Phytophthora medicaginis
| Phytophthora medicaginis | |
|---|---|
| Scientific classification | |
| Domain: | Eukaryota |
| (unranked): | SAR |
| Superphylum: | Heterokonta |
| Class: | Oomycetes |
| Subclass: | Incertae sedis |
| Order: | Pythiales |
| Family: | Pythiaceae |
| Genus: | Phytophthora |
| Species: | P. medicaginis |
| Binomial name | |
|
Phytophthora medicaginis E.M. Hansen & D.P. Maxwell, (1991) |
|
| Synonyms | |
|
Phytophthora megasperma f.sp. medicaginis T.L. Kuan & Erwin, (1980) |
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Phytophthora megasperma f.sp. medicaginis T.L. Kuan & Erwin, (1980)
Phytophthora sojae f.sp. medicaginis Faris
Phytophthora medicaginis is a plant pathogen that causes root rot in alfalfa and chickpea. It is a major disease of these plants and is found wherever they are grown. P. medicaginis causes failure of stand establishment because of seedling death.Phytophthora medicaginis was formerly known as Phytophthora megasperma.
Phytophthora medicaginis (P. medicaginis) is an oomycete pathogen that causes root rot and damping off of seedlings. P. medicaginis is specific to alfalfa and chickpea and can reside in soil or water, but since it is a water mold, it requires free water to infect another plant. This disease is most prevalent in newly seeded fields that experience flooding but can also be found in mature plants. P. medicaginis commonly causes seedling death but if this pathogen is present in mature crops, P. medicaginis causes root rot which limits the plant’s ability to acquire nutrients and water. This leads to secondary symptoms such as chlorosis, wilting, stunting, root decay, lesions and death. This disease is difficult to identify but reddish-brown or black root lesions will exist and oospores, sporangia, zoospores, antheridia, and oogonia are spore types that will be visible under a microscope. An ELISA test can confirm the presence of phytophthora, but to confirm the species, a PCR test is effective. Several host factors will affect disease development including damage/stress to the plant and also the degree of resistance of host cultivar.
The disease cycle “starts” in the early spring as the oospores begin to germinate. Oospores are thick walled survival structures that allow the pathogen to survive winter. The oospores are then stimulated to germinate in the presence of free water and root exudates. Germination produces zoospores and sporangia which can then release more zoospores that infect other seeds. This is the asexual part of the cycle. This production of sporangia and zoospores happens until the end of the season when oogonia and antheridia engage in homothallic sexual reproduction to produce oospores once again. Spore types are disseminated via water such as during flooding. A cool environment also favors disease transmission.
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