The effects of Alzheimer's and Parkinson's disease on 28-day mortality of COVID-19.

We compared the prognosis of inpatients with a known diagnosis of Alzheimer's or Parkinson's disease who have COVID-19 infection with other hospitalized patients with COVID-19. Our cohort study started in October 2020 and ended in May 2021 and included inpatients with COVID-19 infection who were admitted to hospitals. From a total of 67,871 patients with a confirmed diagnosis of COVID-19, a sample of 3732 individuals were selected of which 363 had Alzheimer's, and 259 had Parkinson's disease. All patients had both positive RT-PCR test and positive chest CT for COVID-19. The outcome was dead within 28 days of admission and the predictors were a large number of demographic and clinical features, and comorbidities recorded at patients' bedside. Mortality were 37.5%, 35.1%, and 29.5% in patients with Alzheimer's disease, Parkinson's disease; and in other patients, respectively. The hazard ratio for Alzheimer's disease was 1.27 (95% CI, 1.06-1.53, p=0.010) and for Parkinson's disease was 1.17 (95% CI, 0.94-1.46, p=0.171). Age was a predictor of mortality, hazard ratio=1.04 (95% CI, 1.03-1.05, p<0.001). Patients with Alzheimer's disease and COVID-19 infection were older and more likely to have a loss of consciousness on admission (both p≤0.001). We concluded that inpatients with Alzheimer's disease have an increased risk for 28-day mortality from COVID-19 and healthcare settings should be ready to provide critical care for them such as early intubation and immediate O2 therapy. However, Parkinson's disease does not significantly predict higher mortality of COVID-19.

First Report of Xiphinema rivesi (Nematoda, Longidoridae) in Washington State.

Dagger nematode, Xiphinema rivesi Dalmaso, 1969 reportedly transmits several viruses in North America and Europe (2) leading to severe yield reduction in crops. Soil samples were collected in March 2013 during a survey of cherry orchards in Chelan County, WA; these historically suffer from cherry rasp leaf disease, caused by Cherry rasp leaf virus (CRLV) (genus Cheravirus). Soil samples were transported to the WSDA nematology laboratory in Prosser, WA, where 250-cc subsamples were processed using sucrose centrifugal flotation (1). Dagger nematodes were hand-picked and stored in 0.1% sodium chloride before being sent to the USDA-ARS Nematology Laboratory in Beltsville, MD, for morphological and molecular identification. The morphological and molecular analysis of adult females identified the dagger nematode species as Xiphinema rivesi Dalmaso, 1969 (4). Morphological characters used for identification included female body, and total stylet length (odontostyle and odontophore), location of guiding ring from oral aperture, head and tail shape, various tail measurements, and vulva percentage in relation to body length. Measurements of females (n = 10) include a mean body length of 1,902 ± 162.4 (1,832 to 2,203) µm, odontostyle 83 ± 3.5 (80 to 90) µm, odontophore 54.8 ± 4.2 (50 to 65) µm, total stylet 137.8 ± 4.2 (130 to 145) µm, guiding ring from oral aperture 70 ± 5.1 (60 to 75) µm, tail 30.8 ± 2.5 (27.5 to 35.0) µm, body diameter at anus 24.7 ± 1.7 (22 to 28) µm, J (hyaline portion of tail) 6.0 ± 0.9 (5.0 to 7.5) µm, body diameter at beginning of J 8.5 ± 1.0 (7.5 to 10.5) µm, body diameter at 5 µm from tail terminus 7.5 ± 0.2 (7.0 to 8.0) µm, and V% 52.2 ± 1.8 (49.4 to 55.0) µm. Molecular diagnosis of X. rivesi was confirmed after DNA was extracted from two individual nematodes by mechanical disruption with a micro knife in 20 µl worm lysis buffer containing 500 mM KCl, 100 mM Tris-Cl (pH8.3), 15 mM MgCl2, 10 mM dithiothreitol (DTT), 4.5% Tween 20, and 0.1% gelatin. DNA extracts were stored at -80°C until needed, then thawed, 1 µl proteinase K (from 2 mg/ml stock) was added, and the tubes were incubated at 60°C for 60 min, followed by 95°C for 15 min. The 28S large ribosomal D2-D3 expansion segment was amplified with D2A (5'-ACAAGTACCGTGAGGGAAAGTT-3') and D3B (5'-TCGGAAGGAACCAGCTACTA-3'), and the internal transcribed spacer (ITS) region was amplified with primers TW81 (5'-GTTTCCGTAGGTGAACCTGC-3') and AB28 (5'-ATATGCTTAAGTTCAGCGGGT-3'), as previously described (3). To verify the identity of the sequences generated from PCR, sequenced products were subjected to a database search using BLAST. Sequences from the 28S region were >99% identical to several sequences of X. rivesi sampled from Spain (GenBank Accessions JQ990038, JQ990039, HM921357, and HM921358). Sequences from the ITS region were 97 to 98% identical to X. rivesi sequences (FR878063 to FR878066) obtained from the host Vitis vinifera from Italy. To the best of our knowledge, this is the first report of this nematode from the Washington. The quick and persistent spread of CRLV in most of the orchards visited calls for concern and there is need for urgent control measures against this vector nematode. References: (1) W. R. Jenkins. Plant Dis. Rep. 48:692, 1964. (2) S. Sirca et al. Plant Dis. 91:770, 2007. (3) Skantar et al. J. Nematol. 44:58, 2012. (4) M. R. Wojtowicz. et al. J. Nematol. 14:511, 1982.

