scholarly journals First Report of the Presence of Tomato apical stunt viroid on Tomato in Sénégal

Plant Disease ◽  
2007 ◽  
Vol 91 (3) ◽  
pp. 330-330 ◽  
Author(s):  
T. Candresse ◽  
A. Marais ◽  
F. Ollivier ◽  
E. Verdin ◽  
D. Blancard
Keyword(s):  
Ivory Coast ◽  
Polyacrylamide Gel Electrophoresis ◽  
Potato Spindle Tuber Viroid ◽  
First Report ◽  
Stunt Viroid ◽  
Reverse Transcription Pcr ◽  
New Information ◽  
Leaf Chlorosis ◽  
Viroid Infection ◽  
Leaf Curl Virus

Tomato apical stunt viroid (TASVd) was initially discovered in the Ivory Coast (2). It was later reported in Indonesia and more recently was found to be responsible for severe outbreaks in protected tomatoes in Israel (1) and Tunisia (3). Although not of quarantine status, TASVd is included in the EPPO alert list. In 2005, severe arrest of apical growth and leaf chlorosis were observed in tomato samples from northern Sénégal. Tomato yellow leaf curl virus was initially identified in some samples, but since the symptoms observed were reminiscent of those associated with viroid infection, samples were analyzed by return-polyacrylamide gel electrophoresis and molecular hybridization with a Potato spindle tuber viroid (PSTVd) probe. Positive results prompted a reanalysis by reverse transcription-PCR assays specific for PSTVd or TASVd. Positive amplification was only obtained with the TASVd-specific primers (Vir+ GGGGAAACCTGGAGGAA and Vir- GGGGATCCCTGAAGGAC), and the identity of the viroid confirmed by sequencing of the amplified fragment. The complete genome sequence obtained (GenBank Accession No. EF051631) shows 94 to 96% identity with other TASVd sequences in the databases, the highest homology being with the original Ivory Coast isolate (96%, 11 mutations, and 4 indels for the 362-nt genome). These results provide new information on the diversity of TASVd and of its detrimental potential for tomato crops and represent, to our knowledge, the first report of the presence of TASVd in Sénégal. References: (1) Y. Antignus et al. Phytoparasitica 30:502, 2002. (2) C. R. Walter. Acad. Sci. 292:537, 1981. (3) J. Th. J. Verhoeven et al. Plant Disease 90:528, 2006.

scholarly journals First Report of Hop stunt viroid in Apricot in China

Plant Disease ◽  
2006 ◽  
Vol 90 (6) ◽  
pp. 828-828 ◽  
Author(s):  
Y. A. Yang ◽  
H. Q. Wang ◽  
R. Guo ◽  
Z. M. Cheng ◽  
S. F. Li ◽  
...  
Keyword(s):  
Polyacrylamide Gel Electrophoresis ◽  
Rt Pcr ◽  
First Report ◽  
Republic Of China ◽  
Stunt Viroid ◽  
Hop Stunt Viroid ◽  
Viroid Infection ◽  
Wide Range ◽  
Irregular Border ◽  
Apricot Tree

