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Species Page

common rust of maize

Puccinia sorghi

Distribution

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Host plants / species affected

Main hosts

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Zea mays (maize)
Zea mays subsp. mays (sweetcorn)

List of symptoms / signs

Fruit - extensive mould
Inflorescence - lesions on glumes
Inflorescence - lesions; flecking; streaks (not Poaceae)
Leaves - abnormal colours
Leaves - fungal growth
Leaves - necrotic areas
Stems - mould growth on lesion

Symptoms

P. sorghi is characterized by the presence of golden-brown to cinnamon-brown pustules (uredinial) that can develop on any above-ground plant part including leaves, husks, tassels and stalks. The uredinia are circular to elongate, and develop with approximately equal frequency on the upper and lower leaf surfaces. The initial symptom is the formation of small chlorotic areas. As the uredinia develop they become erumpent, pushing up the epidermal tissue which eventually splits open to expose masses of powdery urediniospores. Spores often collect in and infect the whorls of the plants resulting in a band of infection across the leaf. On varieties containing genes for the production of anthocyanin pigments, the uredinia may be surrounded by a purple halo. When the disease is severe, large areas of the leaves and leaf sheaths can become first chlorotic then necrotic.

Prevention and control

Introduction

P. sorghi is generally controlled with the use of disease-resistant hybrids on maize, and by foliar application of fungicides on high-value crops such as sweet corn, seed corn, and popcorn. Cultural practices may be effective in areas where urediniospores can overwinter on debris or where infected species of Oxalis are a source of inoculum.

Host-Plant Resistance

Host resistance is probably the most feasible means of controlling P. sorghi in many situations. Two general types of resistance to P. sorghi are available in maize. One type involves a quantitative reduction in the numbers of uredinia. This type is often referred to as partial resistance, but has also been called general, slow-rusting, and rate-reducing resistance. The second type of resistance results in a qualitative difference in the disease reaction, with smaller lesions that produce fewer or no urediniospores.

Partial resistance is expressed most noticeably in mature plants, and has been referred to as adult-plant or mature-plant resistance (Hooker, 1985), but it can also be detected in the seedling stage (Pataky, 1986). Partial resistance affects disease development in a number of ways. The number and size of uredinia are reduced, as well as the amount of sporulation (Hooker, 1985; Pataky, 1986; Randle et al., 1984). The germination rates of urediniospores also are lower (Peltz, 1971), and the time between infection and the formation of uredinia may be longer on partially resistant genotypes. These reductions and delays in inoculum production reduce the rate of disease spread and slow the development of epidemics (Headrick and Pataky, 1988). Partial resistance is multi-genic, involving several to many genes, and the resulting disease reactions can range from moderately susceptible to highly resistant, depending on the genes which are present. The gene effects have been found to be largely additive, and the estimates of heritability are high. Partial resistance to P. sorghi is widely used in dent corn grown in the USA, and the level of economic loss due to this rust is generally low (Hooker, 1985; Melching, 1975). Partial resistance is also available in some sweet corn genotypes, but many popular hybrids are highly susceptible (Groth, et al., 1983; Pataky, et al., 1985). Sweet corn hybrids with high levels of partial resistance have been shown to have disease severity values 80% lower than those observed on susceptible hybrids grown under similar conditions (Pataky and Eastburn, 1993).

The qualitative type of resistance is often referred to as race-specific resistance because it is only effective against specific races of the pathogen. It is also called Rp resistance (resistance-puccinia). This type of resistance is simply inherited. Twenty-four dominant resistance factors, mapping to five gene loci, were identified in the 1950s and 1960s (Hooker, 1969). Lesion types on plants with Rp resistance include small chlorotic flecks, small necrotic spots, small pustules surrounded by necrotic tissue, small pustules surrounded by chlorotic tissue, and medium sized sporulating pustules without chlorosis, depending on the specific genes or alleles involved. A cluster of genes (Rp1, Rp5 and Rp6) are found on chromosome 10, and Rp3 and Rp4 are located on chromosomes 3 and 4, respectively. Rp1, Rp3 and Rp4 are known to be multi-allelic, with 14 (labelled A - N), six (A - F), and two (A and B) identified alleles respectively. There is now evidence to indicate that the Rp1 locus is actually a group of closely linked loci, and that two distinct alleles are actually the same allele plus or minus a modifying allele at another locus (Hulbert, 1991). For example, RP1L may actually be RP1c plus another allele. The Rp1D allele is currently widely used against P. sorghi in sweet corn in the continental USA where it provides excellent control (Pataky, 1987b). When the Rp1D allele is present small chlorotic flecks develop at the site of infection, but the lesions do not develop further, nor are any urediniospores produced. However, this allele has been overcome in other regions of the world such as Hawaii, and is not effective for controlling the diseases in these regions.

