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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.
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").
Pinta, the least severe of treponemal infections being limited to the skin, is thought to be transmitted by skin-to-skin contact (similar to bejel and yaws), and after an incubation period of two to three weeks, produces a raised papule, which enlarges and becomes hyperkeratotic (scaly/flaky). Lesions are usually present in the exposed surface of arms and legs. Local lymph nodes might be enlarged. Three to 9 months later, further thickened and flat lesions (pintids) appear all over the body. These generally resolve, but a proportion of people with pinta will go on to develop late-stage disease, characterised by widespread pigmentary change with a mixture of hyperpigmentation and depigmentation which can be disfiguring.
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.
Pinta (also known as Azul, Carate, Empeines, Lota, Mal del Pinto and Tina) is a human skin disease endemic to Mexico, Central America, and South America caused by infection with a spirochete, "Treponema pallidum carateum", which is morphologically and serologically indistinguishable from the bacterium that causes syphilis.
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.
Granuloma inguinale (also known as donovanosis) is a bacterial disease caused by "Klebsiella granulomatis" (formerly known as "Calymmatobacterium granulomatis") characterized by ulcerative genital lesions. It is endemic in many less developed regions. It is also known as donovanosis, granuloma genitoinguinale, granuloma inguinale tropicum, granuloma venereum, granuloma venereum genitoinguinale, lupoid form of groin ulceration, serpiginous ulceration of the groin, ulcerating granuloma of the pudendum, and ulcerating sclerosing granuloma.
The disease often goes untreated because of the scarcity of medical treatment in the countries in which it is found. In addition, the painless genital ulcers can be mistaken for syphilis. The ulcers ultimately progress to destruction of internal and external tissue, with extensive leakage of mucus and blood from the highly vascular lesions. The destructive nature of donovanosis also increases the risk of superinfection by other pathogenic microbes.
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.
Paracoccidioidomycosis (PCM) (also known as "Brazilian blastomycosis," "South American blastomycosis,","Lutz-Splendore-de Almeida disease" and "paracoccidioidal granuloma") is a fungal infection caused by the fungus "Paracoccidioides brasiliensis". Sometimes called "South American blastomycosis", paracoccidioidomycosis is caused by a different fungus than that which causes blastomycosis.
As in the majority of paracoccidioidomycosis cases, pulmonary involvement results in shortness of breath, a productive cough and hemoptysis, as well as general symptoms of weight loss, fever and fatigue. Visually, lesions (as pictured) are often present, most commonly on the face.
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.
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
These ulcers have punched-out edge and slough in floor, resembling gummatous ulcer. Surrounding area might have loss of sensation.
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.
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.
Gummas have a firm, necrotic center surrounded by inflamed tissue, which forms an amorphous proteinaceous mass. The center may become partly hyalinized.
These central regions begin to die through coagulative necrosis, though they also retain some of the structural characteristics of previously normal tissues, enabling a distinction from the granulomas of tuberculosis where caseous necrosis obliterates preexisting structures. Other histological features of gummas include an "intervening zone" containing epithelioid cells with indistinct borders and multinucleated giant cells, and a "peripheral zone" of fibroblasts and capillaries. Infiltration of lymphocytes and plasma cells can be seen in the peripheral zone as well. With time, gummas eventually undergo fibrous degeneration, leaving behind an irregular scar or a round fibrous nodule.
It is restricted to necrosis involving spirochaetal infections that cause syphilis. Growths that have the appearance of gummas are described as gummatous.
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.
A gumma is a soft, non-cancerous growth resulting from the tertiary stage of syphilis. It is a form of granuloma. Gummas are most commonly found in the liver ("gumma hepatis"), but can also be found in brain, heart, skin, bone, testis, and other tissues, leading to a variety of potential problems including neurological disorders or heart valve disease.
Malum perforans (also known as neurotrophic ulcer and trophic ulcer) is a long-lasting, usually painless ulcer that penetrates deep into or through the skin, usually on the sole of the foot (in which case it may be called malum perforans pedis). It is often a complication in diabetes mellitus and other conditions affecting the nerves.
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.
Rhinopharyngitis mutilans, also known as gangosa, is a destructive ulcerative condition that usually originates about the soft palate and spreads into the hard palate, nasopharynx, and nose, resulting in mutilating cicatrices, and outward to the face, eroding intervening bone, cartilage, and soft tissues. It occurs in late stages of yaws, usually 5 to 10 years after first symptoms of infection.