| Picture | Title | Caption | Copyright |
|---|---|---|---|
| Symptoms on maize top leaves | Maize dwarf mosaic potyvirus: mosaic symptoms on maize top leaves. | Malisa Tosic | |
| Symptoms on maize plants | Maize dwarf mosaic potyvirus: a group of infected maize plants showing yellowing, some red discolouration, and tip necrosis. | Malisa Tosic | |
| Symptoms on maize top leaves | Maize dwarf mosaic potyvirus: mosaic symptoms on maize top leaves. | Malisa Tosic | |
| Symptoms on ears of maize | Cobs of maize plants infected with MDMV compared with a healthy cob (on the right). | Malisa Tosic | |
| Symptoms on sorghum leaves | Mosaic symptoms on sorghum leaves due to infection by maize dwarf mosaic potyvirus. | Malisa Tosic | |
| Symptoms on sorghum plants | Shock reaction" of sorghum plants infected with MDMV. The virus-free healthy plant (in the middle) remains green. | Malisa Tosic | |
| Symptoms on sorghum leaves | MDMV: mosaic and red stripes with necrosis on leaves of infected sorghum plants | Malisa Tosic | |
| Symptoms on sorghum crop | Effect of sowing density on red stripe necrosis. The crop is more affected if sowing is sparse. | Malisa Tosic | |
| Symptoms on rhizomes and leaves | Sorghum halepense: rhizomes and leaves showing mosaic due to infection with MDMV. | Malisa Tosic | |
| Symptoms on sorghum leaves | Sorghum cv. Tamaran, one of the differential cultivars showing mosaic when infected with MDMV-A, (including S 3A, BingK, BingH, and R²7 isolates) or necrotic streaks and stripes on inoculated leaves when infected with SCMV-YU (isolates SM1, SM2, SM3, Bac, and S1A). | Malisa Tosic |
Datasheet
Maize dwarf mosaic virus (dwarf mosaic of maize)
Index
- Pictures
- Identity
- Taxonomic Tree
- Notes on Taxonomy and Nomenclature
- Description
- Distribution Table
- Risk of Introduction
- Habitat
- Hosts/Species Affected
- Host Plants and Other Plants Affected
- Growth Stages
- Symptoms
- List of Symptoms/Signs
- Biology and Ecology
- Means of Movement and Dispersal
- Seedborne Aspects
- Plant Trade
- Vectors and Intermediate Hosts
- Impact
- Diagnosis
- Detection and Inspection
- Similarities to Other Species/Conditions
- Prevention and Control
- References
- Distribution Maps
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Top of pageIdentity
Top of pagePreferred Scientific Name
- Maize dwarf mosaic virus
Preferred Common Name
- dwarf mosaic of maize
Other Scientific Names
- European maize mosaic virus
- Indian maize mosaic virus
- maize dwarf mosaic potyvirus
- maize mosaic virus
- maize stripe mosaic virus
- sorghum red stripe virus
Local Common Names
- Argentina: virus del mosaico enanizante del maiz
- Bulgaria: virus karlikovoi mosaika na tsarevitsata; virus mosaika na tsarevitsata; virus na chervenata shrichovatost na tsarevitsata
- Czechoslovakia (former): sorghumrotstreifigdeit virus
- France: virus de la mosaïque du maïs; virus de la mosaïque nanisante du maïis
- Germany: Europäischern Maismosaik virus; Maisstreifenmosaik virus; Maisverzwergungsmosaik virus; Sorghumrotstreifigkeit virus
- Hungary: kukorica csikos mosaik virus; kukorica törpe mosaic virus
- India: maize mosaic virus; sorghum red stripe virus
- Italy: virus del'arrosamento striato del sorgo
- Romania: virusul mosaicul porumbului; virusul striatia ruginie a sorgului
- Russian Federation: virus karlikovoi mozaiki kukuruzy; virus mozaiki kukuruzy
- Slovakia: virus mosaika kukurice
- Ukraine: virus mozaiki kukurudzi
- Venezuela: virus del mosaico enanizante del mais
- Yugoslavia (Serbia and Montenegro): virus mosaika kukuruza; virus mozaicne krzljavosti kukuruza
English acronym
- MDMV
EPPO code
- MDMV00 (Maize dwarf mosaic potyvirus)
Taxonomic Tree
Top of page- Domain: Virus
- Group: "Positive sense ssRNA viruses"
- Group: "RNA viruses"
- Family: Potyviridae
- Genus: Potyvirus
- Species: Maize dwarf mosaic virus
Notes on Taxonomy and Nomenclature
Top of page
In 1963, a new maize disease was recognized in Iowa, USA (Janson and Ellett, 1963), and soon after was shown to be caused by a new virus named Maize dwarf mosaic virus (MDMV) (Janson et al., 1965; Williams and Alexander, 1965). MacKenzie et al. (1966) showed that MDMV was comprised of two different strains, strain A infectious to Johnson grass (Sorghum halepense) (MDMV-A), and strain B non-infectious to Johnson grass (MDMV-B). Strain B (MDMV-B) was later shown not to be MDMV.
On the basis of reactions in N-20 and other maize inbred lines, Louie and Knoke (1975) differentiated four more strains of MDMV and named them C, D, E and F (MDMV-C, -D, -E and -F). Jarjees and Uyemoto (1984) described a new strain of MDMV named Ksl (MDMV-KSl), which differed from MDMV-A, especially in its serology. McDaniel and Gordon (1985) also described a new strain of MDMV and named it O (MDMV-O), on the basis of its infectivity to oats. However, like MDMV-B, both MDMV-KSl and MDMV-O were later shown not to be MDMV.
The taxonomy of MDMV, as an important pathogen of maize, sorghum and sugarcane, has attracted attention worldwide. It was long considered that MDMV was a strain of Sugarcane mosaic virus (SCMV) (Pirone, 1972). However, based on characteristics other than host range and differential host plants, as well as serology, MDMV was shown to be different from SMV. The question was clarified in the last decade when new approaches were applied in the taxonomy of potyviruses infecting maize, sorghum, sugarcane and Johnsongrass. Besides characteristics common for Potyviridae (Shukla et al., 1994) and for the Potyvirus group (Hollings and Brunt, 1981), taxonomy of MDMV is based on: infectivity to Johnsongrass (MacKenzie et al., 1966; Ford et al., 1989); specificity of sorghum differential cultivars (Tosic et al., 1990a); and N-terminus serology, as a consequence of amino-acid sequence in the N-terminus of virus coat protein polypeptide chain (Shukla et al., 1989).
The properties of MDMV led to its differentiation from SCMV, Sorghum mosaic virus (SrMV) and Johnsongrass mosaic virus (JGMV). At that time, the strain of MDMV-B was re-identified as a strain of SCMV (SCMV-MDB), and strains Ksl and O (MDMV-KSl and MDMV-O) were re-identified as strains of JGMV (JGMV-KSl and -O (Shukla et al., 1989; Shukla and Teakle, 1989; Teakle et al., 1989). After these discoveries, MDMV was separated from related viruses and shown to be an independent member of the Potyviridae (Shukla et al., 1994), Potyvirus group (Hollings and Brunt, 1981), and, more specifically, a member of the subgroup of SMV (Shukla et al., 1994).
After this reclassification of the previously described MDMV strain the following strains were identified: MDMV-A (the type strain), MDMV-C, MDMV-D, MDMV-E and MDMV-F (Ford et al., 1989). These five MDMV strains differed in the reactions of N 20 and some other maize inbred lines, their transmissibility by Myzus persicae and Acyrthosiphon pisum, and serologically (Louie and Knoke, 1975; Lenardon et al., 1993).
Some MDMV isolates from different regions and countries were specific and differed from MDMV-A (the type strain), for example, from France (Kerlan et al., 1974), Israel (Antignus, 1987), Venezuela (Toler et al., 1982; Garrido and Trujillo, 1988a) and Spain (Achon et al., 1996). Other isolates from former Yugoslavia were identical to MDMV-A (Tosic and Malak, 1973; Tosic, 1974; Tosic et al., 1977a; Tosic et al., 1990b; Krstic, 1992; Krstic et al., 1995, Krstic and Tosic, 1995). The unclear relationship among these MDMV strains and isolates suggests the need for more attention on the taxonomy of MDMV isolates originating from different countries and regions. They should be compared in simultaneous investigations under the same conditions.
The nomenclature of MDMV is incomplete. The first recognised diseases caused by the virus (now known as MDMV) were sorghum red stripe and maize mosaic which were described in Italy (Goidanich, 1938; Grancini, 1957; Lovisolo, 1957) and in Yugoslavia (Panjan, 1960; Lovisolo and Acimovic, 1961). After becoming epiphytotic in Ohio, USA, in the early 1960s, the disease, as well as the virus were renamed as maize dwarf mosaic and maize dwarf mosaic virus (MDMV), respectively, (Janson and Ellett, 1963; Janson et al., 1965; Williams and Alexander, 1965). The name MDMV has been accepted by most, if not all, researchers worldwide.
On the basis of reactions in N-20 and other maize inbred lines, Louie and Knoke (1975) differentiated four more strains of MDMV and named them C, D, E and F (MDMV-C, -D, -E and -F). Jarjees and Uyemoto (1984) described a new strain of MDMV named Ksl (MDMV-KSl), which differed from MDMV-A, especially in its serology. McDaniel and Gordon (1985) also described a new strain of MDMV and named it O (MDMV-O), on the basis of its infectivity to oats. However, like MDMV-B, both MDMV-KSl and MDMV-O were later shown not to be MDMV.
The taxonomy of MDMV, as an important pathogen of maize, sorghum and sugarcane, has attracted attention worldwide. It was long considered that MDMV was a strain of Sugarcane mosaic virus (SCMV) (Pirone, 1972). However, based on characteristics other than host range and differential host plants, as well as serology, MDMV was shown to be different from SMV. The question was clarified in the last decade when new approaches were applied in the taxonomy of potyviruses infecting maize, sorghum, sugarcane and Johnsongrass. Besides characteristics common for Potyviridae (Shukla et al., 1994) and for the Potyvirus group (Hollings and Brunt, 1981), taxonomy of MDMV is based on: infectivity to Johnsongrass (MacKenzie et al., 1966; Ford et al., 1989); specificity of sorghum differential cultivars (Tosic et al., 1990a); and N-terminus serology, as a consequence of amino-acid sequence in the N-terminus of virus coat protein polypeptide chain (Shukla et al., 1989).
The properties of MDMV led to its differentiation from SCMV, Sorghum mosaic virus (SrMV) and Johnsongrass mosaic virus (JGMV). At that time, the strain of MDMV-B was re-identified as a strain of SCMV (SCMV-MDB), and strains Ksl and O (MDMV-KSl and MDMV-O) were re-identified as strains of JGMV (JGMV-KSl and -O (Shukla et al., 1989; Shukla and Teakle, 1989; Teakle et al., 1989). After these discoveries, MDMV was separated from related viruses and shown to be an independent member of the Potyviridae (Shukla et al., 1994), Potyvirus group (Hollings and Brunt, 1981), and, more specifically, a member of the subgroup of SMV (Shukla et al., 1994).
