Infected fish should be moved into high quality water, where they may recover if their clinical signs are mild.

If disease occurs eradication is required. Once the disease is eradicated good husbandry, surveillance and biosecurity measures are necessary to prevent recurrence. In countries free of epizootic ulcerative syndrome, quarantine and health certificates are necessary for the movement of all live fish to prevent the introduction of the disease.

Often a diagnosis of exclusion, skin biopsy shows a neutrophillic inflammatory infiltrate.

At first, fish develop red spots on the skin. These lesions expand to form ulcers and extensive erosions filled with necrotic tissue and mycelium. This is followed by the development of granulomas on the internal organs and death.

A provisional diagnosis can be made by using squash preparations of the skeletal muscle from beneath an ulcer to identify the septate hyphae of the water mould. Definitive diagnosis can be made based on histopathogical findings and isolation of the pathogen.

NL is diagnosed by a skin biopsy, demonstrating superficial and deep perivascular and interstitial mixed inflammatory cell infiltrate (including lymphocytes, plasma cells, mononucleated and multinucleated histiocytes, and eosinophils) in the dermis and subcutis, as well as necrotising vasculitis with adjacent necrobiosis and necrosis of adnexal structures. Areas of necrobiosis are often more extensive and less well defined than in granuloma annulare. Presence of lipid in necrobiotic areas may be demonstrated by Sudan stains. Cholesterol clefts, fibrin, and mucin may also be present in areas of necrobiosis. Depending on the severity of the necrobiosis, certain cell types may be more predominant. When a lesion is in its early stages, neutrophils may be present, whereas in later stages of development lymphocytes and histiocytes may be more predominant.

First-line therapy for disseminated or localized instances of pyoderma gangrenosum is systemic treatment by corticosteroids and ciclosporin. Topical application of clobetasol, mupirocin, and gentamicin alternated with tacrolimus can be effective.

Pyoderma gangrenosum ulcers demonstrate pathergy, that is, a worsening in response to minor trauma or surgical debridement. Significant care should be taken with dressing changes to prevent potentially rapid wound growth. Many patients respond differently to different types of treatment, for example some benefit from a moist environment, so treatment should be carefully evaluated at each stage.

Papules that begin as small "spouts" can be treated with Dakins Solution to prevent infection and wound clusters also benefit from this disinfectant. Wet to dry applications of Dakins can defeat spread of interior infection. Heavy drainage can be offset with Coban dressings. Grafting is not recommended due to tissue necrosis.

If ineffective, alternative therapeutic procedures include systemic treatment with corticosteroids and mycophenolate mofetil; mycophenolate mofetil and ciclosporin; tacrolimus; thalidomide; infliximab; or plasmapheresis.

There is currently a phase III trial for the use of the IL-1B modulating agent gevokizumab in treating the ulcers of pyoderma gangrenosum.

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.

Ulcerative dermal necrosis (UDN) is a chronic dermatological disease of cold water salmonid fish that had a severe impact on north Atlantic Salmon and sea trout stocks in the late 1960s, the 1970s and 1980.

Affected fish developed severe skin lesions over large parts of their body which penetrated into skeletal muscle. The onset of symptoms only occurred after migration into freshwater. Lesions became quickly infected with overgrowths of "Saprolegnia" fungus giving the affected fish an appearance of being covered in slimy white pustules. The most severely affected fish frequently die before spawning.

Although the worst effects of the disease were seen in the 1970s and 1980, even now large numbers of salmon will succumb to the disease after spawning. This is thought be due in part to their weak post-spawning condition, and lack of food for several months whilst in the river.

Those fish that do make it back to the sea are thought to make a good recovery.

Lichen planus has a unique microscopic appearance that is similar between cutaneous, mucosal and oral. A Periodic acid-Schiff stain of the biopsy may be used to visualise the specimen. Histological features seen include:

- thickening of the stratum corneum both with nuclei present (parakeratosis) and without (orthokeratosis). Parakeratosis is more common in oral variants of lichen planus.

- thickening of the stratum granulosum

- thickening of the stratum spinosum (acanthosis) with formation of colloid bodies (also known as Civatte bodies, Sabouraud bodies) that may stretch down to the lamina propria.

- liquefactive degeneration of the stratum basale, with separation from the underlying lamina propria, as a result of desmosome loss, creating small spaces (Max Joseph spaces).

- Infiltration of T cells in a band-like pattern into the dermis "hugging" the basal layer.

- Development of a "saw-tooth" appearance of the rete pegs, which is much more common in non-oral forms of lichen planus.

