The infection in most instances presents as a painless lump just under the skin. In southern Australia, the presentation is more often as a pimple in the skin (dermis) rather than under it. The infection is mostly in the limbs, most often in exposed areas, but not on the hands or feet. In children, all areas may be involved, including the face or abdomen. A more severe form of infection produces diffuse swelling of a limb, which, unlike the papule or nodule, can be painful and accompanied by fever. Infection may frequently follow physical trauma, often minor trauma such as a small scratch.

Buruli ulcer is an infectious disease caused by "Mycobacterium ulcerans". The early stage of the infection is characterised by a painless nodule or area of swelling. This nodule can turn into an ulcer. The ulcer may be larger inside than at the surface of the skin, and can be surrounded by swelling. As the disease worsens, bone can be infected. Buruli ulcers most commonly affect the arms or legs; fever is uncommon.

"M. ulcerans" releases a toxin known as mycolactone, which decreases immune system function and results in tissue death. Bacteria from the same family also cause tuberculosis and leprosy ("M. tuberculosis" and "M. leprae", respectively). How the disease is spread is not known. Sources of water may be involved in the spread. As of 2013 there is no effective vaccine.

If people are treated early, antibiotics for eight weeks are effective in 80%. The treatment often includes the medications rifampicin and streptomycin. Clarithromycin or moxifloxacin are sometimes used instead of streptomycin. Other treatments may include cutting out the ulcer. After the infection heals, the area typically has a scar.

In 2015 about 2,000 cases were reported. Buruli ulcers occur most commonly in rural sub-Saharan Africa especially Cote d'Ivoire, but can also occur in Asia, the Western Pacific and the Americas. Children are most commonly infected. Cases have occurred in more than 32 countries. The disease also occurs in a number of animals other than humans. Albert Ruskin Cook was the first to describe buruli ulcers in 1897. It is classified as a neglected tropical disease.

The vast majority of the tropical ulcers occur below the knee, usually around the ankle. They may also occur on arms. They are often initiated by minor trauma, and subjects with poor nutrition are at higher risk. Once developed, the ulcer may become chronic and stable, but also it can run a destructive course with deep tissue invasion, osteitis, and risk of amputation. Unlike Buruli ulcer, tropical ulcers are very painful. Lesions begin with inflammatory papules that progress into vesicles and rupture with the formation of an ulcer. Chronic ulcers involve larger area and may eventually develop into squamous epithelioma after 10 years or more.

Tropical ulcer, more commonly known as jungle rot, is a chronic ulcerative skin lesion thought to be caused by polymicrobial infection with a variety of microorganisms, including mycobacteria. It is common in tropical climates.

Ulcers occur on exposed parts of the body, primarily on anterolateral aspect of the lower limbs and may erode muscles and tendons, and sometimes, the bones. These lesions may frequently develop on preexisting abrasions or sores sometimes beginning from a mere scratch.

The initial lesion is a small subcutaneous swelling following minor trauma. Later, sinuses that discharge purulent and seropurulent exudates containing grains which are fungal colonies are formed. Destruction of deeper tissues, and deformity and loss of function in the affected limbs may occur in later stages.

Eumycetoma is a chronic granulomatous fungal disease of humans, affecting mainly the limbs, and sometimes the abdominal and chest walls or the head. "Mycetoma pedis" (mycetoma of the foot), the most common form of mycetoma, is known widely as the Madura foot. The infection is endemic in Africa, India and Central and South America.

Epizootic ulcerative syndrome (EUS), also known as mycotic granulomatosis (MG) or red spot disease (RSD), is a disease caused by the water mould "Aphanomyces invadans". It infects many freshwater and brackish fish species in the Asia-Pacific region and Australia. The disease is most commonly seen when there are low temperature and heavy rainfall in tropical and sub-tropical waters.

Small, painless nodules appear after about 10–40 days of the contact with the bacteria. Later, the nodules burst, creating open, fleshy, oozing lesions. The infection spreads, mutilating the infected tissue. The infection will continue to destroy the tissue until treated. The lesions occur at the region of contact typically found on the shaft of the penis, the labia, or the perineum. Rarely, the vaginal wall or cervix is the site of the lesion. At least one case in India led to partial autoamputation of the penis. The patient tested positive for HIV-2 and had been infected for six years.