After this reclassification of the previously described MDMV strain the following strains were identified: MDMV-A (the type strain), MDMV-C, MDMV-D, MDMV-E and MDMV-F (Ford et al., 1989). These five MDMV strains differed in the reactions of N 20 and some other maize inbred lines, their transmissibility by Myzus persicae and Acyrthosiphon pisum, and serologically (Louie and Knoke, 1975; Lenardon et al., 1993).
Some MDMV isolates from different regions and countries were specific and differed from MDMV-A (the type strain), for example, from France (Kerlan et al., 1974), Israel (Antignus, 1987), Venezuela (Toler et al., 1982; Garrido and Trujillo, 1988a) and Spain (Achon et al., 1996). Other isolates from former Yugoslavia were identical to MDMV-A (Tosic and Malak, 1973; Tosic, 1974; Tosic et al., 1977a; Tosic et al., 1990b; Krstic, 1992; Krstic et al., 1995, Krstic and Tosic, 1995). The unclear relationship among these MDMV strains and isolates suggests the need for more attention on the taxonomy of MDMV isolates originating from different countries and regions. They should be compared in simultaneous investigations under the same conditions.
The nomenclature of MDMV is incomplete. The first recognised diseases caused by the virus (now known as MDMV) were sorghum red stripe and maize mosaic which were described in Italy (Goidanich, 1938; Grancini, 1957; Lovisolo, 1957) and in Yugoslavia (Panjan, 1960; Lovisolo and Acimovic, 1961). After becoming epiphytotic in Ohio, USA, in the early 1960s, the disease, as well as the virus were renamed as maize dwarf mosaic and maize dwarf mosaic virus (MDMV), respectively, (Janson and Ellett, 1963; Janson et al., 1965; Williams and Alexander, 1965). The name MDMV has been accepted by most, if not all, researchers worldwide.
Description
Top of page
MDMV particles, as shown for the first time by Williams and Alexander (1965), are filamentous, ca 750 nm long and 13 nm wide. These findings have been verified by many researchers. Rao et al. (1998b) have reported an improved purification procedure for MDMV.
The virus particles are of nucleoprotein composition. A ssRNA species of ca 3320 kDa (Berger et al., 1989) representing ca 5% of the particle weight (Jones and Tolin, 1972). A single polypeptide species of apparent MW of 30.7 kDa for a native preparation, or 35.5 kDa for a carboxymethylated preparation (Von Baumgarten and Ford, 1981; Jensen et al., 1986) build the protein coat of the virions.
The sedimentation coefficient of the virus particles is 176± 5S and the buoyant density in CsCl is l.3421 (Tosic and Ford, 1974), while the A280/A260 ratio is 0.82 (Langenberg, 1973).
The dilution end-point of MDMV is 0.001 to 0.00001, longevity in vitro at room temperature up to 3 days compared with up to 8 days at 2-3°C, and a thermal inactivation point between 55 and 58°C (Williams and Alexander, 1965; Tosic and Ford, 1974).
The virus particles are of nucleoprotein composition. A ssRNA species of ca 3320 kDa (Berger et al., 1989) representing ca 5% of the particle weight (Jones and Tolin, 1972). A single polypeptide species of apparent MW of 30.7 kDa for a native preparation, or 35.5 kDa for a carboxymethylated preparation (Von Baumgarten and Ford, 1981; Jensen et al., 1986) build the protein coat of the virions.
The sedimentation coefficient of the virus particles is 176± 5S and the buoyant density in CsCl is l.3421 (Tosic and Ford, 1974), while the A280/A260 ratio is 0.82 (Langenberg, 1973).
The dilution end-point of MDMV is 0.001 to 0.00001, longevity in vitro at room temperature up to 3 days compared with up to 8 days at 2-3°C, and a thermal inactivation point between 55 and 58°C (Williams and Alexander, 1965; Tosic and Ford, 1974).
Distribution Table
Top of pageThe distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
Last updated: 25 Feb 2021| Continent/Country/Region | Distribution | Last Reported | Origin | First Reported | Invasive | Reference | Notes |
|---|---|---|---|---|---|---|---|
Africa |
|||||||
| Burkina Faso | Present | ||||||
| Cameroon | Present, Few occurrences | ||||||
| Côte d'Ivoire | Present, Few occurrences | ||||||
| Egypt | Present | ||||||
| Ethiopia | Present | ||||||
| Kenya | Present | ||||||
| Mauritius | Present | ||||||
| Morocco | Present | ||||||
| Niger | Present | ||||||
| Nigeria | Present | ||||||
| South Africa | Present | ||||||
| Zambia | Present | ||||||
| Zimbabwe | Present | ||||||
Asia |
|||||||
| China | Present | ||||||
| -Beijing | Present | ||||||
| -Gansu | Present | ||||||
| -Hebei | Present | ||||||
| -Hubei | Present | ||||||
| -Jiangsu | Present | ||||||
| -Liaoning | Present | ||||||
| -Shaanxi | Present | ||||||
| -Shandong | Present | ||||||
| -Shanxi | Present | ||||||
| Georgia | Present | Original citation: Chaduneli & Menabde, 1972 | |||||
| India | Present | ||||||
| -Maharashtra | Present | ||||||
| -Uttar Pradesh | Present | ||||||
| Iran | Present | ||||||
| Iraq | Present | ||||||
| Israel | Present | ||||||
| Jordan | Present | ||||||
| Kazakhstan | Present | ||||||
| Pakistan | Present | ||||||
| Philippines | Present | ||||||
| South Korea | Present | ||||||
| Taiwan | Present | ||||||
| Turkey | Present | ||||||
| Uzbekistan | Present | ||||||
| Yemen | Present | ||||||
Europe |
|||||||
| Bosnia and Herzegovina | Present, Localized | ||||||
| Bulgaria | Present | ||||||
| Croatia | Present | ||||||
| Czechia | Present | ||||||
| Czechoslovakia | Present, Widespread | ||||||
| Federal Republic of Yugoslavia | Present, Widespread | ||||||
| France | Present | ||||||
| Germany | Present, Few occurrences | ||||||
| Greece | Present | ||||||
| Hungary | Present | ||||||
| Italy | Present | ||||||
| Poland | Present | ||||||
| Romania | Present, Widespread | ||||||
| Russia | Present | ||||||
| -Central Russia | Present, Widespread | ||||||
| -Russia (Europe) | Present, Widespread | ||||||
| Serbia and Montenegro | Present | ||||||
| Spain | Present, Widespread | ||||||
| Ukraine | Present | ||||||
North America |
|||||||
| Canada | Present | ||||||
| -Ontario | Present | ||||||
| Cuba | Present | ||||||
| Haiti | Present | ||||||
| Honduras | Present | ||||||
| Mexico | Present | ||||||
| United States | Present | ||||||
| -Alabama | Present | ||||||
| -Arkansas | Present | ||||||
| -California | Present, Widespread | ||||||
| -Delaware | Present | ||||||
| -Florida | Present | ||||||
| -Georgia | Present | ||||||
| -Hawaii | Present | ||||||
| -Idaho | Present | ||||||
| -Illinois | Present | ||||||
| -Indiana | Present | ||||||
| -Iowa | Present | ||||||
| -Kansas | Present | ||||||
| -Kentucky | Present | ||||||
| -Louisiana | Present | ||||||
| -Maine | Present | ||||||
| -Massachusetts | Present | ||||||
| -Michigan | Present | ||||||
| -Minnesota | Present, Widespread | ||||||
| -Mississippi | Present | ||||||
| -Missouri | Present | ||||||
| -Nebraska | Present | ||||||
| -New Hampshire | Present | ||||||
| -New Jersey | Present, Widespread | ||||||
| -New Mexico | Present | ||||||
| -New York | Present | ||||||
| -North Carolina | Present | ||||||
| -North Dakota | Present | ||||||
| -Ohio | Present | ||||||
| -Oklahoma | Present | ||||||
| -Pennsylvania | Present | ||||||
| -South Carolina | Present | ||||||
| -South Dakota | Present, Widespread | ||||||
| -Tennessee | Present | ||||||
| -Texas | Present | ||||||
| -Vermont | Present | ||||||
| -Virginia | Present | ||||||
| -Washington | Present | ||||||
| -Wisconsin | Present | ||||||
Oceania |
|||||||
| Australia | Present | ||||||
| -Queensland | Present | ||||||
| -Victoria | Present | ||||||
South America |
|||||||
| Argentina | Present | ||||||
| Brazil | Present | ||||||
| -Goias | Present | ||||||
| -Minas Gerais | Present | ||||||
| -Sao Paulo | Present | ||||||
| Chile | Present | ||||||
| Colombia | Present | ||||||
| Peru | Present | ||||||
| Venezuela | Present | ||||||
Risk of Introduction
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RISK CRITERIA CATEGORY
Economic Importance High
Distribution Worldwide
Seedborne Incidence Low
Seed Transmitted Yes
Seed Treatment No
Overall Risk Low
Notes on Phytosanitary Risk
Although MDMV is an economically important plant pathogen, it is already distributed worldwide and has a very low rate of transmission by seed.
Economic Importance High
Distribution Worldwide
Seedborne Incidence Low
Seed Transmitted Yes
Seed Treatment No
Overall Risk Low
Notes on Phytosanitary Risk
Although MDMV is an economically important plant pathogen, it is already distributed worldwide and has a very low rate of transmission by seed.
Habitat
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All host plants, both cultivated and wild, support the maintenance of MDMV under field conditions. When infected, perennial species play the most important role. They provide a permanent source of MDMV, and Johnsongrass (Sorghum halepense) is the most important.
Johnsongrass is a perennial with well-developed rhizomes, which give rise to new tillers every spring. Due to its perennial nature, Johnsongrass accumulates and preserves inoculum of MDMV. Wherever present, Johnsongrass is usually highly infected with MDMV. Many researchers have proved that infected Johnsongrass plants serve as a permanent source of the virus under field conditions (Pop, 1962; Shepherd et al., 1964; Sutic and Tosic, 1966; Tosic and Simova, 1967).
Garrido and Trujillo (1989) found that infected Sorghum verticilliflorum plants play an important part in MDMV maintenance.
The presence of a source of MDMV is crucial for disease occurrence and spread, and often best explains the onset of MDMV in maize and sorghum crops (Louie and Knoke, 1991; Tosic and Mijavec, 1991).
Johnsongrass is a perennial with well-developed rhizomes, which give rise to new tillers every spring. Due to its perennial nature, Johnsongrass accumulates and preserves inoculum of MDMV. Wherever present, Johnsongrass is usually highly infected with MDMV. Many researchers have proved that infected Johnsongrass plants serve as a permanent source of the virus under field conditions (Pop, 1962; Shepherd et al., 1964; Sutic and Tosic, 1966; Tosic and Simova, 1967).