Chemical Control

Due to the variable regulations around (de-)registration of pesticides, we are for the moment not including any specific chemical control recommendations. For further information, we recommend you visit the following resources:


This information is part of a full datasheet available in the Crop Protection Compendium (CPC);www.cabi.org/cpc. For information on how to access the CPC, click here.

Impact

Several studies have assessed the effects of P. sorghi infection on yield and quality of both dent corn and sweet corn. In dent corn the main effect of P. sorghi is a reduction in grain yield, primarily resulting from a reduction in kernel size. However, the disease can also cause reductions in plant height, fresh plant weight, ear length, ear diameter, oil content and protein content, as well as increase the occurrence of stalk rots (Hooker, 1985). In temperate regions, where infection does not usually occur until mid-season, P. sorghi rarely causes significant yield reductions in dent corn. However, yield losses as high as 25% have been measured. A study conducted in the central section of the United States used near isogenic lines of dent corn in order to compare resistant lines with their susceptible counterparts. Disease severity was measured as the percentage of leaf area covered with P. sorghi pustules at 50 days after anthesis. Disease severity values of 10, 30, 50, 60 and 70% resulted in yield reductions of 4, 6, 15, 21 and 24%, respectively (Hooker, 1962; Russell, 1965). In Argentina yield increases of 17.3-18.6% were observed on hybrids protected from P. sorghi infection by the application of foliar fungicides (Martines, 1977) as compared to their unprotected counterparts. P. sorghi severity can be higher in more tropical regions where infection can occur at earlier growth stages. In Hawaii, P. sorghi severity of 80% resulted in an average reduction in grain yield of 35% (Kim and Brewbaker, 1976). Grain yields on some extremely susceptible hybrids were reduced by as much as 75%. In India yield losses resulting from P. sorghi infection as high as 32% have been observed (Sharma et al., 1982).

P. sorghi is a more severe and consistent problem on sweet corn and is now considered to be a major disease of this crop (Randle et al., 1984). Some sweet corn hybrids are more susceptible to P. sorghi than are most dent corn hybrids (Headrick and Pataky, 1987), but differences in the time of planting also influence the severity of infection on sweet corn. Sweet corn plantings are staggered through the spring and early summer in temperate regions to provide a steady and consistent supply of sweet corn for processing and fresh market consumption. The later season plantings are the most severely affected because the plants are relatively young when P. sorghi inoculum is prevalent.

Ear fresh weight and cut kernel weight are usually well correlated, and both have been used in estimating the effects of P. sorghi infection. Yield losses in sweet corn from zero to nearly 50% have been observed (Groth et al., 1983a, b). Host resistance to P. sorghi greatly influences the level of infection severity, and thus the yield loss. In a study looking at the effect of P. sorghi on the yields of three hybrids with varying degrees of resistance, reductions in ear fresh weight of 18, 26 and 49% occurred on the hybrids Sugarloaf, Jubilee, and Style Pak, respectively, when exposed to high levels of P. sorghi infection.

A quantitative relationship between the severity of P. sorghi infection and the level of yield loss in sweet corn has been established (Pataky, 1987a). This model estimates that every 10% of leaf area affected by P. sorghi, measured one week before harvest, corresponds to a 6% reduction in total ear weight, or a 6.5% reduction in the number of marketable ears. Thus, a P. sorghi severity value of 60% leads to an expected yield reduction of 36% in total ear weight or a 39% reduction in the number of marketable ears.