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Deep Learning Technology: Sebastian Arnold, Betty van Aken, Paul Grundmann, Felix A. Gers and Alexander Löser. Learning Contextualized Document Representations for Healthcare Answer Retrieval. The Web Conference 2020 (WWW'20)
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It may have a variety of appearances; most easily identifiable are the enlarging raised red rings with a central area of clearing (ringworm). The same appearances of ringworm may also occur on the scalp (tinea capitis), beard area (tinea barbae) or the groin (tinea cruris, known as jock itch or dhobi itch).
Other classic features of tinea corporis include:
- The edge of the rash appears elevated and is scaly to touch.
- Sometimes the skin surrounding the rash may be dry and flaky.
- Almost invariably, there will be hair loss in areas of the infection.
Infections on the body may give rise to typical enlarging raised red rings of ringworm. Infection on the skin of the feet may cause athlete's foot and in the groin, jock itch. Involvement of the nails is termed onychomycosis, and they may thicken, discolour, and finally crumble and fall off. They are common in most adult people, with up to 20% of the population having one of these infections at any given moment.
Animals such as dogs and cats can also be affected by ringworm, and the disease can be transmitted between animals and humans, making it a zoonotic disease.
Specific signs can be:
- red, scaly, itchy or raised patches
- patches may be redder on outside edges or resemble a ring
- patches that begin to ooze or develop blister
- bald patches may develop, when the scalp is affected
- nails may thicken, discolour or begin to crack
The most common term for the infection, "ringworm", is a misnomer, since the condition is caused by fungi of several different species and not by parasitic worms.
Tinea capitis (also known as "herpes tonsurans", "ringworm of the hair", "ringworm of the scalp", "scalp ringworm", and "tinea tonsurans") is a cutaneous fungal infection (dermatophytosis) of the scalp. The disease is primarily caused by dermatophytes in the "Trichophyton" and "Microsporum" genera that invade the hair shaft. The clinical presentation is typically single or multiple patches of hair loss, sometimes with a 'black dot' pattern (often with broken-off hairs), that may be accompanied by inflammation, scaling, pustules, and itching. Uncommon in adults, tinea capitis is predominantly seen in pre-pubertal children, more often boys than girls.
At least eight species of dermatophytes are associated with tinea capitis. Cases of "Trichophyton" infection predominate from Central America to the United States and in parts of Western Europe. Infections from "Microsporum" species are mainly in South America, Southern and Central Europe, Africa and the Middle East. The disease is infectious and can be transmitted by humans, animals, or objects that harbor the fungus. The fungus can also exist in a carrier state on the scalp, without clinical symptomatology. Treatment of tinea capitis requires an oral antifungal agent; griseofulvin is the most commonly used drug, but other newer antimycotic drugs, such as terbinafine, itraconazole, and fluconazole have started to gain acceptance.
It may appear as thickened, scaly, and sometimes boggy swellings, or as expanding raised red rings (ringworm). Common symptoms are severe itching of the scalp, dandruff, and bald patches where the fungus has rooted itself in the skin. It often presents identically to dandruff or seborrheic dermatitis. The highest incidence in the United States of America is in American boys of school age.
There are three type of tinea capitis, microsporosis, trichophytosis, and favus; these are based on the causative microorganism, and the nature of the symptoms. In "microsporosis", the lesion is a small red papule around a hair shaft that later becomes scaly; eventually the hairs break off 1–3 mm above the scalp. This disease used to be caused primarily by "Microsporum audouinii", but in Europe, "M. canis" is more frequently the causative fungus. The source of this fungus is typically sick cats and kittens; it may be spread through person to person contact, or by sharing contaminated brushes and combs. In the United States, "Trichophytosis" is usually caused by "Trichophyton tonsurans", while "T. violaceum" is more common in Eastern Europe, Africa, and India. This fungus causes dry, non-inflammatory patches that tend to be angular in shape. When the hairs break off at the opening of the follicle, black dots remain. "Favus" is caused by "T. schoenleinii", and is endemic in South Africa and the Middle East. It is characterized by a number of yellowish, circular, cup-shaped crusts (scutula) grouped in patches like a piece of honeycomb, each about the size of a split pea, with a hair projecting in the center. These increase in size and become crusted over, so that the characteristic lesion can only be seen around the edge of the scab.