Weed Hosts of Globodera pallida from Idaho.

The potato cyst nematode, Globodera pallida (PCN), a restricted pest in the United States, was first reported in Bingham and Bonneville counties of Idaho in 2006 (1). The U.S. government and Idaho State Department of Agriculture hope to eradicate it from infested fields. Eradicating PCN will require depriving the nematodes of their hosts over a protracted time period. Functional eradication might be achieved with relatively high, proven to be efficacious dosages of soil fumigants. The presence of host weeds of PCN can play a significant role in the success of the eradication program. To determine the host status of common weeds found in potato fields of the Pacific Northwest, host suitability tests were conducted in a secured greenhouse located at the University of Idaho at Moscow. Reproduction of PCN on nine weeds including hairy nightshade (Solanum physalifolium formerly S. sarrachoides) and cutleaf nightshade (S. triflorum) (biotypes from Idaho and Washington), black nightshade (S. nigrum) (Washington biotype), bittersweet nightshade (S. dulcamara) (Idaho biotype), redroot pigweed (Amaranthus retroflexus), kochia (Kochia scoparia), and common lambsquarters (Chenopodium album) were compared with reproduction on Desiree, Russet Burbank (known hosts), and Santé (poor host) potatoes (S. tuberosum). Plants were grown in 10-cm-diameter clay pots containing sandy loam soil previously fumigated with methyl bromide and inoculated with 10 to 150 cysts that were either collected from infested fields or raised in the secured greenhouse (ample diapause period elapsed). Treatments were replicated five times and each trial lasted 3 months. Cysts were extracted from soil with a Fenwick can, and the reproductive factor (RF = final cyst count ÷ initial inoculum) was determined. While both biotypes of hairy nightshade were suitable hosts of PCN (161-668 ÷ 150; RF = >1), cutleaf biotypes, black, and bittersweet nightshades were poor hosts (1-108 ÷ 150; RF = <1). Russet Burbank (77 ÷ 40; RF = 1.9) and Desiree (21-119 ÷ 75; RF = >1) proved to be suitable hosts and Santé (1-20 ÷ 150; RF = <1) a poor host of Idaho PCN. Although some cysts were recovered from pots containing the remaining weed species, they may have been part of the original inoculum. The significance of nightshade species (whether suitable or poor hosts) in eradication of potato cyst nematode from infested fields cannot be overemphasized. Reference: (1) A. M. Skantar et al. J. Nematol. 39:133, 2007.

Independent resistant reactions expressed in root and tuber of potato breeding lines with introgressed resistance to Meloidogyne chitwoodi.

