.

First Report of Stem Rot in Canola Caused by Sclerotinia minor in Western Australia.

Canola (Brassica napus L.) is a significant oilseed break crop in Western Australia. In late October 2012, canola plants (cv. Jackpot) showing typical symptoms of stem rot with bleached appearance and fluffy white fungal growth on the infected tissues were observed in an experimental plot at Katanning, Western Australia. Severely affected plants were lodged with partially filled pods and shriveled seeds. Small, irregular sclerotia (<2 mm) were found inside the plants and were more concentrated in the root and basal stem than in the upper stem regions. Ten sclerotia from three symptomatic plants were surface sterilized with 1.25% NaOCl for 1 minute, rinsed twice in sterile distilled water and plated on potato dextrose agar (PDA) supplemented with 10 mg liter-1 Aureomycin. Plates were incubated under a black light at 22 ± 2°C. Sclerotinia minor Jagger was consistently isolated as identified by colony morphology, abundant sclerotia on PDA, and size of sclerotia <2 mm (3). A pathogenicity test was conducted on six 7-week-old canola plants cv. Tawriffic. Mycelial plugs (5 mm diameter) were excised from the margins of actively growing 3-day-old cultures and attached on to the 2nd and the 4th internodes of the main stem with Parafilm. Three plants inoculated with agar plugs without mycelium served as controls. Following inoculation, the plants were kept in a misting chamber for 48 h and then transferred to a growth room at 18 ± 2°C with a 12-h photoperiod. Typical lesions of stem rot similar to those observed in the field were noticed 3 days after inoculation. Within a week, all the inoculated plants were completely girdled by the lesions with stems breaking off and collapsing at the point of inoculation. Small sclerotia formed within lesions on the outside of the diseased stems. S. minor was reisolated from the stems of symptomatic plants, fulfilling Koch's postulates. No symptoms developed on the control plants. S. minor has previously been reported on host plants other than canola in Western Australia (4), canola petals in New South Wales, Australia (2), and also on canola stems in Argentina (1). To our knowledge, this is the first report of occurrence of S. minor on canola in Western Australia. Although S. sclerotiorum is the predominant species causing stem rot in canola in Western Australia, S. minor has the potential to cause significant yield losses under favorable environmental conditions. Correct identification and monitoring a shift in pathogens is essential for implementing effective management strategies and breeding resistant varieties. References: (1) S. A. Gaetán et al. Plant Dis. 92:172, 2008. (2) T. Hind-Lanoiselet et al. Aust Plant Pathol. 30:289, 2001. (3) L. M. Kohn. Phytopathology 69:881, 1979. (4) R. Shivas. J. Royal. Soc. Western Australia 72:1, 1989.

First Report of Club Root Caused by Plasmodiophora brassicae on Canola in Australia.

In 2009, a disease survey was conducted in 97 commercial canola (Brassica napus L.) fields in Western Australia by the Department of Agriculture and Food, Western Australia (DAFWA). In about 20% of the fields from the northern agricultural region of Western Australia, small patches were observed where canola plants showed symptoms of stunting and wilting. These plants were collected and roots of affected plants were washed thoroughly and examined for the presence of root disease. Small galls and clublike structures were observed on the secondary roots and sometimes on the main root of the affected plants. Examination of thin free hand sections from the root galls revealed that several cortical cells were enlarged and full of resting spores. The diameter of resting spores ranged between 2.5 and 3.0 µm. Plasmodia and zoosporangia were also observed in the root hairs. The identity of Plasmodiophora brassicae Woronin was confirmed by PCR using a modified method of Cao et al. 2007 (1). DNA from spores and slices of the galls of 14 different samples were extracted using DNeasy plant mini kit (QIAGEN Australia) as per manufacturer's instructions. Samples were disrupted by placing them into MPBIO tube A and placed in the Fast Prep machine at speed of 6 ms-1 for 40 s. This was repeated twice. The species-specific primers TC1F (5'-GTGGTCGAACTTCATTAAATTTGGGCTCTT-3')/TC1R (5'-TTCACCTACGGAACGTATATGTGCATGTGA-3') and TC2F (5'-AAACAACGAGTCAGCTTGAATGCTAGTGTG-3')/TC2R (5'-CTTTAGTTGTGTTTCGGCTAGGATGGTTCG-3') were used (1). The primers TC1F and TC1R failed to produce a PCR product of 548-bp size but using the primers TC2F and TC2R the PCR reaction resulted in a 519- bp fragment. Seven out of 14 samples gave positive results for P. brassicae with primers TC2F and TC2R. This indicates that the P. brassicae pathotype from Western Australia may be different than the one found in Alberta, Canada. However, pathotypes of P. brassicae from brassica vegetables from Australia have been found similar to the populations of P. brassicae present in the United States (2). Pathogenicity of P. brassicae was tested by dipping roots of five 10-day-old canola plants var. Cobbler in a spore suspension (1 × 106 resting spores/ml). Roots of five control plants were dipped in sterile water. Five weeks after inoculation, small galls were observed on the roots of three inoculated plants and the control plants remained symptomless. Resting spores were recovered from the galls developed on the roots of affected plants. Presence of P. brassicae in the affected roots was further confirmed by PCR using the method described above. To our knowledge, this is the first report of club root of canola in Australia. Club root is reported from vegetable brassicas and white mustard (Sinapis alba L.) in Australia. Club root has become a serious disease of canola in Canada since its detection in Alberta in 2006 (3). The resting spores of the fungus can survive for several years in soil, and therefore, this disease could pose a significant threat to canola production in Western Australia. References: (1) Cao et al. Plant Dis. 91:80, 2007. (2) Donald et al. Ann. App. Biol. 148:239, 2006. (3) S. Streklov et al. Can. J. Plant Pathol. 28:467, 2006.