Tinea corporis (also known as ringworm, tinea circinata, and tinea glabrosa) is a superficial fungal infection (dermatophytosis) of the arms and legs, especially on glabrous skin; however, it may occur on any part of the body. It is similar to other forms of tinea.
Athlete's foot is divided into four categories or presentations: chronic interdigital athlete's foot, plantar (chronic scaly) athlete's foot (aka "moccasin foot"), acute ulcerative tinea pedis, and vesiculobullous athlete's foot. "Interdigital" means between the toes. "Plantar" here refers to the sole of the foot. The ulcerative condition includes macerated lesions with scaly borders. Maceration is the softening and breaking down of skin due to extensive exposure to moisture. A vesiculobullous disease is a type of mucocutaneous disease characterized by vesicles and bullae (blisters). Both vesicles and bullae are fluid-filled lesions, and they are distinguished by size (vesicles being less than 5–10 mm and bulla being larger than 5–10 mm, depending upon what definition is used).
Athlete's foot occurs most often between the toes (interdigital), with the space between the fourth and fifth digits most commonly afflicted. Cases of interdigital athlete's foot caused by "Trichophyton rubrum" may be symptomless, it may itch, or the skin between the toes may appear red or ulcerative (scaly, flaky, with soft and white if skin has been kept wet), with or without itching. An acute ulcerative variant of interdigital athlete's foot caused by "T. mentagrophytes" is characterized by pain, maceration of the skin, erosions and fissuring of the skin, crusting, and an odor due to secondary bacterial infection.
Plantar athlete's foot (moccasin foot) is also caused by "T. rubrum" which typically causes asymptomatic, slightly erythematous plaques (areas of redness of the skin) to form on the plantar surface (sole) of the foot that are often covered by fine, powdery hyperkeratotic scales.
The vesiculobullous type of athlete's foot is less common and is usually caused by "T. mentagrophytes" and is characterized by a sudden outbreak of itchy blisters and vesicles on an erythematous base, usually appearing on the sole of the foot. This subtype of athlete's foot is often complicated by secondary bacterial infection by "Streptococcus pyogenes" or "Staphylococcus aureus".
A dermatomycosis is a skin disease caused by a fungus. This excludes dermatophytosis.
Examples of dermatomycoses are tinea and cutaneous candidiasis.
As the disease progresses, the skin may crack, leading to bacterial skin infection and inflammation of the lymphatic vessels. If allowed to grow for too long, athlete's foot fungus may spread to infect the toenails, feeding on the keratin in them, a condition called onychomycosis.
Because athlete's foot may itch, it may also elicit the scratch reflex, causing the host to scratch the infected area before he or she realizes it. Scratching can further damage the skin and worsen the condition by allowing the fungus to more easily spread and thrive. The itching sensation associated with athlete's foot can be so severe that it may cause hosts to scratch vigorously enough to inflict excoriations (open wounds), which are susceptible to bacterial infection. Further scratching may remove scabs, inhibiting the healing process.
Scratching infected areas may also spread the fungus to the fingers and under the fingernails. If not washed away soon enough, it can infect the fingers and fingernails, growing in the skin and in the nails (not just underneath). After scratching, it can be spread to wherever the person touches, including other parts of the body and to one's environment. Scratching also causes infected skin scales to fall off into one's environment, leading to further possible spread.
When athlete's foot fungus or infested skin particles spread to one's environment (such as to clothes, shoes, bathroom, etc.) whether through scratching, falling, or rubbing off, not only can they infect other people, they can also reinfect (or further infect) the host they came from. For example, infected feet infest one's socks and shoes which further expose the feet to the fungus and its spores when worn again.
The ease with which the fungus spreads to other areas of the body (on one's fingers) poses another complication. When the fungus is spread to other parts of the body, it can easily be spread back to the feet after the feet have been treated. And because the condition is called something else in each place it takes hold (e.g., tinea corporis (ringworm) or tinea cruris (jock itch), persons infected may not be aware it is the same disease.