Resistance to Meloidogyne chitwoodi was introgressed from Solanum bulbocastanum into the cultivated gene pool of potato. A single dominant gene is responsible for resistance to race 1 reproduction on the root system. An additional form of resistance was discovered in certain advanced backcross clones. A BC(5) clone, PA99N82-4, resisted invasion of tubers by available nematode juveniles whether supplied by weeds or challenged by several root resistance-breaking pathotypes. This tuber resistance is inherited as a single dominant gene and is linked to R(Mc1(blb)). Because this gene has been mapped to chromosome 11, tuber resistance genetic factors are inferred to be on the same chromosome in coupling phase. Among 153 progeny derived from crosses with PA99N82-4, 42 recombinants, comprising both resistant root/susceptible tuber and susceptible root/resistant tubers, were found while other progeny were doubly resistant (like PA99N82-4) or doubly susceptible. Therefore, the existence of two linked genetic factors controlling independently expressed traits is confirmed. The combination of the two phenotypes is likely to be a sufficient level of resistance to avoid tuber damage from circumstances that provide exogenous juveniles proximal to the tubers in the soil. These factors are weed hosts of M. chitwoodi host races and pathotypes of M. chitwoodi that overcome R(Mc1(blb)). Under field conditions, where a resistance-breaking pathotype of M. chitwoodi was present, tuber-resistant PA99N82-4 breeding line produced tubers which were commercially acceptable and not culled. A related breeding line, root resistant but tuber susceptible, and Russet Burbank were severely tuber damaged and commercially unacceptable.

Pratylenchus neglectus, P. thornei, and Paratylenchus hamatus Nematodes Causing Yield Reduction to Dryland Peas and Lentils in Idaho.

In June 2006, stunted and chlorotic plants were observed in large patches in two 40.5-ha fields of dryland peas (Pisum sativum) in Latah County, Idaho, which resulted in 90 and 75% crop loss. In the same region, a 121.4-ha field of dryland lentils (Lens culinaris) also had plants showing poor growth, wilting, and yellowing in large patches, which resulted in 40% crop loss. Two species of lesion nematodes (Pratylenchus neglectus and P. thornei) and one species of pin nematode (Paratylenchus hamatus) were extracted from rhizosphere soil and the roots of symptomatic plants from these fields. In a subsequent survey of seven dryland pea fields, under cv. Columbian, in Latah and Nez Perce counties and one dryland pea field, under cv. Small Sieve, in Latah County, plant samples had means of 551 and 2,178 mixed species of lesion nematodes per gram of dry root, respectively. Plant samples from 12 lentil fields in Latah County, six planted with cv. Red Chief and six with cv. Pardina, had means of 279 and 987 mixed species of lesion nematodes per gram of dry root, respectively. Soil samples from the same fields had a mean of 628 and 671 pin nematodes, Paratylenchus hamatus, per 250 cm3 soil for Red Chief and Pardina, respectively. Lentils cv. Pardina and peas cv. Columbian were planted separately in six pots, five seeds per pot containing 250 g of infested soil brought from the field to the greenhouse. Fumigated sandy loam soil was used as control. These assays were repeated three times. In addition, peas and lentils were planted to pots infested singly with each of the three nematode species. For this assay, nematodes were extracted from field soil, surface sterilized, and used to infest 250 g of fumigated sandy loam soil at two nematodes per gram of soil. Six plants per nematode species and an uninoculated control were used in the greenhouse assays, which were repeated three times. Nematodes in all of the assays reduced plant growth in comparison with controls; an average of 50 to 70% reduction in plant height was noted. The lesion nematode populations increased in all pots. The greenhouse assays verified the negative impact of these nematodes on growth of dryland peas cvs. Columbian and Small Sieve and lentils cvs. Red Chief and Pardina. P. neglectus, P. thornei, and Paratylenchus spp. previously have been reported from the semi-arid Pacific Northwest (1). However, to our knowledge, this is the first report attributing plant growth and yield reduction of certain cultivars of lentils and peas to these two species of lesion nematodes and pin nematodes, identified to species level as Paratylenchus hamatus. Reference: (1) R. W. Smiley et al. J. Nematol. 36:54, 2004.

Establishing a corky ringspot disease plot for research purposes.

A method to establish two experimental corky ringspot disease (CRS) plots that had no prior CRS history is described. CRS is a serious disease of potato in the Pacific Northwest caused by tobacco rattle virus (TRV) and transmitted primarily by Paratrichodorus allius. 'Samsun NN' tobacco seedlings were inoculated with viruliferous P. allius in the greenhouse before they were transplanted into the field soil at the rate of 3,000 plus seedlings/ha. Care was taken to keep soil around plants in the greenhouse and transplants in the field moist to avoid vector mortality. The vector population in the soil of one of the fields was monitored by extraction, examination under microscope and bioassay on tobacco seedlings to ascertain that they were virus carriers. Presence of virus in tobacco bioassay plants was determined by visual symptoms on tobacco leaves and by testing leaves and roots using ELISA. Although TRV transmission was rapid, there was loss of infectivity in the first winter which necessitated a re-inoculation. After two years of planting infected tobacco seedlings, 100% of soil samples collected from this field contained viruliferous P. allius. In the second field, all five commercial potato cultivars, known to be susceptible, expressed symptoms of CRS disease indicating that the procedure was successful.