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.

The microorganism spreads from one host to another through contact with the open sores.

These are only local and no systemic manifestations are present.

The ulcer characteristically:

- Ranges in size dramatically from 3 to 50 mm (1/8 inch to two inches) across

- Is painful

- Has sharply defined, undermined borders

- Has irregular or ragged borders

- Has a base that is covered with a gray or yellowish-gray material

- Has a base that bleeds easily if traumatized or scraped

- painful swollen lymph nodes occurs in 30 to 60% of patients.

- dysuria (pain with urination) and dyspareunia (pain with intercourse) in females

About half of infected men have only a single ulcer. Women frequently have four or more ulcers, with fewer symptoms.

The initial ulcer may be mistaken as a "hard" chancre, the typical sore of primary syphilis, as opposed to the "soft chancre" of chancroid.

Approximately one-third of the infected individuals will develop enlargements of the inguinal lymph nodes, the nodes located in the fold between the leg and the lower abdomen.

Half of those who develop swelling of the inguinal lymph nodes will progress to a point where the nodes rupture through the skin, producing draining abscesses. The swollen lymph nodes and abscesses are often referred to as buboes.

There are many differences and similarities between the conditions syphilitic chancre and chancroid.

- Similarities

- Both originate as pustules at the site of inoculation, and progress to ulcerated lesions

- Both lesions are typically 1–2 cm in diameter

- Both lesions are caused by sexually transmissible organisms

- Both lesions typically appear on the genitals of infected individuals

- Both lesions can be present at multiple sites and with multiple lesions

- Differences

- Chancre is a lesion typical of infection with the bacterium that causes syphilis, Treponema pallidum

- Chancroid is a lesion typical of infection with the bacterium Haemophilus ducreyi

- Chancres are typically painless, whereas chancroid are typically painful

- Chancres are typically non-exudative, whereas chancroid typically have a grey or yellow purulent exudate

- Chancres have a hard (indurated) edge, whereas chancroid have a soft edge

- Chancres heal spontaneously within three to six weeks, even in the absence of treatment

- Chancres can occur in the pharynx as well as on the genitals

Different types of discharges from ulcer are:

- Serous, usually seen in healing ulcer

- Purulent, seen in infected ulcer. Yellow creamy discharge is observed in staphylococcal infection; bloody opalescent discharge in streptococcal infection, while greenish discharge is seen in pseudomonas ulcer

- Bloody (sanguineous), usually seen in malignant ulcers and in healing ulcers with healthy granulation tissue

- Seropurulent

- Serosanguinous

- Serous with sulphur granules, seen in actinomycosis

- Yellowish, as seen in tuberculous ulcer

Skin ulcers appear as open craters, often round, with layers of skin that have eroded. The skin around the ulcer may be red, swollen, and tender. Patients may feel pain on the skin around the ulcer, and fluid may ooze from the ulcer. In some cases, ulcers can bleed and, rarely, patients experience fever. Ulcers sometimes seem not to heal; healing, if it does occur, tends to be slow. Ulcers that heal within 12 weeks are usually classified as acute, and longer-lasting ones as chronic.

Ulcers develop in stages. In stage 1 the skin is red with soft underlying tissue. In the second stage the redness of the skin becomes more pronounced, swelling appears, and there may be some blisters and loss of outer skin layers. During the next stage, the skin may become necrotic down through the deep layers of skin, and the fat beneath the skin may become exposed and visible. In stage 4, deeper necrosis usually occurs, the fat underneath the skin is completely exposed, and the muscle may also become exposed. In the last two stages the sore may cause a deeper loss of fat and necrosis of the muscle; in severe cases it can extend down to bone level, destruction of the bone may begin, and there may be sepsis of joints.

Chronic ulcers may be painful. Most patients complain of constant pain at night and during the day. Chronic ulcer symptoms usually include increasing pain, friable granulation tissue, foul odour, and wound breakdown instead of healing. Symptoms tend to worsen once the wound has become infected.

Venous skin ulcers that may appear on the lower leg, above the calf or on the lower ankle usually cause achy and swollen legs. If these ulcers become infected they may develop an unpleasant odour, increased tenderness and redness. Before the ulcer establishes definitively, there may be a dark red or purple skin over the affected area as well as a thickening, drying, and itchy skin.