Hop stunt viroid (HSVd), a member of the family Pospiviroidae, was first described as the causal agent of hop stunt disease in Japan. It has since been found in a wide range of hosts including herbaceous and woody hosts (e.g., hop, cucumber, grapevine, citrus, plum, peach, pear, apricot, almond, and pomegranate). It was also detected and characterized in apricot where infection appears to be latent (1). The viroid occurs frequently in apricot. In southeastern Spain, the presence of HSVd was found to infect 81% of apricot trees (2). Apricots originated in China and are extensively cultivated, but HSVd infection in this host has not been reported. In September 2005, a single symptomatic apricot tree, ‘Yin Bai’, one of the most popular and widely grown cultivars in China, was discovered at the Institute of Fruit Science in Changping District in Beijing, Peoples Republic of China. Observed symptoms included a number of yellow spots with an irregular border that scattered in an irregular manner over the leaf surface. Total RNA was extracted and used for return-polyacrylamide gel electrophoresis and reverse transcription-polymerase chain reaction (RT-PCR) (4). Results of both assays were positive for HSVd. A 297-bp full-length DNA fragment was amplified by RT-PCR using primers R1 (5′-GCTGGATTCTGAGAAGAGTT-3′) complementary to HSVd residues 87–106 for the RT reaction, followed by R2 (5′-AACCCGGGGCTCCTTTCTCA-3′) complementary to HSVd residues 67–84 and forward primer F3 (5′-AACCCGGGGCAACTCTTCTC-3′) residues 79–96 for PCR. The primers are located in the strictly conserved central region of the conserved HSVd group and contain the unique endonuclease restriction site SmaI. The amplified products were cloned into pGEM-T (Promega, Madison, WI) and selected for further analysis on the basis of the results of restriction digests. Six individual clones were sequenced and three different sequences were obtained. Nucleic acid sequence (GenBank Accession No. DQ362901) obtained from one clone was 99.3% (nucleotide changes T206→C, C233→T) identical to HSVd.apr8 (GenBank Accession No. Y09349) (3). Sequence (GenBank Accession No. DQ362904) obtained from three clones was 99.7% (nucleotide change C233→T) and a third sequence (GenBank Accession No. DQ362905) obtained from two clones was 99.3% (nucleotide changes G107→A, C233→T) identical to HSVd.apr8. Further investigation is necessary to determine whether the symptoms observed are associated with the viroid infection. To our knowledge, this is the first report of HSVd isolated from apricot in China. References: (1) N. Astruc et al. Eur. J. Plant Pathol. 102:837, 1996. (2) M. C. Cañzres et al. Acta Hortic. 472:581, 1998. (3) S. A. Kofalvi et al. J. Gen. Virol. 78:3177, 1997. (4) S. F. Li et al. Ann. Phytopathol. Soc. Jpn. 61:381, 1995.

Effect of potato spindle tuber viroid on sexual reproduction and viroid transmission in true potato seed

1986 ◽  
Vol 64 (2) ◽  
pp. 336-340 ◽  
Author(s):  
M. E. Grasmick ◽  
S. A. Slack
Keyword(s):  
Fruit Development ◽  
Seed Weight ◽  
Seed Set ◽  
Transmission Rate ◽  
Pollen Viability ◽  
Polyacrylamide Gel Electrophoresis ◽  
Potato Spindle Tuber Viroid ◽  
Potato Seed ◽  
True Potato Seed ◽  
Viroid Infection

The effect of potato spindle tuber viroid infection on pollen viability, fruit-set, botanical seed set, seed weight, and seed germination in potatoes was determined. Pollen collected from the infected cultivar 'Monona' was less viable than pollen collected from healthy plants. Pollen collected from infected plants reduced seed set significantly but did not reduce fruit development or seed set in all cultivars tested. For some cultivars, infected maternal plants increased the frequency of fruit development and seed weight compared with healthy controls. True potato seed from viroid-infected 'Katahdin' × 'Superior' crosses germinated at a higher rate than did seed from comparable uninfected parents. Progeny from viroid-infected parents that exhibited potato spindle tuber viroidlike symptoms did not always test positive for potato spindle tuber viroid by bioassay or polyacrylamide gel electrophoresis tests. Efficiency of potato spindle tuber viroid detection by bioassay was highest for seedlings 2 weeks after imbibition. Potato spindle tuber viroid was detected in 100% of the progeny tested after true potato seed was stored at 4 °C for 12 years. Tests on selfed true potato seed from the viroid-infected cultivar 'Monona' demonstrated a transmission rate of 100% after subinoculation of initial bioassay plants.

scholarly journals First Report of Natural Infection of Greenhouse Tomatoes by Potato spindle tuber viroid in the United States

Plant Disease ◽  
2010 ◽  
Vol 94 (11) ◽  
pp. 1376-1376 ◽  
Author(s):  
K.-S. Ling ◽  
D. Sfetcu
Keyword(s):  
United States ◽  
Potato Spindle Tuber Viroid ◽  
The United States ◽  
Mechanical Transmission ◽  
Rt Pcr ◽  
Tomato Plants ◽  
First Report ◽  
Viroid Infection ◽  
Plant Pathol ◽  
Greenhouse Tomatoes

