The best way to manage SDS is with a resistant variety. One issue is that most resistant varieties are only partially resistant so yield reductions may still occur. Another issue is that the plant needs resistance for SDS and SCN in order to gain true resistance because of their synergistic relationship and most varieties do not have resistance for both. Aside from resistance, the only other ways to control SDS are management practices.

These include:

- Avoid planting in cool, wet conditions

- Plant later when the soil has warmed up

- Try avoiding soil compaction as it creates wet spots in the soil that can increase plant stress and SDS infection rates

- Managing for SCN as this nematode often occurs alongside "F. virguliforme"

- Deep tillage to break up compaction and help the soil warm faster

One common management tactic used in other pathogen management plans is crop rotation. In some cases, disease severity can be reduced but most often it is not effective. This is because of chlamydospores and macroconidia as they can persist in soils for many years.

Fungicides are another common product used to control fungal pathogens. In-furrow applications and seed treatments with fungicides have some effect in decreasing disease instance but in most cases, the timing isn't right and the pathogen can still infect the plants. Foliar applications of fungicides have no effect on disease suppression for SDS because the fungi are found in the soil and mainly the roots of the plants. Most foliar fungicides do not move downward through plants, therefore having no effect on the pathogen.

The bacteria can survive in the rhizosphere of other crops such as tomato, carrots, sweet potato, radish, and squash as well as weed plants like lupin and pigweed, so it is very hard to get rid of it completely. When it is known that the bacterium is present in the soil, planting resistant varieties can be the best defense against the disease. Many available beet cultivars are resistant to "Pectobacterium carotovorum" subsp. "betavasculorum", and some examples are provided in the corresponding table. A comprehensive list is maintained by the USDA on the Germplasm Resources Information Network.

Even though some genes associated with root defense response have been identified, the specific mechanism of resistance is unknown, and it is currently being researched.

"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.

Sudden Death Syndrome (SDS) in Soybean plants quickly spread across the southern United States in the 1970s, eventually reaching most agricultural areas of the US. SDS is caused by a Fusarium fungi, more specifically the soil borne root pathogen "Fusarium virguliforme," formerly known as "Fusarium solani" f. sp. "glycines"."." Losses could exceed hundreds of millions of dollars in US soybean markets alone making it one of the most important diseases found in Soybeans across the US

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.

Some bacteriophages, viruses that infect bacteria, have been used as effective controls of bacterial diseases in laboratory experiments. This relatively new technology is a promising control method that is currently being researched. Bacteriophages are extremely host-specific, which makes them environmentally sound as they will not destroy other, beneficial soil microorganisms. Some bacteriophages identified as effective controls of "Pectobacterium carotovorum" subsp. "betavasculorum" are the strains ΦEcc2 ΦEcc3 ΦEcc9 ΦEcc14. When mixed with a fertilizer and applied to inoculated calla lily bulbs in a greenhouse, they reduced diseased tissue by 40 to 70%. ΦEcc3 appeared to be the most effective, reducing the percent of diseased plants from 30 to 5% in one trial, to 50 to 15% in a second trial. They have also been used successfully to reduce rotting in lettuce caused by "Pectobacterium carotovorum" subsp. "carotovorum", a different bacterial species closely related to the one that causes beet vascular necrosis.

While it is more difficult to apply bacteriophages in a field setting, it is not impossible, and laboratory and greenhouse trials are showing bacteriophages to potentially be a very effective control mechanism. However, there are a few obstacles to surmount before field trials can begin. A large problem is that they are damaged by UV light, so applying the phage mixture during the evening will help promote its viability. Also, providing the phages with susceptible non-pathogenic bacteria to replicate with can ensure there is adequate persistence until the bacteriophages can spread to the targeted bacteria. The bacteriophages are unable to kill all the bacteria, because they need a dense population of bacteria in order to effectively infect and spread, so while the phages were able to decrease the number of diseased plants by up to 35%, around 2,000 Colony Forming Units per milliliter (an estimate of living bacteria cells) were able to survive the treatment. Lastly, the use of these bacteriophages places strong selection on the host bacteria, which causes a high probability of developing resistance to the attacking bacteriophage. Thus it is recommended that multiple strains of the bacteriophage be used in each application so the bacteria do not have a chance to develop resistance to any one strain.

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.

