Made by DATEXIS (Data Science and Text-based Information Systems) at Beuth University of Applied Sciences Berlin
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)
Funded by The Federal Ministry for Economic Affairs and Energy; Grant: 01MD19013D, Smart-MD Project, Digital Technologies
The symptoms of this disease include:
- Severe pruritus
- Pain
- Inflammation and swelling
- Lesions and ulcerations, with black dots in the center
Left untreated, secondary infections, such as bacteremia, tetanus, and gangrene, can occur.
In all cases, tungiasis by itself only caused morbidity, though secondary infection may lead to mortality. The life cycle section presents the Fortaleza stages from the flea’s developmental perspective. It should be noted that the discussion is specific to symptoms of human infection. The clinical presentation in humans follows the Fortaleza Classification as the stage of infection will determine the symptoms present. The following discussion will give an overview of the symptoms beginning in stage 2 because patients are not likely to present themselves at the early stages of infection, mostly because the flea’s burrowing is usually not felt. This may be due to a keratolytic enzyme secreted during stage 1.
The patient with a single flea may present as early as stage 2 when, though the erythema is barely perceptible, a boring pain and the curious sensation of pleasant itching occur. This inflammatory reaction is the initial immunological response to the infestation. Heavily infested patients may not notice a stage 2 infection due to the other fleas’ causing irritation as well. Feces may be seen, but this is more common in the 3rd stage.
Around the third day after penetration, erythema and skin tenderness are felt, accompanied by pruritus (severe itching) and a black furuncular nodule surrounded by a white halo of stretched skin caused by the expansion of the flea. Fecal coils may protrude from the center of the nodule where the flea’s anus is facing upward. They should be washed off quickly as the feces may remain in the skin unless removed. During this 3a substage, pain can be severe, especially at night or, if the nodule is on the foot, while walking. Eggs will also begin to be released and a watery secretion can be observed. The radical metamorphosis during the 3rd to 6th day after penetration, or neosomy, precedes the formation of a small caldera-like rim rampart as a result of the increased thickness of the flea’s chitin exoskeleton. During the caldera formation, the nodule shrinks a bit and it looks as if it is beginning to dry out; this takes 2 weeks and comprises substage 3b.
At the third week after penetration and substage 4a, the eggs’ release will have stopped and the lesion will become smaller and more wrinkled. As the flea is near death, fecal and water secretion will stop altogether. Pain, tenderness, and skin inflammation will still be present. Around the 25th day after penetration, the lesion looks like a black crust and the flea’s carcass is removed by host repair mechanisms and the skin begins to heal. With the flea gone, inflammation may still persist for a while.
Although patients would not present within the 5th stage of tungiasis as the flea would be dead and no longer in the body, this stage is characterized by the reorganization of the skin (1–4 weeks) and a circular residue of 5–10 mm in diameter around the site in penetration. An intraepithelial abscess, which developed due to the presence of the flea, will drain and later heal. Although these disease residues would persist for a few months, tungiasis is no longer present.
In severe cases, ulcers are common, as well as complete tissue and nail deformation. A patient may be unable to walk due to severe pain if too many of the lesions are present in the feet. Suppuration (pus formation), auto-amputation of digits (via ainhum), and chronic lymphedema may also be seen.
If the patient is not vaccinated, tetanus is often a complication due to secondary infection. Gangrene is another common complication of severe infestation and superinfection. Staphylococcus aureus and Wolbachia endobacteria can be transmitted by the chigoe flea, as well as nearly 150 other different pathogens. For these reasons, the chigoe flea should be removed as soon as possible.
Tungiasis (also known as "nigua", "pio" and "bicho de pie", or "pique" or sand flea disease) is an inflammatory skin disease caused by infection with the female ectoparasitic "Tunga penetrans" (also known as chigoe flea, jigger, nigua or sand flea), found in the tropical parts of Africa, the Caribbean, Central and South America, and India. "Tunga penetrans" is the smallest known flea, measuring 1 mm across. It is also known in Latin America as the "nigua" and "bicho de pie" (Spanish) or "bicho de pé" (Portuguese), literally ""foot bug"". "Tunga penetrans" is a member of the genus "Tunga", which comprises 13 species.
Tungiasis causes skin inflammation, severe pain, itching, and a lesion at the site of infection that is characterized by a black dot at the center of a swollen red lesion, surrounded by what looks like a white halo. Desquamation of the skin is always seen, especially after the flea expands during hypertrophy.
