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 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.

Post-kala-azar dermal leishmaniasis (PKDL) is a recurrence of kala-azar that may appear on the skin of affected individuals months and up to 20 years after being partially treated, untreated or even in those considered adequately treated. In Sudan, they can be demonstrated in up to 60% of treated cases. They manifest as hypopigmented skin lesions (such as macules, papules, nodules), or facial redness. Though any organism causing kala-azar can lead to PKDL, it is commonly associated with "Leishmania donovani" which gives different disease patterns in India and Sudan. In the Indian variant, nodules enlarge with time and form plaques but rarely ulcerate, but nodules from the African variety often ulcerate as they progress. Nerve involvement is common in African variety but rare in Indian subcontinent. Histology demonstrates a mixture of chronic inflammatory cells; there can be macrophage or epitheloid granuloma. Parasite concentration is not consistent among studies, perhaps reflecting low sensitivity of diagnostic methods used in earlier entries.

Current approach to diagnosis involves 1. demonstration of parasite by microscopy, "in vitro" culture or animal inoculation; 2. immunodiagnosis of parasite antigen; 3. detection of parasite DNA in tissue. Newer PCR based tools have higher sensitivity and specificity. Emergence of PKDL has been reported in HIV affected individuals and may become a problem in future.

Sodium stibogluconate alone or in combination with rifampicin is used for the treatment of PKDL for a long course of up to 4 months. Compliance can be an issue for such a long course.

Cutaneous leishmaniasis (also known as oriental sore, tropical sore, chiclero ulcer, chiclero's ulcer or Aleppo boil) is the most common form of leishmaniasis affecting humans. It is a skin infection caused by a single-celled parasite that is transmitted by the bite of a phlebotomine sandfly. There are about twenty species of "Leishmania" that may cause cutaneous leishmaniasis.

This disease is considered to be a zoonosis (an infectious disease that is naturally transmissible from vertebrate animals to humans), with the exception of "Leishmania tropica" — which is often an anthroponotic disease (an infectious disease that is naturally transmissible from humans to vertebrate animals).

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 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.

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.

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.

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

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.

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 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.

Within 90 days (but usually less than a month) of infection a painless but distinctive "mother yaw" nodule appears, which enlarges and becomes warty in appearance. Nearby "daughter yaws" may also appear simultaneously.

This primary stage resolves completely within six months. The secondary stage occurs months to years later, with typically widespread skin lesions that vary in appearance, including "crab yaws" on the palms of the hands and soles of the feet with desquamation. These secondary lesions frequently ulcerate and are then highly infectious, but heal after six months or more. About 10% of people then go on to develop tertiary disease within five to ten years (during which further secondary lesions may come and go), with widespread bone, joint and soft tissue destruction, which may include extensive destruction of the bone and cartilage of the nose (Rhinopharyngitis mutilans or "gangosa").

Affected feet may become numb, by erythema (turning red) or cyanosis (turning blue) as a result of poor blood supply, and may begin emanating a decaying odor if the early stages of necrosis (tissue death) set 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 may require amputation. If trench foot is treated properly, complete recovery is normal, though it is marked by severe short-term pain when feeling returns.

"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.

Acanthocheilonemiasis is a rare tropical infectious disease caused by a parasite known as "Acanthocheilonema perstans". It can cause skin rashes, abdominal and chest pains, muscle and joint pains, neurological disorders and skin lumps. It is mainly found in Africa. The parasite is transmitted through the bite of small flies. Studies show that there are elevated levels of white blood cells.

Acanthocheilonemiasis belongs to a group of parasitic diseases known as filarial disease (nematode), all of which are classified as Neglected Tropical Diseases. Filarial disease results when microfilariae, which are nematode larvae, reach the lymphatic system; microfilariae reside in the serous cavities of humans. They have a five-stage life cycle that includes birth to thousands of live microfilariae within the host (i.e. human body), and then translocation via blood meal to the dermis layer of the skin. It is here that microfilariae cause major symptoms, which are edema and thickening of the skin and underlying connective tissues. It can also cause skin rashes, abdominal and chest pains, muscle (myalgia) and joint pains, neurological disorders and skin lumps. In addition, it causes spleen and liver enlargement, which is called hepatosplenomegaly. Studies show elevated levels of leukocytes, or white blood cells, which is referred to as eosinophilia. It is mainly found in Africa. The parasite is transmitted through the bite of small flies ("A. coliroides").