Immediate treatment consists of rinsing the bite site in cold water. If not too painful, ice the bite site. This constricts the blood vessels so the venom does not spread. Also recommended is papain, an enzyme that breaks down protein. Papain can be found in meat tenderizer and papaya. This deactivates the majority of the centipede venom's proteins. Depending on the type of centipede and level of envenomation, this treatment may not degrade the entire venom dose and residual pain will remain.

Individuals who are bitten by centipedes are sometimes given a urine test to check for muscle tissue breakdown and/or an EKG to check for heart and vascular problems.

Reassurance and pain relief is often given in the form of painkillers, such as non-steroidal anti-inflammatory medications, antihistamines and anti-anxiety medications. In a severe case the affected limb can be elevated and administered diuretic medications.

Wound care principles and sometimes antibiotics are used to keep the wound itself from becoming infected or necrotic.

In Barbados, a folk remedy involves applying a freshly cut onion to the site of the injury "bite" for 10 minutes. Repeat until relief is obtained.

"Warm water immersion foot" is a skin condition of the feet that results after exposure to warm, wet conditions for 48 hours or more and is characterized by maceration ("pruning"), blanching, and wrinkling of the soles, padding of toes (especially the big toe) and padding of the sides of the feet.

Foot maceration occur whenever exposed for prolong periods to moist conditions. Large watery blisters appear which are painful when they open and begin to peel away from the foot itself. The heels, sides and bony prominences are left with large areas of extremely sensitive, red tissue, exposed and prone to infection. As the condition worsens, more blisters develop due to prolonged dampness which eventually covers the entire heel and/or other large, padded sections of the foot, especially the undersides as well as toes. Each layer in turn peels away resulting in deep, extremely tender, red ulcerations.

Healing occurs only when the feet are cleansed, dried and exposed to air for weeks. Scarring is permanent with dry, thin skin that appears red for up to a year or more. The padding of the feet returns but healing can be painful as the nerves repair with characteristics of diabetic neuropathy. Antibiotics and/or antifungal are sometimes prescribed.

Foot immersion is a common problem with homeless individuals wearing one pair of socks and shoes for extensive periods of time, especially wet shoes and sneakers from rain and snow. The condition is exacerbated by excessive dampness of the feet for prolonged periods of time. Fungus and bacterial infections prosper in the warm, dark, wet conditions and are characterized by a sickly odor that is distinct to foot immersion.

Immersion foot syndromes are a class of foot injury caused by water absorption in the outer layer of skin. There are different subclass names for this condition based on the temperature of the water to which the foot is exposed. These include trench foot, tropical immersion foot, and warm water immersion foot. In one 3-day military study, it was found that submersion in water allowing for a higher skin temperature resulted in worse skin maceration and pain.

If a horse is suspected of choke, a veterinarian will often pass a stomach tube down the animal's esophagus to determine if there is a blockage. Failure to access the stomach with the tube indicates a complete obstruction; difficulty passing the tube may represent a stenosis, or narrowing; or a partial obstruction. Radiography and endoscopy are also used in refractory cases.

There is no diagnostic test for calciphylaxis. The diagnosis is a clinical one. The characteristic lesions are the ischemic skin lesions (usually with areas of skin necrosis). The necrotic skin lesions (i.e. the dying or already dead skin areas) typically appear as violaceous (dark bluish purple) lesions and/or completely black leathery lesions. They can be extensive. The suspected diagnosis can be supported by a skin biopsy. It shows arterial calcification and occlusion in the absence of vasculitis. Sometimes the bone scintigraphy can show increased tracer accumulation in the soft tissues. In certain patients, anti-nuclear antibody may play a role.

Raised inflammatory markers (high ESR, CRP) are common but nonspecific. Examination of the coughed up mucus is important in any lung infection and often reveals mixed bacterial flora. Transtracheal or transbronchial (via bronchoscopy) aspirates can also be cultured. Fiber optic bronchoscopy is often performed to exclude obstructive lesion; it also helps in bronchial drainage of pus.

After the material has passed, a veterinarian may try to prevent the onset of aspiration pneumonia by placing the horse on broad-spectrum antibiotics. The animal should be monitored for several days to ensure that it does not develop pneumonia, caused by inhalation of bacteria-rich food material into the lungs.

The material caught in a horse's throat usually causes inflammation, which may later lead to scarring. Scarring reduces the diameter of the esophagus (a stenosis or stricture), which increases the chance that the horse may choke again. The veterinarian may therefore place the horse on a course of NSAIDs, to help to control the inflammation of the esophagus.

