Fusarium wilt is a common vascular wilt fungal disease, exhibiting symptoms similar to Verticillium wilt. The pathogen that causes Fusarium wilt is "Fusarium oxysporum" ("F. oxysporum"). The species is further divided into forma specialis based on host plant.

Panama disease is a plant disease of the roots of banana plants. It is a type of Fusarium wilt, caused by the fungal pathogen "Fusarium oxysporum f. sp. cubense" (Foc). The pathogen is resistant to fungicide and cannot be controlled chemically.

During the 1950s, Panama disease wiped out most commercial Gros Michel banana production. The Gros Michel banana was the dominant cultivar of bananas, and the blight inflicted enormous costs and forced producers to switch to other, disease-resistant cultivars. New strains of Panama disease currently threaten the production of today's most popular cultivar, Cavendish.

Laurel wilt, also called laurel wilt disease, is a vascular disease caused by the fungus "Raffaelea lauricola", which is transmitted by the invasive redbay ambrosia beetle, "Xyleborus glabratus". The disease affects and kills members of the laurel family. The avocado is perhaps the most commercially valuable plant affected by laurel wilt.

Some redbay trees may be resistant to the disease, and future research will investigate factors associated with resistance, in the hope that tolerant varieties can be identified and developed.

Bacterial wilt of turfgrass is the only known bacterial disease of turf. The causal agent is the Gram negative bacterium Xanthomonas campestris pv. graminis. The first case of bacterial wilt of turf was reported in a cultivar of creeping bentgrass known as Toronto or C-15, which is found throughout the midwestern United States. Until the causal agent was identified in 1984, the disease was referred to simply as C-15 decline. This disease is almost exclusively found on putting greens at golf courses where extensive mowing creates wounds in the grass which the pathogen uses in order to enter the host and cause disease.

Creeping bentgrass ("Agrostis stolonifera") and annual bluegrasses ("Poa annua") are the makeup of most putting greens, as well as the preferred hosts of this pathogen. Specifically, Toronto (C-15), Seaside, and Nemisilla are the cultivars of creeping bentgrass most commonly affected. The bacteria enter the plant host and interfere with water and nutrient flow, causing the plant to look drought stressed and to take on a blueish-purple color. Additionally, symptoms of bacterial wilt of turf grass include yellow leaf spots, tan or brown spots, water soaked lesions, elongated yellow leaves and shriveling of aforementioned blue or dark green leaves.Since putting greens are not a pure stand of turf, some grass blades may be resistant to the bacterium and thus remain unharmed while the surrounding turf dies, rendering the putting surface inconsistent and unsightly, especially at high-end golf courses.

"F. oxysporum" is a major wilt pathogen of many economically important crop plants. It is a soil-borne pathogen, which can live in the soil for long periods of time, so rotational cropping is not a useful control method. It can also spread through infected dead plant material, so cleaning up at the end of the season is important.

One control method is to improve soil conditions because "F. oxysporum" spreads faster through soils that have high moisture and bad drainage. Other control methods include planting resistant varieties, removing infected plant tissue to prevent overwintering of the disease, using soil and systemic fungicides to eradicate the disease from the soil, flood fallowing, and using clean seeds each year. Applying fungicides depends on the field environment. It is difficult to find a biological control method because research in a greenhouse can have different effects than testing in the field. The best control method found for "F. oxysporum" is planting resistant varieties, although not all have been bred for every forma specialis.

"F. oxysporum" f. sp. "batatas" can be controlled by using clean seed, cleaning up infected leaf and plant material and breeding for resistance. Fungicides can also be used, but are not as effective as the other two because of field conditions during application. Fungicides can be used effectively by dip treating propagation material.

Different races of "F. oxysporum" f. sp. "cubense", Panama disease on banana, can be susceptible, resistant and partially resistant. It can be controlled by breeding for resistance and through eradication and quarantine of the pathogen by improving soil conditions and using clean plant material. Biological control can work using antagonists. Systemic and soil fungicides can also be used.

The main control method for "F. oxysporum" f. sp. "lycopersici", vascular wilt on tomato, is resistance. Other effective control methods are fumigating the infected soil and raising the soil pH to 6.5-7.

The most effective way to control "F. oxysporum" f. sp. "melonis" is to graft a susceptible variety of melon to a resistant root-stock. Resistant cultivars, liming the soil to change soil pH to 6-7, and reducing soil nitrogen levels also help control "F. oxysporum" f. sp. "melonis".

The fungus "Trichoderma viride" is a proven biocontrol agent to control this disease in an environment friendly way.

Two external symptoms help characterize Panama disease of banana:

- Yellow leaf syndrome, the yellowing of the border of the leaves which eventually leads to bending of the petiole.