"Tropical immersion foot" (also known as "Paddy foot", and "Paddy-field foot") is a skin condition of the feet seen after continuous immersion of the feet in water or mud of temperature above 22 degrees Celsius (roughly 72 degrees Fahrenheit ) for two to ten days.

The primary symptom of podoconiosis is swelling and disfigurement of the lower extremities. The swelling can either be soft and fluid or hard and fibrotic. Multiple firm nodules may develop over time, as well as hyperkeratotic papillomata that resemble moss, which has led to the disease's alternate name of Mossy Foot. The edema of podoconiosis is usually bilateral and asymmetric. Prior to the development of lymphatic failure and frank lymphedema, a prodrome consisting of itching, burning, hyperkeratosis, plantar edema, and rigid digits may occur. As with other forms of tropical lymphedema, chronic disease can lead to fusion of the toes, ulceration, and bacterial superinfection. The disease has an acute component, and sufferers may experience recurrent episodes of lower extremity warmth, firmness, and pain.

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.

Yaws is a tropical infection of the skin, bones and joints caused by the spirochete bacterium "Treponema pallidum pertenue". The disease begins with a round, hard swelling of the skin, 2 to 5 centimeters in diameter. The center may break open and form an ulcer. This initial skin lesion typically heals after three to six months. After weeks to years, joints and bones may become painful, fatigue may develop, and new skin lesions may appear. The skin of the palms of the hands and the soles of the feet may become thick and break open. The bones (especially those of the nose) may become misshapen. After five years or more large areas of skin may die, leaving a scar.

Yaws is spread by direct contact with the fluid from a lesion of an infected person. The contact is usually of a non-sexual nature. The disease is most common among children, who spread it by playing together. Other related treponemal diseases are bejel ("Treponema pallidum endemicum"), pinta ("Treponema pallidum carateum"), and syphilis ("Treponema pallidum pallidum"). Yaws is often diagnosed by the appearance of the lesions. Blood antibody tests may be useful but cannot separate previous from current infections. Polymerase chain reaction (PCR) is the most accurate method of diagnosis.

Prevention is, in part, by curing those who have the disease thereby decreasing the risk of transmission. Where the disease is common, treating the entire community is effective. Improving cleanliness and sanitation will also decrease spread. Treatment is typically with antibiotics including: azithromycin by mouth or benzathine penicillin by injection. Without treatment, physical deformities occur in 10% of cases.

Yaws is common in at least 14 tropical countries as of 2012. The disease only infects humans. In the 1950s and 1960s the World Health Organization (WHO) nearly eradicated yaws. Since then the number of cases has increased and there are renewed efforts to globally eradicate the disease by 2020. The last estimate of the number of people infected was more than 500,000 in 1995. Although one of the first descriptions of the disease was made in 1679 by Willem Piso, archaeological evidence suggests that yaws may have been present among humans as far back as 1.6 million years ago.

This most common form of impetigo, also called nonbullous impetigo, most often begins as a red sore near the nose or mouth which soon breaks, leaking pus or fluid, and forms a honey-colored scab, followed by a red mark which heals without leaving a scar. Sores are not painful, but they may be itchy. Lymph nodes in the affected area may be swollen, but fever is rare. Touching or scratching the sores may easily spread the infection to other parts of the body.

Skin ulcers with redness and scarring also may result from scratching or abrading the skin.

Bullous impetigo, mainly seen in children younger than 2 years, involves painless, fluid-filled blisters, mostly on the arms, legs, and trunk, surrounded by red and itchy (but not sore) skin. The blisters may be large or small. After they break, they form yellow scabs.

Podoconiosis, also known as nonfilarial elephantiasis, is a disease of the lymph vessels of the lower extremities that is caused by chronic exposure to irritant soils. It is the second most common cause of tropical lymphedema after filariasis, and it is characterized by prominent swelling of the lower extremities, which leads to disfigurement and disability.

Generally speaking, acanthocheilonemiasis does not show initial symptoms. However, if symptoms do arise, it is typically in individuals who are visiting highly infected areas rather than natives to those areas. A major common laboratory finding is an increase in specialized white blood cells, which is called eosinophilia.

Other symptoms include itchy skin, neurological symptoms, abdominal and chest pain, muscle pain, and swelling underneath the skin. If there are abnormally high levels of white blood cells, then a physical examination will most likely find an enlarged spleen or liver.

In certain scenarios, nematodes may physically lodge into the chest or abdomen, resulting in an inflammation. Diagnosis of this condition usually occurs via a blood smear examination under light microscopy.