A New Pathotype of Meloidogyne chitwoodi Race 1 from Washington State.

Meloidogyne chitwoodi Golden et al. is a serious pest of potato (Solanum tuberosum L.), and is widespread in the Pacific Northwest United States. M. chitwoodi is currently reported to consist of two host races and one pathotype (2,3) that are not distinguished morphologically. Host race 1 reproduces on Chantenay carrot but not on Thor alfalfa and host race 2 reproduces on alfalfa but not on carrot. Both races fail to reproduce on roots of S. bulbocastanum, a wild potato species used as a source of resistance in our breeding program (1). The resistance to race 1 in S. bulbocastanum is attributed to Rmc1(blb) gene. Pathotype 1 of race 2 breaks resistance and reproduces on S. bulbocastanum (2). We have tested resistant breeding lines repeatedly in Prosser, WA field plots infested with MC race 1 and harvested tubers free from M. chitwoodi damage. In 2004 however, tubers of some resistant lines were damaged by the M. chitwoodi population that did not cause damage in the past. Populations of M. chitwoodi were established on tomato by adding peels obtained from the infected tubers of resistant lines. The reproductive factor, final number of eggs ÷ initial inoculum, of the new population was determined on five replications of 3-week-old Chantenay carrot and Thor alfalfa. Five thousand eggs were extracted from nematode cultures reared on tomatoes and then were added around the root system of the test plants. The plants were maintained in the greenhouse for 55 days before the nematode eggs were extracted and RF (reproductive factor = final/initial population) values determined. Like the MC race 1, new populations reproduced on Chantenay carrot (RF > 1) but failed to reproduce on Thor alfalfa (RF < 0.1). Unlike MC race 1, the new populations reproduced on roots of all breeding lines that carried Rmc1(blb) gene (RF > 1). These results suggest that the selected population of M. chitwoodi in the Prosser site is a new pathotype, which is designated pathotype 1 of MC race 1. References: (1) C. R. Brown et al. Am. J. Potato Res. 83:1, 2006. (2) H. Mojtahedi et al. J. Nematol. 30:506, 1998. (3) G. S. Santo et al. Plant Dis. 69:361, 1985.

Evidence for the expression of the EGF receptor on human monocytic cells.

Several malignancies over-express the epidermal growth factor receptor, ligation of which results in cellular differentiation and multiplication. Mononuclear phagocytes secrete this cytokine and its receptor has been detected on microglial cells. This communication describes the expression (and its regulation) of epidermal growth factor receptor (EGFR) on U937 cells. We have shown that a few are EGFR-positive, with expression being up regulated by interleukin 6 (IL-6). Also, when cultured in the presence of serum with the monoclonal anti-EGFR, ICR62, U937s showed a reduced growth rate. By contrast, ICR9 caused a significant increase in cellular proliferation. Both antibodies induced cycle arrest in late G(1)/S phase. When the cells were cultured in the absence of serum, low antibody concentration (10 microg/ml) showed an early inhibitory effect on cell proliferation. By contrast, at high antibody concentrations (50 micro/ml), ICR62 significantly increased the proliferation of U937 cells. We suggest that these results provide indirect evidence for an autocrine action of EGF on U937 cells.

Genetic Analysis of Resistance to Meloidogyne chitwoodi Introgressed from Solanum hougasii into Cultivated Potato.

An accession of Solanum hougasii, a wild tuber-bearing potato species native to Mexico, was found to be resistant to races 1 and 2 of Meloidogyne chitwoodi. A resistant selection was selfed and its progeny possessed the same combined resistance uniformly. A selected resistant seedling from the selfed progeny was crossed to cultivated tetraploid potato (S. tuberosum) to form an F hybrid, and was backcrossed to cultivated tetraploid potato to form a BC population in which resistance to the two races segregated. Progeny of the BC were tested in inoculation experiments with four replicates for each progeny genotype for each race of nematode. Resistance was evaluated on the basis of extracted egg counts from the entire root system of pot-grown plants. Considering resistance to each race separately, for race 1, non-host (Rf

Effect of the Mi Gene in Tomato on Reproductive Factors of Meloidogyne chitwoodi and M. hapla.