Garrido and Trujillo (1989) found that infected Sorghum verticilliflorum plants play an important part in MDMV maintenance.
The presence of a source of MDMV is crucial for disease occurrence and spread, and often best explains the onset of MDMV in maize and sorghum crops (Louie and Knoke, 1991; Tosic and Mijavec, 1991).
Hosts/Species Affected
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In addition to maize (Zea mays), including field maize, sweetcorn, popcorn and maize inbred lines (seed crop), MDMV has been isolated from the following naturally-infected plant species:
Sorghum (Sorghum bicolor) is the other very important host of MDMV. Crops of grain sorghum, silage sorghum, as well as of broomcorn (technical sorghum) are susceptible to damage by MDMV.
Sugarcane (Saccharum officinarum) is also an important host of MDMV. The virus adversely affects sugarcane crops.
Johnsongrass (Sorghum halepense) is the most important perennial wild host. Infected plants serve as a permanent source of the virus under field conditions. Other wild hosts are less important, but they also contribute to virus ecology and epidemiology.
In addition to these natural hosts, many plant species in the Poaceae are susceptible to MDMV when mechanically inoculated. MDMV has a very broad host range which includes ca 250 plant species in 81 genera of six subfamilies of Poaceae. MDMV has been isolated from ca 40 plant species infected under field conditions.
Sorghum (Sorghum bicolor) is the other very important host of MDMV. Crops of grain sorghum, silage sorghum, as well as of broomcorn (technical sorghum) are susceptible to damage by MDMV.
Sugarcane (Saccharum officinarum) is also an important host of MDMV. The virus adversely affects sugarcane crops.
Johnsongrass (Sorghum halepense) is the most important perennial wild host. Infected plants serve as a permanent source of the virus under field conditions. Other wild hosts are less important, but they also contribute to virus ecology and epidemiology.
In addition to these natural hosts, many plant species in the Poaceae are susceptible to MDMV when mechanically inoculated. MDMV has a very broad host range which includes ca 250 plant species in 81 genera of six subfamilies of Poaceae. MDMV has been isolated from ca 40 plant species infected under field conditions.
Host Plants and Other Plants Affected
Top of page| Plant name | Family | Context | References |
|---|---|---|---|
| Avena sativa (oats) | Poaceae | Other | |
| Bromus catharticus (prairiegrass) | Poaceae | Wild host | |
| Chloris barbata (purpletop chloris) | Poaceae | Wild host | |
| Panicum miliaceum (millet) | Poaceae | Other | |
| Paspalum conjugatum (buffalo grass) | Poaceae | Wild host | |
| Pennisetum glaucum (pearl millet) | Poaceae | Wild host | |
| Saccharum officinarum (sugarcane) | Poaceae | Other | |
| Sorghum bicolor (sorghum) | Poaceae | Main | |
| Sorghum halepense (Johnson grass) | Poaceae | Wild host | |
| Sorghum sudanense (Sudan grass) | Poaceae | Wild host | |
| Stenotaphrum secundatum (buffalo grass) | Poaceae | Wild host | |
| Tripsacum dactyloides (eastern gamagrass) | Poaceae | Wild host | |
| Urochloa plantaginea (marmeladegrass) | Poaceae | Wild host | |
| Zea mays (maize) | Poaceae | Main | |
| Zea mays subsp. mays (sweetcorn) | Poaceae | Main |
Symptoms
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Symptoms of MDMV on maize and sorghum are similar. Virus-infected plants are discoloured, exhibit dwarfing, sterility, and sometimes premature death. The severity of symptoms depends primarily on the susceptibility of the genotype being grown, and on the time of infection.
Early infection leads to severe and more pronounced symptoms. Field maize usually shows less severe symptoms than sweetcorn or inbred lines.
Mosaic usually appears first at the base of the youngest leaf still unfolding in the sheath. On one (or both) sides of the main leaf vein, chlorotic dots and streaks appear, which gradually enlarge and spread over the blade of the growing leaf. Streaks and dots can merge into chlorotic stripes or lines, which run along the leaf blade. Normal green colour may remain as streaks, stripes or lines, usually along the leaf veins. Upper leaves which appear after infection became chlorotic and yellowish. Chlorotic-yellow plant apices are a very reliable symptom of MDMV infection of maize plants.
Sweetcorn and maize inbred lines, sometimes also field maize, exhibit mosaic and yellowing of leaves accompanied by a reddish-violet colour. Such discoloration usually appears when infection takes place early in the growing season, when maize seedlings are very young. Reddish-violet discoloration can be dots, streaks, or stripes along the margins, or starting from the leaf tips. Such discoloration is more often on older leaves after an early infection. The leaf tissue showing reddish-violet discoloration may become necrotic. Such symptoms are usually accompanied by severe dwarfing of infected plants. Necrosis overcomes most, or all, of the diseased plant. Such premature necrosis characterises early infected plants of maize inbred lines.
All discoloration occurs on leaves which were growing when infection occurs, or on leaves grown after infection. Leaves which had completed their growth before infection remained symptomless. It is possible to estimate at what state of plant growth the infection occurred.
Growth of maize plants is also affected by infection with MDMV. All internodes on the stalk of infected maize plants, grown after infection, are shorter and sometimes become rosette-like at the apices. The degree of growth reduction also depends on the maize genotype and on the time of infection. Early infection correlates with severe dwarfing under experimental conditions (Genter et al., 1973).
With field maize and when infection is not too early, the height of infected maize plants is decreased by 20-25% (Tosic and Misovic, 1967). When either maize inbred lines or sweetcorn are infected with MDMV they are often short, frequently less than 1 m (Tosic et al., 1990a).
Maize plants infected with MDMV exhibit obvious delayed growth. The mid-silk stage and fertilization may be delayed by 2 weeks or more (Dimitrijevic, 1969; Scott and Nelson, 1972). Ears of maize MDMV-infected plants are not usually ripe at harvest time, but are in transition between the milk and waxy stage, or are just in the waxy stage.
Sterility is a symptom commonly accompanying MDMV infection in maize. Sterility of maize plants infected with the virus occurs due to a delay of the silking and tasseling stages compared with healthy plants (Dimitijevic, 1969; Scott and Nelson, 1972). Lower pollen viability and shorter pollen germ tubes of maize plants infected with MDMV (Mikel et al., 1982) also contribute to the sterility.
Sterility of field maize plants infected with MDMV can often reach 25% or more (Tosic and Misovic, 1967). With maize inbred lines, especially after an early infection, sterility can be much higher, leading to a complete yield loss. Severely infected maize seed crops are therefore usually ploughed under (Tosic et al., 1990a).
Incomplete fertilisation of ears of maize plants is also a symptom of MDMV infection. Due to the symptoms listed (dissimultaneous stages of growth, lower viability of pollen of infected maize) entire rows of grain are incomplete on those ears originating from maize plants infected with MDMV (Tosic and Misovic, 1967).
Some other changes in maize plants infected with MDMV include reduced photosynthesis plus increased respiration (Tu and Ford, 1968), reduced transpiration (Lindsey and Gudauskas, 1975), cell inclusions of pinwheel and scroll types (Krass and Ford, 1969; Moline, 1972; Langenberg and Schroeder, 1973; Edwardson, 1974; Krstic, 1992; Lesemann et al., 1992).
Sorghum reactions to infection with MDMV can be more diverse than those on maize and they depend not only on plant genotype susceptibility but also on climatic conditions. They include discoloration, dwarfing, tillering and necrosis.
Mosaic is a very common symptom on different sorghum genotypes infected with MDMV. The first signs of mosaic can be seen on the base of the youngest leaf, still in the sheath. Chlorotic dots and streaks first appearing later on, merge and spread over the leaf blade forming chlorotic stripes or lines.
Under cool conditions, mosaic on sorghum plants can be accompanied by red stripes. The disease was therefore named sorghum red stripe and the virus sorghum red stripe virus. Red stripes on leaves of sorghum plants infected with MDMV usually became necrotic (Persley et al., 1977; Martin and Hackerott, 1982; Jarjees and Uyemoto, 1983; Mijavec, 1991; Berenji et al., 1996) especially under cool conditions. After such a shock reaction, diseased sorghum plants can recover but the yield of these plants is very reduced and of poor quality.
Dwarfing of sorghum plants infected with MDMV is more pronounced than with infected maize, especially those plants which suffered from the shock reaction.
Tillering is also a common phenomenon which accompanies MDMV infection in sorghum. Plants subjected to leaf necrosis tiller more than those which are healthy or those not subjected to the shock reaction.
Brushes of broom maize plants infected with MDMV are underdeveloped and very often reddish. This results in brushes of lower quality.
Symptoms on Johnsongrass are similar to those on sorghum. Chlorotic streaks of different length and intensity run along the veins of the leaves, and often they turn reddish-violet. The mosaic disappears as the Johnsongrass leaves age. Only the top two or three leaves exhibit sharp mosaic symptoms.
Early infection leads to severe and more pronounced symptoms. Field maize usually shows less severe symptoms than sweetcorn or inbred lines.
Mosaic usually appears first at the base of the youngest leaf still unfolding in the sheath. On one (or both) sides of the main leaf vein, chlorotic dots and streaks appear, which gradually enlarge and spread over the blade of the growing leaf. Streaks and dots can merge into chlorotic stripes or lines, which run along the leaf blade. Normal green colour may remain as streaks, stripes or lines, usually along the leaf veins. Upper leaves which appear after infection became chlorotic and yellowish. Chlorotic-yellow plant apices are a very reliable symptom of MDMV infection of maize plants.
Sweetcorn and maize inbred lines, sometimes also field maize, exhibit mosaic and yellowing of leaves accompanied by a reddish-violet colour. Such discoloration usually appears when infection takes place early in the growing season, when maize seedlings are very young. Reddish-violet discoloration can be dots, streaks, or stripes along the margins, or starting from the leaf tips. Such discoloration is more often on older leaves after an early infection. The leaf tissue showing reddish-violet discoloration may become necrotic. Such symptoms are usually accompanied by severe dwarfing of infected plants. Necrosis overcomes most, or all, of the diseased plant. Such premature necrosis characterises early infected plants of maize inbred lines.
All discoloration occurs on leaves which were growing when infection occurs, or on leaves grown after infection. Leaves which had completed their growth before infection remained symptomless. It is possible to estimate at what state of plant growth the infection occurred.
Growth of maize plants is also affected by infection with MDMV. All internodes on the stalk of infected maize plants, grown after infection, are shorter and sometimes become rosette-like at the apices. The degree of growth reduction also depends on the maize genotype and on the time of infection. Early infection correlates with severe dwarfing under experimental conditions (Genter et al., 1973).
