In a September 2008 study, a possible fungicide was tested. The abstract of the study reads as follows:

In this study, the systemic fungicide propiconazole completely inhibited mycelial growth of Raffaelea spp. in vitro at concentrations 0.1 parts per million (ppm) or greater and was fungitoxic at 1 ppm or greater, whereas the fungicide thiabendazole was less inhibitory. None of the ten mature redbay trees that received root-flare injections of propiconazole developed crown wilt symptoms for at least 30 weeks after being inoculated with Raffaelea spp., whereas nine of ten untreated control trees wilted in more than one-third of their crowns. Propiconazole was retained in the stem xylem for at least 7.5 months after injection but was more frequently detected in samples from trees injected 4.5 months earlier and was not well detected in small-diameter branches. Results suggest that propiconazole may be useful in preventing laurel wilt in redbay, but limitations and questions regarding duration of efficacy, rate of uptake, and efficacy under different levels of disease pressure remain.

In 2011, the EPA granted a Section 18 Emergency Exemption allowing the use of Tilt (a formulation of propiconazole) on commercial avocado trees to prevent laurel wilt disease. However, questions remain about the efficacy and cost-effectiveness of this treatment in commercial groves

"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.

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.

General biocides such as copper, Junction, or ZeroTol offer a potential solution to bacterial wilt of turf grass, however such chemical control ages must be applied after every mowing which may be economically impractical and ultimately phytotoxic. If bacterial wilt is present of the golf course, the best option may be to designate a mower for use on infected greens only in order to prevent the spread of the pathogen to other greens. Other viable methods include simply limiting the number of wounds the plant incurs, thereby limiting entry sites for the pathogen. A simple example would be less frequent mowing. It has also been proven that the disease is most devastating in grass cut to a length of between 1/8 and 3/16 of an inch, but less so in grass over 1/4 of an inch in length or longer, which presents an additional argument for limiting mowing. Another example is limiting sand topdressing as this is also a very abrasive technique which can create small wounds which allow entry of bacteria into the plant.

A major factor complicating the control of Xanthomonas campestris pv. graminis is weather. While it is not possible to control the weather per se, a study found great decreases in pathogen efficacy at temperatures below 20 °C, suggesting that cooling measures may be effective in combating this pathogen.

Ideally, resistant strains of the host plant should be used to control such a plant pathogen, however no resistant cultivars of turf grass have been identified to date. While no completely resistant cultivars exist, golf course owners can find solace in the fact that certain cultivars such as Penncross and Penneagle are more resistant to bacterial wilt and may thus reduce the need for frequent chemical applications and other cultural controls. Researchers are making gains towards the identification of resistant cultivars as evidenced by the finding that variation in genetic linkage groups 1, 4, and 6 accounted for over 43% of resistance among Italian rye grass.

A 1987 study found evidence of a possible biocontrol strategy for bacterial wilt of turf grass. The researchers found that antiserum to Pseudomonas fluorescens or Erwinia herbicola from hosts which have survived infections by the corresponding pathogens is capable of reducing wilt symptoms in turf grass caused by Xanthomonas campestris pv. graminis. The researchers did note, however, that while it is important to ensure the presence of a higher number of competing bacterial cells in order to reduce symptoms, one should take care to avoid over-infecting the host with a new bacterial pathogen.

Further gains towards host resistance were made in 2001 when researchers found that inoculation of meadow fescue during breeding with a single aggressive strain of the bacterial wilt pathogen greatly increased resistance in offspring, thereby demonstrating the potential of selective breeding to reduce bacterial wilt pathogenesis on turf and rye grasses.

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.

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.

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.

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 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.

"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.

Diagnosis of the cause of a physiological disorder (or disease) can be difficult, but there are many web-based guides that may assist with this. Examples are: "Abiotic plant disorders: Symptoms, signs and solutions"; "Georgia Corn Diagnostic Guide"; "Diagnosing Plant Problems" (Kentucky); and "Diagnosing Plant Problems" (Virginia).

Some general tips to diagnosing plant disorders:

- Examine where symptoms first appear on a plant—on new leaves, old leaves or all over?

- Note the pattern of any discolouration or yellowing—is it all over, between the veins or around the edges? If only the veins are yellow deficiency is probably not involved.

- Note general patterns rather than looking at individual plants—are the symptoms distributed throughout a group of plants of the same type growing together. In the case of a deficiency all of the plants should be similarly effected, although distribution will depend on past treatments applied to the soil.

- Soil analysis, such as determining pH, can help to confirm the presence of physiological disorders.

- Consider recent conditions, such as heavy rains, dry spells, frosts, etc., may also help to determine the cause of plant disorders.

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 process was started before the arch of the foot had a chance to develop fully, usually between the ages of 4 and 9. Binding usually started during the winter months since the feet were more likely to be numb, and therefore the pain would not be as extreme.

First, each foot would be soaked in a warm mixture of herbs and animal blood; this was intended to soften the foot and aid the binding. Then, the toenails were cut back as far as possible to prevent in-growth and subsequent infections, since the toes were to be pressed tightly into the sole of the foot. Cotton bandages, 3 m long and 5 cm wide (10 ft by 2 in), were prepared by soaking them in the blood and herb mixture. To enable the size of the feet to be reduced, the toes on each foot were curled under, then pressed with great force downwards and squeezed into the sole of the foot until the toes broke.

The broken toes were held tightly against the sole of the foot while the foot was then drawn down straight with the leg and the arch of the foot was forcibly broken. The bandages were repeatedly wound in a figure-eight movement, starting at the inside of the foot at the instep, then carried over the toes, under the foot, and around the heel, the freshly broken toes being pressed tightly into the sole of the foot. At each pass around the foot, the binding cloth was tightened, pulling the ball of the foot and the heel together, causing the broken foot to fold at the arch, and pressing the toes underneath the sole. The binding was pulled so tightly that the girl could not move her toes at all and the ends of the binding cloth were then sewn so that the girl could not loosen it.

The girl's broken feet required a great deal of care and attention, and they would be unbound regularly. Each time the feet were unbound, they were washed, the toes carefully checked for injury, and the nails carefully and meticulously trimmed. When unbound, the broken feet were also kneaded to soften them and the soles of the girl's feet were often beaten to make the joints and broken bones more flexible. The feet were also soaked in a concoction that caused any necrotic flesh to fall off.

Immediately after this agonizing procedure, the girl's broken toes were folded back under and the feet were rebound. The bindings were pulled even tighter each time the girl's feet were rebound. This unbinding and rebinding ritual was repeated as often as possible (for the rich at least once daily, for poor peasants two or three times a week), with fresh bindings. It was generally an elder female member of the girl's family or a professional foot binder who carried out the initial breaking and ongoing binding of the feet. It was considered preferable to have someone other than the mother do it, as she might have been sympathetic to her daughter's pain and less willing to keep the bindings tight.

For most the bound feet eventually became numb. However, once a foot had been crushed and bound, attempting to reverse the process by unbinding is painful, and the shape could not be reversed without a woman undergoing the same pain all over again.