Some individuals may experience an allergic response to the fungus called an id reaction in which blisters or vesicles can appear in areas such as the hands, chest, and arms. Treatment of the underlying infection typically results in the disappearance of the id reaction.
Gram-negative toe web infection is a cutaneous condition that often begins with dermatophytosis.
Although there are a multitude of varying appearances, the id reaction often presents with symmetrical red patches of eczema with papules and vesicles, particularly on the outer sides of the arms, face and trunk which occur suddenly and are intensely itchy occur a few days to a week after the initial allergic or irritant dermatitis. Most commonly, athletes foot can lead to localised vesicles on hands, bacterial infections to erythema nodosum and herpes simplex virus to erythema multiforme.
The diagnosis is frequently made by treating the initial triggering skin problem and observing the improvement in the eczematous rash. Both the initial skin problem and the id reaction must be observed to make the diagnosis.
All dyshidrotic rashes are not id reactions, but id reactions are often dishydrotic-like.
Initial tests may include isolating a fungus by taking a swab and sending it for culture. Patch testing may be considered if there is suspicion of allergic contact dermatitis.
A skin biopsy is rarely necessary, but if done mostly shows an interstitial granulomatous dermatitis, some lesions being spongiotic. Id reactions cannot be distinguished from other skin diseases by histopathology. However, they can be distinguished from other id reactions by histopathology.
Id reactions (also known as "disseminated eczema," and "generalized eczema") are types of acute dermatitis developing after days or weeks at skin locations distant from the initial inflammatory or infectious site. They can be localised or generalised. This is also known as an 'autoeczematous response' and there must be an identifiable initial inflammatory or infectious skin problem which leads to the generalised eczema. Often, intensely itchy, the red papules and pustules can also be associated with blisters and scales and are always remote from the primary lesion. It is most commonly a blistering rash with itchy vesicles on the sides of fingers and feet as a reaction to fungal infection on the feet, athlete's foot. Stasis dermatitis, Allergic contact dermatitis, Acute irritant contact eczema and Infective dermatitis have been documented as possible triggers, but the exact cause and mechanism is not fully understood. Several other types of id reactions exist including erythema nodosum, erythema multiforme, Sweet's syndrome and urticaria.
Body lice are a nuisance in themselves and cause intense itching. They are also vectors (transmitters) of other diseases and can spread epidemic typhus, trench fever, and louse-borne relapsing fever.
Body lice frequently lay their eggs on or near the seams of clothing. They must feed on blood and usually only move to the skin to feed. They exist worldwide and infest people of all races and can therefore spread rapidly under crowded living conditions where hygiene is poor (homeless, refugees, victims of war or natural disasters).
Some diseases are inherent abnormalities of skin structure or function. These include skin fragility syndrome (Ehlers-Danlos), hereditary hypotrichosis and congenital or hereditary alopecia.
Cat skin disorders are among the most common health problems in cats.
Skin disorders in cats have many causes, and many of the common skin disorders that afflict people have a counterpart in cats. The condition of a cat's skin and coat can also be an important indicator of its general health. Skin disorders of cats vary from acute, self-limiting problems to chronic or long-lasting problems requiring life-time treatment. Cat skin disorders may be grouped into categories according to the causes.
There are two expressions of this condition, one for long or double coated breeds and one for short coated breeds, both with differing presentations.
- For long- or double-coated breeds such as Poodles, Akitas and Samoyeds, the condition often presents itself with silvery dandruff which adheres to the coat, hair loss (not to be confused with moulting or "blowing coat"), a dull and brittle coat, and later on skin lesions along the back and ears as well as thickened skin and a musty or rancid odour.
- For short-coated breeds such as Vizslas, the condition causes facial swellings, nodular skin lesions, fine dandruff which does not adhere to the coat, and a general "moth-eaten" appearance to the coat.