With field maize and when infection is not too early, the height of infected maize plants is decreased by 20-25% (Tosic and Misovic, 1967). When either maize inbred lines or sweetcorn are infected with MDMV they are often short, frequently less than 1 m (Tosic et al., 1990a).
Maize plants infected with MDMV exhibit obvious delayed growth. The mid-silk stage and fertilization may be delayed by 2 weeks or more (Dimitrijevic, 1969; Scott and Nelson, 1972). Ears of maize MDMV-infected plants are not usually ripe at harvest time, but are in transition between the milk and waxy stage, or are just in the waxy stage.
Sterility is a symptom commonly accompanying MDMV infection in maize. Sterility of maize plants infected with the virus occurs due to a delay of the silking and tasseling stages compared with healthy plants (Dimitijevic, 1969; Scott and Nelson, 1972). Lower pollen viability and shorter pollen germ tubes of maize plants infected with MDMV (Mikel et al., 1982) also contribute to the sterility.
Sterility of field maize plants infected with MDMV can often reach 25% or more (Tosic and Misovic, 1967). With maize inbred lines, especially after an early infection, sterility can be much higher, leading to a complete yield loss. Severely infected maize seed crops are therefore usually ploughed under (Tosic et al., 1990a).
Incomplete fertilisation of ears of maize plants is also a symptom of MDMV infection. Due to the symptoms listed (dissimultaneous stages of growth, lower viability of pollen of infected maize) entire rows of grain are incomplete on those ears originating from maize plants infected with MDMV (Tosic and Misovic, 1967).
Some other changes in maize plants infected with MDMV include reduced photosynthesis plus increased respiration (Tu and Ford, 1968), reduced transpiration (Lindsey and Gudauskas, 1975), cell inclusions of pinwheel and scroll types (Krass and Ford, 1969; Moline, 1972; Langenberg and Schroeder, 1973; Edwardson, 1974; Krstic, 1992; Lesemann et al., 1992).
Sorghum reactions to infection with MDMV can be more diverse than those on maize and they depend not only on plant genotype susceptibility but also on climatic conditions. They include discoloration, dwarfing, tillering and necrosis.
Mosaic is a very common symptom on different sorghum genotypes infected with MDMV. The first signs of mosaic can be seen on the base of the youngest leaf, still in the sheath. Chlorotic dots and streaks first appearing later on, merge and spread over the leaf blade forming chlorotic stripes or lines.
Under cool conditions, mosaic on sorghum plants can be accompanied by red stripes. The disease was therefore named sorghum red stripe and the virus sorghum red stripe virus. Red stripes on leaves of sorghum plants infected with MDMV usually became necrotic (Persley et al., 1977; Martin and Hackerott, 1982; Jarjees and Uyemoto, 1983; Mijavec, 1991; Berenji et al., 1996) especially under cool conditions. After such a shock reaction, diseased sorghum plants can recover but the yield of these plants is very reduced and of poor quality.
Dwarfing of sorghum plants infected with MDMV is more pronounced than with infected maize, especially those plants which suffered from the shock reaction.
Tillering is also a common phenomenon which accompanies MDMV infection in sorghum. Plants subjected to leaf necrosis tiller more than those which are healthy or those not subjected to the shock reaction.
Brushes of broom maize plants infected with MDMV are underdeveloped and very often reddish. This results in brushes of lower quality.
Symptoms on Johnsongrass are similar to those on sorghum. Chlorotic streaks of different length and intensity run along the veins of the leaves, and often they turn reddish-violet. The mosaic disappears as the Johnsongrass leaves age. Only the top two or three leaves exhibit sharp mosaic symptoms.
List of Symptoms/Signs
Top of page| Sign | Life Stages | Type |
|---|---|---|
| Leaves / abnormal patterns | ||
| Whole plant / dwarfing |
Biology and Ecology
Top of page
MDMV sources under field conditions are infected plants and, to a lesser extent, infected seed, (less than 0.01%). Among the host plants which serve as a natural source of the virus are many species from the Poaceae. Among them, the most important are Johnsongrass (Sutic and Tosic, 1966; Tosic and Simova, 1967; Onazi and Wilde, 1974) and Sorghum verticilliflorum (Garrido and Trujillo, 1989).
The virus is transmitted by numerous aphids from infected wild or cultivated host plants. S. halepense is the best source of the virus (Onazi and Wilde, 1974), but other researchers (Thongmeearkom et al., 1976) found no difference between Johnsongrass and maize seedlings as sources of MDMV. Maize is the most likely food-plant to become infected (Onazi and Wilde, 1974).
Many aphid species are involved in MDMV transmission. The following species are proven vectors of MDMV: Acyrthosiphon pisum, Aphis citricola, A. craccivora, A. decepta, A. fabae, A. gossypii, A. helianthi, A. maidiradicis, Brevicoryne brassicae, Hysteroneura setariae, Macrosiphum euphorbiae, Metopolophium festucae, Myzus persicae, Rhopalosiphum maidis, R. padi, Rhopalomyzus poae, Schizaphis graminum, Sitobion avenae, Therioaphis trifolii forma maculata and Uroleucon ambrosiae (Tosic and Simova, 1967; Tosic and Sutic. 1968; Koike, 1977; Ferro et al., 1980; Berger et al., 1983; Madden et al., 1983; Rest and Splittstoesser., 1985; Ford et al., 1989; Mijavec, 1991; Garrido and Cermeli, 1994).
Aphid vectors transmit MDMV in a non-persistent manner. Acquisition and inoculation feedings are between 10 sec. to 2 min, with no latent period. Persistence of MDMV in aphids is usually between 30 minutes and 4 h, but can be 6 h (Tosic and Sutic, 1968; Shaunak and Pitre, 1973; Thongmeearkom et al., 1976). It was also shown that aphids' biotypes differ in efficiency of MDMV transmission (Berger et al., 1983).
Virus concentrations and age of the source plant/tissue can also affect MDMV aphid transmission (Tu and Ford, 1971; Thongmeearkom et al., 1976).
Persistence of MDMV in aphid vectors for a few hours can allow long distance transmission. Such a phenomenon was hypothesised for an epidemic of MDMV in maize in 1977 in Minnesota, USA (Zeyen et al., 1987).
Increase of MDMV transmission and more frequent incidence of the disease is correlated with an increase of aphid populations at sites of the virus source (Knoke et al., 1983). Peaking of MDMV spread coincided with mass flight of aphid vectors, which can happen in May-June (Leclant, 1974), July (Knoke et al., 1974; Tosic and Sutic, 1974) or even in August (Madden et al., 1986).
Spread of MDMV by aphid vectors is not influenced by wind, topography or by orientation of plant rows (Damsteegt, 1976).
It has been reported that MDMV may be spread by urediospores of Puccinia sorghi (Wechmar et al., 1992).
The incidence of MDMV is also affected by cultural practices. It has been shown that the incidence of MDMV infection is negatively correlated with density of sowing (Popov, 1978). On non-tilled plots incidence of MDMV infection is higher than on plots with tillage (All et al., 1977).
The incubation period in infected plants usually lasts 6-10 days, but under certain conditions, can last up to 4 weeks (Tosic and Sutic, 1968), depending on the susceptibility of the plant genotype and the environment. Resistant genotypes, when inoculated during the winter, develop symptoms in ca 10 days, but in summer the appearance of symptoms is delayed and symptoms are milder (Jones and Tolin, 1972). It has also been shown that pigment-deficient maize mutants supported MDMV replication (Mayhew et al., 1973). However, it was shown that chloroplasts are involved in MDMV replication (Mayhew et al., 1972).
The concentration of MDMV in infected maize plants varies greatly and depends on the cultivar susceptibility, temperature, age, leaf position and other factors. With resistant maize genotypes during the summer, the concentration of virus is lower and often restricted to certain areas which show symptoms of streaking and banding (Jones and Tolin, 1972). It was also shown experimentally that MDMV reaches higher concentrations at 15° than at 25 or at 35°C (Jensen et al., 1985).
During maturation of the seeds, or when leaves are senescing, the virus concentration declines (Jensen et al., 1985). Concentration of MDMV in infected plants is also influenced by other factors.
Acute doses of sulfur dioxide (262 or 524 µg/m³) for 5-10 h increase MDMV concentration (Laurence et al., 1981). However, nitrogen stress has the most important effect on the decrease of MDMV concentration (Vangessel and Coble, 1993).
MDMV is readily transmitted by sap inoculation. Optimal conditions for mechanical inoculation with MDMV are: source plants should be inoculated 10 days before use; infective juice should be diluted 10x with 0.01 M phosphate buffer at pH 7.0, or in tap water; inoculation of test plants can be done on the first leaf 6 days after plant emergence, on the second leaf 2 days later, or on the third leaf ca 2 weeks after plant emergence (Seifers, 1984).
Inoculation on the lower leaf surface is more effective than on the upper leaf surface (Rosenkranz and Scott, 1987).
Test plants once inoculated should be incubated at 25°C and symptoms will be visible in 6-10 days.
Mechanical inoculation can be applied under field conditions. It can be performed by airbrush (Lindner and Kirkpatrick, 1959) or by solid-stream (Louie et al., 1983) at pressures of 2.1 to 12.7 kg/cm².
Washings from MDMV-infected seedliners show greater conductivity, higher concentrations of K+ and Ca++, and ninhydrin-positive substances (Stevens and Gudauskas, 1982).
Mixed infections of MDMV with Sugarcane mosaic virus, Maize chlorotic dwarf virus, Barley yellow dwarf virus and Cucumber mosaic virus occur frequently (Panjan, 1966; Louie et al., 1974; Belli et al., 1980; Uyemoto et al., 1981; Knox et al., 1987; Fuchs et al., 1990a; Ivarovic et al., 1992; Krstic, 1992; Krstic and Tosic, 1995). The mixed infection is usually followed by a more depressive effect on plant growth and development (Ivanovic et al., 1992).
Maize plants infected with MDMV are of higher susceptibility to stalk rot (caused by Gibberella spp.) (Tosic et al., 1977b, 1979; El-Meleigi, 1989) and root rot (caused by Gibberella spp., Helminthosporium pedicelluatum) (Tu and Ford, 1971). Infected maize plants are also more susceptible to Ustilago maydis [Ustilago zeae] (Ivanovic, 1979), Puccinia sorghi (Arny et al., 1980), Helminthosporium maydis [Cochliobolus heterostrophus] (Beniwal and Gudauskas, 1974), Cercospora zeae-mais (Genter et al., 1973) and to other pathogens. C. heterostrophus sporulates sooner and more abundantly on maize plants infected with MDMV (Beniwal and Gudauskas, 1974; Stevens and Gudauskas, 1983). Conidia of C. heterostrophus borne on maize leaves infected with MDMV are longer, have more septa and are of higher viability than those formed on MDMV-free plants (Stevens and Gudauskas, 1983).