As of 2009, tungiasis is present worldwide in 88 countries with varying degrees of incidence. This disease is of special public health concern in highly endemic areas such as Nigeria, Trinidad and Tobago, and Brazil, where its prevalence, especially in poor communities, has been known to approach 50%.
The chigoe flea is properly classified as a member of the order Siphonaptera as it is a flea. Although commonly referred to as chiggers, true chiggers are mites which are minute arachnids. Mites penetrate the skin and feed on skin cells that are broken down by an enzyme they secrete from their mouthparts, but they do not lay eggs in the host as "T. penetrans" does. Moreover, in mites, the adult and the larval forms both feed on other animals. This is not the case with "T. penetrans", as only the adults feed on mammals and it is only the female that stays attached to the host.
"Tunga penetrans" is also known by the following names: chigoe flea, sand flea, nigua, chigger flea, jigger flea, bicho de pé, pico, sikka, kuti, and piqui, among many others.
Dracunculiasis is diagnosed by seeing the worms emerging from the lesions on the legs of infected individuals and by microscopic examinations of the larvae.
As the worm moves downwards, usually to the lower leg, through the subcutaneous tissues, it leads to intense pain localized to its path of travel. The burning sensation experienced by infected people has led to the disease being called "the fiery serpent". Other symptoms include fever, nausea, and vomiting. Female worms cause allergic reactions during blister formation as they migrate to the skin, causing an intense burning pain. Such allergic reactions produce rashes, nausea, diarrhea, dizziness, and localized edema. When the blister bursts, allergic reactions subside, but skin ulcers form, through which the worm can protrude. Only when the worm is removed is healing complete. Death of adult worms in joints can lead to arthritis and paralysis in the spinal cord.
Dracunculiasis, also called Guinea-worm disease (GWD), is an infection by the Guinea worm. A person becomes infected when they drink water that contains water fleas infected with guinea worm larvae. Initially there are no symptoms. About one year later, the person develops a painful burning feeling as the female worm forms a blister in the skin, usually on a lower limb. The worm then emerges from the skin over the course of a few weeks. During this time, it may be difficult to walk or work. It is very uncommon for the disease to cause death.
In humans, the only known cause is "Dracunculus medinensis". The worm is about one to two millimeters wide, and an adult female is 60 to 100 centimeters long (males are much shorter at ). Outside of humans, the young form can survive up to three weeks, during which they must be eaten by water fleas to continue to develop. The larva inside water fleas may survive up to four months. Thus, in order for the disease to remain in an area, it must occur each year in humans. A diagnosis of the disease can usually be made based on the signs and symptoms.
Prevention is by early diagnosis of the disease followed by keeping the person from putting the wound in drinking water to decrease spread of the parasite. Other efforts include improving access to clean water and otherwise filtering water if it is not clean. Filtering through a cloth is often enough. Contaminated drinking water may be treated with a chemical called temefos to kill the larva. There is no medication or vaccine against the disease. The worm may be slowly removed over a few weeks by rolling it over a stick. The ulcers formed by the emerging worm may get infected by bacteria. Pain may continue for months after the worm has been removed.
In 2015 there were 22 reported cases of the disease while in 2016 there were 25. This is down from an estimated 3.5 million cases in 1986. In 2016 the disease occurred in three countries, all in Africa, down from 20 countries in the 1980s. It will likely be the first parasitic disease to be globally eradicated. Guinea worm disease has been known since ancient times. The method of removing the worm is described in the Egyptian medical Ebers Papyrus, dating from 1550 BC. The name dracunculiasis is derived from the Latin "affliction with little dragons", while the name "guinea worm" appeared after Europeans saw the disease on the Guinea coast of West Africa in the 17th century. Other "Dracunculus" species are known to infect various mammals, but do not appear to infect humans. Dracunculiasis is classified as a neglected tropical disease. Because dogs may also become infected, the eradication program is monitoring and treating dogs as well.
