Symptoms include yellowing, stunting, and death of seedlings and yellowing and stunting of older plants. Infected plants wilt readily, lower leaves yellow and dry, the xylem tissues turn brown, and the plant may die. In the early stages of disease, the roots are not rotted.
Clinical presentation includes refractory fever (> 90%), skin lesions and sino-pulmonary infections (∼75%). Type of skin lesions includes ecthyma-like, target, and multiple subcutaneous nodules. Skin lesions lead to diagnosis in >50% of patients and precede fungemia by ∼5 days.
There is no effective fungicide or other cure for Fusarium wilt. The pathogen nearly always kills infected hosts. Prevention and exclusion are the only effective management strategies. Avoid this problem by replanting at that site using species from different genera than plants previously infected there by Fusarium.
Colonies are usually fast growing, pale or bright-coloured (depending on the species) with or without a cottony aerial mycelium. The colour of the thallus varies from whitish to yellow, pink, red or purple shades. Species of Fusarium typically produce both macro- and microconidia from slender phialides.
The pathogen most often enters through root wounds caused by cultivation or by nematode feeding. Fusarium wilt can be seed borne, but it is rare in commercial seed. The fungus can be introduced on infected transplants or spread on equipment contaminated with infested soil.
A PCR detection based on the intergenic spacer (IGS) region has been developed for different agricultural important Fusarium species (complexes) that can also distinguish clinical species complexes like Fusarium equiseti and F. sporotrichioides because different-sized fragments are produced [47].
Synthetic fungicides are widely used to control wilt diseases. Thiophanate-methyl was found to be effective against Fusarium wilt disease when applied as a soil drench and a seed dresser3.
In humans, Fusarium species cause a broad spectrum of infections, including superficial (such as keratitis and onychomycosis), locally invasive, or disseminated infections, with the last occurring almost exclusively in severely immunocompromised patients (74).
Natamycin is active against Fusarium species both in vitro and in vivo, and is used along with voriconazole as the mainstay of treatment for Fusarium keratitis. Onychomycosis is treated with terbinafine, voriconazole and sometimes itraconazole.
Another easy way to detect Fusarium is to smell the bulbs. Infected bulbs have a distinct sour smell as a result of the fungus degrading the bulbs' tissue.
In general, control of Fusarium wilt disease can be accomplished by improving soil conditions, planting disease-resistant varieties, removing infected plant tissues, using clean seeds, and using soil and fungicides.
Fusarium can survive in soil for 5-10 years, surviving as saprophytes (lives on dead/decaying organic matter) in plant debris in soil indefinitely and producing dormant and tough resting spores.
Plants in the Solanaceae family that were evaluated include Nicotiana glauca, Solanum aculeastrum, Solanum mauritianum and Solanum seaforthianum. Leaf extracts from these plants demonstrated potent in vitro activities (minimum inhibitory concentrations <1.0 mg/mL) against nine Fusarium species (Table 2).
Fusarium species are filamentous fungi commonly found in the environment, particularly in soil, on plants, and in water systems and can cause a spectrum of diseases in humans ranging from superficial, invasive, and disseminated infections via inhalation, ingestion, or direct inoculation.
Symptoms include yellowing, stunting, and death of seedlings and yellowing and stunting of older plants. Infected plants wilt readily, lower leaves yellow and dry, the xylem tissues turn brown, and the plant may die. In the early stages of disease, the roots are not rotted.
AMB considered being the most effective drug against Fusarium, followed by VRC. Posaconazole can be used for refractory cases. Nonetheless, the usage of monotherapy for the treatment of systemic fusariosis is unsatisfactory owing to high rates of resistance against antifungal agents.
Fusarium colonies are usually pale or brightly colored (depending on the species) and may have a cottony aerial mycelium. Their color varies from whitish to yellow, brownish, pink or reddish. Species of Fusarium typically produce spores (called macro- and microconidias) for reproduction and dissemination.
Fusarium species, in particular, Fusarium solani, are common causes of keratitis. They are also common causes of onychomycosis, endophthalmitis, and skin and musculoskeletal infections. The disseminated form of infection most commonly occurs in patients with acute leukemia and prolonged neutropenia.
T-2 and HT-2 toxins are mycotoxins produced by Fusarium molds. These toxins are found in contaminated grains, such as wheat, rye, oat, and barley. Contamination generally occurs when these foods are not stored and/or dried properly.
Saxitoxins are also known as paralytic shellfish poisons (PSPs). Most human saxitoxin toxicoses have been associated with the ingestion of marine shellfish, which accumulate saxitoxins produced by marine dinoflagellates.
Terbinafine is another option to treat some Fusarium species, but this compound is only registered to treatment of superficial infections [39]. Natamycin (5%) and/or topical amphotericin B (0.5%) are first-line treatment of fungal keratitis in some countries.
Use an effective fungicide. These include: metconazole (Caramba®), prothioconazole + tebuconazole (Prosaro®), prothioconazole (Proline®), and adepidyn (Miravis Ace®). Apply an effective fungicide at the correct time. The most effective application window is from flowering (anthesis; Feekes 10.5.
There are different methods to detect Fusarium by PCR including conventional and real-time (hybridization or hydrolysis probe based) PCR [6,13,14,15], which are limited by their high turnaround time, detection of some selected species, or uncommon real-time PCR formats.