Some correlation was found between MDMV infection of maize and the borer Chilo partellus (Paliwal, 1971) and between MDMV and the nematode Pratylenchus zeae (Nath et al., 1979).
Several methods have been used to purify MDMV. Those methods mainly differ in extraction media and in extract clarification. Shepherd (1965) purified MDMV from leaves of maize plants 3-4 weeks after inoculation. Infected tissue was homogenised in 0.5% mercaptoethanol, and clarification was done by emulsification with chloroform (ratio 1:1, extract:chloroform, v/v).
Differential centrifugation was used by Sehgal (1968). Infected leaf tissue was chilled at 4°C for 10-12 h then extracted in 67 mM phosphate buffer pH 7.0 with 10 mM NaDIECA. Extract clarification was achieved by acidification to pH 5.3 and DEAE cellulose treatment.
Jones and Tolin (1972) extracted virus in 0.1 sodium citrate containing 0.5 M mercaptoethanol, and clarification was done by emulsification with half volume of chloroform. Langenberg (1973) applied 0.1 M TAC (Triscitric acid-PVP-2-mercaptoethanol) pH 8.2 with 1.3 propane diamine for virus extraction. Clarification was done using CaCl2 and K2HPO4, and the virus was pelleted using PEG.
Tosic et al. (1974) purified MDMV from maize leaves which had been chilled at 4°C for 12-16 h, 3 weeks after inoculation. Extraction was performed in 0.01 M phosphate buffer at pH 7.0, also in a cool room. Extract was clarified by acidification to pH 4.7 (with 1.0 N HCl) and emulsification with a low volume of chloroform (3%, v/v), after which differential centrifugation, sucrose density gradient or centrifugation through 30% of sucrose were applied.
Von Baumgarten and Ford (1981) purified MDMV from maize leaves 10-12 daus after inoculation. Extraction was done in 60 mM sodium phosphate buffer pH 9.2 containing 10 mM NaDIECA. Clarification was performed with low volume (5%, v/v) of chloroform. The virus was pelleted using PEG with the addition of NaCl up to 0.3 M.
Means of Movement and Dispersal
Top of pageVector transmission
Many aphid species are involved in MDMV transmission. The following species are proven vectors of MDMV: Acyrthosiphon pisum, Aphis citricola, A. craccivora, A. decepta, A. fabae, A. gossypii, A. helianthi, A. maidiradicis, Brevicoryne brassicae, Hysteroneura setariae, Macrosiphum euphorbiae, Metopolophium festucae, Myzus persicae, Rhopalosiphum maidis, R. padi, Rhopalomyzus poae, Schizaphis graminum, Sitobion avenae, Therioaphis trifolii forma maculata and Uroleucon ambrosiae (Tosic and Simova, 1967; Tosic and Sutic. 1968; Koike, 1977; Ferro et al., 1980; Berger et al., 1983; Madden et al., 1983; Rest and Splittstoesser., 1985; Ford et al., 1989; Mijavec, 1991; Garrido and Cermeli, 1994).
Seedborne Aspects
Top of page
Incidence
MDMV has been detected at levels of about 0.5% in maize seeds (Shepherd and Holdeman, 1965; Williams et al., 1968; Boothroyd, 1977; Hill et al., 1974; Mikel et al., 1984b). There is some indication that newer strains might be transmitted at higher rates than older ones (Knoke and Louie, 1981). In sweetcorn plants leaf-inoculated by a mixture of strains A and B, MDMV was detected in the pericarp, but rarely in the endosperm and embryo of seeds at 21 days after pollination. In mature seeds, MDMV was occasionally detected in the pericarp and endosperm, but not in the embryo (Mikel et al., 1984b). With respect to the process of infection of seeds, Nemchinov et al. (1990) showed that MDMV is present in all floral meristems of male and female reproductive structures of all stages of organogenesis of ears and cobs of infected maize. The virus was also found in suspensions from mature pollen grains as well as in all parts of the mature seed. Mikel et al. (1982) proved that MDMV is present in the silks, but did not find the virus in pollen grains. They also showed that pollen from infected maize plants develops shorter germ tubes in vitro as well as in vivo. Mikel et al. (1984b) showed that MDMV is also present in glumes, anthers and unfertilized or fertilized kernels.
Miao HongQin et al. (1998) studied the effects of time of plant infection by MDMV on seedborne infection as follows: in an insect-proof greenhouse, three maize inbred lines (Huangye 4-3, 7922 and 81515) were inoculated with MDMV at the 3 to 5, 6 to 8, 9 to 11 and 13 to 15-leaf stages. Bioassays showed that the rate of seedborne MDMV was 0% in Huangye 4-3 (a resistant line), 1.65% in 7922 (a susceptible line) and 0% in 81515 (a resistant line). The rates of MDMV infection at the four growth stages (from seedling to booting) in line 7922 were 100, 100, 63.6 and 10.1%, disease indexes were 95.6, 82.4, 63.6 and 11.1 and the rates of seedborne MDMV were 2.3, 1.5, 3.3 and 0.78%, respectively. Evaluation of the three inbred lines suggested that resistance levels were related to infected plant growth periods. The younger the plants, the lower the resistance they showed to MDMV infection.
Effect on Seed Quality
One report indicated that germination of seed from MDMV-infected plants was not suppressed, but shoot and root growth was reduced (Panayotou, 1981). Another study showed that both germination and root development were reduced (Stakic and Savic, 1984). More recently, Achon and Sin (1998) artificially infected two inbred lines, Mo17 (susceptible) and B73 (tolerant) and their hybrids with MDMV. Virus infection reduced the number of seeds produced on infected plants. The reductions were 30-33% on Mo17, 20.9% on Mo17XB73, 7.5-7.7% on B73 and 4.4-8.3% on B73XMo17.
Pathogen Transmission
Transmission of MDMV from infected maize seeds to seedlings has been demonstrated in sterilized soil (Shepherd and Holdeman, 1965; Williams et al., 1968; Hill et al., 1974; Mikel et al., 1984b). The virus could not be transmitted through seeds of infected sorghum (Madhulika Mishra et al., 1998).
Weed hosts, in particular Johnsongrass (Knoke et al., 1983), and aphids (Knoke and Louie, 1981; Knoke et al., 1983; Rest et al., 1985; Scott, 1985) are considered to be major inoculum sources. Aphids transmit the pathogen nonpersistently.
Seed Treatment
No known seed treatment will eliminate MDMV infection. Imidacloprid seed treatment has been investigated, but control under field conditions by reduction of aphid transmission of MDMV was not demonstrated (Epperlein et al., 1995).
Seed Health Tests
Grow-out: seeds are grown in sterile soil and examined for symptom development (Shepherd and Holdeman, 1965; Williams et al., 1968; Hill et al., 1974; Mikel et al., 1984).
Serological: ELISA successfully detected the pathogen in seed parts (Mikel et al., 1984). Other ELISA tests (Reeves et al., 1978) have not been applied to seeds. Monoclonal antibodies have been developed to the virus (Hill et al., 1984).
Iowa State University Seed Health Testing Laboratory has adapted a diagnostic kit manufactured by Agdia Unc, Elkhart, Indiana, USA, to test for MDMV in seeds. The method is available on the USDA National Seed Health System website, www.seedhealth.org.
MDMV has been detected at levels of about 0.5% in maize seeds (Shepherd and Holdeman, 1965; Williams et al., 1968; Boothroyd, 1977; Hill et al., 1974; Mikel et al., 1984b). There is some indication that newer strains might be transmitted at higher rates than older ones (Knoke and Louie, 1981). In sweetcorn plants leaf-inoculated by a mixture of strains A and B, MDMV was detected in the pericarp, but rarely in the endosperm and embryo of seeds at 21 days after pollination. In mature seeds, MDMV was occasionally detected in the pericarp and endosperm, but not in the embryo (Mikel et al., 1984b). With respect to the process of infection of seeds, Nemchinov et al. (1990) showed that MDMV is present in all floral meristems of male and female reproductive structures of all stages of organogenesis of ears and cobs of infected maize. The virus was also found in suspensions from mature pollen grains as well as in all parts of the mature seed. Mikel et al. (1982) proved that MDMV is present in the silks, but did not find the virus in pollen grains. They also showed that pollen from infected maize plants develops shorter germ tubes in vitro as well as in vivo. Mikel et al. (1984b) showed that MDMV is also present in glumes, anthers and unfertilized or fertilized kernels.
Miao HongQin et al. (1998) studied the effects of time of plant infection by MDMV on seedborne infection as follows: in an insect-proof greenhouse, three maize inbred lines (Huangye 4-3, 7922 and 81515) were inoculated with MDMV at the 3 to 5, 6 to 8, 9 to 11 and 13 to 15-leaf stages. Bioassays showed that the rate of seedborne MDMV was 0% in Huangye 4-3 (a resistant line), 1.65% in 7922 (a susceptible line) and 0% in 81515 (a resistant line). The rates of MDMV infection at the four growth stages (from seedling to booting) in line 7922 were 100, 100, 63.6 and 10.1%, disease indexes were 95.6, 82.4, 63.6 and 11.1 and the rates of seedborne MDMV were 2.3, 1.5, 3.3 and 0.78%, respectively. Evaluation of the three inbred lines suggested that resistance levels were related to infected plant growth periods. The younger the plants, the lower the resistance they showed to MDMV infection.
Effect on Seed Quality
One report indicated that germination of seed from MDMV-infected plants was not suppressed, but shoot and root growth was reduced (Panayotou, 1981). Another study showed that both germination and root development were reduced (Stakic and Savic, 1984). More recently, Achon and Sin (1998) artificially infected two inbred lines, Mo17 (susceptible) and B73 (tolerant) and their hybrids with MDMV. Virus infection reduced the number of seeds produced on infected plants. The reductions were 30-33% on Mo17, 20.9% on Mo17XB73, 7.5-7.7% on B73 and 4.4-8.3% on B73XMo17.
Pathogen Transmission
Transmission of MDMV from infected maize seeds to seedlings has been demonstrated in sterilized soil (Shepherd and Holdeman, 1965; Williams et al., 1968; Hill et al., 1974; Mikel et al., 1984b). The virus could not be transmitted through seeds of infected sorghum (Madhulika Mishra et al., 1998).
Weed hosts, in particular Johnsongrass (Knoke et al., 1983), and aphids (Knoke and Louie, 1981; Knoke et al., 1983; Rest et al., 1985; Scott, 1985) are considered to be major inoculum sources. Aphids transmit the pathogen nonpersistently.
Seed Treatment
No known seed treatment will eliminate MDMV infection. Imidacloprid seed treatment has been investigated, but control under field conditions by reduction of aphid transmission of MDMV was not demonstrated (Epperlein et al., 1995).
Seed Health Tests
Grow-out: seeds are grown in sterile soil and examined for symptom development (Shepherd and Holdeman, 1965; Williams et al., 1968; Hill et al., 1974; Mikel et al., 1984).