The effect of the Mi gene on the reproductive factor of Meloidogyne chitwoodi and M. hapla, major nematode pests of potato, was measured on nearly isogenic tomato lines differing in presence or absence of the Mi gene. The Mi allele controlled resistance to reproduction of race 1 of M. chitwoodi and to one of two isolates of race 2. No resistance to race 3 of M. chitwoodi or to M. hapla was found. Variability in response to isolates of race 2 may reflect diversity of virulence genotypes heretofore undetected. Resistance to race 1 of M. chitwoodi could be useful in potato if the Mi gene were functional following transferral by gene insertion technology into potato. Since the Mi gene is not superior to RMc derived from Solarium bulbocastanum, the transferral by protoplast fusion appears to offer no advantage.

RFLP analysis of resistance to Columbia root-knot nematode derived from Solanum bulbocastanum in a BC2 population.

The mapping of resistance toMeloidogyne chitwoodi derived from Solarium bulbocastanum is reported. A population suitable for mapping was developed as follows. A somatic hybrid of nematode-resistant S. bulbocastanum and cultivated tetraploid potato was produced. This was backcrossed to tetraploid potato, and a single resistant BC1 was selected and backcrossed again to the same recurrent tetraploid parent. The mapping population consisted of 64 BC2 progeny scored for restriction fragment length polymorphic (RFLP) markers and 62 of these were evaluated for the reproductive efficiency of race 1 of M. chitwoodi. Forty-eight polymorphic RFLP markers, originally derived from tomato and mapped in diploid cultivated potato, were assigned to 12 chromosomes of S. bulbocastanum. Of the 62 progeny screened for nematode resistance, 18 were non-hosts and four were poor hosts. The rest were highly susceptible (good hosts). Analysis of the resistance (including non-hosts and poor hosts) as both a qualitative trait and as a meristic trait on which QTL analysis was applied supported the same genetic hypothesis. Genetic control was localized solely to factor(s) lying at one end of chromosome 11. The level of expression of resistance in the S. bulbocastanum parent and the resistant portion of the BC2 was essentially the same. This fact, together with the highly significant LOD scores for one end of the chromosome-11 marker array, supports a genetic model equivalent to monogenic dominant control.

Characterization of Resistance in a Somatic Hybrid of Solanum bulbocastanum and S. tuberosum, to Meloidogyne chitwoodi.

A somatic hybrid, CBP-233, between resistant Solanum bulbocastanum (SB-22) and susceptible S. tuberosum (R4) was tested for resistance to Meloidogyne chitwoodi race 1. One week after inoculation, only 0.04-0.4% of the initial inoculum (Pi, 5,000 eggs) as second stage-juveniles infected SB-22 and CBP-233 root systems, compared to 2% in R4. After 8 weeks, the number of M. chitwoodi in SB-22 and CBP-233 roots remained lower (0.3-1.5% of Pi) compared to R4, which increased from 2% to ca. 27%. Development of M. chitwoodi was delayed on SB-22 and CBP-233 by at least 2 weeks, and only half of the infective nematodes established feeding sites and matured in resistant clones compared to 99% in susceptible R4. Necrotic tissue surrounded nematodes that failed to develop in SB-22 and CBP-233. The reproductive factor (ratio of final number of eggs recovered from roots to Pi) was <0.01 for both SB-22 and CBP-233 and 46.8 for R4. Delaying inoculation of CBP-233 from 1 to 3 months after planting did not increase the chance or rate of tuber infection. Only a few M. chitwoodi developed to maturity on CBP-233 tubers and deposited a small number of eggs. SB-22 rarely produced tubers in these experiments, and like CBP-233 were resistant to M. chitwoodi. It appeared that the mechanisms of resistance to M. chitwoodi in roots and tubers of CBP-233 are similar.

Suppression of Meloidogyne chitwoodi with Sudangrass Cultivars as Green Manure.

