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.

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

Beet vascular necrosis and rot is a soft rot disease caused by the bacterium Pectobacterium carotovorum" subsp. "betavasculorum, which has also been known as "Pectobacterium betavasculorum" and "Erwinia carotovora" subsp. "betavasculorum". It was classified in the genus "Erwinia" until genetic evidence suggested that it belongs to its own group; however, the name Erwinia is still in use. As such, the disease is sometimes called Erwinia rot today. It is a very destructive disease that has been reported across the United States as well as in Egypt. Symptoms include wilting and black streaks on the leaves and petioles. It is usually not fatal to the plant, but in severe cases the beets will become hollowed and unmarketable. The bacteria is a generalist species which rots beets and other plants by secreting digestive enzymes that break down the cell wall and parenchyma tissues. The bacteria thrive in warm and wet conditions, but cannot survive long in fallow soil. However, it is able to persist for long periods of time in the rhizosphere of weeds and non-host crops. While it is difficult to eradicate, there are cultural practices that can be used to control the spread of the disease, such as avoiding injury to the plants and reducing or eliminating application of nitrogen fertilizer.

Most of the SDS symptoms can be confused with other factors like nutrient deficiencies and some other diseases like brown stem rot and stem canker. Usually the first symptom seen is interveinal chlorosis, which is the yellowing of the plant material between the leaf veins. When leaves begin to die, puckering and mottling can also be observed along with the chlorosis. As severity increases, necrosis (death of cells) occurs and eventually these leaves will fall off, leaving only petioles left on the stem. If the conditions are right (cool and wet), these symptoms can appear suddenly, causing large yield reductions. Normally, this is seen in mid or late July around the time of flowering and pod production.

In addition to foliar symptoms, the stem of the soybean plant can show symptoms as well. If a soybean stem with SDS is split, the pith will be visibly white while the cortical tissue around the pith will be tan to light brown in color. If the pith is brown in color (or if the whole stem looks brown on the inside), it is likely that the plant has brown stem rot, rather than SDS

Along with the above ground foliar and stem symptoms, the roots usually show some kind of rotting and decrease in vigor compared to other healthy soybean roots. If soil conditions are moist, roots are also likely to show blue masses of spores (macroconidia) around the taproot just below the soil surface. Blue fungal masses, found along with the foliar and stem symptoms, are strong diagnostic indicators for SDS

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.

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.

Symptoms can be found on both beet roots and foliage, although foliar symptoms are not always present. If present, foliar symptoms include dark streaking along petioles and viscous froth deposits on the crown which are a by-product of bacterial metabolism. Petioles can also become necrotic and demonstrate vascular necrosis. When roots become severely affected, wilting also occurs. Below ground symptoms include both soft and dry root rot. Affected vascular bundles in roots become necrotic and brown, and tissue adjacent to necrosis becomes pink upon air contact. The plants that do not die completely may have rotted-out, cavernous roots.

Various pathogens can cause root rot in beets; however the black streaking on petioles and necrotic vascular bundles in roots and adjacent pink tissue help to distinguish this disease from others such as Fusarium Yellows. Additionally, sampling from the rhizosphere of infected plants and serological tests can confirm the presence of "Erwinia caratovora" subs.

"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.

"Trench foot " is a medical condition caused by prolonged exposure of the feet to damp, unsanitary, and cold conditions. The use of the word "trench" in the name of this condition is a reference to trench warfare, mainly associated with World War I. Affected feet may become numb, affected by erythrosis (turning red) or cyanosis (turning blue) as a result of poor vascular supply, and feet may begin to have a decaying odour due to the possibility of the early stages of necrosis setting in. As the condition worsens, feet may also begin to swell. Advanced trench foot often involves blisters and open sores, which lead to fungal infections; this is sometimes called tropical ulcer (jungle rot).

If left untreated, trench foot usually results in gangrene, which can cause the need for amputation. If trench foot is treated properly, complete recovery is normal, though it is marked by severe short-term pain when feeling returns. As with other cold-related injuries, trench foot leaves sufferers more susceptible to it in the future.

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.

The history of a centipede bite is fairly straightforward; the victim typically sees and identifies the characteristic centipede before, or soon after being bitten.