Bumblefoot is so named because of the characteristic "bumbles" or lesions, as well as swelling of the foot pad, symptomatic of an infection. Topical antiseptics in addition to oral or injected antibiotics may be used to combat the infection, which if left untreated may be fatal.

The differential diagnosis for OLP includes:

- Other oral vesiculo-ulcerative conditions such as Pemphigus vulgaris and Benign mucous membrane pemphigoid

- Lupus erythematosus, with lesions more commonly occur on the palate and appear as centrally ulcerated or erythematous with radiating white striae. In contrast, OLP and lichenoid reactions rarely occur on the palate, and the striae are randomly arranged rather than radial.

- Chronic ulcerative stomatitis

- Frictional keratosis and Morsicatio buccarum (chronic cheek biting)

- Oral leukoplakia

- Oral candidiasis

Extensive treatments have been used on domestic animals more than on wild animals, probably because infected domestic animals are easier to identify and treat than infected wildlife. Treatment plans and management vary across taxa because this disease tends to affect each species differently. Antifungal drugs are the first line of defense to kill the agents causing phaeohyphomycosis, but despite the significant progress made in the last two decades and a 30% increase in available antifungal drugs since 2000, many drugs are not effective against black fungi. Diseases caused black fungi are hard to treat because the fungi are very difficult to kill. This high resilience may be contributed to the presence of melanin in their cell walls. Current antifungal agents the fungi are not resistant to are posaconazole, voriconazole, and azole isavuconazole.

In 2006, a free-living Eastern box turtle, "Terrapene carolina carolina", was found with a form of phaeohyphomycosis and was brought in the Wildlife Center of Virginia. Its symptom was swelling of the right hindfoot; it was diagnosed as having chromomycosis by histopathology. The center provided a series of antimicrobial treatments and a one-month course of 1 mg itraconazole, administered orally once a day. The eastern box turtle was euthanized due to further complications and the caretakers’ belief that the turtle would not be able to survive if placed back in the wild.

A recent case of a form of phaeohyphomycosis infection was found in a dog in 2011. The Journal of the American Veterinary Medical Association published a case study in which researchers successfully managed an intracranial phaeohyphomycotic fungal granuloma in a one-year-old male Boxer dog. Veterinarians of the Department of Veterinary Clinical Sciences at Tufts University surgically removed the granuloma in the right cerebral hemisphere. The patient was treated with fluconazole for 4 months, and was followed with voriconazole for 10 months. Both are medications used to treat fungal infections. Based on magnetic resonance imaging and cerebrospinal fluid (CSF) analysis 8 months after the surgery, the male Boxer’s outcome was considered excellent.

Emphasis has been placed on how to manage this disease through careful management practices including: proper handling, preventing crowding situation with animals, and transportation. Both the animals and the environment should be treated thoroughly to hinder the spread and control the fungal infection. This is especially important since humans can also contract this disease.

There is no clearly defined cure for necrobiosis. NLD may be treated with PUVA therapy and improved therapeutic control.

Although there are some techniques that can be used to diminish the signs of necrobiosis such as low dose aspirin orally, a steroid cream or injection into the affected area, this process may be effective for only a small percentage of those treated.

The spider biting apparatus is short and bites are only possible in experimental animals with pressure on the spider's back. Thus many bites occur when a spider is trapped in a shirt or pant sleeve. There is no commercial chemical test to determine if the venom is from a brown recluse. The bite itself is not usually painful. Many necrotic lesions are erroneously attributed to the bite of the brown recluse. (See Note). Skin wounds are common and infections will lead to necrotic wounds. Thus many terrible skin infections are attributed falsely to the brown recluse. Many suspected bites occurred in areas outside of its natural habitat. A wound found one week later may be misattributed to the spider. The diagnosis is further complicated by the fact that no attempt is made to positively identify the suspected spider. Because of this, other, non-necrotic species are frequently mistakenly identified as a brown recluse. Several certified arachnologists are able to positively identify a brown recluse specimen on request.

Reports of presumptive brown recluse spider bites reinforce improbable diagnoses in regions of North America where the spider is not endemic such as Florida, Pennsylvania, and California.

A new mnemonic device, "NOT RECLUSE", has been suggested as a tool to help professionals more objectively exclude skin lesions that were suspected to be loxosceles.

Numerous, Occurrence( wrong geography) Timing( wrong season), Red Center, Elevated, Chronic, Large (more than 10 cm), Ulcerates too quickly (less than a week), Swollen, Exudative

The "Severity of Illness Score for Toxic Epidermal Necrolysis" (SCORTEN) is a scoring system developed to assess the severity of TEN and predict mortality in patients with acute TEN.