Serological: ELISA successfully detected the pathogen in seed parts (Mikel et al., 1984). Other ELISA tests (Reeves et al., 1978) have not been applied to seeds. Monoclonal antibodies have been developed to the virus (Hill et al., 1984).
Iowa State University Seed Health Testing Laboratory has adapted a diagnostic kit manufactured by Agdia Unc, Elkhart, Indiana, USA, to test for MDMV in seeds. The method is available on the USDA National Seed Health System website, www.seedhealth.org.
Plant Trade
Top of page| Plant parts liable to carry the pest in trade/transport | Pest stages | Borne internally | Borne externally | Visibility of pest or symptoms |
|---|---|---|---|---|
| Flowers/Inflorescences/Cones/Calyx | Yes | Pest or symptoms usually invisible | ||
| Leaves | Yes | Pest or symptoms usually visible to the naked eye | ||
| Roots | Yes | Pest or symptoms usually invisible | ||
| Seedlings/Micropropagated plants | Yes | Pest or symptoms usually visible to the naked eye | ||
| Stems (above ground)/Shoots/Trunks/Branches | Yes | Pest or symptoms usually invisible | ||
| True seeds (inc. grain) | Yes | Pest or symptoms usually visible to the naked eye |
| Plant parts not known to carry the pest in trade/transport |
|---|
| Bark |
| Bulbs/Tubers/Corms/Rhizomes |
| Fruits (inc. pods) |
| Growing medium accompanying plants |
| Wood |
Vectors and Intermediate Hosts
Top of page| Vector | Source | Reference | Group | Distribution |
|---|---|---|---|---|
| Acyrthosiphon pisum | Ford et al. (1989) | Insect | ||
| Aphis craccivora | Ford et al. (1989) | Insect | ||
| Aphis decepta | Insect | |||
| Aphis fabae | Ford et al. (1989) | Insect | ||
| Aphis gossypii | Ford et al. (1989) | Insect | ||
| Aphis maidiradicis | Ford et al. (1989) | Insect | ||
| Aphis spiraecola | Insect | |||
| Brevicoryne brassicae | Ford et al. (1989) | Insect | ||
| Hysteroneura setariae | Insect | |||
| Macrosiphum euphorbiae | Ford et al. (1989) | Insect | ||
| Metopolophium festucae | Mijavec (1991) | Insect | ||
| Myzus persicae | Ford et al. (1989) | Insect | ||
| Rhopalomyzus poae | Insect | |||
| Rhopalosiphum maidis | Ford et al. (1989) | Insect | ||
| Rhopalosiphum padi | Ford et al. (1989) | Insect | ||
| Schizaphis graminum | Ford et al. (1989) | Insect | ||
| Sitobion avenae | Ford et al. (1989) | Insect | ||
| Therioaphis trifolii | Ford et al. (1989) | Insect | ||
| Uroleucon ambrosiae | Insect |
Impact
Top of page
MDMV causes economic losses in maize, including field maize, sweetcorn and maize inbred lines (seed crop), as well as sorghum, including silage sorghum, grain sorghum and broom maize. Infection on maize plants affects growth stages of development, leaf area, fertility and mature weights, number of seeds and rows, yield (seed yield, total yield), 1000 grain weight, seed quality (viability), and susceptibility of infected plants to other pathogens/diseases.
The extent of pathological changes induced by MDMV mainly depends on cultivar susceptibility, time of infection, water conditions, nutrients etc.
Early infection with MDMV delays all stages of maize development, for ca 2 weeks or more (Dimitrijevic, 1969; Scott and Nelson, 1972; Mikel et al., 1981).
The height of maize plants infected with MDMV is reduced by up to 23% (Tosic and Misovic, 1967; Popov, 1972; Sum et al., 1979; Olsen et al., 1990). In extreme cases, especially with maize inbred lines, the diseased plants are 25-50% of the height of healthy plants (Jansen and Ellet, 1963; Tosic et al., 1990a).
Leaf area reduction in maize plants infected with MDMV is up to 11%, but after early infection and early water stress, the leaf area could be reduced by 33% or more (Olsen et al., 1990). Leaf area reduction, along with a decrease in plant height, have a large influence on crop productivity.
Sterility, which is more frequent with infected maize plants, contributes to the economic impact of MDMV. Reduced growth and development, and changes in some plant development stages (Dimitrijevic, 1969; Scott and Nelson, 1972; Mikel et al., 1981) can lead to sterility in up to 25% of infected plants (Tosic and Misovic, 1967), but in the case of maize inbred lines the sterility can be even higher (Tosic et al., 1990a).
The number of ears per plant, especially of marketable ears of sweetcorn crops, is markedly reduced by MDMV infection (Gregory and Ayers, 1982; Mikel et al., 1982). Fresh weight of ears can be reduced by 30% or more by MDMV infection. (Anzola et al., 1980; Mikel et al., 1981; Antignus, 1987). Ear length reduction due to MDMV infection ranges by up to 25.6% (Tosic and Misovic, 1967; Mikel et al., 1981; Peti, 1983). The diameter of ears of maize plants infected with MDMV is also affected (Mikel et al., 1981). Ear yield can be drastically reduced by MDMV, especially after an early infection. The reduction in ear weight caused by MDMV infection can be nearly 50% (Tosic and Misovic, 1967; Antignus, 1987; Fuchs et al., 1990b; Olsen et al., 1990). Ears of maize plants infected with MDMV are poorly filled and the number of kernels and rows of kernels are reduced (Tosic and Misovic, 1967; Olsen et al., 1990; Kovacs et al., 1994).
Kernels of maize plants infected by MDMV are usually smaller, especially at the basal portion of the ear (Mikel et al., 1981). Consequently, the 1000 grain weight can be reduced by up to 26% (Peti, 1983; Kovacs et al., 1994).
The total yield of maize can be very much affected by MDMV infection. Yield reduction per fertile field maize plant infected with MDMV can be up to 42% (Tosic and Misovic, 1967). However, with maize inbred lines or with sweetcorn, especially after later sowing, the yield can be reduced by 75% or more (Forster et al., 1980).
Germinability of seeds formed on maize plants infected with MDMV may be reduced by nearly 20%, while the length and width of primary roots are smaller by 7.4 and 20.0%, respectively (Stakic and Savic, 1984).
Sorghum is the second main crop which can be affected by MDMV. Symptoms on sorghum plants infected with MDMV can be more severe than those caused by the same virus on maize plants. The symptoms on sorghum depends on cultivar susceptibility, time of infection, and environmental conditions (mainly temperature). Besides mosaic and growth reduction, infected sorghum plants show red stripes and necrosis. Red stripe is a common symptom, characteristic of sorghum plants infected by MDMV. Necrosis usually appears after a low temperature period, when the temperature falls to 15-16°C and below. After a such cool period the leaves of sorghum plants infected with MDMV, and showing mosaic and red stripes symptoms, became necrotic. It appears as a shock reaction, after which plants usually recover but they yield less than healthy plants (Berenji et al., 1996).
Yield of grain sorghum due to MDMV infection can be reduced by 15% (Toler, 1985) or up to 79% (Giorda and Toler, 1986). With broomcorn, depending on the cultivar, yield decrease can range from 32 to 59% (Tosic and Mijavec, 1991).
The extent of pathological changes induced by MDMV mainly depends on cultivar susceptibility, time of infection, water conditions, nutrients etc.
Early infection with MDMV delays all stages of maize development, for ca 2 weeks or more (Dimitrijevic, 1969; Scott and Nelson, 1972; Mikel et al., 1981).
The height of maize plants infected with MDMV is reduced by up to 23% (Tosic and Misovic, 1967; Popov, 1972; Sum et al., 1979; Olsen et al., 1990). In extreme cases, especially with maize inbred lines, the diseased plants are 25-50% of the height of healthy plants (Jansen and Ellet, 1963; Tosic et al., 1990a).
Leaf area reduction in maize plants infected with MDMV is up to 11%, but after early infection and early water stress, the leaf area could be reduced by 33% or more (Olsen et al., 1990). Leaf area reduction, along with a decrease in plant height, have a large influence on crop productivity.
Sterility, which is more frequent with infected maize plants, contributes to the economic impact of MDMV. Reduced growth and development, and changes in some plant development stages (Dimitrijevic, 1969; Scott and Nelson, 1972; Mikel et al., 1981) can lead to sterility in up to 25% of infected plants (Tosic and Misovic, 1967), but in the case of maize inbred lines the sterility can be even higher (Tosic et al., 1990a).
The number of ears per plant, especially of marketable ears of sweetcorn crops, is markedly reduced by MDMV infection (Gregory and Ayers, 1982; Mikel et al., 1982). Fresh weight of ears can be reduced by 30% or more by MDMV infection. (Anzola et al., 1980; Mikel et al., 1981; Antignus, 1987). Ear length reduction due to MDMV infection ranges by up to 25.6% (Tosic and Misovic, 1967; Mikel et al., 1981; Peti, 1983). The diameter of ears of maize plants infected with MDMV is also affected (Mikel et al., 1981). Ear yield can be drastically reduced by MDMV, especially after an early infection. The reduction in ear weight caused by MDMV infection can be nearly 50% (Tosic and Misovic, 1967; Antignus, 1987; Fuchs et al., 1990b; Olsen et al., 1990). Ears of maize plants infected with MDMV are poorly filled and the number of kernels and rows of kernels are reduced (Tosic and Misovic, 1967; Olsen et al., 1990; Kovacs et al., 1994).
Kernels of maize plants infected by MDMV are usually smaller, especially at the basal portion of the ear (Mikel et al., 1981). Consequently, the 1000 grain weight can be reduced by up to 26% (Peti, 1983; Kovacs et al., 1994).
The total yield of maize can be very much affected by MDMV infection. Yield reduction per fertile field maize plant infected with MDMV can be up to 42% (Tosic and Misovic, 1967). However, with maize inbred lines or with sweetcorn, especially after later sowing, the yield can be reduced by 75% or more (Forster et al., 1980).
Germinability of seeds formed on maize plants infected with MDMV may be reduced by nearly 20%, while the length and width of primary roots are smaller by 7.4 and 20.0%, respectively (Stakic and Savic, 1984).
Sorghum is the second main crop which can be affected by MDMV. Symptoms on sorghum plants infected with MDMV can be more severe than those caused by the same virus on maize plants. The symptoms on sorghum depends on cultivar susceptibility, time of infection, and environmental conditions (mainly temperature). Besides mosaic and growth reduction, infected sorghum plants show red stripes and necrosis. Red stripe is a common symptom, characteristic of sorghum plants infected by MDMV. Necrosis usually appears after a low temperature period, when the temperature falls to 15-16°C and below. After a such cool period the leaves of sorghum plants infected with MDMV, and showing mosaic and red stripes symptoms, became necrotic. It appears as a shock reaction, after which plants usually recover but they yield less than healthy plants (Berenji et al., 1996).
