A Handbook of Rice Seedborne Fungi TW Mew and P ... - IRRI books

Table 4. Germination (%) of untreated and treated seeds using paper towel and in-soil germination methods (400seeds each; randomized complete block design).Normal a Abnormal Dead seedsVarieties Paper In-soil Paper In-soil Paper In-soiltowel test towel test towel testUntreatedIR62 79.7 ab 91.7 a 16.0 a 5.3 a 4.3 a 3.0 bSARBON 65.3 b 75.7 ab 20.3 a 12.0 a 14.3 a 12.3 abC22 94.0 a 84.0 ab 4.3 b 10.3 a 1.7 a 5.7 abBS1-10 68.0 b 72.7 b 18.3 a 11.0 a 13.7 a 16.3 aHot-water treatmentIR62 86.7 a 85.3 a 5.0 b 7.7 b 8.3 b 7.0 bSARBON 46.3 b 50.3 c 19.7 a 10.3 b 34.0 a 39.3 aC22 92.3 a 94.3 a 5.0 b 4.0 b 2.7 b 1.7 bBS1-10 76.3 a 67.7 b 13.7 ab 25.0 a 10.0 a 7.3 baIn a column under each treatment, means followed by a common letter are not significantly different at the 5% level by Duncan’s multiple rangetest.Relationship between seedborne inoculumand disease development in the fieldIn determining the importance of a seedborne pathogen,it is essential to relate inoculum production andthe efficiency of the secondary spread to the inoculumthreshold and disease severity after establishment.For a monocyclic disease, initial infectionshould be closely related to the initial inoculum providedby the seed. For a polycyclic disease, a lowlevel of seedborne inoculum is adequate to begininfection from the seedbed to the main field, and increasedisease intensity if climatic or crop-growingconditions are favorable. For instance, in rice blastcaused by P. oryzae with low detection and infectionfrequencies, seed-carried inoculum is more importantin temperate or subtropical environments than ina tropical lowland environment. In the former environments,the likelihood of seed-carried inoculumbeginning an infection and producing a sufficientamount of inoculum for secondary infection is higher(Ou 1985).Inoculum level and inoculum thresholdsIn seed health testing for certification, the inoculumthreshold of seedborne pathogens is defined as theamount of seed infection or infestation that can causea disease in the field under conducive conditions andlead to economic losses (Kuan 1988). We believethat this should mean a minimal amount of seed infectionor infestation. In principle and as Gabrielson(1988) indicated, one infected seed may give rise toone infected plant, but, under field conditions, this ishardly the case. The values of the inoculum thresholdfor different crop-pathogen combinations in differentcountries vary widely (Gabrielson 1988).Our experience with rice has shown that thepotential of a seedborne pathogen to cause a diseaseis determined by the type of pathogen in relation tothe crop growth environment. Under conditions in awet-bed nursery for rice seedlings, the likelihood of afungal pathogen beginning an infection appears lessthan under tropical conditions. Perhaps this is becauseof the microbial competition or antagonism.On the other hand, if the level of seedborne inoculumis high (we have not had it quantified), then the probabilityof it causing infection is also high. As one infectedseed begins one disease focus and this focalpoint expands, the probability of infection increases.In reality, disease establishment is affected by inoculumdensity and the crop cultivation environment.The more infected seeds there are (inoculum level),the higher the probability of having an infection.We have monitored detection levels of seedbornefungal pathogens from imported seed lots byplanting them in the field after seed treatment forpostentry plant quarantine observation. Diseases observedwere not related to seedborne pathogens(Table 2). Pathogens from harvested seeds fromthese plants were detected, but we are not surewhether these fungal pathogen populations were thesame as those carried by the original seed or if theycame from other sources in the field.9