In April 2009, a large number of tomato plants (Solanum lycopersicum L.) grown in a commercial greenhouse facility near Los Angles, CA exhibited general plant stunting (short internodes) and foliar symptoms that included distortion, chlorosis, and scattered necrotic spotting. Over time, the leaves began to exhibit a purple color and curling. Diseased plants were often elongated and frail with spindly shoots. The disease resulted in a significant yield loss due to reduced fruit size. Disease symptoms described above are generally different from those of Pepino mosaic virus (PepMV) infection, which causes yellow mosaic or patches on leaves and marbling of fruits. The disease was initially localized in certain areas in a greenhouse despite using a number of cultural management efforts including vigorous scouting, roguing of diseased plants, and strict hygiene and cleaning practices. The disease was also observed in neighboring greenhouses by the spring of 2010. A standard panel of tests for common tomato viruses and viroids were conducted using the appropriate serological or PCR assays. Reverse transcription (RT) PCR analysis of nine symptomatic plants with pospiviroid-specific primers, Pospil-RE and Pospil-FW (3), produced an amplicon of the expected size (~196 bp) while three healthy looking tomato plants did not. Subsequently, full viroid genomic sequences were obtained through RT-PCR with primer sets specific for Potato spindle tuber viroid (PSTVd), 3H1/2H1 (2), as well as for the pospiviroid genus, MTTVd-F and MTTVd-R (1). Sequences obtained from direct sequencing of amplicons or cloned PCR products from one isolate were identical and consisted of a full viroid genome of 358 nt, which was named PSTVd-CA1 (GenBank Accession No. HM753555). BLASTn queries of the NCBI database showed that this isolate had a high sequence identity (98%) to other PSTVd isolates (i.e., EF044304, X52037, and Y09577). The disease was reproducible upon mechanical transmission (1) on three tomato ‘Moneymaker’ plants, which expressed symptoms that were similar to those on the source plants. Recovery of PSTVd on the inoculated tomato plants was confirmed by RT-PCR and sequencing. Because of its susceptibility to viroid infection, tomato ‘Moneymaker’ plants are commonly used as indicators for the study of pospiviroids, including PSTVd. Natural PSTVd infection on greenhouse tomatoes has been reported in Europe (3) and New Zealand. Although a number of reports in the United States have been published on naturally occurring PSTVd infections of potatoes, to our knowledge, this is the first report of a natural PSTVd infection on tomatoes in the United States. The exact source of the PSTVd inoculum in the current disease outbreak is unknown, but it could have been introduced from infected potato or ornamental plants (4) or through infected tomato seeds. The disease epidemic might have been enhanced by frequent hands-on activities in greenhouse tomato production and the environmental conditions (high temperature and intense lighting) in the greenhouse that favor symptom expression. References: (1) K.-S. Ling and W. Zhang, Plant Dis. 93:1216, 2009. (2). A. M. Shamloul et al. Can. J. Plant Pathol. 19:89, 1997. (3) J. Th. J. Verhoeven et al. Eur. J. Plant Pathol. 110:823, 2004. (4) J. Th. J. Verhoeven et al. Plant Pathol. 59:3, 2010.

scholarly journals First Report of Mixed Infection of Hop stunt viroid and Peach latent mosaic viroid on Peach

Plant Disease ◽  
2002 ◽  
Vol 86 (3) ◽  
pp. 329-329 ◽  
Author(s):  
M. Tessitori ◽  
A. Reina ◽  
R. La Rosa
Keyword(s):  
Polyacrylamide Gel Electrophoresis ◽  
First Report ◽  
Stunt Viroid ◽  
Phenol Extraction ◽  
Detection And Identification ◽  
Rna Probes ◽  
Hop Stunt Viroid ◽  
Fruit Disease ◽  
Specific Disorders ◽  
Peach Trees

Hop stunt viroid (HSVd), belonging to the family Pospiviroidae, was first reported in hop, but infects several plant species, including herbaceous and woody hosts (e.g., grapevine, pear, peach, plum [2], apricot, almond, and pomegranate). In grapevine and apricot, the viroid appears to be latent. However, in other species, the viroid is associated with specific disorders: hop stunt, dapple fruit disease of plum and peach (2), and citrus cachexia. During spring 2000, stunted trees exhibiting delayed budbreak were observed in peach, cv. Redhaven, orchards in Sicily. In the summer of 2000, peach leaves were collected from symptomatic trees, triturated, and used to purify total nucleic acids by phenol extraction followed by CF-11 cellulose-chromatography. Viroid RNAs were detected by sequential polyacrylamide gel electrophoresis (sPAGE) and silver staining. Citrus exocortis viroid (371 nt) and Citrus viroid IIIb (294 nt) were used as standards. Nonradioactive hybridizations with digoxigenin (DIG)-labeled, Peach latent mosaic viroid (PLMVd) and HSVd RNA probes were used in viroid detection and identification. Predicted sizes of the viroid RNAs calculated in sPAGE and DIG probe hybridization demonstrated that ‘Redhaven’ peach trees were infected with PLMVd and HSVd. These results provide the first evidence of the contemporary presence of HSVd and PLMVd in peach trees. To our knowledge, this is the first report of HSVd in peach trees in Italy. Molecular characterization of this HSVd isolate is in progress to determine the nucleotide sequence of some of the variants in the population and to decide to which of the five proposed HSVd groups (1) this isolate should be assigned. Reference: (1) S. A. Kofalvi et al. J. Gen. Virol. 78:3177, 1997. (2) T. Sano et al. J. Gen. Virol. 70:1311, 1989.