Meloidogyne chitwoodi race 1 reproduced on Piper sudangrass (Sorghum bicolor (L.) Moench), 332 (sudangrass hybrid), and P855F and P877F (sorghum-sudangrass hybrids), but failed to reproduce efficiently on Trudan 8, Trudex 9 (sudangrass hybrids), and Sordan 79, SS-222, and Bravo II (sorghum-sudangrass hybrids). Meloidogyne chitwoodi race 2 behaved similarly and reproduced more efficiently on Piper, P855F, and P877F than on Trudan 8, Trudex 9, or Sordan 79. The mean reproductive factor for M. chitwoodi races on the poorer hosts ranged from <0.1 to 0.9 under greenhouse and field conditions. Meloidogyne hapla failed to reproduce on any of the cultivars tested. In the laboratory, leaves of each cultivar chopped and incorporated as green manure reduced the M. chitwoodi population in infested soil more than unamended or wheat green manure treatments. Trudan 8, although limited to the zone of incorporation, protected this zone from colonization of upward migrating second stage juveniles (J2) for up to 6 weeks. Leaves of Trudan 8 but not roots were effective against M. chitwoodi, and J2 appeared to be more sensitive than egg masses. Trudan 8 and Sordan 79 as green manure reduced M. chitwoodi in bucket microplots under field conditions.

Seasonal Migration of Meloidogyne chitwoodi and its Role in Potato Production.

Seasonal vertical migration of Meloidogyne chitwoodi through soil and its impact on potato production in Washington and Oregon was studied. Nematode eggs and second-stage juveniles (J2) were placed at various depths (0-180 cm) in tubes filled with soil and buried vertically or in holes dug in potato fields. Tubes were removed at intervals over a 12-month period and soil was bioassayed on tomato roots. Upward migration began in the spring after water had percolated through the tubes. Nematodes were detected in the top 5 cm of tubes within 1-2 months of burial, depending on depth of placement. Potatoes were grown in field plots for 4 or 5 months before the tubers were evaluated for infection. One hundred eggs and J2 per gram soil placed at 60 and 90 cm caused significant tuber damage at the Washington and Oregon sites, respectively. At the Washington site, inoculum placed at 90, 120, and 150 cm caused potato root infection without serious impact on tuber quality, but inoculum diluted 2-8 times and placed at 90 cm did not cause root or tuber infection. Nematode migration was dependent on soil texture; 9 days after placement at the bottoms of tubes, J2 had moved up 55 cm in sandy loam soil (Oregon) but only 15 cm in silt loam (Washington). Thus, the importance of M. chitwoodi which occur deep in a soil profile may depend on soil texture, population density, and length of the growing season.

Suppression of Root-knot Nematode Populations with Selected Rapeseed Cultivars as Green Manure.

Meloidogyne chitwoodi races 1 and 2 and M. hapla reproduced on 12 cultivars of Brassica napus and two cultivars of B. campestris. The mean reproductive factors (Rf), Rf = Pf at 55 days / 5,000, for the three nematodes were 8.3, 2.2, and 14.3, respectively. All three nematodes reproduced more efficiently (P < 0.05) on B. campestris than on B. napus. Amending M. chitwoodi-infested soil in plastic bags with chopped shoots of Jupiter rapeseed reduced the nematode population more (P < 0.05) than amendment with wheat shoots. Incorporating Jupiter shoots to soil heavily infested with M. chitwoodi in microplots reduced the nematode population more (P < 0.05) than fallow or corn shoot treatments. The greatest reduction in nematode population density was attained by cropping rapeseed for 2 months and incorporating it into the soil as a green manure.

Population Dynamics of Meloidogyne chitwoodi on Russet Burbank Potatoes in Relation to Degree-day Accumulation.

Population dynamics of Meloidogyne chitwoodi were studied for 2 years in a commercial potato field and microplots. Annual second-stage juvenile (J2) densities peaked at harvest in mid-fall, declined through the winter, and were lowest in early summer. In the field and in one microplot study, population increase displayed trimodal patterns during the 1984 and 1985 seasons. Overwintering nematodes produced egg masses on roots by 600-800 degree-days base 5 C (DD) after planting. Second-generation and third-generation eggs hatched by 950-1,100 DD and 1,500-1,600 DD, respectively, and J2 densities rapidly increased in the soil. A fourth generation was observed at 2,150 DD in 1985 microplot studies. Tubers were initiated by 450-500 DD, but J2 were not observed in the tubers until after the second generation hatched at 988-1,166 DD. A second period of tuber invasion was observed when third generation J2 hatched. The regional variation in M. chitwoodi damage on potato may be explained by degree-day accumulation in different potato production regions of the western United States.

