Plant disease is the abnormal growth and development of a plant. A diseased plant is incapable of carrying out its normal physiological functions to the best of its genetic potential. Individual parasite or pathogen strains infect some host strains more readily than others causing diseases in such hosts. This may be due to the production of virulent factor(s) that is/are specific to that particular host variety by such a pathogen or due to the presence of some essential nutrients needed by the pathogen in the host variety (Hammond-kosack et al., 2003).

Specificity has to do with both the factors that determine virulence in the pathogen and also those that confer resistance in the host. Pathogen virulence and host resistance may both be determined by more than one factor. Most pathogens exhibit a high degree of host-specificity. Non-host plant species are often said to express non-host resistance (Jones et al.,2006T). The term host resistance is used when a pathogen species can be pathogenic on the host species but certain strains of that plant species resist certain strains of the pathogen species. There can be overlap in the causes of host resistance and non-host resistance. Pathogen host range can change quite suddenly if, for example, the capacity to synthesize a host-specific toxin or effector is gained by gene shuffling/mutation, or by horizontal gene transfer from a related or relatively unrelated organism (Friedman et al.,2007).

Good knowledge of specificity in plant diseases is important in controlling of plant diseases caused by pathogens either through producing specialized chemicals which will attack the structural integrity or metabolic activities of these pathogens or through better techniques for breeding and deploying resistant crops.


















Specificity in plant diseases entails the fact that some microbes are able to cause infection in a wide range of hosts while others can infect only one or a few host species. Specificity includes a distinction between hosts and non-host species. In some cases, a pathogen may be restrticted to particular host tissues or organs. Such tissue specificity is alluded to in many common names for pathogens, for example root rot, leaf mould and vascular wilt. Though, the factors controlling these patterns of colonization are poorly understood (Dickson et al., 1982).



Host–pathogen specificity means that the relative infectiousness of a pathogen to different host strains will vary from strain to strain inthe pathogen. In a simple two-strain system, for example, one pathogen strain might infecthost strain 1 more readily than host strain 2, while the other pathogen strain mightinfect host strain 2 more readily than host strain 1. Similarly, one pathogen strain might betwice as infectious as the other to host strain 1, but four times as infectious as the other tohost strain 2. In cases like these, the rate of disease transmission will be specific to eachcombination of host and pathogen strains, in a way that cannot be expressed as the simpleproduct of each pathogen’s overall infectiousness (to all host strains) and each host’s overallsusceptibility (to all pathogen strains) (Borowicz et al., 1991). The genetic basis of this strong specificity is explained by the gene-for-gene elicitor-receptor model. This model takes into account a virulence (avr) genes in the pathogen which are homologous to the resistance (R) genes in the host plant. A complementary combination of avr and R genes results in an incompatible host-pathogen interaction (rejection) and triggers defense mechanisms in the host cells. By contrast, a non-complementary combination of avr and R genes (compatible) results in infection (Clarke, D.D. 1997).

 A group of genes has been implicated consisting of the hypersensitivity reaction (HR) and pathogenicity (hrp) genes which control the capacity of pathogens to develop HR in non-host plants. The transcription of hrp genes is controlled by a hostsystem. A second group of genes, the avirulence (avr) genes, code for most of the virulence-associated proteins introduced into the host cell by the type III secretion system controlled by the HRP system, and trigger programmed plant defense responses such as HR (De Wit, 1997).

Host–pathogen specificity is widespread in nature, but little is known about its impact on the evolution of virulence. A simple host–parasite model was used to explore how the fitness consequences of pathogen infectiousness and lethality are influenced by the genetic specificity of host–parasite interactions (Kirchner et al., 2002).

2.2    THE MODEL

The analysis is based on a variant of the host–pathogen model developed by Kirchner and Roy (2001). The model contains two host strains and two pathogen strains. The model can be generalized straightforwardly for more complex systems. The equations assume haploid genetics for the hosts and pathogens. Thus, the equations are formally equivalent to those for ecological competition between separate host and pathogen species and could be used in that context as well. In the model, uninfected host populations are denoted Xi, where i = 1 . . . 2 denotes the host strain. Infected host populations are denoted Yik, where i denotes the host strain and k = 1 . . . 2 denotes the pathogen strain that it is infected. The pathogens cannot survive without hosts, so they need not be modelled explicitly; instead, their dynamics are represented by the infected host population. All of the host populations are expressed as fractions of the carrying capacity.


In specific host-pathogen interactions, the invading pathogen usually produces a toxin which affects the host normal metabolic processes. These toxins are called host-specific toxins (Kirchner et al., 2002).





These are low molecular weight compounds which are injurious to plants. Their production is usually triggered off when a virulent strain of a pathogen infects a particular susceptible host strain.  An example of such a toxin is Victorin which is isolated from Helminthosporium victoriae, the cause of blight disease in Oats. The fungus was especially virulent on one known variety known as Victoria. Although the pathogen was particularly localized in the basal portion of the plant, symptoms extended into the leaves which often collapsed. This shows that the toxin is mobile within the plant and thus acted at a distance from the actual site of infection. Victorin is a peptide linked to a tricyclic amine and it does not affect resistant Oat cultivars (Dickson et al.,1982).

Table 1: Some host-specific toxins involved in plant disease.






Helminthosporium victoriae


T toxin

Helminthosporium maydis Race T



Helminthosporium sacchari


PC toxin

Periconia circinata




Alternaria kikuchiana

Japanese pear



The most important attribute of host-specific toxins is that they are agents of virulence, a fungus that produces a host-specific toxin cause more disease on its host than one that is otherwise identical but does not produce the host-specific toxin. Plant insensitivity to a host specific toxin confers increased resistance to the producing organism. Most host-specific toxins are secondary metabolites, they show great diversity in their chemistry ant their biological effects. Known host-specific toxins include cyclic peptides, terpenoids, oligosaccharides, polyketides, and compounds of unknown biogenisis. (Macdonald et al.2002).








Plant viruses are obligate symbionts that depend on their host plants for reproduction. To colonize new hosts, most plant viruses also require vectors, which may include insects, mites, nematodes, or fungi. Although some viruses can be transmitted intergenerationally from parent to offspring in the seed, transmission by vectors clearly plays an important role in determining fitness for most viruses, and it can result in extremely rapid spread of a virus (Kado, 2000). Viruses vary in the number of possible hosts that they can infect, and in the number of vectors that can transmit them effectively. Viruses must take over the reproductive machinery of a cell, a process that requires specific receptors. Similarly, recent research has demonstrated that vector transmission requires highly specific viral transport mechanisms in the vector.

Vector Specificity versus Host Specificity.

Patterns of host and vector specificity differ significantly among types of vectors. Of the 474 viruses transmitted by vectors, 86.7% are transmitted by insects, 5.5% by fungi, 4.0% by nematodes, and 1.8% by mites. Because insects are the most common vectors, the patterns of specificity for the subset of insect-transmitted viruses are similar to those for all vectored viruses. Again, viruses have much more specialized relations with their insect vectors than with their hosts at the level of species, genus, and family.  Among insect-transmitted viruses, 54.9% have a single vector species, and only 10.8% have a single host plant. Viruses that have more intimate associations with their insect vectors might be expected to be the most vector specific.

Virus distribution is constrained more by the specificity of virus-vector relations

than by the specificity of virus-host plant relations. Many viruses have a very narrow range of vectors but a large host range. In contrast, no viruses have a narrow range of host plants if they have many vector species. The feeding range of the vector determines in large part the host range of the virus, suggesting that viruses can adapt to new hosts fairly readily (Jones et al., 2006).

Table 2 : Some viruses and their vectors.




Tomato spotted wilt virus (TSWV)



, Grapevine fanleaf virus (GFLV)

Xiphinema index (nematode)


Tomato yellow leaf curlv virus(TYLCV)

Bemisa tabaci





Plant host resistance mechanisms are characterized by a combination of constitutive and inducible responses usually referred to as passive and active resistance mechanisms respectively. Passive resistance mechanisms are anatomical or chemical barriers preventing establishment of the pathogen. These barriers are present prior to infection and therefore represent a constitutive feature of the host. In contrast, active resistance mechanisms are induced by challenge with a micro organism and cannot be detected in healthy plants prior to inoculation.












