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.

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.

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.

The fungal pathogen "Fusarium oxysporum" affects a wide variety of hosts of any age. Tomato, tobacco, legumes, cucurbits, sweet potatoes and banana are a few of the most susceptible plants, but it will also infect other herbaceous plants. "Fusarium oxysporum" generally produces symptoms such as wilting, chlorosis, necrosis, premature leaf drop, browning of the vascular system, stunting, and damping-off. The most important of these is vascular wilt. Fusarium wilt starts out looking like vein clearing on the younger leaves and drooping of the older lower leaves, followed by stunting of the plant, yellowing of the lower leaves, defoliation, marginal necrosis and death of the plant. On older plants, symptoms are more distinct between the blossoming and fruit maturation stages.

"Fusarium oxysporum" is split into divisions called "formae speciales" (singular "forma specialis", abbreviated "f.sp."). There are over 100 formae speciales divisions, each with one or two different races. Each forma specialis within the species are host-specific (i.e. specific to a certain plant) and produce different symptoms:

"F. oxysporum" f. sp. "batatas" affects sweet potato. The symptoms include leaf chlorosis, stunting, and leaf drop. It is transmitted through the soil and through vascular wounds in plant material.

"Fusarium oxysporum" f. sp. "canariensis" causes Fusarium wilt of Canary Island date palm and other propagated palms. The disease is spread through contaminated seed, soil, and pruning tools.

"F. oxysporum" f. sp. "cubense" causes Panama disease on banana. It is found everywhere bananas are grown in Africa, Asia, Central and South America. It attacks banana plants of all ages and spreads mainly through the soil. It causes wilting and yellowing of the leaves.

"F. oxysporum" f. sp. "lycopersici" causes vascular wilt in tomato. The disease starts out as yellowing and drooping on one side of the plant. Leaf wilting, plant stunting, browning of the vascular system, leaf death, and lack of fruit production also occur.

"F. oxysporum" f. sp. "melonis" attacks muskmelon and cantaloupe. It causes damping-off in seedlings and causes chlorosis, stunting and wilting in old plants. Necrotic streaks can appear on the stems.

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.

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.

Symptoms of laurel wilt include wilted stems and leaves and dark streaking in the wood. Laurel wilt can spread in at least two ways: one is via the beetle's natural reproduction and migration. A second way is through the sale and transport of beetle-infested wood, a result of redbay's use as firewood and for outdoor grilling.

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" spp. attack a very large host range including more than 350 species of vegetables, fruit trees, flowers, field crops, and shade or forest trees. Most vegetable species have some susceptibility, so it has a very wide host range. A list of known hosts is at the bottom of this page.

The symptoms are similar to most wilts with a few specifics to "Verticillium". Wilt itself is the most common symptom, with wilting of the stem and leaves occurring due to the blockage of the xylem vascular tissues and therefore reduced water and nutrient flow. In small plants and seedlings, "Verticillium" can quickly kill the plant while in larger, more developed plants the severity can vary. Some times only one side of the plant will appear infected because once in the vascular tissues, the disease migrates mostly upward and not as much radially in the stem. Other symptoms include stunting, chlorosis or yellowing of the leaves, necrosis or tissue death, and defoliation. Internal vascular tissue discoloration might be visible when the stem is cut.

In "Verticillium", the symptoms and effects will often only be on the lower or outer parts of plants or will be localized to only a few branches of a tree. In older plants, the infection can cause death, but often, especially with trees, the plant will be able to recover, or at least continue living with the infection. The severity of the infection plays a large role in how severe the symptoms are and how quickly they develop.

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 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.