Turf melting out is caused by the fungal pathogen "Dreschlera poae", in the family Dematiaceae. It is a common problem on turfgrass and affects many different species. The disease infects all parts of the plant most commonly on golf course roughs, sports fields, and home lawns. There are two stages of the disease: the leaf blade infection and the crown and root infection Melting out occurs during the cool weather of April and May and is encouraged by high nitrogen fertility. The disease is spread by wind-blown or water splashed spores and survive in thatch.

Necrotic ring spot is a common disease of turf caused by soil borne fungi (Ophiosphaerella korrae) that mainly infects roots (4). It is an important disease as it destroys the appearance of turfgrasses on park, playing fields and golf courses. Necrotic Ring Spot is caused by a fungal pathogen that is an ascomycete that produces ascospores in an ascocarp (6). They survive over winter, or any unfavorable condition as sclerotia. Most infection occurs in spring and fall when the temperature is about 13 to 28°C (5). The primary hosts of this disease are cool-season grasses such as Kentucky bluegrass and annual bluegrass (6). Once turf is infected with "O. korrae", it kills turf roots and crowns. Symptoms of the disease are quite noticeable since they appear as large yellow ring-shaped patches of dead turf. Management of the disease is often uneasy and requires application of multiple controls. The disease can be controlled by many different kind of controls including chemicals and cultural.

Turf melting out begins as black to purple spots on the leaf blades. These spots eventually appear on the leaf sheaths. The fungus then begin to move down and invade the crowns and the roots of the plants. From far away, the turf appears yellow or blackish brown. The colors that appear on the turf directly reflect the nitrogen levels in the plant. When turfgrass has low levels of nitrogen it turns yellow and when it has high nitrogen levels, it turns blackish brown. As the disease progresses, the infected turf becomes thin and brown. These symptoms are related to wilted turf. Unless the turfgrass is properly treated by fungicides, the grass will be replaced by broadleaf weeds and invasive grasses.

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.

Snow mold is a type of fungus and a turf disease that damages or kills grass after snow melts, typically in late winter. Its damage is usually concentrated in circles three to twelve inches in diameter, although yards may have many of these circles, sometimes to the point at which it becomes hard to differentiate between different circles. Snow mold comes in two varieties: pink or gray. While it can affect all types of grasses, Kentucky bluegrass and fescue lawns are least affected by snow mold.

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.

Red thread disease is a fungal infection found on lawns and other turfed areas. It is caused by the corticioid fungus "Laetisaria fuciformis" and has two separate stages. The stage that gives the infection its name is characterised by very thin, red, needle-like strands extending from the grass blade. These are stromata, which can remain viable in soil for two years. After germinating, the stromata infect grass leaf blades through their stomata. The other stage is visible as small, pink, cotton wool-like mycelium, found where the blades meet. It is common when both warmth and humidity are high.

Environment

"Laetisaria fuciformis", the fungus that causes red thread disease develops more often in cool (59-77°F) and wet conditions. These conditions are more present in the spring and fall when rainfall is higher and temperatures are slightly lower. Turf grass that is poor in nutrition and are slow growing are areas that are more susceptible to red thread disease. The fungus grows from the thread like red webbing structures called sclerotia. The sclerotia can survive in leaf blades, thatch, and soil for months to years. These areas that have been infected spread the disease by water, wind, and contaminated equipment. Since this fungus can survive for long periods of time it is essential to cure the infected area so further spreading of the disease does not occur.

Management

Managing red thread disease first starts by providing conditions that are not favorable for the fungal disease to develop. Having a balanced and adequate nitrogen fertilization program helps suppress the disease. This includes applying mild to substantial amounts of phosphorus and potassium to the turf. Other than properly fertilizing the turf, it is very important to maintain a soil pH between 6.5 and 7. Having a more basic pH creates less favorable conditions for a fungus to form. Reducing shade on turf areas also reduces chances of the fungal disease to form because shaded areas create a higher humidity near the turfs surface. Another technique to suppressing red thread disease is top dressing with compost. Suppression of the disease increases with the increase of compost used on the turf. Fungicides are not recommended to control red thread because the cost of chemical control is expensive and turf grasses usually recover from the disease quickly. If the use of fungicides is necessary, products containing strobilurins can be applied and can be very effective if applied before symptoms occur.

Hosts and symptoms

The hosts of the red thread disease only include turf grass. Turf grass is primarily present on home lawns and athletic fields. Some of these turf grass species include annual bluegrass, creeping bentgrass, Kentucky bluegrass, pereninial ryegrass, fine fescue, and bermudagrass. These species of grass are not the only types of turf that can be diagnosed with red thread disease but are the most common hosts. Noticeable symptoms of red thread disease are irregular yellow patches on the turf that are 2 to 24 inches in diameter. Affected areas are diagnosed with faintly pinkish web like sclerotia on the leaf blades. This sclerotia is the fungus growing on the leaf blades. This sclerotia has a reddish to pink spider web look to it.

The first signs of infection are small irregular patches of brown/yellowing grass. Upon closer inspection, either the tiny red needles or the pink fluffy mycelium will be visible. As the infection spreads, the small patches will join to form large brown areas.