Amphibians infected with "B. dendrobatidis" have been known to show many different clinical signs. Perhaps the earliest sign of infection is anorexia, occurring as quickly as 8 days after being exposed . Individuals infected are also commonly found in a lethargic state, characterized by slow movements, and refuse to move when stimulated. Excessive shedding of skin is seen in most frog species affected by "B. dendrobatidis". These pieces of shed skin are described as opaque, gray-white, and tan. Some of these patches of skin are also found adhered to the skin of the amphibians. These signs of infection are often seen 12–15 days following exposure. The most typical symptom of chytridiomycosis is thickening of skin, which promptly leads to the death of the infected individuals because those individuals cannot take in the proper nutrients, release toxins, or, in some cases, breathe. Other common signs are reddening of the skin, convulsions, and a loss of righting reflex . In tadpoles "B. dendrobatidis" affects the mouthparts, where keratin is present, leading to abnormal feeding behaviors or discoloration of the mouth.
Chytridiomycosis is an infectious disease in amphibians, caused by the chytrid "Batrachochytrium dendrobatidis", a nonhyphal zoosporic fungus. Chytridiomycosis has been linked to dramatic population declines or even extinctions of amphibian species in western North America, Central America, South America, eastern Australia, East Africa (Tanzania) and Dominica and Montserrat in the Caribbean. Much of the New World is also at risk of the disease arriving within the coming years.
The fungus is capable of causing sporadic deaths in some amphibian populations and 100% mortality in others. No effective measure is known for control of the disease in wild populations. Various clinical signs are seen by individuals affected by the disease. A number of options are possible for controlling this disease-causing fungus, though none has proved to be feasible on a large scale. The disease has been proposed as a contributing factor to a global decline in amphibian populations that apparently has affected about 30% of the amphibian species of the world.
Trombiculosis, trombiculiasis, or trombiculidiasis is a rash caused by trombiculid mites which is often referred to as a chigger bite.
Pulicosis (also known as "flea bites") is a skin condition caused by several species of fleas, including the cat flea ("Ctenocephalides felis") and dog flea ("Ctenocephalides canis"). This condition can range from mild irritation to severe irritation. In some cases, 48 to 72 hours after being bitten, a more severe rash-like irritation may begin to spread across the body. Symptoms include swelling of the bitten area, erythema, ulcers of the mouth and throat, restlessness, and soreness of the areolae. In extreme cases, within 1 week after being bitten, the condition may spread through the lymph nodes and begin affecting the central nervous system. Permanent nerve damage can occur.
If they receive an excessive number of bites, pets can also develop flea allergy dermatitis, which can potentially be fatal if no actions are taken. However, dogs and cats are not the only ones that are at risk. Humans can suffer from flea bites and, depending on a variety of factors, the bites can cause much pain and discomfort.
Bacillary angiomatosis (BA) is a form of angiomatosis associated with bacteria of the "Bartonella" genus.
Cutaneous BA is characterised by the presence of lesions on or under the skin. Appearing in numbers from one to hundreds, these lesions may take several forms:
- papules or nodules which are red, globular and non-blanching, with a vascular appearance
- purplish nodules sufficiently similar to Kaposi's sarcoma that a biopsy may be required to verify which of the two it is
- a purplish lichenoid plaque
- a subcutaneous nodule which may have ulceration, similar to a bacterial abscess
While cutaneous BA is the most common form, it can also affect several other parts of the body, such as the brain, bone, bone marrow, lymph nodes, gastrointestinal tract, respiratory tract, spleen, and liver. Symptoms vary depending on which parts of the body are affected; for example, those whose livers are affected may have an enlarged liver and fever, while those with osseous BA experience intense pain in the affected area.
Areas affected are those the cat can access most easily, including the abdomen, legs, flank, and chest.
- Baldness, usually beginning with the abdomen
- Obvious over-grooming (although some cats may only engage in the behavior in the absence of owners)
- Redness, rashes, pus, scabs on the bald area or areas traumatized by over-grooming
- A highly irritable cat may even cut its face with the claw of its hind foot if over-zealously scratching the back of its head.
Murine typhus (also called endemic typhus) is a form of typhus transmitted by fleas (Xenopsylla cheopis), usually on rats. (This is in contrast to epidemic typhus, which is usually transmitted by lice.) Murine typhus is an under-recognized entity, as it is often confused with viral illnesses. Most people who are infected do not realize that they have been bitten by fleas.
The flea found most commonly on both dogs and cats with a flea infestation is the cat flea, "Ctenocephalides felis". Pets that develop FAD have an allergic response to flea saliva injected during flea feeding. The itch associated with just one flea bite persists long after that flea is gone and leads to significant self-trauma.
