NEMATODE DISEASE
COMPLEXES
Introduction
■ Plant parasitic nematodes can be the sole pathogens or may interact with other
plant pathogens or nematodes to cause a disease complex.
■ Nematodes frequently form disease complexes with wilt-inducing and root-rot
fungi.
■ Infection by Meloidogyne spp., Pratylenchus and Rotylenchulus reniformis
nematodes, for example, increases the incidence and severity of Fusarium,
Verticillium spp, Pythium spp. wilt in a number of plants. Meloidogyne spp.,
Pratylenchus, Anguina and Ditylenchus interact with disease causing bacteria,
Clavibacter Pseudomonas and Agrobacterium to increase the severity of the
disease.
Cont..
■ Tomatoes grown in soils infested with nemaodes, were attacked by Ralstonia solanacearum but
in nematode free soils they remained healthy.
■ Nematodes serve as vectors of other plant pathogens, and/or wounding agents that increase the
susceptibility of the host.
■ Plant parasitic nematodes enhance host susceptibility leading to increased rate of development
and severity of wilt and fungal rot diseases.
■ The root exudates from root knot nematode (RKN) infected plants stimulate the fungal pathogens
and suppress actinomycetes, which are antagonists of the wilt fungus (Fusarium spp.).
■ The physiological change of RKN- infected plants also enhances penetration by the fungus and
wilt development.
■ Root knot nematode infection increases the pathogenicity of the wilt fungus and consequently
the severity of the disease.
How nematodes interfere with plant
physical and chemical defense system.
■ The nematodes establish their feeding sites in the xylem parenchyma cells,
bringing about significant changes in the morphology, anatomy and biochemistry
of the plant.
■ Giant cells induced by RKN remain in a state of high metabolic activity through
continuous stimulation by the nematode.
■ The high concentrations of sugars, hemi - cellulose, organic acids, free amino
acids, proteins and lipids benefits the fungal pathogens.
■ The giant cells remain in a perpetual juvenile state which delays maturation and
suberisation of other vascular tissues and thus fusarium successfully penetrates
and establishes in the xylem elements
Cont..
■ Inhibition of phytoalexins by the nematodes implies loss of resistance to the wilt
fungus.
■ Inhibition of tyloses formation by the RKN on tomato is a possible mechanism for
increased wilt.
■ Tyloses formed in the xylem vessels by the expansion of xylem parenchyma
through the pits do not develop from xylem parenchyma cells which are
transformed into giant cells or physiologically altered adjacent cells.
Nematodes and virus transmition
■ Nematodes are important vectors of viruses. Xiphinema and Longidorus
transmit nepoviruses (family secoviridae subfamily comovirinae, are
transmitted by nematodes).
■ Trichodorus and Paratrichodorus vector the tobraviruses (in the family
vigaviridae).
■ Xiphinema index and X. americanum, for example transmits grapevine fan
leaf and tomato ring spot viruses, respectively.
■ Longidorus elongatus transmits the raspberry ringspot virus, Trichodorus
cylindricus, the tobacco rattle virus and Paratrichodorus minor, the pepper
ringspot virus.
■ The nematodes transmit viruses in a non-circulative manner being the
ingestion-egestion type of transmission.
Nematodes and virus transmition
■ The nematode acquires/ingests the virus particles while feeding on the virus infected plant,
retains the particles at specific sites within the nematode and egest them by dissociation
from the sites of retention.
■ The virus retention sites differ among the nematode genera.
■ In Xiphinema, for example, the site is the cuticular lining of the odontophore, the
oesophagus and the oesophageal pump while in Longidorus, the site is the inner surface of
the cuticular ondontostyle and its guiding sheath.
■ In Trichodorus and Paratrichodorus the site is in the lining of the oesophagus from the
most anterior region to the cardia (oesophageal-intestinal valve) but not associated with
the onchiostyle.
■ All these surfaces are shed during moulting and therefore the virus particles do not pass
from one stage of the nematode to another during development.
Nematodes and bacteria diseases
■ Bacteria can be transmitted by nematodes externally on their body surfaces or
internally within their alimentary canal.
■ Anguina tritici is closely associated with Clavibacter tritici causing the yellow ear
rot or “tundu” in India.
■ The bacterium is associated with the body surface of the juveniles inside the seed
galls.
■ Ditylenchus dipsaci transmits Clavibacter michiganense pv. insidiosum which
causes wilt in alfalfa.
■ The bacterium is carried on the body of the nematodes into the crown buds and is
placed in conducive infection courts.
Nematodes and fungal disease
■ Nematodes have also been reported to transmit fungal pathogens.
■ Anguina tritici is a vector of spores of Dilophospora alopecuri which
attacks aerial parts of cereals.
■ The nematode while moving between the leaf sheaths to reach the
growing point takes the fungal conidia and deposits them on a
growing point.
■ Further, the nematode by feeding on the tender leaves helps in the
penetration and establishment of the fungus.
Conclusion
■ All PPN wound plants either by a simple micro-puncture or by rupturing or separating
cells.
■ They may thereby either introduce a pathogen on or within their bodies or aid the entry
of a pathogen already present on the plant cell surface.
■ Wounding is particularly important for bacteria as they enter plants mainly through
wounds.
■ Besides creating wounds the nematodes also modify the host tissue to enrich the
substrate nutritionally to the advantage of the bacteria.
■ For example Meloidogyne modifies tomato tissues and makes them more susceptible
to bacterial canker (Clavibacter michiganense) and bacterial wilt (Ralstonia
solanacearum) especially when the nematodes are inoculated before the bacterium.