Although skin ulcers do not seem of great concern at a first glance, they are worrying conditions especially in people suffering from diabetes, as they are at risk of developing diabetic neuropathy.

Ulcers may also appear on the cheeks, soft palate, the tongue, and on the inside of the lower lip. These ulcers usually last from 7 to 14 days and can be painful.

The most common presentation is a single large, deep ulcer (although several smaller ulcers may occur) in the internal surface of one or both labia minora. The labia majora may be affected, as may the vagina and urethra. The ulcer develops very quickly, and is usually preceded by sudden onset of fever and malaise.

The diagnosis is mainly clinical and centred in eliminating other more common causes for vulvar ulcers. Nevertheless, it has been proposed that Epstein-Barr detection using polymerase chain reaction for virus genome can help to reach sooner a diagnosis.

People usually complain of intense pain that may seem excessive given the external appearance of the skin. People initially have signs of inflammation, fever and a fast heart rate. With progression of the disease, often within hours, tissue becomes progressively swollen, the skin becomes discolored and develops blisters. Crepitus may be present and there may be a discharge of fluid, said to resemble "dish-water". Diarrhea and vomiting are also common symptoms.

In the early stages, signs of inflammation may not be apparent if the bacteria are deep within the tissue. If they are "not" deep, signs of inflammation, such as redness and swollen or hot skin, develop very quickly. Skin color may progress to violet, and blisters may form, with subsequent necrosis (death) of the subcutaneous tissues.

Furthermore, people with necrotizing fasciitis typically have a fever and appear sick. Mortality rates are as high as 73% if left untreated. Without surgery and medical assistance, such as antibiotics, the infection will rapidly progress and will eventually lead to death.

When it affects the groin it is known as Fournier gangrene.

The definitions of the four pressure ulcer stages are revised periodically by the National Pressure Ulcer Advisor Panel (NPUAP) in the United States and the European Pressure Ulcer Advisor Panel (EPUAP) in Europe. Briefly, they are as follows:

- Stage 1: Intact skin with non-blanchable redness of a localized area usually over a bony prominence. Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area. The area differs in characteristics such as thickness and temperature as compared to adjacent tissue. Stage 1 may be difficult to detect in individuals with dark skin tones. May indicate "at risk" persons (a heralding sign of risk).

- Stage 2: Partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough. May also present as an intact or open/ruptured serum-filled blister. Presents as a shiny or dry shallow ulcer without slough or bruising. This stage should not be used to describe skin tears, tape burns, perineal dermatitis, maceration or excoriation.

- Stage 3: Full thickness tissue loss. Subcutaneous fat may be visible but bone, tendon or muscle are not exposed. Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunneling. The depth of a stage 3 pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have (adipose) subcutaneous tissue and stage 3 ulcers can be shallow. In contrast, areas of significant adiposity can develop extremely deep stage 3 pressure ulcers. Bone/tendon is not visible or directly palpable.

- Stage 4: Full thickness tissue loss with exposed bone, tendon or muscle. Slough or eschar may be present on some parts of the wound bed. Often include undermining and tunneling. The depth of a stage 4 pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have (adipose) subcutaneous tissue and these ulcers can be shallow. Stage 4 ulcers can extend into muscle and/or supporting structures (e.g., fascia, tendon or joint capsule) making osteomyelitis likely to occur. Exposed bone/tendon is visible or directly palpable. In 2012, the NPUAP stated that pressure ulcers with exposed cartilage are also classified as a stage 4.

- Unstageable: Full thickness tissue loss in which actual depth of the ulcer is completely obscured by slough (yellow, tan, gray, green or brown) and/or eschar (tan, brown or black) in the wound bed. Until enough slough and/or eschar is removed to expose the base of the wound, the true depth, and therefore stage, cannot be determined. Stable (dry, adherent, intact without erythema or fluctuance) eschar on the heels is normally protective and should not be removed.

- Suspected Deep Tissue Injury: A purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer or cooler as compared to adjacent tissue. A deep tissue injury may be difficult to detect in individuals with dark skin tones. Evolution may include a thin blister over a dark wound bed. The wound may further evolve and become covered by thin eschar. Evolution may be rapid exposing additional layers of tissue even with optimal treatment.

