# Fusing _Fusarium_ Pathogens in the Era of Climate Change: A Conceptual Approach
## 2 FHB Counteracting and Preventive Measures  
In order to reduce the FHB risks and grain TCTB mycotoxin accumulation, several control practices have been shown to be efficient. The se control strategies rely on plant resistance breeding and on reducing the levels of primary pathogen inocula through management strategies like crop rotation, tillage, and the use of fungicides. Breaking the fungal disease cycle by adapting the sowing period [19; 24] has proven to be a good measure too. However, the period when spraying of fungicides is effective might be very short and, depending on appropriate weather conditions, difficult to handle [19; 25]. Additionally, the efficacy of the fungicide application determines if all _Fusarium_ species which are present and pathogenic under particular conditions can be controlled. Sometimes the application of a fungicide which works excellently against some specific pathogenic species might not be effective against other species, which subsequently become dominant [19; 21]. The se factors of inefficient treatment lead to variable success in controlling FHB by application of fungicides [19; 21].  
Plant FHB resistance breeding is an extremely complex task because multiple genes control the disease quantitative traits. Additionally, the resistance breeding outcome depends on the genotype and environmental interactions [19; 26; 27; 28; 29; 30]. Early studies on FHB resistance have demonstrated that the resistance can be broken down into two components: type I resistance that operates against initial infection, and type II resistance that operates against the spread of the pathogen within the host [28; 29; 30]. Later, three additional components were differentiated: a resistance to kernel infection (type III), a tolerance to infection (type IV), and a resistance to DON accumulation (type V) [28; 29; 30]. Over 100 quantitative trait loci (QTL) for FHB resistance in wheat (_Triticum aestivum_) have been identified so far [26; 29; 30]. QTL for FHB disease linked with the heading date, plant height, spikelet morphology, kernel discoloration were found in all wheat chromosomes except chromosome 7D [26; 28; 29; 30; 31]. Wheatgrass _Thinopyrum elongatum_ is an important wild relative of wheat with many excellent resistance traits and can be an effective source for FHB resistance breeding. The perennial plant was sequenced, and chromosomal locations of genes along with genetic markers identified. After multiple crosses and silencing the candidate genes individually it was found that one, Fhb7 codes for an enzyme, glutathione S-transferase, which is required for wheat FHB resistance [31].  
It is clear that environmental change will impact not only the crop plant-pathogen interactions but also other aspects of the plant cropping system that ultimately will affect the _Fusarium_ inoculation potential and host plant susceptibility [22]. The economic severity of the disease depends on the disease geographic distribution, climatic conditions, and crop susceptibility [32]. Recently, changes in FHB population composition dynamics and disease virulence have been recorded [33], suggesting that the knowledge of FHB resistance needs to be updated. Furthermore, a detailed understanding of the climatic controls on pathosystem is required for the development of effective management strategies [33].