Yield of grain sorghum due to MDMV infection can be reduced by 15% (Toler, 1985) or up to 79% (Giorda and Toler, 1986). With broomcorn, depending on the cultivar, yield decrease can range from 32 to 59% (Tosic and Mijavec, 1991).
Diagnosis
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MDMV can be differentiated from sugarcane mosaic potyvirus, sorghum mosaic potyvirus and Johnson grass mosaic potyvirus in several ways. The quickest and most reliable methods are infectivity (bioassays), serology (serodiagnosis) (Ford et al., 1989) and, more recently, RT-PCR (Marie-Jeanne et al., 2000).
Maize, and especially sweetcorn seedlings, are very reliable test plants in mechanical as well as in inoculation tests with aphid vectors. Johnsongrass, oat and maize seedlings should be used as test plants. Johnsongrass seedling test plants would differentiate MDMV from Sugarcane mosaic virus and sorghum mosaic virus. MDMV readily infects Johnsongrass (Ford et al., 1989) while Sugarcane mosaic virus and Sorghum mosaic virus only rarely infect Johnsongrass (Tippett and Abbott, 1968; Koike and Gillaspie, 1976; Teakle et al., 1989; Shukla et al., 1994).
Oats are only susceptible to Johnsongrass mosaic virus (Tosic et al., 1990a). Oats cultivar Garland is the best test plant (McDaniel and Gordon, 1985). In addition to Johnsongrass and oats, MDMV can also be identified and differentiated by inoculating a set of sorghum cultivars inoculating Atlas Rio, BTX398, NM31, SA8735, R430, OKY8, Tarman, Aunis, Trudex and TX2786. When infected with MDMV, seedlings of these sorghum varieties develop mosaic, but Altas Rio, NM31, R430 and Aunis may also show rare necrosis on new leaves (Tosic et al., 1990a). Reliable results can be obtained by using Johnsongrass, sorghum cultivar Atlas, oats, and maize seedlings as test plants.
Test plants for bioassays are best used at the 3-leaf stage. The first leaf can be inoculated on the 6th day after plant emergence, the second leaf 2 days later, and the third leaf 2 weeks after plant emergence. Inoculated test plants should be incubated at 25°C (Seifers, 1984). Although either is satisfactory, mechanical inoculation is more efficient when performed on the lower leaf surface (Rosenkranz and Scott, 1987).
Serological analysis is very fast, can be applied to many samples, and, when properly done, is dependable. A prerequisite is a good antiserum. MDMV is a good immunogen and prepared antisera have high titers (1/258-1/516 in slide agglutination tests) (Tosic and Ford, 1974).
Many serological methods have been used for MDMV detection. Those most used are ELISA (Reeves et al., 1978; Sum et al., 1979a; Jarjees and Uyemoto, 1984) and electro-blot immunoassay (EBIA) (Shukla et al., 1989a; Lenardon et al., 1993). However, slide agglutination (Tosic, 1974; Tosic and Ford, 1974; Tosic et al., 1977), as well as agar-gel-double diffusion tests (Gordon et al., 1976; Novikov et al., 1984; An et al., 1992; Garrido et al., 1993) have been successfully used. More recently, RT-PCR has been used for identification and differentiation (e.g. Marie-Jeanne et al., 2000).
Maize, and especially sweetcorn seedlings, are very reliable test plants in mechanical as well as in inoculation tests with aphid vectors. Johnsongrass, oat and maize seedlings should be used as test plants. Johnsongrass seedling test plants would differentiate MDMV from Sugarcane mosaic virus and sorghum mosaic virus. MDMV readily infects Johnsongrass (Ford et al., 1989) while Sugarcane mosaic virus and Sorghum mosaic virus only rarely infect Johnsongrass (Tippett and Abbott, 1968; Koike and Gillaspie, 1976; Teakle et al., 1989; Shukla et al., 1994).
Oats are only susceptible to Johnsongrass mosaic virus (Tosic et al., 1990a). Oats cultivar Garland is the best test plant (McDaniel and Gordon, 1985). In addition to Johnsongrass and oats, MDMV can also be identified and differentiated by inoculating a set of sorghum cultivars inoculating Atlas Rio, BTX398, NM31, SA8735, R430, OKY8, Tarman, Aunis, Trudex and TX2786. When infected with MDMV, seedlings of these sorghum varieties develop mosaic, but Altas Rio, NM31, R430 and Aunis may also show rare necrosis on new leaves (Tosic et al., 1990a). Reliable results can be obtained by using Johnsongrass, sorghum cultivar Atlas, oats, and maize seedlings as test plants.
Test plants for bioassays are best used at the 3-leaf stage. The first leaf can be inoculated on the 6th day after plant emergence, the second leaf 2 days later, and the third leaf 2 weeks after plant emergence. Inoculated test plants should be incubated at 25°C (Seifers, 1984). Although either is satisfactory, mechanical inoculation is more efficient when performed on the lower leaf surface (Rosenkranz and Scott, 1987).
Serological analysis is very fast, can be applied to many samples, and, when properly done, is dependable. A prerequisite is a good antiserum. MDMV is a good immunogen and prepared antisera have high titers (1/258-1/516 in slide agglutination tests) (Tosic and Ford, 1974).
Many serological methods have been used for MDMV detection. Those most used are ELISA (Reeves et al., 1978; Sum et al., 1979a; Jarjees and Uyemoto, 1984) and electro-blot immunoassay (EBIA) (Shukla et al., 1989a; Lenardon et al., 1993). However, slide agglutination (Tosic, 1974; Tosic and Ford, 1974; Tosic et al., 1977), as well as agar-gel-double diffusion tests (Gordon et al., 1976; Novikov et al., 1984; An et al., 1992; Garrido et al., 1993) have been successfully used. More recently, RT-PCR has been used for identification and differentiation (e.g. Marie-Jeanne et al., 2000).
Detection and Inspection
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Dwarf mosaic on maize and sorghum plants is easily observed. At least three surveys should be undertaken in order to detect the disease and to estimate its intensity in maize or sorghum crops. The best time for the first survey is when plants have 5-7 leaves, the second should be performed around the stage of silking and heading, and the third should be later in the season, before plants start to senesce and change colour.
Mosaic symptoms are obvious on younger leaves and younger plants within 1-2 weeks after inoculation. Mosaic symptoms are also more visible early in the morning or when it is cloudy. High temperature and drought make mosaic symptoms more difficult to observe.
Mosaic symptoms on maize or sorghum crops can be detected by long distance photography (aerial detection) (Ausmuss and Hilty, 1972).
Mosaic symptoms are obvious on younger leaves and younger plants within 1-2 weeks after inoculation. Mosaic symptoms are also more visible early in the morning or when it is cloudy. High temperature and drought make mosaic symptoms more difficult to observe.
Mosaic symptoms on maize or sorghum crops can be detected by long distance photography (aerial detection) (Ausmuss and Hilty, 1972).
Similarities to Other Species/Conditions
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MDMV is a member of the Potyvirus genus of the Potyviridae family, and has a close relationship to the subgroup of Sugarcane mosaic virus. Other viruses in this taxon are similar in morphology and particle structure, and for some there is also a close similarity in natural methods of transmission.
The viruses of the MDMV subgroup are Sugarcane mosaic virus (SCMV), Sorghum mosaic virus (SrMV) and Johnsongrass mosaic virus (JGMV). They are similar in particle morphology, physical and biophysical properties, ways of transmission (mechanically and by aphids in a nonpersistent manner), serology and, with a few exceptions, in host range.
Because of these similarities, MDMV was once considered to be a strain of SCMV (Shepherd, 1965; Stefanac, 1967; Snazelle et al., 1971; Pirone, 1972). New approaches in taxonomy of these viruses and the development and application of N-terminus serology (Shukla et al., 1989a) showed that MDMV differed from SCMV, SrMV, JGMV and even from the former strain B of MDMV (MDMV-B) which was re-identified as a new strain of SCMV, SCMV-MDB (Shukla et al, 1989b).
MDMV differs from other viruses in the Sugarcane mosaic virus subgroup of potyviruses as follows:
1. Infectivity to Johnsongrass. MDMV and Johnsongrass mosaic virus readily infect Johnsongrass, while Sugarcane mosaic virus and Sorghum mosaic virus do not (Tippett and Abbott, 1968; Koike and Gillaspie, 1976; Teakle et al., 1989; Shukla et al., 1994).
2. Infectivity to oats. MDMV, like Sugarcane mosaic virus and Sorghum mosaic virus, does not infect oats, whilst Johnsongrass mosaic virus does infect oats (McDaniel and Gordon, 1985; Tosic et al., 1990a).
3. Serology. MDMV is serologically related via the conserved central section of the protein coat to Sugarcane mosaic virus, Sorghum mosaic virus and Johnsongrass mosaic virus, but is easily differentiated by purified antiserum which only contains antibodies reacting specifically to the N-terminus of the protein (Shukla et al., 1989a).
4. Reaction of sorghum differential cultivars. MDMV infects all sorghum differential genotypes, Atlas, Rio, BTX 398, NM31, SA 8735, R430, OKY8, Tamaran, Aunis and Turdex. MDMV causes mosaic on these cultivars and on Atlas, Rio, NM31, R430 and Aunis, also causes rare necrosis on new leaves (Tosic et al., 1990a).
5. Cell inclusions. MDMV, like Johnsongrass mosaic virus and Sorghum mosaic virus, induces pinwheels and scrolls, while Sugarcane mosaic virus in addition to those two types of cell inclusions, induces laminated aggregates (Lesemann et al., 1992).
The viruses of the MDMV subgroup are Sugarcane mosaic virus (SCMV), Sorghum mosaic virus (SrMV) and Johnsongrass mosaic virus (JGMV). They are similar in particle morphology, physical and biophysical properties, ways of transmission (mechanically and by aphids in a nonpersistent manner), serology and, with a few exceptions, in host range.
Because of these similarities, MDMV was once considered to be a strain of SCMV (Shepherd, 1965; Stefanac, 1967; Snazelle et al., 1971; Pirone, 1972). New approaches in taxonomy of these viruses and the development and application of N-terminus serology (Shukla et al., 1989a) showed that MDMV differed from SCMV, SrMV, JGMV and even from the former strain B of MDMV (MDMV-B) which was re-identified as a new strain of SCMV, SCMV-MDB (Shukla et al, 1989b).
MDMV differs from other viruses in the Sugarcane mosaic virus subgroup of potyviruses as follows:
1. Infectivity to Johnsongrass. MDMV and Johnsongrass mosaic virus readily infect Johnsongrass, while Sugarcane mosaic virus and Sorghum mosaic virus do not (Tippett and Abbott, 1968; Koike and Gillaspie, 1976; Teakle et al., 1989; Shukla et al., 1994).
