Қызылшаң – Claviceps туысының саңырауқұлақтары

Group of fungi of the genus Claviceps
the fungi

Ergot ('/ɜr//g//ə//t/ URgət) or ergot fungi refers to a group of fungi of the genus Claviceps. The most prominent member of this group is Claviceps purpurea ("rye ergot fungus"). This fungus grows on rye and related plants, and produces alkaloids that can cause ergotism in humans and other mammals who consume grains contaminated with its fruiting structure (called ergot sclerotium). Claviceps includes about 50 known species, mostly in the tropical regions. Economically significant species include C. purpurea (parasitic on grasses and cereals), C. fusiformis (on pearl millet, buffel grass), C. paspali (on dallis grass), C. africana (on sorghum), and C. lutea (on paspalum). C. purpurea most commonly affects outcrossing species such as rye (its most common host), as well as triticale, wheat, and barley. It affects oats only rarely. C. purpurea has at least three races or varieties, which differ in their host specificity:
G1 — land grasses of open meadows and fields;
G2 — grasses from moist, forest, and mountain habitats;
G3 (C. purpurea var. spartinae) — salt marsh grasses (Spartina, Distichlis).

An ergot kernel, called a sclerotium, develops when a spore of fungal species of the genus Claviceps infects a floret of flowering grass or cereal. The infection process mimics a pollen grain growing into an ovary during fertilization. Infection requires that the fungal spore have access to the stigma; consequently, plants infected by Claviceps are mainly outcrossing species with open flowers, such as rye (Secale cereale) and ryegrasses (genus Lolium). The proliferating fungal mycelium then destroys the plant ovary and connects with the vascular bundle originally intended for seed nutrition. The first stage of ergot infection manifests itself as a white soft tissue (known as sphacelia) producing sugary honeydew, which often drops out of the infected grass florets. This honeydew contains millions of asexual spores (conidia), which insects disperse to other florets. Later, the sphacelia convert into a hard dry sclerotium inside the husk of the floret. At this stage, alkaloids and lipids accumulate in the sclerotium. Claviceps species from tropic and subtropic regions produce macro and microconidia in their honeydew. Macroconidia differ in shape and size between the species, whereas microconidia are rather uniform, oval to globose (5×3 μm). Macroconidia are able to produce secondary conidia. A germ tube emerges from a macroconidium through the surface of a honeydew drop and a secondary conidium of an oval to pearlike shape is formed, to which the contents of the original macroconidium migrates. Secondary conidia form a white, frost like surface on honeydew drops and spread via the wind. No such process occurs in Claviceps purpurea, Claviceps grohii, Claviceps nigricans, and Claviceps zizaniae, all from northern temperate regions. When a mature sclerotium drops to the ground, the fungus remains dormant until proper conditions (such as the onset of spring or a rain period) trigger its fruiting phase. It germinates, forming one or several fruiting bodies with heads and stipes, variously coloured (resembling a tiny mushroom). In the head, threadlike sexual spores form, which are ejected simultaneously when suitable grass hosts are flowering. Ergot infection causes a reduction in the yield and quality of grain and hay, and if livestock eat infected grain or hay it may cause a disease called ergotism. Black and protruding sclerotia of C. purpurea are well known. However, many tropical ergots have brown or greyish sclerotia, mimicking the shape of the host seed. For this reason, the infection is often overlooked. Insects, including flies and moths, carry conidia of Claviceps species, but it is unknown whether insects play a role in spreading the fungus from infected to healthy plants.

Ergotism is the earliest recorded example of mycotoxicosis, or poisoning caused by toxic molds. Early references to ergotism date back as far as 600 BC, an Assyrian tablet referred to it as a "noxious pustule in the ear of grain." In 350 BC, the Parsees described "noxious grasses that cause pregnant women to drop the womb and die in childbed." England is noticeably absent from the historical regions affected by ergotism as its main source of food was wheat, which is resistant to ergot fungi. In 994, a massive outbreak of potentially attributed to ergotism caused 40,000 deaths in the regions of Aquitaine, Limousin, Périgord, and Angoumois in France.

Mankind has known about Claviceps purpurea for a long time, and its appearance has been linked to extremely cold winters that were followed by rainy summers. The sclerotial stage of C. purpurea conspicuous on the heads of ryes and other such grains is known as ergot. Favorable temperatures for growth are in the range of 18–30 °C. Temperatures above 37 °C cause rapid germination of conidia. Sunlight has a chromogenic effect on the mycelium, with intense coloration. Cereal mashes and sprouted rye are suitable substrates for growth of the fungus in the laboratory.

Claviceps africana infects sorghum. In sorghum and pearl millet, ergot became a problem when growers adopted hybrid technology, which increased host susceptibility. C. africana caused ergot disease that caused a famine in 1903 1906 in Northern Cameroon, West Africa, and also occurs in eastern and southern Africa, especially Zimbabwe and South Africa. Male sterile sorghums (also referred to as A lines) are especially susceptible to infection, as first recognized in the 1960s, and massive losses in seed yield have been noted. Infection is associated with cold night temperatures that are below 12 °C occurring two to three weeks before flowering. Sorghum ergot caused by Claviceps africana Frederickson, Mantle and De Milliano is widespread in all sorghum growing areas, whereas the species was formerly restricted to Africa and Asia where it was first recorded more than 90 years ago, it has been spreading rapidly and by the mid 1990s it reached Brazil, South Africa, and Australia. By 1997, the disease had spread to most South American countries and the Caribbean including Mexico, and by 1997 had reached Texas in the United States.