First Report of Charcoal Rot on Canola Caused by Macrophomina phaseolina in Western Australia.

In the spring of 2006, canola (Brassica napus L.) plants suffering from wilt were observed in an experimental plot at Merredin, Western Australia. Symptoms on the affected plants were tan-brown, longitudinal streaks along the main stem and on some lateral branches. Lesions on the stem were predominantly unilateral but sometimes covered the entire stem. Some of the lateral branches were completely wilted, and if present, pods were either shriveled or contained small seed. At the base of the stem, the lesions were grayish brown streaks that caused longitudinal splitting of the stem base. Small spherical (55 to 75 µm in diameter) and elongated (75 to 120 µm long) microsclerotia were seen in the pith and vascular region. Roots appeared to be symptomless, but upon removing the epidermis, grayish streaks were also seen on the roots and small sclerotia were observed in the pith and the vascular region of roots. One hundred and four small pieces (1 to 2 cm) of stem and root from 10 symptomatic plants were surface sterilized with 1.25% NaOCl, rinsed twice in sterile distilled water, and plated on potato dextrose agar (PDA) supplemented with 10 ppm of aureomycin. These were incubated under a blacklight at 22°C. Macrophomina phaseolina (Tassi) Goid. was isolated from 80% of the pieces as identified by colony morphology and the size of microsclerotia that ranged between 50 and 190 µm (3). Eight-three isolates were obtained. None of the isolates produced pycnidia on PDA. However, pycnidia (100 to 190 µm) with pycnidiospores (17.5 to 30 × 7.5 to 10 µm) were produced on the affected stems collected from the field. Pathogenicity tests with one of the isolates were conducted on seven 2-week-old canola plants (cv. Stubby). Three uninoculated plants served as the control. Roots of 2-week-old plants were dipped in an aqueous conidial suspension (1 × 104 conidia/ml) of M. phaseolina for an hour while roots of control plants were dipped in sterile water. Inoculated and control plants were repotted in separate pots and transferred to a glasshouse. A week after inoculation, M. phaseolina produced chlorosis of the leaves, and subsequently, complete wilting and death of the inoculated plants. M. phaseolina was successfully reisolated from roots and stems of symptomatic plants. No symptoms developed on the control plants. Pathogenicity was also tested by soaking seeds of cv. Stubby with an aqueous conidial suspension of M. phaseolina for one-half hour and incubating on agar media after drying. Germinating seeds were colonized by the growing mycelium and seedlings were completely killed within a week. Abundant microsclerotia were produced on the dead seedlings. M. phaseolina has been previously reported on canola in the United States (1) and Argentina (2) and more recently has been reported on canola in eastern Australia (4). To our knowledge, this is the first record of occurrence of M. phaseolina on canola in Western Australia and its impact on canola yield needs to be determined. References: (1) R. E. Baird et al. Plant Dis. 78:316, 1994. (2) S. A. Gaetán et al. Plant Dis. 90:524, 2006. (3) P. Holliday and E. Punithalingam. Macrophomina phaseolina. No. 275 in: Descriptions of Plant Pathogenic Fungi and Bacteria. CMI, Kew, Surrey, UK, 1970. (4) M. Li et al. Aust. Plant Dis. Notes 2:93, 2007.

Epidemiology of Blackleg (Leptosphaeria maculans) of Canola (Brassica napus) in Relation to Maturation of Pseudothecia and Discharge of Ascospores in Western Australia.