Efficacy of Ethoprop on Meloidogyne hapla and M. chitwoodi and Enhanced Biodegradation in Soil.

Responses of egg masses, free eggs, and second-stage juveniles (J2) ofMeloidogyne hapla and M. chitwoodi to ethoprop were evaluated. The results indicated that J2 were the most sensitive, followed by free eggs and egg masses. In general, M. chitwoodi was more susceptible to ethoprop than M. hapla. Ethoprop at 7.2 mug a.i./g soil protected tomato roots from upward migrating M. chitwoodi for 5 weeks. The zone of protection was extended to 10 and 20 cm below the root zone when 3.6 and 7.2 cm water were applied over 8 days. Ethoprop at 1.8, 3.6, and 7.2 mug a.i./g soil degraded faster and killed fewer M. chitwoodi J2 in potato field soil previously exposed to ethoprop than in unexposed soil or sterilized exposed soil. The enhanced biodegradation property of the exposed soil lasted 17 months after the last application of ethoprop. The limited downward movement of ethoprop in the soil, migration of M. chitwoodi J2 into the treated zone, presence of resistant life stage(s) at the time of application, and loss of efficacy due to enhanced biodegradation may have a significant effect on the performance of ethoprop.

Differential Response of Thor Alfalfa to Meloidogyne chitwoodi Races and M. hapla.

Second-stage juveniles (J2) of races 1 and 2 of Meloidogyne chiiwoodi and M. hapla readily penetrated roots of Thor alfalfa and Columbian tomato seedlings; however, few individuals of M. chitwoodi race 1 were able to establish feeding sites and mature on alfalfa. Histopathological studies indicate that J2 of race 1 either failed to initiate feeding sites or they caused cell enlargement without typical cell wall thickening. The protoplasm of these cells coagulated, and juveniles of race 1 did not develop beyond the swollen J2 stage. A few females of race 1 fed on small giant cells and deposited a few eggs at least 20 and 30 days later than M. chitwoodi race 2 and M. hapla, respectively. Failure of race 1 to establish feeding sites was related to egression of J2 from the roots. The M. chitwoodi race 1 J2 egression from alfalfa roots was higher than egression of race 2 and M. hapla. Egression of J2 of M. chitwoodi races 1 and 2 from tomato roots was similar and higher than that of M. hapla. Thus egression plays an important role in the host-parasite relationship of M. chitwoodi and alfalfa.

Host Tests to Differentiate Meloidogyne chitwoodi Races 1 and 2 and M. hapla.

The reproductive factor (R = final egg density at 55 days / 5,000, initial egg density) of Meloidogyne chitwoodi race 2 (alfalfa race) on 46 crop cultivars ranged from 0 to 130. The reproductive efficiency of M. chitwoodi race 1 (non-alfalfa race) and M. chitwoodi race 2 was compared on selected crop cultivars. The basic difference between the two races lay in their differential reproduction on Thor alfalfa and Red Cored Chantenay carrot. M. chitwoodi race 2 reproduced on alfalfa but not on carrot. Conversely, alfalfa was a poor host and carrots were suitable for M. chitwoodi race 1. Based on host responses to M. chitwoodi races and M. hapla, a new differential host test was proposed to distinguish the common root-knot nematode species of the Pacific Northwest.

Host-parasite Relationship of Carrot Cultivars and Meloidogyne chitwoodi Races and M. hapla.

Most of the 15 carrot cultivars tested were moderate to good hosts to Meloidogyne chitwoodi race 1, whereas all except Orlando Gold were nonhosts or poor hosts for M. chitwoodi race 2. All carrot cultivars were good hosts for M. hapla. The plant weights of the carrot cultivars Red Cored Chantenay and Orlando Gold infected with either race of M. chitwoodi were significantly less than uninoculated checks in pots. Under field microplot conditions, however, detrimental effects on quality were rarely observed. M. hapla was pathogenic to both cultivars in the greenhouse and the field. The tolerance level of Orlando Gold to M. hapla was lower than Red Cored Chantenay.