Often the horse will only be fed softened food for a few days, allowing the esophagus to heal, before it is allowed to gradually resume its normal diet (e.g. hay and unsoaked grain). Horses with re-occurring chokes may require their diet to be changed.

This disease is caused by problems in the circulatory system, so when it is presented, in the beginning it is important to follow several recommendations. The person needs to keep the legs elevated as much as possible to help the return of the blood. Whenever sitting down, the person needs to keep the legs on a foot stool. At night it is advisable to sleep with a pillow under the lower legs. In the evening, t is not unusual for legs to be swollen. The volume of the lower leg can increase to up to 100ml after a long working day or up to 200ml after a long-haul flight without moving.

In the example of the 41-year-old Japanese man the lesions were much improved by washing and topical use of corticosteroids for two months, also oral antibiotics like cephalexin are used if cellulitis is present. Moist exudative inflammation and moist ulcers respond to tepid wet compresses of Burow’s solution or just saline or water for 30 to 60 minutes several times a day. But in worse cases, edema that does not disappear spontaneously within a few hours or after a walk, is described as pathological, so it needs to have a special treatment. It is very important to say that Papillamitosis, bilateral and marked edema with few symptoms is mostly caused by the systemic circulation (heart, kidneys, liver).

Papillamitosis is associated, as has been mentioned before, with symptoms and/or clinical signs such as dilated superficial veins, varicose veins and changes in the skin. Edema and its complication Papillamitosis are only partially reversible and soon becomes hard, which is mainly confirmed on palpation. All skin structures are affected and this is characterized by the term. Lymphoedema may develop in many cases accompanied by acral thickening of the skin folds, hyperkeratosis and papillomatosis.

Gas gangrene (also known as clostridial myonecrosis and myonecrosis) is a bacterial infection that produces gas in tissues in gangrene. This deadly form of gangrene usually is caused by "Clostridium perfringens" bacteria. It is a medical emergency. About 1000 cases of gas gangrene occur yearly in the United States.

Myonecrosis is a condition of necrotic damage, specific to muscle tissue. It is often seen in infections with "C. perfringens" or any of myriad soil-borne anaerobic bacteria. Bacteria cause myonecrosis by specific exotoxins. These microorganisms are opportunistic and, in general, enter the body through significant skin breakage. Gangrenous infection by soil-borne bacteria was common in the combat injuries of soldiers well into the 20th century, because of nonsterile field surgery and the basic nature of care for severe projectile wounds.

Other causes of myonecrosis include envenomation by snakes of the "Bothrops" genus (family Viperidae), ischemic necrosis, caused by vascular blockage (e.g., diabetes type II), tumours that block or hoard blood supply, and disseminated intravascular coagulation or other thromboses.

A centipede bite is an injury resulting from the action of a centipede's forcipules, pincer-like appendages that pierce the skin and inject venom into the wound. Such a wound is not technically a bite, as the forcipules are modified first pair of legs rather than true mouthparts. Clinically, the wound is viewed as a cutaneous condition characterized by paired hemorrhagic marks that form a chevron shape caused by the large paired forcipules of the centipede.

The centipede's venom causes pain and swelling in the area of the bite, and may cause other reactions throughout the body. The majority of bites are not life-threatening to humans and present the greatest risk to children and those who develop allergic reactions.

Treatment is usually debridement and excision, with amputation necessary in many cases. Water-soluble antibiotics (such as penicillin) alone are not effective because they do not penetrate ischaemic muscles sufficiently to be effective. Penicillin is effective against C. perfringens. When gas gangrene occurs in such regions as the abdominal cavity, the patient can be treated in a hyperbaric chamber. which contains a pressurized oxygen-rich atmosphere. The oxygen saturates the infected tissues and thereby prevents the growth of the obligately anaerobic clostridia. The growth of C. perfringens is inhibited when the availability of oxygen is equivalent to a partial pressure of around 9–10 kPa (compare to 4–5 kPa in venous blood under normal conditions, with 11–13 kPa in arteries and 21 kPa in air at sea level), so if the treatment is started early, this condition can mostly be cured.

Erythromelalgia is a difficult condition to diagnose as there are no specific tests available. However, reduced capillary density has been observed microscopically during flaring; and reduced capillary perfusion is noted in the patient. Another test that can be done is to have the patient elevate their legs, and note the reversal (from red to pale) in skin color. Tests done at universities include quantitative sensory nerve testing, laser evoked potentials, sweat testing and epidermal sensory nerve fiber density test (which is an objective test for small fiber sensory neuropathy). Due the aforementioned factors, patients may face delays in diagnosis.