scholarly journals First Report of Chrysanthemum stunt viroid in Various Cultivars of Argyranthemum frutescens in France

Plant Disease ◽  
2011 ◽  
Vol 95 (9) ◽  
pp. 1196-1196 ◽  
Author(s):  
A. Marais ◽  
C. Faure ◽  
J. M. Deogratias ◽  
T. Candresse
Keyword(s):  
The United States ◽  
Full Length ◽  
The European Union ◽  
Rt Pcr ◽  
First Report ◽  
Chrysanthemum Stunt Viroid ◽  
Stunt Viroid ◽  
Viroid Infection ◽  
Mother Plants ◽  
The Difference

Described for the first time in Chrysanthemum indicum in the United States, Chrysanthemum stunt viroid (CSVd) was reported to naturally infect species in the Asteraceae family (1,3), as well a few hosts in other families. In May 2010 in a nursery in southwest France, the occurrence of stunted A. frutescens plantlets of cv. Butterfly showing yellow deformed leaves with terminal necrosis, which resembled the growth reduction, flower distortion or leaf necrosis symptoms reported for CSVd in Argyranthemum spp. (3), was reported. Mother plants from which the plantlets originated were asymptomatic. Reverse transcription (RT)-PCR with universal pospiviroid primers Pospi1-FW/RE (4) was performed on five symptomatic plants. A fragment of expected size (197 bp) was obtained in all cases. Viroid infection was confirmed by RT-PCR with two sets of primers: Vid-FW/RE using a 59°C annealing temperature instead of the recommended 62°C (4) and Vir-plus/minus that allows the amplification of the full-length viroid genome (2). Sequences of the three different uncloned amplicons were determined and a 355-nt contig was assembled (GenBank No. JF938538). A BLAST analysis of this full-length sequence revealed 99% identity with CSVd isolates from Chrysanthemum from Korea and Germany (GenBank Accession Nos. AF394452 and X16408). The Argyranthemum CSVd sequence differed from the Chrysanthemum ones by an A insertion at position 289 and substitutions (A to T) at positions 65 and 299. The insertion at position 289 is currently unique among CSVd sequences in GenBank. Thirty-five symptomless mother plants of A. frutescens cv. Butterfly were tested by PCR and all were shown to be infected. The difference in symptomatology observed between the mother plants and the commercial potting plants cannot be explained at this stage, but may reflect the different physiologies or growing conditions of the two kinds of plants, since these are known to affect CSVd symptoms in other hosts (1). To estimate the extent of CSVd contamination in A. frutescens, samples of 11 other cultivars originating from different nurseries were similarly analyzed. In addition to Butterfly, cvs. Sonnenstral, Maya Bofinger, Lili, Blanc Double, and Daisy Solenio were found to be infected by CSVd in the absence of clear symptomatology. The CSVd-free cultivars were Angelic Bordeaux, Dark Pink, Pink Delight, Angelic White, Dana, and Summer. The Pospi1-FW/RE amplicons from Blanc Double, Lili, and Daisy Solenio were identical to the Butterfly isolate sequence while the Maya Bofinger sequence showed one substitution (C to T) at position 256 and Sonnenstral had one substitution (T to A) at position 254. Although CSVd infection of Butterfly had been reported from Germany (3), to our knowledge, the results reported here represent the first report of CSVd in Argyranthemum for France and implicate a range of cultivars. CSVd being classified as a quarantine pest in Chrysanthemum spp. in the European Union, the finding of its significant prevalence in A. frutescens cultivars, frequently in the absence of clear symptomatology, raises the possibility that contaminated Argyranthemum may constitute a reservoir for future Chrysanthemum contamination. References: (1) I. Bouwnen and A. van Zaayen. Page 281 in: Viroids. Science Publishers, Enfield, NH, 2003. (2) T. Candresse et al. Plant Dis. 91:330, 2007. (3) W. Mentzel and E. Maiss. Z. Pflanzenk. Pfanzenschutz 107:548, 2000. (4) J. Th. J. Verhoeven et al. Eur. J. Plant Pathol. 110:823, 2004.