ABSTRACT The timing of maturation of pseudothecia and discharge of ascospores of the blackleg fungus (Leptosphaeria maculans) is critical in relation to infection early in the cropping season of canola. During 1998 to 2000, development of pseudothecia was investigated on residues of the previous year's canola crop collected from four agroclimatically different locations: Mount Barker (southern high rainfall), Wongan Hills (central medium rainfall), Merredin (central low rainfall), and East Chapman (northern low rainfall) in Western Australia. The pseudothecia matured on residues at different times after harvest in various regions. In general, pseudothecia maturity occurred earlier in the high-rainfall areas than in medium- and low-rainfall areas. An ascospore discharge pattern was investigated from residues of crop from the previous year (6-month-old residues) at three locations-Mount Barker, Wongan Hills, and East Chapman in Western Australia-and from 18-month-old residues that were burnt and raked in the previous year at Mount Barker and East Chapman. Ascospore discharge commenced earlier in high-rainfall (>450 mm) areas (Mount Barker) and late in northern low-rainfall (<325 mm) areas (East Chapman). The major ascospore showers took place during May (late autumn) and June (early winter) at Mount Barker and during July and August (mid- to late winter) at East Chapman. The number of ascospores discharged was extremely low at East Chapman compared with Mount Barker. At both locations, the number of ascospores discharged from 18-month-old residues that were raked and burnt in the previous year were only approximately 10% of those discharged from previous year's residues left undisturbed. The discharge of ascospores on any given day was negatively correlated with accumulated temperatures, maximum temperature, evaporation, minimum and maximum soil temperatures, and solar radiation and was positively correlated with the minimum temperature, rain, and minimum relative humidity. This is the first report describing how pseudothecia mature on residues in different rainfall areas in Western Australia, and it potentially can be used in developing a forecasting system to avoid the synchronization of major ascospore showers with the maximum susceptibility period of canola seedlings.

Strains of Leptosphaeria maculans with the Capacity to Cause Crown Canker on Brassica carinata are Present in Western Australia.

Blackleg, caused by Leptosphaeria maculans (Desm.) Ces. et de Not., is the most important disease of canola (Brassica napus L.) in Australia, Europe, Canada, and North America (2). During the early 1990s, new cultivars of canola with resistance to blackleg were released in Australia. Despite good adult-plant resistance, these cultivars still suffered significant yield losses from blackleg under high disease pressure. Potential new sources of blackleg resistance such as B. nigra L., B. carinata L., and Sinapis alba L. are being evaluated. B. carinata is believed to be highly resistant to blackleg by virtue of its B-genome. However, some L. maculans isolates that can attack B. carinata have been reported from Germany (1). During the 2003 growing season, 22 isolates of L. maculans were collected from different canola-growing areas of Western Australia and tested for their reaction on 24 seedlings of each of various Brassica genotypes, including B. carinata, in a controlled environment chamber. Twenty-four seeds per genotype were sown in 100-ml plastic pots (12 seeds per pot) and both cotyledons of 10-day-old seedlings were wound inoculated with a conidial suspension (1 × 107 conidia/ml) of each isolate of L. maculans. Disease assessments were made 2 weeks after inoculation. The majority of isolates induced a noninvasive hypersensitive reaction on B. carinata without pycnidial development. However, four of the isolates caused lesions with abundant pycnidia on B. carinata cotyledons. The lesion size ranged between 3 and 7 mm and appeared similar to that on susceptible B. napus cultivars. B. carinata seedlings were grown for another 8 weeks in a glasshouse, and crown cankers were observed from plants inoculated with three of the four seedling virulent isolates. The severity of crown cankers as percent of stem circumference (percent disease index) ranged between 20 and 54%. Twenty-five stem pieces from mature B. carinata plants infected with one of the three isolates were plated on V8 juice agar and L. maculans was recovered from 70% of pieces. Abundant pycnidia were also observed on these stem pieces. These results have important implications for using B. carinata as a source of blackleg resistance in canola breeding. To our knowledge, this is the first report of L. maculans isolates with the capacity to induce crown cankers on B. carinata in Australia. References: (1) C. Sjöidin and K. Glimelius. J. Phytopathol. 123:322, 1988. (2) J. West et al. Plant Pathol. 51:454, 2002.

Blackleg sporacle: a model for predicting onset of pseudothecia maturity and seasonal ascospore showers in relation to blackleg of canola.

ABSTRACT A simple model has been developed to predict the onset of pseudothecia maturity and seasonal ascospore showers in relation to blackleg disease in canola, caused by the fungus Leptosphaeria maculans. The model considers a combination of two weather factors, daily mean temperature and daily total rainfall, to drive progress of maturity of pseudothecia on the infested canola stubble left from past crops. Each day is categorized as suitable or not suitable for progress of the maturation process. The onset of pseudothecia maturity occurs when approximately 43 suitable days have occurred. Following the onset of maturity, ascospore showers are triggered when daily rainfall exceeds a threshold. The model satisfactorily predicted the timing of the onset of pseudothecia maturity when tested with 3 years of field observations at four locations in Western Australia, which characteristically has a Mediterranean climate. The model also agreed reasonably well with the daily pattern of ascospore release observed in two locations. Sensitivity analysis was performed to show the relative importance of the parameters that describe the onset of pseudothecia maturity.