Gray snow mold ("Typhula" spp. or Typhula blight) is the less damaging form of snow mold. While its damage may appear widespread, it typically does little damage to the grass itself, only to the blades. Unlike most plant pathogens, it is able to survive throughout hot summer months as sclerotia under the ground or in plant debris. Typhula blight is commonly found in United States in the Great Lakes region and anywhere with cold winter temperatures and persistent snow fall.

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.

Turf necrotic ring spot is known to infect various bluegrass and turfgrass species, especially the cool-season grasses. The fungus also infects fescues and bentgrasses (11). It is common in sodded lawns, rapidly growing lawns, and lawns with layered soil (3). The pathogen produces circular patches of bald spots that are tan or yellow in color (12). These patches are about 5 to 10 cm in diameter, but can grow to be about 1 meter in diameter. Eventually, as the infected turf dies, the spots turn brown. Within the patch, there may be areas of living grass at the center, creating a frog-eye appearance that this pathogen is known for. This is the result of the turf in the center surviving or being recolonized by healthy grass (3).

While the infection happens during cooler seasons, such as fall and spring, the symptoms can carry into summer (7). Should the disease continue through the summer, it may cause the crown and roots to become blackened with visible mycelium (11). As previously mentioned, this disease alters the grass by creating patches of yellow or tan dead grass (1). Another possible symptom is leaf lesions. Leaf lesions are often common among fungal diseases. If there are leaf lesions on the blade, the lesions will be inconsistent in terms of size and shape. The lesions may also be varying colors, such as yellow, tan, or dark brown (11).

Lethal yellowing (LY) is a phytoplasma disease that attacks many species of palms, including some commercially important species such as the coconut and date palm. In the Caribbean it is spread by the planthopper "Haplaxius crudus" (former name "Myndus crudus") which is native to Florida, parts of the Caribbean and Central America. The only effective cure is prevention, i.e. planting resistant varieties of coconut palm and preventing a park or 'golf course like' environments which attracts the planthopper. Some cultivars, such as the Jamaica Tall coconut cultivar, nearly died out by lethal yellowing. Heavy turf grasses and similar green ground cover will attract the planthopper to lay its eggs and the nymphs develop at the roots of these grasses. The planthoppers' eggs and nymphs may pose a great threat to coconut growing countries' economies, into which grass seeds for golf courses and lawns are imported from the Americas.

It is not clearly understood how the disease was spread to East Africa as the planthopper "Haplaxius crudus" is not native in East Africa.

The only explanation is that it was imported with grass seed from Florida that was used to create golf courses and lawns in beach resorts. There is a direct connection between green lawns and the spread of lethal yellowing in Florida. Even so-called 'resistant cultivars' such as the Malayan Dwarf or the Maypan hybrid between that dwarf and the Panama Tall were never claimed to have a 100% immunity. The nymphs of the planthoppers develop on roots of grasses, hence the areas of grass in the vicinity of palm trees is connected with the spread of this phytoplasma disease. The problem arose as a direct result of using coconut and date palms for ornamental and landscaping purposes in lawns, golf courses and gardens together with these grasses. When these two important food palms were grown in traditional ways (without grasses) in plantations and along the shores, the palm groves were not noticeably affected by lethal yellowing. There is no evidence that disease can be spread when instruments used to cut an infected palm are then used to cut or trim a healthy one. Seed transmission has never been demonstrated, although the phytoplasma can be found in coconut seednuts, but phytosanitary quarantine procedures that prevent movement of coconut seed, seedlings and mature palms out of an LY epidemic area should be applied to grasses and other plants that may be carrying infected vectors.

Beside coconut palm ("Cocus nucifera"), more than 30 palm species have also been reported as susceptible to lethal phytoplasmas around the globe.

The most obvious sign of thrush is usually the odor that occurs when picking out the feet. Additionally, the infected areas of the hoof will be black in color (even on a dark-horned hoof), and will easily break or crumble when scraped with a hoof pick. When picking the hooves around thrush areas, the differences between healthy and infected areas can be seen when white/gray tissue (healthy frog) is surrounding a dark, smelly (infected) area.

Most horses do not become lame if infected with thrush. However, if left untreated, the bacteria may migrate deeper into the sensitive parts of the hoof, which will result in lameness. Then, the horse may also react when its feet are picked out, and blood may be seen.

Typically the first symptom of starfish wasting disease is white lesions that appear on the surface of the starfish and spread rapidly, followed by decay of tissue surrounding the lesions. Next the animal becomes limp as the water vascular system fails and it is no longer able to maintain its internal hydrostatic balance. The body structure begins to break down, signs of stretching appear between the arms which may twist and fall off, and the animal dies. The arms may continue to crawl around for a while after being shed. Progression of these events can be rapid, leading to death within a few days.

A deflated appearance can precede other morphological signs of the disease. All of these symptoms are also associated with ordinary attributes of unhealthy stars and can arise when an individual is stranded too high in the intertidal zone (for example) and simply desiccates. "True" wasting disease will be present in individuals that are found in suitable habitat, often in the midst of other individuals that might also be affected.