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Nematode disease complexes

  • 1.
  • 2.
    Introduction ■ Plant parasiticnematodes can be the sole pathogens or may interact with other plant pathogens or nematodes to cause a disease complex. ■ Nematodes frequently form disease complexes with wilt-inducing and root-rot fungi. ■ Infection by Meloidogyne spp., Pratylenchus and Rotylenchulus reniformis nematodes, for example, increases the incidence and severity of Fusarium, Verticillium spp, Pythium spp. wilt in a number of plants. Meloidogyne spp., Pratylenchus, Anguina and Ditylenchus interact with disease causing bacteria, Clavibacter Pseudomonas and Agrobacterium to increase the severity of the disease.
  • 3.
    Cont.. ■ Tomatoes grownin soils infested with nemaodes, were attacked by Ralstonia solanacearum but in nematode free soils they remained healthy. ■ Nematodes serve as vectors of other plant pathogens, and/or wounding agents that increase the susceptibility of the host. ■ Plant parasitic nematodes enhance host susceptibility leading to increased rate of development and severity of wilt and fungal rot diseases. ■ The root exudates from root knot nematode (RKN) infected plants stimulate the fungal pathogens and suppress actinomycetes, which are antagonists of the wilt fungus (Fusarium spp.). ■ The physiological change of RKN- infected plants also enhances penetration by the fungus and wilt development. ■ Root knot nematode infection increases the pathogenicity of the wilt fungus and consequently the severity of the disease.
  • 4.
    How nematodes interferewith plant physical and chemical defense system. ■ The nematodes establish their feeding sites in the xylem parenchyma cells, bringing about significant changes in the morphology, anatomy and biochemistry of the plant. ■ Giant cells induced by RKN remain in a state of high metabolic activity through continuous stimulation by the nematode. ■ The high concentrations of sugars, hemi - cellulose, organic acids, free amino acids, proteins and lipids benefits the fungal pathogens. ■ The giant cells remain in a perpetual juvenile state which delays maturation and suberisation of other vascular tissues and thus fusarium successfully penetrates and establishes in the xylem elements
  • 5.
    Cont.. ■ Inhibition ofphytoalexins by the nematodes implies loss of resistance to the wilt fungus. ■ Inhibition of tyloses formation by the RKN on tomato is a possible mechanism for increased wilt. ■ Tyloses formed in the xylem vessels by the expansion of xylem parenchyma through the pits do not develop from xylem parenchyma cells which are transformed into giant cells or physiologically altered adjacent cells.
  • 6.
    Nematodes and virustransmition ■ Nematodes are important vectors of viruses. Xiphinema and Longidorus transmit nepoviruses (family secoviridae subfamily comovirinae, are transmitted by nematodes). ■ Trichodorus and Paratrichodorus vector the tobraviruses (in the family vigaviridae). ■ Xiphinema index and X. americanum, for example transmits grapevine fan leaf and tomato ring spot viruses, respectively. ■ Longidorus elongatus transmits the raspberry ringspot virus, Trichodorus cylindricus, the tobacco rattle virus and Paratrichodorus minor, the pepper ringspot virus. ■ The nematodes transmit viruses in a non-circulative manner being the ingestion-egestion type of transmission.
  • 7.
    Nematodes and virustransmition ■ The nematode acquires/ingests the virus particles while feeding on the virus infected plant, retains the particles at specific sites within the nematode and egest them by dissociation from the sites of retention. ■ The virus retention sites differ among the nematode genera. ■ In Xiphinema, for example, the site is the cuticular lining of the odontophore, the oesophagus and the oesophageal pump while in Longidorus, the site is the inner surface of the cuticular ondontostyle and its guiding sheath. ■ In Trichodorus and Paratrichodorus the site is in the lining of the oesophagus from the most anterior region to the cardia (oesophageal-intestinal valve) but not associated with the onchiostyle. ■ All these surfaces are shed during moulting and therefore the virus particles do not pass from one stage of the nematode to another during development.
  • 8.
    Nematodes and bacteriadiseases ■ Bacteria can be transmitted by nematodes externally on their body surfaces or internally within their alimentary canal. ■ Anguina tritici is closely associated with Clavibacter tritici causing the yellow ear rot or “tundu” in India. ■ The bacterium is associated with the body surface of the juveniles inside the seed galls. ■ Ditylenchus dipsaci transmits Clavibacter michiganense pv. insidiosum which causes wilt in alfalfa. ■ The bacterium is carried on the body of the nematodes into the crown buds and is placed in conducive infection courts.
  • 9.
    Nematodes and fungaldisease ■ Nematodes have also been reported to transmit fungal pathogens. ■ Anguina tritici is a vector of spores of Dilophospora alopecuri which attacks aerial parts of cereals. ■ The nematode while moving between the leaf sheaths to reach the growing point takes the fungal conidia and deposits them on a growing point. ■ Further, the nematode by feeding on the tender leaves helps in the penetration and establishment of the fungus.
  • 10.
    Conclusion ■ All PPNwound plants either by a simple micro-puncture or by rupturing or separating cells. ■ They may thereby either introduce a pathogen on or within their bodies or aid the entry of a pathogen already present on the plant cell surface. ■ Wounding is particularly important for bacteria as they enter plants mainly through wounds. ■ Besides creating wounds the nematodes also modify the host tissue to enrich the substrate nutritionally to the advantage of the bacteria. ■ For example Meloidogyne modifies tomato tissues and makes them more susceptible to bacterial canker (Clavibacter michiganense) and bacterial wilt (Ralstonia solanacearum) especially when the nematodes are inoculated before the bacterium.
  • 11.