scholarly journals First Report of Potato spindle tuber viroid Naturally Infecting Greenhouse Tomatoes in North Carolina

Plant Disease ◽  
2013 ◽  
Vol 97 (1) ◽  
pp. 148-148 ◽  
Author(s):  
K.-S. Ling ◽  
R. Li ◽  
D. R. Panthee ◽  
R. G. Gardner
Keyword(s):  
North Carolina ◽  
Real Time ◽  
Potato Spindle Tuber Viroid ◽  
Seed Sample ◽  
Rt Pcr ◽  
Tomato Plants ◽  
First Report ◽  
Viroid Infection ◽  
Leaf Tissues ◽  
The U.S

In spring 2012, a severe disease was observed on a limited number of tomato plants (Solanum lycopersicum L.) in a research greenhouse facility in western North Carolina. The first symptoms noted were downward curling of the terminal leaves accompanied by a rough puckered darker green texture. This was followed in time by greater distortion of the leaves with pale green on leaf margins. Older leaves with symptoms developed necrosis, with necrotic spots and streaks appearing on a few fruits. On some of these affected fruits, stems, peduncles, pedicels, and sepals also showed symptoms. Infected plants were badly stunted, and fruits in the upper parts of plants displaying severe symptoms remained very small. In just a few months, the disease spread to other tomato plants inside the greenhouse. A survey in May 2012 showed a disease incidence of 18% (156 symptomatic plants out of a total of 864) in this greenhouse. Initial screenings for possible viruses using ELISA (Agdia, Elkhart, IN), as well as a reverse transcription (RT)-PCR panel of 15 common tomato viruses in our laboratory were negative. Because of the symptoms and negative results for viruses, a viroid infection was suspected. Total plant RNA was prepared using TRIzol reagent (Invitrogen, Carlsbad, CA) from leaf tissues of eight diseased plants and one seed sample. Using real-time RT-PCR developed against Potato spindle tuber viroid (PSTVd) and some related pospiviroids (1), positive signals were observed with a mean Ct = 13.24 for leaf tissues and Ct = 19.91 for the seed sample. To obtain a full viroid genome, RT-PCR using two different sets of primers, one specific for PSTVd (PSTVd-F and PSTVd-R) (2), and a universal primer set for pospiviroids (MTTVd-F and MTTVd-R) (3) was performed. RT-PCR generated amplicons with expected size of ~360 bp from all eight leaf and one seed samples, but not from a healthy control. PCR products were cloned using the TOPO TA cloning kit (Invitrogen, Carlsbad, CA). A total of 22 full genomic sequences were obtained. A multi-sequence alignment generated a consensus sequence of 360 nt, designated as NC12-01 (GenBank Accession No. JX280944). BLASTn search in the NCBI database revealed the highest sequence identity of 96.9% to Australian (AY962324) and UK (AJ583449) isolates of PSTVd and 95.9% identity to the tomato isolate of PSTVd-CA1 (HM753555). Similar disease symptoms were observed on two ‘Rutgers’ tomato plants 2 weeks post mechanical inoculation and the presence of PSTVd was confirmed by real-time RT-PCR (1). A mock-inoculated plant did not show any symptoms. In the U.S., natural infection of PSTVd on tomato was first identified in California in 2010 (3). To our knowledge, this is the first report of a natural occurrence of PSTVd on tomato in the eastern U.S. The diseased plants were contained, properly disposed of, and eradicated in this location. The broader geographic distribution of PSTVd on tomato in the U.S., and the potential latent infection in potato and a number of ornamentals (4), emphasizes the need for better plant and seed health tests for viroids on these plants. References: (1) N. Boonham et al. J. Virol. Methods 116:139, 2004. (2) H. Bostan et al. J. Virol. Methods 116:189, 2004. (3) K.-S. Ling and D. Sfetcu. Plant Dis. 94:1376, 2010. (4) R. A. Owens and J. Th. J. Verhoeven. The Plant Health Instructor. DOI: 10.1094/PHI-I-2009-0804-01, 2009.

scholarly journals First Report of Hop stunt viroid Infecting Hop in Slovenia

Plant Disease ◽  
2012 ◽  
Vol 96 (4) ◽  
pp. 592-592 ◽  
Author(s):  
S. Radisek ◽  
A. Majer ◽  
J. Jakse ◽  
B. Javornik ◽  
J. Matoušek
Keyword(s):  
North America ◽  
Direct Sequencing ◽  
First Report ◽  
Stunt Viroid ◽  
Reverse Transcription Pcr ◽  
Plant Soil ◽  
Hop Stunt Viroid ◽  
Agricultural Business ◽  
Phytosanitary Measures ◽  
La Jolla

Hop (Humulus lupulus), of the Cannabaceae family, is a dioecious perennial climbing plant that is native to Asia, North America, and Europe and is commercially grown in many countries for its use in brewing and the pharmaceutical industry. Slovenia has a more than 100-year-old hop-growing tradition and it is an important national agricultural business, with 90% of production exported to foreign markets. Since 2007, symptoms similar to Hop stunt viroid (HSVd) infection have been observed in several hop gardens with cvs. Celeia, Bobek, and Aurora in the Savinja Valley and Koroška Region. Symptoms include stunting, leaf curl, small cone formation, and dry root rot. In the first year of finding the disease, the incidence varied from 1 to 30% and increased rapidly (by as much as 10%) each subsequent year, predominantly along plant rows. For molecular identification of the pathogen, RNA was extracted from leaves and cones of symptomatic and asymptomatic plants from two different hop gardens with cv. Celeia using Tri Reagent (T9424; Sigma-Aldrich, St Louis, MO). Reverse transcription-PCR was carried out using two pairs of specific HSVd primers, HSVdI/HSVdII and HSVdeI/HSVdeII (3,4). Both primer pairs gave a single PCR product from tissue from symptomatic plants, with expected lengths of ~300 bp, but no amplicons were produced using samples from asymptomatic plants. PCR products from HSVdI/HSVdII were subjected to direct sequencing and HSVdeI/HSVdeII products were cloned in PCR Script SK (+) (Stratagene, La Jolla, CA) vector and sequenced. Five sequences (EMBL Accession Nos. HE575344, HE575345, HE575346, HE575347, and HE575348) were obtained, which revealed 96 to 99% sequence identity with various HSVd variants (grapevine, citrus, and cucumber) reported in GenBank of the National Centre for Biotechnology Information (NCBI). HSVd belonging to the Hostuviroid genus, Pospiviroidae family, has been previously reported in hop in Japan, South Korea, North America, and China (1,2). To our knowledge, this is the first report of the detection of HSVd on hop in Europe. Strict phytosanitary measures have been taken to prevent further spread and to eradicate HSVd infections. References: (1) K. C. Eastwell and T. Sano. Hop Stunt. Page 48 in: Compendium of Hop Diseases and Pests. W. F. Mahaffee et al., eds. The American Phytopathological Society, St. Paul, MN, 2009. (2) L. Guo et al. Plant Pathol. 57:764, 2008. (3) J. Matoušek et al. Plant Soil Environ. 49:168, 2003. (4) J. Matoušek et al. J. Virol. Methods 122:153, 2004.

scholarly journals Viroid Prevalence in Tunisian Citrus

Plant Disease ◽  
2004 ◽  
Vol 88 (11) ◽  
pp. 1286-1286 ◽  
Author(s):  
A. Najar ◽  
N. Duran-Vila
Keyword(s):  
Sweet Orange ◽  
Polyacrylamide Gel Electrophoresis ◽  
Sour Orange ◽  
Citrus Industry ◽  
Stunt Viroid ◽  
Hop Stunt Viroid ◽  
Washington Navel ◽  
Viroid Infection ◽  
Csiro Publishing ◽  
The Mediterranean Basin

The citrus industry in Tunisia is based mainly on the production of local cultivars of sweet orange (Citrus sinensis), common mandarin (C. reticulata), clementine (C. clementina), and lemon (C. limon). Sour orange (C. aurantium) is the only rootstock presently being used in the major growing area located at Cap Bon where 80% of citrus is being produced. The presence of tristeza disease in the Mediterranean basin is a threat to the Tunisian citrus industry, and new rootstocks giving tristeza tolerant rootstock/scion combinations are urgently needed as an alternative to sour orange. Since some promising rootstocks are known to be sensitive to viroids (1), a survey was conducted to determine if the cultivars grown presently in Tunisia were infected with viroids. Following a preliminary report (2), an extensive survey was conducted from 1995-2001 that included 174 symptomless sources being grown at Cap Bon: 26 Maltaise demi-sanguine, 9 Maltaise sanguine, 20 Maltaise blonde, 4 orange doublefine, 16 Washington navel, 12 Valencia late, 29 common mandarin, 42 Cassar clementine, 5 Lunari lemon, and 11 Eureka lemon. These sources were graft-inoculated into Etrog citron that subsequently developed symptoms characteristic of viroid infection. Sequential polyacrylamide gel electrophoresis analysis and molecular hybridization using viroid-specific probes (1) revealed that all sources were infected with at least two viroids. Citrus exocortis viroid (CEVd), Hop stunt viroid (HSVd), and Citrus viroid III (CVd-III) were widespread and accounted for 68.4, 67.8, and 81.0% of the sources tested, respectively. Citrus bent leaf viroid (CBLVd) and Citrus viroid IV (CVd-IV) were only found in 32.7 and 2.3% of the sources. The most frequent viroid combinations were CEVd+HSVd+CVd-III (17.8%) and CEVd+CVd-III (17,2%), whereas HSVd+CVd-IV and CEVd+CBLVd+CVd-III+CVd-IV were found in a single source (0.6%). References: (1) N. Duran-Vila and J. S. Semancik. Pages 178–194 in: Viroids. CSIRO Publishing, Australia, 2003. (2) A. Najar et al. Pages 398–400 in: Proc. 15th Conf. Int. Org. Citrus Virol, 2002.

scholarly journals First Report of a Brugmansia sp. Infected by Tomato apical stunt viroid in Belgium

Plant Disease ◽  
2011 ◽  
Vol 95 (4) ◽  
pp. 495-495 ◽  
Author(s):  
T. Olivier ◽  
E. Demonty ◽  
J. Govers ◽  
K. Belkheir ◽  
S. Steyer ◽  
...  
Keyword(s):  
Plant Protection ◽  
Ornamental Plants ◽  
Potato Spindle Tuber Viroid ◽  
Bumble Bees ◽  
Yield Losses ◽  
Rt Pcr ◽  
Leaf Sample ◽  
First Report ◽  
Stunt Viroid ◽  
Mediterranean Plant

During a routine screening of ornamentals by the Federal Agency for the Safety of the Food Chain (FASFC) in Belgium, a pospiviroid was detected in a symptomless Brugmansia sp. (angel's trumpets) coming from the Netherlands. Detection was performed on a leaf sample by reverse transcription (RT)-PCR, first using universal pospiviroid primer pair (2) VIR1/VIR2 and subsequently with semispecific primer pair (3) CEVd-FW/RE, to amplify the whole viroid genome. Amplicons of expected sizes (260 and 360 bp, respectively) were detected and the sequencing of the CEVd-FW/RE amplicon (GenBank Accession No. FN994891) revealed that the viroid from a Brugmansia sp. was a Tomato apical stunt viroid (TASVd) showing 99.7% similarity with the Sj1 isolate found in Solanum jasminoides (GenBank Accession No. AM777161). Diluted-sap inoculation attempts on tomato from lyophilized material were unsuccessful in agreement with previous results obtained with a Brugmansia isolate of Potato spindle tuber viroid (4). TASVd is mentioned on the alert list of EPPO (European and Mediterranean Plant Protection Organization) because of the heavy yield losses it can induce in tomato, its asymptomatic presence on different ornamental plants (S. jasminoides, Lycianthes rantonnetii, and Streptosolen jamesonii), and its capacity to be transmitted by contact to different Solanaceae as well as by bumble bees to tomato (1). The contaminated plants found in the survey by FASFC have been destroyed to avoid accidental transmission to potato and tomato. To our knowledge, this is the first report of TASVd in a Brugmansia sp. References: (1) Y. Antignus et al. Plant Dis. 91:47, 2007. (2) R. A. Mumford et al. EPPO Bulletin 30:431, 2000. (3) N. Önelge. Turk. J. Agric. For. 21:419, 1997. (4) J. Th. J. Verhoeven. Ph.D. thesis. Wageningen University, Netherlands, 2010.

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