- Green leaf syndrome, which occurs in certain cultivars, marked by the persistence of the green color of the leaves followed by the bending of the petiole as in yellow leaf syndrome. Internally, the disease is characterized by vascular discoloration. This begins in the roots and rhizomes with a yellowing that proceeds to a red or brown color in the pseudostem.

These symptoms often get confused with the symptoms of bacterial wilt of banana, but there are ways to differentiate between the two diseases:

- Fusarium wilt proceeds from older to younger leaves, but bacterial wilt is the opposite.

- Fusarium wilt has no symptoms on the growing buds or suckers, no exudates visible within the plant, and no symptoms in the fruit. Bacterial wilt can be characterized by distorted or necrotic buds, bacterial ooze within the plant, and fruit rot and necrosis.

Once a banana plant is infected, it will continue to grow and any new leaves will be pale in color. Recovery is rare, but if it does occur any new emerging suckers will already be infected and can propagate disease if planted.

"Fusarium oxysporum f. sp. cubense" (Foc) is most prominent in banana and plantain, but some other similar relatives are also susceptible to infection. Different races of the disease are used to classify different major hosts affected by Foc. Race 1 was the initial outbreak which destroyed much of the world's Gros Michel bananas. Cavendish bananas are resistant to race 1, but tropical race 4 (or subtropical race 4) is the classification for Foc which affects Cavendish. Race 2 affects a cooking and dessert banana, Bluggoe.

Verticillium wilt is a wilt disease of over 350 species of eudicot plants caused by six species of Verticillium genus, "V. dahliae", "V. albo-atrum", "V. longisporum", V. nubilum, V. theobromae and

V. tricorpus. (See, for example, Barbara, D.J. & Clewes, E. (2003). "Plant pathogenic Verticillium species: how many of them are there?" Molecular Plant Pathology 4(4).297-305. Blackwell Publishing.) Many economically important plants are susceptible including cotton, tomatoes, potatoes, oilseed rape, eggplants, peppers and ornamentals, as well as others in natural vegetation communities. Many eudicot species and cultivars are resistant to the disease and all monocots, gymnosperms and ferns are immune.

Symptoms are superficially similar to "Fusarium" wilts. There is no chemical control for the disease but crop rotation, the use of resistant varieties and deep plowing may be useful in reducing the spread and impact of the disease.

Dutch elm disease (DED) is caused by a member of the sac fungi (Ascomycota) affecting elm trees, and is spread by elm bark beetles. Although believed to be originally native to Asia, the disease was accidentally introduced into America and Europe, where it has devastated native populations of elms that did not have resistance to the disease. It has also reached New Zealand. The name "Dutch elm disease" refers to its identification in 1921 and later in the Netherlands by Dutch phytopathologists Bea Schwarz and Christine Buisman who both worked with Professor Johanna Westerdijk. The disease affects species in the genera "Ulmus" and "Zelkova", therefore it is not specific to the Dutch elm hybrid.

The causative agents of DED are ascomycete microfungi. Three species are now recognized:

- "Ophiostoma ulmi", which afflicted Europe from 1910, reaching North America on imported timber in 1928.

- "Ophiostoma himal-ulmi", a species endemic to the western Himalaya.

- "Ophiostoma novo-ulmi", an extremely virulent species from Japan which was first described in Europe and North America in the 1940s and has devastated elms in both continents since the late 1960s.

DED is spread in North America by three species of bark beetles (Family: Curculionidae, Subfamily: Scolytinae):

- The native elm bark beetle, "Hylurgopinus rufipes".

- The European elm bark beetle, "Scolytus multistriatus".

- The banded elm bark beetle, "Scolytus schevyrewi".

In Europe, while "S. multistriatus" still acts as a vector for infection, it is much less effective than the large elm bark beetle, "S. scolytus". "H. rufipes" can be a vector for the disease, but is inefficient compared to the other vectors. "S. schevyrewi" was found in 2003 in Colorado and Utah.

Other reported DED vectors include "Scolytus sulcifrons", "S. pygmaeus", "S. laevis", "Pteleobius vittatus" and "Р. kraatzi". Other elm bark beetle species are also likely vectors.

"Verticillium" wilt begins as a mild, local infection, which over a few years will grow in strength as more virile strains of the fungus develop. If left unchecked the disease will become so widespread that the crop will need to be replaced with resistant varieties, or a new crop will need to be planted altogether.

Control of "Verticilium" can be achieved by planting disease free plants in uncontaminated soil, planting resistant varieties, and refraining from planting susceptible crops in areas that have been used repeatedly for solanaceous crops. Soil fumigation can also be used, but is generally too expensive over large areas.

In tomato plants, the presence of ethylene during the initial stages of infection inhibits disease development, while in later stages of disease development the same hormone will cause greater wilt. Tomato plants are available that have been engineered with resistant genes that will tolerate the fungus while showing significantly lower signs of wilting.