The final result is a white, mushy blob, which no longer seems to be a sea star.

Thrush is a very common bacterial infection that occurs on the hoof of a horse, specifically in the region of the frog. The bacterium involved is" Fusobacterium necrophorum", and occurs naturally in the animal's environment — especially in wet, muddy, or unsanitary conditions, such as an unclean stall — and grows best with low oxygen. Horses with deep clefts, or narrow or contracted heels are more at risk of developing thrush.

Sea star wasting disease or starfish wasting syndrome is a disease of starfish and several other echinoderms that appears sporadically, causing mass mortality of affected starfish. There are around 40 different species of sea stars that have been affected by this disease. The disease seems to be associated with raised water temperatures. It starts with the emergence of lesions, followed by body fragmentation and death. In 2014 it was shown that the disease is associated with a densovirus now known as the sea star-associated densovirus (SSaDV).

Vulvovaginal health is the health and sanitation of the human vulva and vagina.

Problems affecting this area include vulva diseases, vaginal diseases and urinary tract infections.

Symptoms of hair loss include hair loss in patches usually in circular patterns, dandruff, skin lesions, and scarring. Alopecia areata (mild – medium level) usually shows in unusual hair loss areas e.g. eyebrows, backside of the head or above the ears where usually the male pattern baldness does not affect. In male-pattern hair loss, loss and thinning begin at the temples and the crown and either thins out or falls out. Female-pattern hair loss occurs at the frontal and parietal.

People have between 100,000 and 150,000 hairs on their head. The number of strands normally lost in a day varies, but on average is 100. In order to maintain a normal volume, hair must be replaced at the same rate at which it is lost. The first signs of hair thinning that people will often notice are more hairs than usual left in the hairbrush after brushing or in the basin after shampooing. Styling can also reveal areas of thinning, such as a wider parting or a thinning crown.

Thallium and its compounds are often highly toxic. Contact with skin is dangerous, and adequate ventilation should be provided when melting this metal. Many thallium(I) compounds are highly soluble in water and are readily absorbed through the skin. Exposure to them should not exceed 0.1 mg per m of skin in an 8-hour time-weighted average (40-hour work week). Thallium is a suspected human carcinogen.

Part of the reason for thallium's high toxicity is that, when present in aqueous solution as the univalent thallium(I) ion (Tl), it exhibits some similarities with essential alkali metal cations, particularly potassium (due to similar ionic radii). It can thus enter the body via potassium uptake pathways. Other aspects of thallium's chemistry differ strongly from that of the alkali metals, such as its high affinity for sulfur ligands. Thus, this substitution disrupts many cellular processes (for instance, thallium may attack sulfur-containing proteins such as cysteine residues and ferredoxins). Thallium's toxicity has led to its use (now discontinued in many countries) as a rat and ant poison.

Among the distinctive effects of thallium poisoning are hair loss (which led to its initial use as a depilatory before its toxicity was properly appreciated) and damage to peripheral nerves (victims may experience a sensation of walking on hot coals), although the loss of hair only generally occurs in low doses; in high doses the thallium kills before this can take effect. Thallium was once an effective murder weapon before its effects became understood and an antidote (Prussian blue) discovered. Indeed, thallium poisoning has been called the "poisoner's poison" since thallium is colorless, odorless and tasteless; its slow-acting, painful and wide-ranging symptoms are often suggestive of a host of other illnesses and conditions.

A substantially blemished face, back and limbs could point to cystic acne. The most severe form of the condition, cystic acne arises from the same hormonal imbalances that cause hair loss, and is associated with dihydrotestosterone production. Seborrheic dermatitis, a condition in which an excessive amount of sebum is produced and builds up on the scalp (looking like an adult cradle cap) is also a symptom of hormonal imbalances, as is an excessively oily or dry scalp. Both can cause hair thinning.

Nummular dermatitis is characterized by chronic or relapsing itchy coin-sized ovoid-shaped red plaques. They can occur on the trunk, limbs, face, and hands.

Nummular dermatitis (also known as "discoid dermatitis," "discoid eczema," "microbial eczema," "nummular eczema," and "nummular neurodermatitis") is one of the many forms of dermatitis. it is characterized by round or oval-shaped itchy lesions. The name comes from the Latin word "nummus," which means "coin."

Rapunzel syndrome, an extreme form of trichobezoar in which the "tail" of the hair ball extends into the intestines, can be fatal if misdiagnosed. In some cases, surgery may be required to remove the mass; a trichobezoar weighing was removed from the stomach of an 18-year-old woman with trichophagia.

Trichophagia is characterized by the person eating hair, usually their own; primarily after pulling it out. Most often, hair is pulled out and then the ends of the root bulb are eaten, or occasionally the hair shaft itself. The hair eventually collects in the gastrointestinal tract (on occasion, and depending upon severity of symptoms) causing indigestion and stomach pain. Ritual is a strong factor, and may involve touching the root bulb to the lips, tasting the hair, and occasionally chewing it. Sometimes those with the disorder may even eat the hair of others. In the psychiatric field it is considered a compulsive psychological disorder.