Once it has been established that it is not secondary erythromelalgia — see below — a programme of management can be put in place.

Some diseases present with symptoms similar to erythromelalgia. Complex regional pain syndrome (CRPS), for instance, presents with severe burning pain and redness except these symptoms are often unilateral (versus symmetric) and may be proximal instead of purely or primarily distal. Furthermore, attacks triggered by heat and resolved by cooling are less common with CRPS.

Erythromelalgia is sometimes caused by other disorders. A partial list of diseases known to precipitate erythromelalgia is below.

Unfortunately, response to treatment is not guaranteed. Also, the necrotic skin areas may get infected, and this then may lead to sepsis (i.e. infection of blood with bacteria; sepsis can be life-threatening) in some patients. Overall, the clinical prognosis remains poor.

Differentiation between this and SCC would be based on a history of recent trauma or dental treatment in the area.

Immunohistochemistry may aid the diagnosis. If the lesion is NS, there will be focal to absent immunoreactivity for p53, low immunoreactivity for MIB1 (Ki-67), and the presence of 4A4/p63- and calponin-positive myoepithelial cells.

Most cases respond to antibiotics and prognosis is usually excellent unless there is a debilitating underlying condition. Mortality from lung abscess alone is around 5% and is improving.

Stasis Papillomatosis is similar to AGEP (Acute generalized exanthematous pustulosis) from pustular psoriasis; criteria for histopathologic distinction have been proposed: papillary edema, vasculitis, exocytosis of eosinophils and single-cell necrosis of keratinocytes in AGEP and acanthosis and papillomatosis in pustular psoriasis.

An example that illustrates the difference between SP and Stasis Papillomatosis and the histology diagnosis is … “a markedly obese, 41-year-old Japanese man who had suffered from psoriasis vulgaris for several years visited hospital with elephantiasis-like swelling of his lower legs of three months' duration. His right lower leg showed marked papillomatosis with thick scales, and the left lower leg was eroded and papillomatous. Although direct lymphography of his lower extremities showed no abnormality, indirect lymphography revealed local lymphatic damage in the involved skin”. Histological examination showed hyperkeratosis, marked papillomatosis, proliferation of capillaries in the upper dermis, and lymphectasia in the lower dermis. It was suspected that obesity and the preceding psoriatic lesions caused local lymphatic disturbances, followed by the development of stasis papillomatosis.

Surgical removal of all dead tissue is the mainstay of treatment for gangrene. Often, gangrene is associated with underlying infection, and thus the gangrenous tissue must be debrided to hinder the spread of the associated infection. The extent of surgical debridement needed depends on the extent of the gangrene, and may be limited to the removal of a finger, toe, or ear, but in severe cases may involve a limb amputation

Dead tissue alone does not require debridement, and in some cases, such as dry gangrene, the affected falls off ("auto-amputates"), making surgical removal not necessary.

As there is often infection associated with gangrene, antibiotics are often a critical component of the treatment of gangrene. The life-threatening nature of gangrene requires treatment with intravenous antibiotics in an inpatient setting.

After the gangrene is treated with debridement and antibiotics, the underlying cause of gangrene can be treated. In the case of gangrene due to critical limb ischemia, revascularization can be performed to treat the underlying peripheral artery disease.

Ischemic disease of the legs is the most common reason for amputations. In about a quarter of these cases the other side requires amputation in the next three years.

In 2005, an estimated 1.6 million individuals in the United States were living with the loss of a limb caused by either trauma, cancer or vascular disease; these estimates are expected to more than double to 3.6 million such individuals by 2050. Antibiotics alone are not effective because they may not penetrate infected tissues sufficiently. Hyperbaric oxygen therapy (HBOT) treatment is used to treat gas gangrene. HBOT increases pressure and oxygen content to allow blood to carry more oxygen to inhibit anaerobic organism growth and reproduction. A regenerative medicine therapy was developed by Dr. Peter DeMarco to treat diabetic gangrene to avoid amputations. Growth factors, hormones, and skin grafts have also been used to accelerate healing for gangrene and other chronic wounds.

Angioplasty should be considered if severe blockage in lower leg vessels (tibial and peroneal artery) leads to gangrene.