Cat-scratch disease commonly presents as tender, swollen lymph nodes near the site of the inoculating bite or scratch or on the neck, and is usually limited to one side. This condition is referred to as regional lymphadenopathy and occurs 1–3 weeks after inoculation. Lymphadenopathy in CSD most commonly occurs in the arms, neck, or jaw, but may also occur near the groin or around the ear. A vesicle or an erythematous papule may form at the site of initial infection. Most patients also develop systemic symptoms such as malaise, decreased appetite, and aches. Other associated complaints include headache, chills, muscular pains, joint pains, arthritis, backache, and abdominal pain. It may take 7 to 14 days, or as long as two months, for symptoms to appear. Most cases are benign and self-limiting, but lymphadenopathy may persist for several months after other symptoms disappear. The disease usually resolves spontaneously, with or without treatment, in one month.
In rare situations, CSD can lead to the development of serious neurologic or cardiac sequelae such as meningoencephalitis, encephalopathy, seizures, or endocarditis. Endocarditis associated with "Bartonella" infection has a particularly high mortality. Parinaud's oculoglandular syndrome is the most common ocular manifestation of CSD, and is a granulomatous conjunctivitis with concurrent swelling of the lymph node near the ear. Optic neuritis or neuroretinitis is one of the atypical presentations.
Immunocompromised patients are susceptible to other conditions associated with "B. henselae" and "B. quintana", such as bacillary angiomatosis or bacillary peliosis. Bacillary angiomatosis is primarily a vascular skin lesion that may extend to bone or be present in other areas of the body. In the typical scenario, the patient has HIV or another cause of severe immune dysfunction. Bacillary peliosis is caused by "B. henselae" that most often affects patients with HIV and other conditions causing severe immune compromise. The liver and spleen are primarily affected, with findings of blood-filled cystic spaces on pathology. In 2015 a Toledo, Ohio woman lost eyesight in an eye after a cat licked it.
Cat-scratch disease (CSD) is a common and usually benign infectious disease caused by the bacterium "Bartonella henselae". It is most commonly found in children following a scratch or bite from a cat within about one to two weeks.
Symptoms of endemic typhus include headache, fever, muscle pain, joint pain, nausea and vomiting. 40–50% of patients will develop a discrete rash six days after the onset of signs. Up to 45% will develop neurological signs such as confusion, stupor, seizures or imbalance.
Symptoms may resemble those of measles, rubella, or possibly Rocky Mountain spotted fever. These symptoms are likely caused by a vasculitis caused by the rickettsia.
Flea allergy dermatitis, FAD, is an eczematous itchy skin disease of dogs and cats. For both of these domestic species, flea allergy dermatitis is the most common cause of skin disease. Affected animals develop allergic reactions to chemicals in flea saliva. Symptoms of this reaction include erythema (redness), papules (bumps), pustules (pus-filled bumps), and crusts (scabs). If severe, hair loss will occur in the affected area. Dogs with flea allergy dermatitis often show hair loss and eczematous skin rash on the lower back, upper tail, neck, and down the back of the legs. Cats with flea allergy dermatitis may develop a variety of skin problems, including feline eosinophilic granuloma, miliary dermatitis, or self-inflicted alopecia from excessive grooming.
Psychogenic alopecia, also called "over-grooming" or "psychological baldness," is a compulsive behavior that affects domestic cats. Generally, psychogenic alopecia does not lead to serious health consequences or a decreased lifespan.
Sylvatic plague is an infectious bacterial disease caused by the bacterium "Yersinia pestis" that primarily affects rodents such as prairie dogs. It is the same bacterium that causes bubonic and pneumonic plague in humans. Sylvatic, or sylvan, means 'occurring in wildlife,' and refers specifically to the form of plague in rural wildlife. Urban plague refers to the form in urban wildlife.
It is primarily transmitted among wildlife through flea bites and contact with infected tissue or fluids. Sylvatic plague is most commonly found in prairie dog colonies and some mustelids like the black-footed ferret.
Depending on the site of infection, tularemia has six characteristic clinical variants: ulceroglandular (the most common type representing 75% of all forms), glandular, oropharyngeal, pneumonic, oculoglandular, and typhoidal.
The incubation period for tularemia is one to 14 days; most human infections become apparent after three to five days. In most susceptible mammals, the clinical signs include fever, lethargy, loss of appetite, signs of sepsis, and possibly death. Nonhuman mammals rarely develop the skin lesions seen in people. Subclinical infections are common, and animals often develop specific antibodies to the organism. Fever is moderate or very high, and tularemia bacilli can be isolated from blood cultures at this stage. The face and eyes redden and become inflamed. Inflammation spreads to the lymph nodes, which enlarge and may (mimicking bubonic plague). Lymph node involvement is accompanied by a high fever.