One point is given for each of the following factors:

- age >40

- heart rate >120 beats/minute

- carrying diagnosis of cancer

- separation of epidermis on more than ten percent of body surface area (BSA) on day 1.

- Blood Urea Nitrogen >28 mg/dL

- Glucose >252 mg/dL (14 mmol/L)

- Bicarbonate <20mEq/L

In 2016, thermography was used to identify and evaluate bumblefoot lesions in 67 captive penguins from three species.

Definitive diagnosis of TEN often requires biopsy confirmation. Histologically, early TEN shows scattered necrotic keratinocytes. In more advanced TEN, full thickness epidermal necrosis is visualized, with a subepidermal split, and scant inflammatory infiltrate in the papillary dermis. Epidermal necrosis found on histology is sensitive but not specific finding for TEN.

In cases where a large dermonecrotic lesion has developed, sometimes surgery is attempted to remove the dead tissue. This is not ideal, since it will usually leave a large open sore behind, but in certain cases, still occurs. Skin graft to cover the ulcer are rarely needed but may help with appearance.

Human’s clinical signs consisted of swelling and eye infections. There were nodules underneath the skin, abscesses or cysts, and lesions running throughout the body. There were papules, plaques and granulomatous damages on the body. In extreme cases there were deep infections within the eyes, bones, heart and central nervous system.

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.

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.

Actinic granuloma (also known as "O'Brien granuloma") is a cutaneous condition characterized histologically by a dermal infiltrate of macrophages.

Actinic granuloma is an asymptomatic granulomatous reaction that affects sun-exposed skin, most commonly on the face, neck, and scalp.

It is characterized by annular or polycyclic lesions that slowly expand centrifugally and have an erythematous elevated edge and a hypopigmented, atrophic center.

Advise to reduce exposure to the sun and to use sunscreen.

Treatment with topical halometasone cream, pimecrolimus cream.

LINES was first described in a 54-year-old male with history of hypothyroidism who presented to an urgent care facility with bilateral axillary adenopathy and severe malaise. Incision and drainage of the nodes was performed and he was discharged home with sulfamethoxazole/trimethoprim for presumed Methicillin-resistant Staphylococcus aureus (MRSA) infection.

The patient subsequently developed a temperature of 37.5°C, expressed rigors, and night sweats. He returned to the ED the next day and on further history admitted to 3 weeks of “snorting 6-8 lines of coke a day” and smoking marijuana every evening to “come down.” He was hospitalized and treated with cefepime, doxycycline, and fluconazole empirically. The next day erythematous painful papules appeared on his trunk, arms, face, and ears. Blood cultures were negative. There was prominent necrosis of the malar region, nose, and lips with complete sparing of the back. Skin biopsy revealed extensive small vessel thrombosis throughout the superficial and deep dermal plexuses with perivascular mononuclear inflammatory infiltrate and a few neutrophils surrounding the vessels. ESR was elevated at 35 mm/hour; cardiolipin IgM was weakly positive at 16.3;C4 was decreased at 10 mg/dl; antinuclear antibodies were negative and p-ANCA was reactive. Coagulation studies were within normal limits. There was an elevated d-dimer of 17.54 mg/mL and platelets were slightly decreased. The patient’s urine drug screen was positive for cannabis but not cocaine.

Methylprednisolone was started and wound care was initiated. Epidermal necrosis then evolved to myonecrosis extending from midthigh to the foot which necessitated below knee amputation of the right extremity.The patient also required allografts to his chest and abdomen and autografts to his face and left lower extremity.

Diagnosis is made primarily through physical assessment of the skin, family history of Mongolian spots, and subjective data given by the care giver. No tests are currently available for diagnosing Mongolian spots.

William Becker first described an association between NME and glucagonoma in 1942 and since then, NME has been described in as many as 70% of individuals with a glucagonoma. NME is considered part of the glucagonoma syndrome, which is associated with hyperglucagonemia, diabetes mellitus, and hypoaminoacidemia.

When NME is identified in the absence of a glucagonoma, it may be considered "pseudoglucagonoma syndrome". Less common than NME with glucagonoma, pseudoglucagonoma syndrome may occur in a number of systemic disorders:

- Celiac disease

- Ulcerative colitis

- Crohn's disease

- Hepatic cirrhosis

- Hepatocellular carcinoma

- Lung cancer, including small cell lung cancer

- Tumors that secrete insulin- or insulin-like growth factor 2

- Duodenal cancer

Neutrophilic dermatosis of the dorsal hands (also known as "Pustular vasculitis of the dorsal hands") is a skin condition that presents with edematous pustular or ulcerative nodules or plaques localized to the dorsal hands.