"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.

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.

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.

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

Currently, fungicides and other chemical and biological control agents have proven fairly unsuccessful, or only successful in vitro or in greenhouses, in the face of Panama disease of bananas. The most commonly used practices include mostly sanitation and quarantine practices to prevent the spread of Panama disease out of infected fields. However, the most effective tool against Panama disease is the development of banana trees resistant to "Fusarium oxysporum f. sp. Cubense". Unfortunately, the clonal reproduction of banana has led to a consequential lack of other varieties. Efforts are being made to produce resistant varieties, but with bananas being triploids which do not produce seeds, this is not an easy task. Creating clones from tissue cultures, rather than suckers, has proven somewhat successful in breeding resistant varieties, however these tend to have decreased success in stress-tolerance, yield, or other beneficial traits necessary for commercial varieties. Nevertheless, these efforts are leading to the best control measure for Panama disease of banana.

Recently, an R gene (RGA2) was transformed into Cavendish bananas which confers disease resistance to Fusarium wilt tropical race 4. This is the first case of successful resistance in the field and is a promising step towards preventing the loss of the Cavendish cultivars that are a huge portion of banana export production and subsistence of many communities.

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.

When Dutch elm disease spread away from the Atlantic coast, control focused on controlling the bark beetle by means of such insecticides as DDT and dieldrin, which were sprayed heavily across all parts of elm trees, usually twice a year in the spring and again at a lower concentration in the summer. In its early years it was generally thought by observers that pesticides did slow the spread of the disease across the United States but as early as 1947 concern was raised that many bird species were killed in large numbers via ingesting poisoned invertebrates. In areas sprayed during the 1950s local people observed birds such as the American woodcock, American robin, white-breasted nuthatch, brown creeper and various "Poecile" species dying. Biologist Rachel Carson consequently argued against spraying elms and for improved sanitation, which she saw as having been more effective in areas with earlier and greater experience countering Dutch elm disease. Although modern critics of Carson have argued that the bird deaths were caused by other factors such as mercury poisoning in the soil, spraying against elm bark beetles declined very rapidly after 1962, a trend aided by fungicides without dangerous side-effects being discovered for the first time after many years of research.

Lignasan BLP (carbendazim phosphate), introduced in the 1970s, was the first fungicide used to control Dutch elm disease. This had to be injected into the base of the tree using specialized equipment, and was never especially effective. It is still sold under the name "Elm Fungicide". Arbotect (thiabendazole hypophosphite) became available some years later, and it has been proven effective. Arbotect must be injected every two to three years to provide ongoing control; the disease generally cannot be eradicated once a tree is infected.

Arbotect is not effective on root graft infections from adjacent elm trees. It is more than 99.5% effective for three years from beetle infections, which is the primary mode of tree infection.

Alamo (propiconazole) has become available more recently, though several university studies show it to be effective for only the current season it is injected. Alamo is primarily recommended for treatment of oak wilt.

Multistriatin is a pheromone produced by female elm bark beetles, which can be produced synthetically. It has potential in being used to trap male beetles, which carry the fungus.

"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.

The first sign of infection is usually an upper branch of the tree with leaves starting to wither and yellow in summer, months before the normal autumnal leaf shedding. This progressively spreads to the rest of the tree, with further dieback of branches. Eventually, the roots die, starved of nutrients from the leaves. Often, not all the roots die: the roots of some species, notably the English elm, "Ulmus procera", can engage in repeatedly putting up suckers which flourish for approximately 15 years, after which they too succumb.

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.

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.

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.

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.