Gram-negative toe web infection is a relatively common infection. It is commonly found on people who are engaged in athletic activities while wearing closed-toe or tight fitting shoes. It grows in a moist environment. Gram-negative is mixed bacterial infection with the following organisms:
- Moraxella
- Alcaligenes
- Acinetobacter
- Pseudomonas
- Proteus
- Erwinia
This mixing of infection and organisms may also cause a mild secondary infection of tinea pedis.
Sebaceous adenitis in an uncommon skin disease found in some breeds of dog, and more rarely in cats, rabbits and horses. characterised by an inflammatory response against the dog's sebaceous glands (glands found in the hair follicles in the skin dermis), which can lead to the destruction of the gland. It was first described in veterinary literature in the 1980s.
The condition can be known medically as bromhidrosis, apocrine bromhidrosis, osmidrosis, ozochrotia, fetid sweat, body smell, or malodorous sweating.
Osmidrosis or bromhidrosis is defined by a foul odor due to a water-rich environment that supports bacteria, which is caused by an abnormal increase in perspiration (hyperhidrosis). This can be particularly strong when it happens in the axillary region (underarms). In this case, the condition may be referred to an axillary osmidrosis.
Trimethylaminuria (TMAU), also known as fish odor syndrome or fish malodor syndrome, is a rare metabolic disorder where trimethylamine is released in the person's sweat, urine, and breath, giving off a strong fishy odor or strong body odor.
Body odor (American English) or body odour (British English; see spelling differences) is present in animals and humans, and its intensity can be influenced by many factors (behavioral patterns, survival strategies). Body odor has a strong genetic basis both in animals and humans, but it can be also strongly influenced by various diseases and physiological conditions. Body odor is generally considered to be an unpleasant odor among many human cultures.
"Rabbits, Hares & Lagomorphs"
Usually there do not appear to be any clinical signs. Subcutaneous cysts, warbles, may present upon larval deposition out of the body at maturation.
"Felines & Canines"
There are three forms in which Cuterebriasis may present:
- Myasis
- Cerebrospinal
- Respiratory
Myasis involves subcutaneous cyst formation due to 3rd larval instar maturation, occurring ~30 days post-entry into the body. Cysts are often found on the face, neck and trunk, but location varies with larval migration within the host. Serous discharge may be observed from these cysts, which are typically 3-5mm in diameter and include a central pore through which the larvae respire. This pore also serves as a means of exit for the larvae, which occurs anywhere between 3 and 8 weeks post-entry.
Cerebrospinal cuterebriasis results from larval migration to the brain. This is seen in cats, and is the proposed cause for feline ischemic encephalopathy and a suggestive causative agent of feline idiopathic vestibular disease. Symptoms of this type of presentation include lethargy, seizures, blindness, abnormal vocalization or gait, circling, and abnormal or no reflex responses. When affecting the central nervous system, cats are known to exhibit violent sneezing attacks that can onset weeks prior to manifestation of other clinical signs.
Respiratory disease results when larval migration occurs through the trachea, pharynx, diaphragm, or lungs. Cuterebriasis has been increasingly noted as a cause for dyspnea in felines.
Cuterebriasis is a parasitic disease affecting rodents, lagomorphs (hares, rabbits, pikas), felines and canines. The etiologic agent is the larval development of bot flies within the "Cuterebra" or "Trypoderma" genera, which occurs obligatorily in rodents and lagomorphs, respectively. Felines and canines serve as accidental hosts, but research suggests only by "Trypoderma" spp. Entrance into the body by first instar larva occurs via mucous membranes of natural orifices or open wounds as opposed to direct dermic penetration.
Muscardine is a disease of insects. It is caused by many species of entomopathogenic fungus. Many muscardines are known for affecting silkworms. Muscardine may also be called calcino.
While studying muscardine in silkworms in the 19th century, Agostino Bassi found that the causal agent was a fungus. This was the first demonstration of the germ theory of disease, the first time a microorganism was recognized as an animal pathogen.
There are many types of muscardine. They are often named for the color of the conidial layer each fungus leaves on its host.
Yellow red muscardine is caused by "Paecilomyces fumosoroseus". It can produce reddish patches on the external body and powdery masses of spores internally.