The symptoms of fungal keratitis are blurred vision, a red and painful eye that does not improve when contact lenses are removed, or on antibiotic treatment, increased sensitivity to light (photophobia), and excessive tearing or discharge. The symptoms are markedly less as compared to a similar bacterial ulcer.

Signs: The eyelids and adnexa involved shows edema and redness, conjuctiva is chemosed. Ulcer may be present. It is a dry looking corneal ulcer with satellite lesions in the surrounding cornea. Usually associated with fungal ulcer is hypopyon, which is mostly white fluffy in appearance. Rarely, it may extend to the posterior segment to cause endophthalmitis in later stages, leading to the destruction of the eye. (Note: Fungal endophthalmitis is extremely rare)

The primary skin lesion usually starts with a macule that is painless, round and erythematous. Then, it develops into a pustule, and then a bulla with central hemorrhagic focus. The bullae progresses into an ulcer which extends laterally. Finally it becomes a gangrenous ulcer with central black eschar surrounded by erythematous halo.

The lesion may be single or multiple. They are most commonly seen in perineum and under arm pit. However, it can occur in any part of the body.

Infectious keratitis can be bacterial, fungal, viral, or protozoal. Remarkable differences in presentation of the patient allows presumptive diagnosis by the eye care professional, helping in institution of appropriate anti-infective therapy.

A genital ulcer is located on the genital area, usually caused by a sexually transmitted disease such as genital herpes, syphilis, chancroid, or "Chlamydia trachomatis". Some other signs of having genital ulcers include enlarged lymph nodes in the groin area, or vesicular lesions, which are small, elevated sores or blisters. The syndrome may be further classified into penile ulceration and vulval ulceration for males and females respectively.

Genital ulcers are not strictly a sign of an STD. They can occur in patients with Behcet's syndrome, lupus, and some forms of rheumatoid arthritis (all non-communicable diseases). Genital tuberculosis, often caused by direct genital contact with infected sputum, can also present as genital ulcer.

Pressure ulcers can trigger other ailments, cause considerable suffering, and can be expensive to treat. Some complications include autonomic dysreflexia, bladder distension, bone infection, pyarthroses, sepsis, amyloidosis, anemia, urethral fistula, gangrene and very rarely malignant transformation (Marjolin's ulcer - secondary carcinomas in chronic wounds). Sores may recur if those with pressure ulcers do not follow recommended treatment or may instead develop seromas, hematomas, infections, or wound dehiscence. Paralyzed individuals are the most likely to have pressure sores recur. In some cases, complications from pressure sores can be life-threatening. The most common causes of fatality stem from kidney failure and amyloidosis.

Pressure ulcers are also painful, with individuals of all ages and all stages of pressure ulcers reporting pain.

These ulcers have punched-out edge and slough in floor, resembling gummatous ulcer. Surrounding area might have loss of sensation.

Necrotizing fasciitis (NF), commonly known as flesh-eating disease, is an infection that results in the death of the body's soft tissue. It is a severe disease of sudden onset that spreads rapidly. Symptoms include red or purple skin in the affected area, severe pain, fever, and vomiting. The most commonly affected areas are the limbs and perineum.

Typically the infection enters the body through a break in the skin such as a cut or burn. Risk factors include poor immune function such as from diabetes or cancer, obesity, alcoholism, intravenous drug use, and peripheral vascular disease. It is not typically spread between people. The disease is classified into four types, depending on the infecting organism. Between 55% and 80% of cases involve more than one type of bacteria. Methicillin-resistant "Staphylococcus aureus" (MRSA) is involved in up to a third of cases. Medical imaging is helpful to confirm the diagnosis.

Prevention is by good wound care and handwashing. It is usually treated with surgery to remove the infected tissue and intravenous antibiotics. Often a combination of antibiotics are used such as penicillin G, clindamycin, vancomycin, and gentamicin. Delays in surgery are associated with a higher risk of death. Despite high quality treatment the risk of death is between 25% and 35%.

Necrotizing fasciitis affects 0.4 to 1 person per 100,000 per year. Both sexes are affected equally. It becomes more common among older people and is very rare in children. Necrotizing fasciitis has been described at least since the time of Hippocrates. The term "necrotising fasciitis" first came into use in 1952.