"B. henselae" is the etiologic agent for peliosis hepatis, which is defined as a vascular proliferation of sinusoid hepatic capillaries resulting in blood-filled spaces in the liver in HIV patients and organ transplant recipients. Peliosis hepatis can be associated with peliosis of the spleen, as well as bacillary angiomatosis of the skin in HIV patients.
Spotted fever can be very difficult to diagnose in its early stages, and even experienced doctors who are familiar with the disease find it hard to detect.
People infected with "R. rickettsii" usually notice symptoms following an incubation period of one to two weeks after a tick bite. The early clinical presentation of Rocky Mountain spotted fever is nonspecific and may resemble a variety of other infectious and non-infectious diseases.
Initial symptoms:
- Fever
- Nausea
- Emesis (vomiting)
- Severe headache
- Muscle pain
- Lack of appetite
- Parotitis in some cases (somewhat rare)
Later signs and symptoms:
- Maculopapular rash
- Petechial rash
- Abdominal pain
- Joint pain
- Conjunctivitis
- Forgetfulness
The classic triad of findings for this disease are fever, rash, and history of tick bite. However, this combination is often not identified when the patient initially presents for care. The rash has a centripetal, or "inward" pattern of spread, meaning it begins at the extremities and courses towards the trunk.
The rash first appears two to five days after the onset of fever, and it is often quite subtle. Younger patients usually develop the rash earlier than older patients. Most often the rash begins as small, flat, pink, non-itchy spots (macules) on the wrists, forearms, and ankles. These spots turn pale when pressure is applied and eventually become raised on the skin. The characteristic red, spotted (petechial) rash of Rocky Mountain spotted fever is usually not seen until the sixth day or later after onset of symptoms, but this type of rash occurs in only 35 to 60% of patients with Rocky Mountain spotted fever. The rash involves the palms or soles in as many as 80% of the patients. However, this distribution may not occur until later on in the course of the disease. As many as 15 percent of patients may never develop a rash.
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.
"B. henselae" and "B. quintana" can cause bacillary angiomatosis, a vascular proliferative disease involving mainly the skin, and other organs. The disease was first described in human immunodificiency virus (HIV) patients and organ transplant recipients. Severe, progressive and disseminated disease may occur in HIV patients. Differential diagnoses include Kaposi´s sarcoma, pyogenic granuloma, hemangioma, "verruga Peruana", and subcutanous tumors. Lesions can affect bone marrow, liver, spleen, or lymph nodes.
Chiggers are commonly found on the tip of blades of grasses to catch a host, so keeping grass short, and removing brush and wood debris where potential mite hosts may live, can limit their impact on an area. Sunlight that penetrates the grass will make the lawn drier and make it less favorable for chigger survival.
Chiggers seem to affect warm covered areas of the body more than drier areas. Thus, the bites are often clustered behind the knees, or beneath tight undergarments such as socks, underwear, or brassieres. Areas higher in the body (chest, back, waist-band, and under-arms) are affected more easily in small children than in adults, since children are shorter and are more likely than adults to come in contact with low-lying vegetation and dry grass where chiggers thrive. An exceptional case has been described in the eye, producing conjunctivitis.
Application of repellent to the shoes, lower trousers and skin is also useful. Because they are found in grass, staying on trails, roads, or paths can prevent contact. Dusting sulfur is used commercially for mite control and can be used to control chiggers in yards. The dusting of shoes, socks and trouser legs with sulfur can be highly effective in repelling chiggers.
Another good strategy is to recognize the chigger habitat to avoid exposure in the first place. Chiggers in North America thrive late in summer, in dry tall grasses and other thick, unshaded vegetation. Insect repellents containing one of the following active ingredients are recommended: DEET, catnip oil extract (nepetalactone), citronella oil or eucalyptus oil extract. However, in 1993 issue a study reported on tests of two commercial repellents: DEET and citrus oil: "All chiggers exposed on the filter papers treated with DEET died and did not move off the treated papers. None of the chiggers that were placed on papers treated with citrus oil were killed." It was concluded that DEET was more effective than citrus oil.
Chiggers can also be treated using common household vinegar (5% acetic acid).