"Verticillium albo-altrum", "Verticilium dahliae" and "V. longisporum" can overwinter as melanized mycelium or microsclerotia within live vegetation or plant debris. As a result, it can be important to clear plant debris to lower the spread of disease. "Verticilium dahliae" and "V. longisporum" are able to survive as microsclerotia in soil for up to 15 years.

Susceptible tomato seedlings inoculated with arbuscular mycorrhizal fungi and "Trichoderma Harzianum" show increased resistance towards "Verticillium" wilt.

Physiological plant disorders are caused by non-pathological conditions such as poor light, adverse weather, water-logging, phytotoxic compounds or a lack of nutrients, and affect the functioning of the plant system. Physiological disorders are distinguished from plant diseases caused by pathogens, such as a virus or fungus. While the symptoms of physiological disorders may appear disease-like, they can usually be prevented by altering environmental conditions. However, once a plant shows symptoms of a physiological disorder it is likely that that season’s growth or yield will be reduced.

Poor growth and a variety of disorders such as leaf discolouration (chlorosis) can be caused by a shortage of one or more plant nutrients. Poor plant uptake of a nutrient from the soil (or other growing medium) may be due to an absolute shortage of that element in the growing medium, or because that element is present in a form that is not available to the plant. The latter can be caused by incorrect pH, shortage of water, poor root growth or an excess of another nutrient. Plant nutrient deficiencies can be avoided or corrected using a variety of approaches including the consultation of experts on-site, the use of soil and plant-tissue testing services, the application of prescription-blend fertilizers, the application of fresh or well-decomposed organic matter, and the use of biological systems such as cover crops, intercropping, improved fallows, ley cropping, permaculture, or crop rotation.

Nutrient (or mineral) deficiencies include:

- Boron deficiency

- Calcium deficiency

- Iron deficiency

- Magnesium deficiency

- Manganese deficiency

- Molybdenum deficiency

- Nitrogen deficiency

- Phosphorus deficiency

- Potassium deficiency

- Zinc deficiency

Foot binding was the custom of applying tight binding to the feet of young girls to modify the shape of their feet. The practice possibly originated among upper class court dancers during the Five Dynasties and Ten Kingdoms period in 10th century China, then became popular among the elite during the Song dynasty and eventually spread to all social classes by the Qing dynasty. Foot binding became popular as a means of displaying status (women from wealthy families, who did not need their feet to work, could afford to have them bound) and was correspondingly adopted as a symbol of beauty in Chinese culture. Foot binding limited the mobility of women, resulting in them walking in a swaying unsteady gait, although some women with bound feet working outdoor had also been reported. The prevalence and practice of foot binding varied in different parts of the country. Feet altered by binding were called lotus feet.

It has been estimated that by the 19th century, 40–50% of all Chinese women may have had bound feet, and up to almost 100% among upper class Han Chinese women. The Manchu Kangxi Emperor tried to ban foot binding in 1664 but failed. In the later part of the 19th century, Chinese reformers challenged the practice but it was not until the early 20th century that foot binding began to die out as a result of anti-foot-binding campaigns. Foot-binding resulted in lifelong disabilities for most of its subjects, and a few elderly Chinese women still survive today with disabilities related to their bound feet.

The most common problem with bound feet was infection. Despite the amount of care taken in regularly trimming the toenails, they would often in-grow, becoming infected and causing injuries to the toes. Sometimes for this reason the girl's toenails would be peeled back and removed altogether. The tightness of the binding meant that the circulation in the feet was faulty, and the circulation to the toes was almost cut off, so any injuries to the toes were unlikely to heal and were likely to gradually worsen and lead to infected toes and rotting flesh. The necrosis of the flesh would also initially give off a foul odour, and later the smell may come from various microorganisms that colonized the folds.

If the infection in the feet and toes entered the bones, it could cause them to soften, which could result in toes dropping off; although, this was seen as a benefit because the feet could then be bound even more tightly. Girls whose toes were more fleshy would sometimes have shards of glass or pieces of broken tiles inserted within the binding next to her feet and between her toes to cause injury and introduce infection deliberately. Disease inevitably followed infection, meaning that death from septic shock could result from foot-binding, and a surviving girl was more at risk for medical problems as she grew older. It is thought that as many as 10% of girls may have died from gangrene and other infections due to footbinding.

At the beginning of the binding, many of the foot bones would remain broken, often for years. However, as the girl grew older, the bones would begin to heal. Even after the foot bones had healed, they were prone to re-breaking repeatedly, especially when the girl was in her teenage years and her feet were still soft. Bones in the girls' feet would often be deliberately broken again in order to improve the size or the shape of the feet. This was especially the case with the toes, as small toes were especially desirable. Older women were more likely to break hips and other bones in falls, since they could not balance securely on their feet, and were less able to rise to their feet from a sitting position. Other issues that might arise from foot binding included paralysis and muscular atrophy.