Figure 1: Passive resistance mechanism









Figure 2 : Active resistance mechanism

Constitutive responses consist of general barriers or preexisting biochemical defenses. Inducible responses can be localized or systemic and are more sophisticated because they involve the recognition of the pathogen by the host plant, signal transduction, and the expression of several genes (Casadevall et al., 2002). In a localized response, plant tissues react against pathogens by a type of programmed cell death consisting essentially of electrolyte leakage from the cytoplasm and an oxidative burst. In systemic defense, a signal spreads from the site of interaction as a response to chemicals, microorganisms, insects, mechanical damage or stress. The signal is mediated by several molecules which function as messengers in plants (Baker et al.,1997). These messengers interact with specific binding proteins that are implicated in the transcriptional activation of pathogenesisrelated (PR) genes in response to pathogen aggression. The products of several of these genes are enzymes, e.g. peroxidases, lipo-oxygenases, superoxide dismutases, and phenylalanine-ammonia-lyase (PAL), involved in the secondary metabolism of plants and specifically in the synthesis of phenolic compounds, or are phytoalexins, glucanases and chitinases, with antimicrobial activity (. Gutterson,1990).



Phytoalexins are antimicrobial compounds of low molecular weight synthesized by and accumulate in plants after exposure to microorganisms. They are produced at sufficient speed and in sufficiently high concentration to inhibit fungal pathogens and in some cases bacteria. Some chemical compounds stimulate the production of phytoalexins in some plants thereby helping in disease resistance indirectly, for example Calcium Chloride and Mercury Chloride stimulate the production of Pisatin in Pisum sativum (Dickson et al., 1982).  

Importance of phytoalexins in disease resistance.

1       They act as soldiers warding off pathogens in plants.

2       They prevent pathogens from colonizing plants and damaging them, for example, Pisatin produced from the pods, stem and leaves of Pea in response to attack by Monilinia fructicola and Aschochy pisi protected the plant from destruction.

Table 2 : Some phytoalexins produced in plants.


Plant host





Pisum sativum

Monilinia fructicola, Aschochy pisi


Solanum tuberosum


Phytophthora infestans

Caffeic acid

Solanum tuberosum


Phytophthora infestans




Rhizoctonia repens


Phaseolus vulgaris


Uromyces phaseoli





The Genetics of Stalk Rot Resistance

Nyhus et al (1989) demonstrated that recurrent selection for Diplodia stalk rot resistance led to improvements in anthracnose stalk rot resistance. One study of the inheritance of resistance for anthracnose stalk rot indicated that additive effects were most significant, while another suggested additive, dominance and epistatic effects were important. Similarly, additive effects have been reported to be most significant for Diplodia stalk rot resistance. A major gene for Gibberella stalk rot resistance has been reported on chromosome 6. Jung et al (1994) reported one major  Quantitative Trait Loci (QTL) for resistance to anthracnose stalk rot, which explained over 50% of the variation in an F 2:3 population. As mentioned above this QTL has also been described as the major gene Rcg1 and encodes an RGA (Broglie et al., 2006) . Arguably, this discovery represents the first report of the sequence of a gene underlying a plant disease resistance QTL.


 The Genetics of Aspergillus  Ear Rot Resistance

The primary cause of Aspergillus ear rot is the fungus Aspergillus flavus Link:Fr., which produces a mycotoxin called aflatoxin. Several studies have reported QTL for resistance to aflatoxin accumulation and to Aspergillus ear rot. In general most of QTL identified were of low to moderate effect, though two explained at least 20% of the phenotypic variation and were found in multiple environments (Brooks et al., 2005) . A recent study showed high correlations, both phenotypic and especially genotypic, between Fusarium ear rot, Aspergillus ear rot and accumulation of aflatoxin and fumonisin in a set of recombinant inbred lines (Robertson-Hoyt et al., 2007) . This suggests that common resistance mechanisms may function for the two diseases, and, conceivably, that breeding for Fusarium resistance may lead to a correlated response for Aspergillus resistance or vice-versa.