Symptoms which are most likely to develop include:

- severe pain, which is usually in proportion to the size of the centipede

- swelling and redness. Possible 'bullseye'

- skin necrosis

- swollen, painful lymph nodes in the regions of the bitten limb

- headache

- palpitations or a racing pulse

- nausea and vomiting

- anxiety

- local itching and burning sensations

The wound left by the bite may be accompanied by swelling, redness, and small puncture wounds which may form a circular pattern. This wound may be susceptible to local ulcerations and necrosis.

A severe bite from a large centipede on a child, senior or person with a weakened heart can cause heart attack if untreated. This is exceptionally rare.

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.

Gas gangrene can cause myonecrosis (muscle tissue death), gas production, and sepsis. Progression to toxemia and shock is often very rapid. It can easily be noticed by the large, blackened sores that form, as well as a degree of loud and distinctive crepitus caused by gas escaping the necrotic tissue.

Choke is a condition in horses in which the esophagus is blocked, usually by food material. Although the horse is still able to breathe, it is unable to swallow, and may become severely dehydrated. A secondary condition, aspiration pneumonia, may also develop if food material and saliva accumulate in the pharynx, spilling into the trachea and into the lungs. Choke is one of the "top 10" emergencies received by equine veterinarians.

The condition is seen in other Equidae like mules and donkeys.

Onset of symptoms is often gradual, but in necrotizing staphylococcal or gram-negative bacillary pneumonias patients can be acutely ill. Cough, fever with shivering, and night sweats are often present. Cough can be productive of foul smelling purulent mucus (≈70%) or less frequently with blood in one third of cases). Affected individuals may also complain of chest pain, shortness of breath, lethargy and other features of chronic illness.

Those with a lung abscess are generally cachectic at presentation. Finger clubbing is present in one third of patients. Dental decay is common especially in alcoholics and children. On examination of the chest there will be features of consolidation such as localized dullness on percussion and bronchial breath sounds.

Chewing: Horses may develop choke if they do not chew their food properly. Therefore, horses with dental problems (e.g. acquired or congenital malocclusion, loose or missing teeth, or excessively sharp dental ridges) that do not allow them to completely grind their food are particularly at risk. In addition, horses that bolt their feed and do not take the time to chew properly are more likely to suffer from choke.

Dry Food: Dry foods may cause choke, especially if the horse does not have free access to water, or if the horse has other risk factors linked to choking. While pelleted or cubed feeds in general fall in this category, horse owners sometimes express particular concerns about beet pulp. However, while horses have choked on beet pulp, a university study did not document that beet pulp is a particular problem. It is believed that choke related to beet pulp is linked to the particle size and the horse's aggressive feeding behaviour, rather than the actual feed itself. Research suggests that horses that bolt their feed without sufficient chewing, or who do not have adequate access to water, are far more likely to choke, regardless of the type of feed, compared to horses that eat at a more leisurely rate. The risk of choke associated with any dry feed can be reduced by soaking the ration prior to feeding.

Foreign Objects: Horse may ingest non-edible materials such as pieces of wood. Cribbers may be more prone to this type of choke, if they happen to swallow a piece of wood or other material while cribbing.

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.

The most prominent symptoms of erythromelalgia are episodes of erythema, swelling, a painful deep-aching of the soft tissue (usually either radiating or shooting) and tenderness, along with a painful burning sensation primarily in the extremities. These symptoms are often symmetric and affect the lower extremities more frequently than the upper extremities. Symptoms may also affect the ears and face. For secondary erythromelalgia, attacks typically precede and are precipitated by the underlying primary condition. For primary erythromelalgia, attacks can last from an hour to months at a time and occur infrequently to frequently with multiple times daily. Common triggers for these episodes are exertion, heating of the affected extremities, and alcohol or caffeine consumption, and any pressure applied to the limbs. In some patients sugar and even melon consumption have also been known to provoke attacks. Many of those with primary erythromelalgia avoid wearing shoes or socks as the heat this generates is known to produce erythromelalgia attacks. Raynaud's phenomenon often coexists in patients with Erythromelalgia. Symptoms may present gradually and incrementally, sometimes taking years to become intense enough for patients to seek medical care. In other cases symptoms emerge full blown with onset.

Rare nowadays but include spread of infection to other lung segments, bronchiectasis, empyema, and bacteremia with metastatic infection such as brain abscess.