2. Infectivity to oats. MDMV, like Sugarcane mosaic virus and Sorghum mosaic virus, does not infect oats, whilst Johnsongrass mosaic virus does infect oats (McDaniel and Gordon, 1985; Tosic et al., 1990a).
3. Serology. MDMV is serologically related via the conserved central section of the protein coat to Sugarcane mosaic virus, Sorghum mosaic virus and Johnsongrass mosaic virus, but is easily differentiated by purified antiserum which only contains antibodies reacting specifically to the N-terminus of the protein (Shukla et al., 1989a).
4. Reaction of sorghum differential cultivars. MDMV infects all sorghum differential genotypes, Atlas, Rio, BTX 398, NM31, SA 8735, R430, OKY8, Tamaran, Aunis and Turdex. MDMV causes mosaic on these cultivars and on Atlas, Rio, NM31, R430 and Aunis, also causes rare necrosis on new leaves (Tosic et al., 1990a).
5. Cell inclusions. MDMV, like Johnsongrass mosaic virus and Sorghum mosaic virus, induces pinwheels and scrolls, while Sugarcane mosaic virus in addition to those two types of cell inclusions, induces laminated aggregates (Lesemann et al., 1992).
Prevention and Control
Top of pageDue to the variable regulations around (de)registration of pesticides, your national list of registered pesticides or relevant authority should be consulted to determine which products are legally allowed for use in your country when considering chemical control. Pesticides should always be used in a lawful manner, consistent with the product's label.
Introduction
The economic importance, due to damage caused in maize and sorghum production, make control of MDMV mandatory. Since it has a wide host range of ca 250 different plant species and more than 20 aphid vectors, control of MDMV is not easy. Therefore, many measures which can contribute to disease control have to be applied. Integrated MDMV control management should comprise three basic measures: destruction of Johnsongrass plus other wild hosts (the source of MDMV under field conditions); control of aphid vectors; and breeding of resistant maize and sorghum genotypes (Milinko et al., 1979; Gorbunova et al., 1980).
Johnsongrass is usually infected by up to 100% with MDMV (Pop, 1962; Shepherd et al., 1964; Sutic and Tosic, 1966; Reeves et al., 1978). Such a high incidence of infection is due to inoculum accumulation in the perennial Johnsongrass. Therefore, Johnsongrass serves as a permanent source (one of the best) of MDMV under field conditions (Tosic and Simova, 1967; Onazi and Wilde, 1974).
Although nearby sources of MDMV inoculum are the most important (Damsteegt, 1976; Madden et al., 1986), sudden epidemics of MDMV in areas without Johnsongrass was hypothesised by long distance aphid vector movement (Zeyen et al., 1987). Therefore, Johnsongrass should be destroyed wherever possible.
Johnsongrass should be controlled as early as possible after emergence (Vangessel and Coble, 1993). When Johnsongrass is controlled late in the season a higher incidence of MDMV occurs, especially on maize hybrids susceptible to MDMV (Eberwine and Hagood, 1995).
MDMV control by systemic insecticides against aphid vectors is also a big challenge. MDMV is transmitted nonpersistently group of viruses. Thus, viruliferous aphids can inoculate healthy plants before being affected by insecticide. It is suggested that the application of insecticides to source plants of the virus would lead to better results.
Oil application weekly or twice-a-week gave better, but not consistent, results (Ferro et al., 1980; Szatmari-Goodman and Nault, 1983).
Host Plant Resistance
The crucial measures for controlling MDMV is breeding resistance genotypes in maize and sorghum. For this, it is necessary to determine a source of resistance and then to transfer and incorporate the resistance into maize and sorghum genotypes growing in production. Mikel et al. (1984) transferred genetic resistance from Pa405 field maize inbred into sweetcorn.
The resistance against MDMV in maize or in sorghum can be recognised by: (1) the absence of infection or mild symptom expression (Kuhn and Smith, 1977; Fuchs and Bedri, 1993); (2) a lower percentage of plants developing symptoms (Kuch and Smith, 1977; Fuchs and Bedri, 1993); (3) a long incubation period (Kuhn and Smith, 1977; Fuchs and Bedri, 1993); (4) suppressed virus translocation-movement within the infected plant (Jones and Tolin, 1972; Ford and Hill, 1976; Kuhn and Smith, 1977; Law et al., 1987; Fuchs and Bedri, 1993); (5) virus presence restricted to certain leaf areas showing symptoms (stripes, bands etc.) (Jones and Tolin, 1972); and (6) a low virus titre (Fuchs and Bedri, 1993).
Resistance to MDMV should be tested both under greenhouse and field conditions. In some cases, similar results were obtained (Kuhn and Smith, 1977; Kovacs et al., 1993) but different results were obtained in others (Kuhn and Jellum, 1970; Louie et al., 1990; Kovacs et al., 1993; Kovacs et al., 1994). The results concerning resistance to MDMV, and obtained under greenhouse conditions, can be used to predict possible resistance under field conditions (Zuber et al., 1973). Selection of parental lines should be based on the results obtained under both greenhouse and field experiments (Naidu and Josephson, 1976).
Many maize genotypes were shown to possess the resistance gene. Examples of resistant genotypes are Pa405, B68, Ph1EP, 0H7B, Ga209, Oh514, Oh514, Oh07, I11A, W70, Oh28, 38-11, C103, A632, A634, B64, PI536518 and PI536519 (Nault et al., 1971; Findley et al., 1973; Findley et al., 1977; Roane et al., 1983; Mikel et al., 1984; Davis et al., 1988; Roane et al., 1989; Poneleit et al., 1990; Ivanovic, 1991; Kovacs et al., 1994). The resistance of some genotypes can be improved by the incorporation of germplasm from a local population (Ivanovic, 1991).
Zea diploperennis, a relative of maize, is immune to MDMV (Podol'skaya, 1988). The diploid teosinte can serve as a source of resistance for maize. Transfer of resistance to MDMV from the source to maize genotypes for growing purposes, can be achieved by crossing (Josephson and Naidu, 1971; Naidu and Josephson, 1976; Juvik and D'Arcy, 1988). In most cases resistance to MDMV is dominantly inherited (Brewbaker, 1975; Findley et al., 1977; Roane et al., 1983; Heo et al., 1985; Roane et al., 1989; Ivanovic et al., 1992; Kovacs et al., 1993; Kovacs et al., 1994) and is probably controlled by one dominant gene (Josephson and Naidu, 1971; Findley et al., 1977; Roane et al., 1983). In this case, crossing two resistant lines, or one resistant with one susceptible line, usually results in resistant hybrids, while crossing two susceptible lines results in a susceptible hybrid (Giorda and Toler, 1985). After crossing two resistant lines there is no, or very little, segregation in the F1 and F2 generations (Mikel et al., 1984).
In some cases resistance to MDMV is partial (Naidu and Josephson, 1976), and is controlled by few genes, one of which is mandatory (Josephson and Naidu, 1971; Mike et al., 1984). Different types of inheritance of resistance against MDMV with the same inbred line (maize genotype) was also shown to occur. It was dominant under field conditions but intermediate under greenhouse conditions (Kovacs et al., 1994).
In order to transfer and to incorporate resistance against MDMV in maize genotypes, back-crossing, alternative back-crossing and selfing or sib-pollination should be applied as well as crossing (Josephson and Naidu, 1971; Naidu and Josephson, 1976). Selection in F1 and BC1 generations, as well as recurrent selection, should be also be applied (Josephson and Naidu, 1976; Kovacs et al., 1990).
The resistance of inbred lines, their combining abilities (general and specific) and inheritance of resistance should be checked before crossing (Popov and Popova, 1976; Heo et al., 1985). Different maize inbred lines, resistant to MDMV, behave differently when crossing (Heo et al., 1985).
Some results have shown that the gene(s) controlling maize resistance against MDMV is located at chromosome 6, on either the short arm or the proximal region of the long arm (Roane et al., 1989; Louie et al., 1991; Simcox et al., 1993, 1995; Ignjatovic et al., 1995). Transgenic maize plants expressing sugarcane mosaic virus-MDB (former MDMV-B) coat protein were also resistant to MDMV-A (Murry et al., 1993).
The most important control measure is breeding sorghum resistant to MDMV. Reaction of sorghum genotypes to MDMV infection markedly differ (Fazli et al., 1970). Many sorghum genotypes, like RS 621, Tx 414, RS 625, BTx 399 (wheatland) and Tx 398 (Martin) are tolerant (Toler, 1985). A good level of resistance against MDMV exists in sorghum lines NM 960, Mer 75-6, Mer 76-1, Mer 77-2, and Mer 77-7 (Zummo et al., 1981). Many sorghum genotypes, like Tx2536, RTx 430 (Toler et al., 1982), Tx 2726 (Miller and Toler, 1984), RTx 435 (Miller, 1986) and RTx 2858 (Miller and Toler, 1990), are resistant to MDMV.
A high level of resistance (immunity) occurs in some sorghum genotypes derived from a cross of grain sorghum and Johnsongrass (2n=20) x Sorghum roxburghii (2n=20) (Krishnasway et al., 1956); i.e., Krish genotype containing the Krish type of resistance. The Krish resistance was transferred and incorporated into sorghum lines called QL lines, which serve as a good source of resistance (Mijavic, 1991). Among QL lines the most used are QL 11, QL 3-Tx and QL 3-India, which are immune to MDMV (Giorda et al., 1985; Giorda and Toler, 1985; Langham et al., 1985; Mijavec, 1989). Sorghum hybrids with RTx 2858 are highly resistant to MDMV.
Ways of transferring the resistance against MDMV in sorghum are the same as those for maize.
Cultural Control
MDMV can also be controlled by some agricultural practices. A lower incidence of disease is correlated with a good tillage system (All et al., 1977), greater plant density (Popov, 1978), early sowing (Scott and Rosenkranz, 1974; Popov, 1979; Forster et al., 1980), polyculture and wide crop rotation (Piper et al., 1996).
On controlling MDMV incidence (and harmfulness) in sorghum, including broomcorn, similar approaches should be effective. The destruction of virus sources, spraying against aphid vectors and agricultural practices can effect MDMV incidence in sorghum as they do in maize.
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Distribution References
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Paliwal YC, Raychaudhuri SP, 1966. Electron microscopic study of maize mosaic virus. In: Indian Journal of Microbiology, 5 69-70.
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Teyssandier EE, Nome SF, Dal Bo E, 1983. Maize virus diseases in Argentina. [Proceedings of the International Maize Virus Disease Colloquium and Workshop, 2-6 August 1982, The Ohio State University, Wooster, Ohio: Ohio Agricultural Research and Development Center], [ed. by Gordon DT, Knoke JK, Nault LR, Ritter RM]. 93-99.
Tosic M, 1962. A contribution to the study of virus diseases of maize in PR Serbia. In: Agronomski Glasnik, 5-7 418-421.
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