**4. Fusarium diseases in animals**

h) To discuss genetic diversity, genetic resistance and molecular markers to investigate

(i) To discuss the environmental conditions that enable the opportunistic growth of *Fusarium* (j) To discuss the distribution and evolution of the genes responsible for mycotoxin

(m) To discuss development of *Fusarium*-resistant cultivars to reduce the diseases caused by

*Fusarium* attacks numerous plants and cereals that are important for human and animal nutrition. It specifically infects certain parts of them, such as grains, seedlings, heads, roots or stem, and causes various diseases, reduced commercial yield, and decrease in product quality [1]. *Fusarium* head blight (FHB) [2, 3], foot (FR) and root rot (RR) [4] and crown rot (CR) are among the major diseases caused by them. FHB produced by *F. graminearum* (teleomorph Gibberella zeae, Schwabe) causes starch and protein losses in cereals [5]. *Fusarium* species are saprophytic and are found commonly growing on the plants as a pathogen. *F. proliferatum* is a plant pathogen that is capable of infecting many important crops. *F. oxysporum* f.sp. *cubense* (FOC) causes *Fusarium* wilt, which is the most destructive disease of banana [6]. Many *Fusarium* species from the *F. solani* species complex (FSSC) are pathogenic and virulent. FSSC causes diseases in many agriculturally important crops, such as FR and/or RR of the infected host plant and causes necrosis. Symptoms, such as wilting, stunting and chlorosis, vary widely according to FSSC pathogenesis and the host plant species. Necrosis depends on the severity of fungal development [4]. Two of the most serious diseases of wheat known globally are *Fusarium* CR and *Fusarium* FHB. Stephens et al. [7] investigated the CR disease in wheat infected by *F. graminearum* and reported that CR developed in three stages. In the first stage, the *F. graminearum* biomass significantly increased within 2 days after inoculation. At this stage, there was germination of spores and superficial hyphal growth on the leaf sheath. In the second stage, the fungal biomass significantly decreased over 2 weeks. At this stage, the fungus penetrated from the outer parts of the leaf sheath to the leaf sheath base. In the third stage, biomass of *F. graminearum* increased significantly, and this increase correlated with fungal colonization on wheat and showed that the fungal biomass was being formed as fungal colonization on wheat crown parenchyma.

Fusarium species cause superficial, locally invasive and diffuse infections in humans. Although *Fusarium verticillioides*, including *F. moniliforme* and *F. fujikuroi* species complex [8],

(k) To discuss the steps that can be taken to prevent toxin production

2 Fusarium - Plant Diseases, Pathogen Diversity, Genetic Diversity, Resistance and Molecular Markers

(l) To discuss suitable approaches for *Fusarium* species disease management

population diversity

*Fusarium* species on a wide scale

**2. Plant pathogens and cereals**

**3. Fusarium infections in humans**

biosynthesis

*Fusarium* mycotoxins affect the growth, reproduction and hormonal condition of the animal. The effect of these mycotoxins on animals depends on the quantity of mycotoxin intake. After intake, these mycotoxins arrive at the gastrointestinal epithelial cell layer which is covered by the mucous secreted from goblet cells [13, 14].

Although deoxynivalenol (DON) and fumonisin-B1 (FB1) increase the permeability of intestinal epithelial cell layer in humans, animals and birds, they worsen the viability and proliferation of intestinal epithelial cells. High doses of mycotoxins may cause abdominal distress, diarrhea, cardiac insufficiency, emesis and even death in pigs and equine leukoencephalomalacia (ELEM) in horses [15]. Through *in vivo* and *in vitro* experimental studies, Cortinovis et al. [16] demonstrated that ZEN and its metabolites markedly up-regulated estrogen secretion in the reproductive organs.

ZEN is closely associated with infertility, decreased milk production and hyperestrogenism [17]. Cortinovis et al. [16] reported that ZEN directly affect ovarian cells and alter oocyte maturation under in vitro conditions; conversely, under in vivo conditions, this mycotoxin affected ovulation and puberty onset and caused morphological and functional disorders. T-2 toxin (T-2) causes cutaneous lesions in the mount and intestinal membrane and reduces egg production in poultry [18].