The Genetics of Gray Leaf Spot

The causal agent of gray leaf spot is Cercospora zeae-maydis (Tehon and Daniels). This disease has increased in importance over the past 15 years due to increased practice of conservation tillage which allows plant residue to remain on the soil surface and act as a spore reservoir. Gray leaf spot  resistance has been reported to be moderate to highly heritable and based largely on additive effects (Gordon et al., 2006) . Several studies have identified QTL for gray leaf spot resistance (Gordon et al., 2004). There is also a report of a major gene for gray leaf spot resistance but a subsequent study contradicted this


The Genetics of Southern Rust

Southern rust is caused by the biotrophic fungus Puccinia polysora Underw.  Rpp9 a major gene for southern rust resistance has been mapped to the short arm of chromosome 10 . Other major genes for southern rust resistance have also been mapped to this region but their allelic relationships to Rpp9 have not been established. QTL for southern rust have been mapped in three populations with no colocalization of QTL across studies (Wisser et al., 2006) . While major genes have been effective so far (Pratt and Gordon, 2006) , it would appear that in the absence of constant disease pressure, the use of marker assisted selection (MAS) would be a feasible approach.



Plants previously infected by a microorganism may become systemically more

resistant to subsequent pathogen attack. Two types of systemic responses have been extensively characterized in dicotyledonous systems; systemic acquired resistance (SAR) and induced systemic resistance (ISR) (Pratt et al., 2006). SAR is a response to necrotizing pathogens and confers a broad-spectrum resistance. It is associated with induction of a number of pathogenesis-related (PR) genes and the NPR1 gene has been shown to be a key regulator of the process . Salicylic acid (SA) appears to be the local inducer of SAR and methyl salicylate (MS) has been implicated as the mobile signal which induces SAR systemically (Park et al., 2007). It is thought that MS is produced at the site(s) of infection, transported throughout the plant in the phloem and is converted to SA at the site of action. ISR is induced by symbiotic micro-organisms in the rhizosphere (Vallad and Goodman, 2004) . It also confers broad-spectrum resistance but the pathway is regulated by jasmonate and ethylene rather than SA and PR-genes are not induced.










Plant resistance to pathogens depends upon timely recognition of the invading pathogen and rapid activation of defense responses via a number of signal transduction pathways. Several signal molecules have been identified in different plant species (Staswick and Lehman 1999). Plants have evolved different highly effective mechanisms to guard themselves and ward off microbial attacks. Pathogens, in turn, have developed enough strategies for by passing these mechanisms. Diseases are only established when the resistance mechanisms (passive and active) of the plant host is breeched by the pathogen. Invading  pathogens must be able to overcome these barriers to gain entrance into the host cells. However, there is differences in the degree of agility and aggressiveness of pathogens as they differ in their genetic constitutions which determines their level of virulence and specificity in plant diseases.










Baker, B., Zambryski, P., Staskawicz, B. and Dinesh-Kumar, S. P. (1997). Signalling in plant-microbe interactions. Science 276:726–733.


Borowicz, V.A. and Juliano, S.A. (1991). Specificity in Host–Fungus    Associations: Do Mutualists Differ from Antagonists? Evol. Ecol., 5: 385–               392.

Broglie, K., Butler, K., Conceicao, A., Frey, T., Hawk, J., Multani, D. and Wolters, P. (2006). Polynucleotides and Methods for Making Plants Resistant to Fungal Pathogens. USA 2006.

Brooks , T.D. , Williams , W.P., Windham , G.L., Willcox , M.C., Pauls, K.P. Abbas, H.K . 2005 .Quantitative Trait Loci Contributing Rresistance to Aflatoxin Accumulation in the Maize Inbred Mp313E . Crop Science 45 : 171 – 174 .

Casadevall, A. and Pirofski, L. (2001). Host–Pathogen Interactions: The

Casadevall, A. & Pirofski, L. A. (2002) What is a Pathogen? Ann. Med. 34(1), 2–4.

Clarke, D.D. (1997). The Genetic Structure of Natural Pathosystems. In The Gene-for-Gene Relationship in Plant–Parasite Interactions (I.R. Crute, E.B. Holub and


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  1. Pingback: The role of genetic and phenotypic diversity in maize and its effects on aflatoxin accumulation by the fungus Aspergillus flavus. · WWW.DBESTREVIEW.COM

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