Chronic inflammation can cause long term lymphatic obstruction. Typically, patients have disorders that present local nodes, primary lymphedema and chronic venous insufficiency. Erysipelas and trauma are major risk factors. Lymphatic edema can be developed in many acral cases accompanied by a thickening of the folds of the skin, hyperkeratosis and papillomatosis. Chronic venous edema is only partially reversible and soon becomes hard, especially confirming tenderness. All structures of the skin are affected. Dilated dermal lymphatic vessels with consequent superior organization and fibrosis result in papillomatosis. As dermal lymphatic stasis progreses, these skin changes become more marked and known as elephantiasis. Occasionally, tissue fibrosis and thickening may become so marked in the later stages of lymphedema that pitting is absent. Recurrent cellulitis, erysipelas and dermato-LAM-adenitis are complications of chronic lymphedema.

The first skin changes in calciphylaxis lesions are mottling of the skin and induration in a livedo reticularis pattern. As tissue thrombosis and infarction occurs, a black, leathery eschar in an ulcer with adherent black slough are found. Surrounding the ulcers is usually a plate-like area of indurated skin. These lesions are always extremely painful and most often occur on the lower extremities, abdomen, buttocks, and penis. Because the tissue has infarcted, wound healing seldom occurs, and ulcers are more likely to become secondarily infected. Many cases of calciphylaxis end with systemic bacterial infection and death.

Calciphylaxis is characterized by the following histologic findings:

1. systemic medial calcification of the arteries, i.e. calcification of tunica media. Unlike other forms of vascular calcifications (e.g., intimal, medial, valvular), calciphylaxis is characterized also by

2. small vessel mural calcification with or without endovascular fibrosis, extravascular calcification and vascular thrombosis, leading to tissue ischemia (including skin ischemia and, hence, skin necrosis).

Erythromelalgia can be found in several billing codes systems and other systems. Erythromelalgia is generally classified as a disease of the circulatory system, falling under the class of "other peripheral vascular disease", as the following two billing code systems will show:

ICD-9-CM

According to the ICD-9-CM database (International Classification of Diseases, Ninth Revision, Clinical Modification), Erythromelalgia is listed under Diseases of the Circulatory System and is identified by number 443.82.

ICD-9-CM Diagnosis Codes > Diseases of the circulatory system (390-459) > Diseases of arteries, arterioles, and capillaries (440-449) > Other peripheral vascular disease (443) > Other specified peripheral vascular disease (443.8) > Erythromelalgia (443.82).

ICD-10-CM

According to the ICD-10-CM database (International Classification of Diseases, Tenth Revision, Clinical Modification), Erythromelalgia is listed under Diseases of the circulatory system and is identified by I73.81.

ICD-10-CM Diagnosis Codes > Diseases of the circulatory system (I00-I99) > Diseases of arteries, arterioles and capillaries (I70-I79) > Other peripheral vascular diseases (173-9) > Erythromelalgia (I73.81)

Mesh

According to the MESH database (Medical Subject Headings), Erythromelalgia is classified under the unique ID number of D004916.

OMIM

According to the OMIM database (NCBI - Online Mendelian Inheritance in Man), Primary Erythromelalgia is listed under the number: 133020.

The condition most commonly is located at the junction of the hard and soft palate. However, the condition may arise anywhere minor salivary glands are located. It has also been occasionally reported to involve the major salivary glands. It may be present only on one side, or both sides. The lesion typically is 1–4 cm in diameter.

Initially, the lesion is a tender, erythematous (red) swelling. Later, in the ulcerated stage, the overlying mucosa breaks down to leave a deep, well-circumscribed ulcer which is yellow-gray in color and has a lobular base.

There is usually only minor pain, and the condition is often entirely painless. There may be prodromal symptoms similar to flu before the appearance of the lesion.

Calciphylaxis most commonly occurs in patients with end-stage renal disease who are on hemodialysis or who have recently received a renal (kidney) transplant. Yet calciphylaxis does not occur only in end-stage renal disease patients. When reported in patients without end-stage renal disease, it is called non-uremic calciphylaxis by Nigwekar et al. Non-uremic calciphylaxis has been observed in patients with primary hyperparathyroidism, breast cancer (treated with chemotherapy), liver cirrhosis (due to alcohol abuse), cholangiocarcinoma, Crohn's disease, rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE).