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
Usually called "swayback," soft back, or low back, an excessive downward bend in the back is an undesirable conformation trait. Swayback is caused in part from a loss of muscle tone in both the back and abdominal muscles, plus a weakening and stretching of the ligaments. As in humans, it may be influenced by bearing young; it is sometimes seen in a broodmare that has had multiple foals. However, it is also common in older horses whose age leads to loss of muscle tone and stretched ligaments. It also occurs due to overuse or injury to the muscles and ligaments from excess work or loads, or from premature work placed upon an immature animal. Equines with too long a back are more prone to the condition than those with a short back, but as a longer back is also linked to smoother gaits, the trait is sometimes encouraged by selective breeding. It has been found to have a hereditary basis in the American Saddlebred breed, transmitted via a recessive mode of inheritance. Research into the genetics underlying the condition has several values beyond just the Saddlebred breed as it may "serve as a model for investigating congenital skeletal deformities in horses and other species."
Swayback refers to abnormal bent-back postures in humans and in quadrupeds, especially horses.
Porocephaliasis is a condition associated with species in the closely related genera "Porocephalus" and "Armillifer". (The term "pentastomiasis" encompasses all diseases of Pentastomida, which includes Porocephaliasis and Linguatulosis.)
Porocephaliasis is associated with contact with snakes. (This is in contrast with Linguatulosis, which is associated with contact with dogs or wolves.)
It has been reported from Africa, Malaysia and the Middle East. Its occurrence has been rare in Europe and North America where it has been found in immigrants and travelers.
"A. phagocytophilum" is transmitted to humans by "Ixodes" ticks. These ticks are found in the US, Europe, and Asia. In the US, "I. scapularis" is the tick vector in the East and Midwest states, and "I. pacificus" in the Pacific Northwest. In Europe, the "I. ricinus" is the main tick vector, and "I. persulcatus" is the currently known tick vector in Asia.
The major mammalian reservoir for "A. phagocytophilum" in the eastern United States is the white-footed mouse, "Peromyscus leucopus". Although white-tailed deer and other small mammals harbor "A. phagocytophilum", evidence suggests that they are not a reservoir for the strains that cause HGA. A tick that has a blood meal from an infected reservoir becomes infected themselves. If an infected tick then latches onto a human the disease is then transmitted to the human host and "A." "phagocytophilum" symptoms can arise.
"Anaplasma phagocytophilum" shares its tick vector with other human pathogens, and about 10% of patients with HGA show serologic evidence of coinfection with Lyme disease, babesiosis, or tick-borne meningoencephalitis.
It is prevalent in parts of Africa and Asia where eating snake meat is common. In Africa it has also been associated with groups who use the snake as a totem. Unlike linguatuliasis, humans are only ever an accidental intermediate host for "Armillifer", i.e. the larvae establish themselves in the visceral organs causing human visceral pentastomiasis, but adults do not occur in the human respiratory system. After a while the larvae die within the host and sometimes calcify, leaving characteristic crescent-shaped structures seen in X-ray. In extreme cases a heavy parasite burden can have serious medical consequences and can even be fatal.
Currently, there is no vaccine against human granulocytic anaplasmosis, so antibiotics are the only form of treatment. The best way to prevent HGA is to prevent getting tick bites.
Berserk llama syndrome or berserk male syndrome (as it is more pronounced in males) is a psychological condition suffered by human-raised llamas and alpacas that can cause them to exhibit dangerously aggressive behavior toward humans. The term has been overused, however, and is sometimes inappropriately applied to llamas with aggressive personalities that are not truly "berserk".
The condition is a result of the llama imprinting on its human handlers to such a degree that it considers them to be fellow llamas. Imprinting can be caused by bottle feeding and by isolation from other llamas. Adult male inter-llama interaction can be rough, including chest-ramming and biting, and they are strongly territorial. Male llamas suffering from this condition become dangerous when this behavior is directed toward humans and they usually have to be euthanised. Female llamas can also suffer from berserk llama syndrome but their behavior is usually limited to spitting and difficult handling.
Berserk llama syndrome can be prevented in males through castration before puberty.
Helminths are extremely successful parasites capable of establishing long-lasting infections within a host. During this time, helminths compete with the host organism's cells for nutrient resources and thus possess the potential to cause harm. However, the number of organisms hosted by individuals undergoing helminthic therapy is very small and any side effects are typically only encountered in the first three months of infection. In the long term, the vast majority of clinically infected individuals are asymptomatic, with no significant nutrient loss. In fact, nutrient uptake can be enhanced in some subjects who are hosting a small number of helminths. If the side effects from helminthic therapy were to become unmanageable, they can be alleviated by the use of anthelminthic medications.[1][7][8] The most common clinical symptoms which may be encountered while undergoing helminthic therapy can include:
- Fatigue
- Gastrointestinal discomfort
- Anemia
- Fever
- Abdominal pain
- Weight loss
- Anorexia
- Diarrhea
- General malaise
Cynanthropy (sometimes spelled "kynanthropy") is, in medicine, the pathological delusion of real persons that they are dogs and in anthropology and folklore, the supposed magical practice of shape-shifting alternately between canine and human form, or the possession of combined canine and human anatomical features, a form of therianthropy.
The Greeks spoke of cynanthropy ("kyon", dog). The term existed by at least 1901, when it was applied to myths from China about humans turning into dogs, dogs becoming people, and sexual relations between humans and canines (De Groot, 184). After lycanthropy, cynanthropy is the best known term for a specific variety of therianthropy.
Anthropologist David Gordon White called Central Asia the "vortex of cynanthropy" because races of dog-men were habitually placed there by ancient writers. Hindu mythology puts races of "Dog Cookers" to the far north of India, the Chinese placed the "Dog Jung" and other human/canine barbarians to the extreme west, and European legends frequently put the dog men called Cynocephali in unmapped regions to the east. Some of these races were described as humans with dog heads, others as canine shapeshifters (White, 114-15).
The weredog or cynanthrope is also known in Timor. It is described as a human/canine shapeshifter who is also capable of transforming other people into animals against their wills. These transformations are usually into prey animals such as goats, so that the cynanthrope can devour them without discovery of the crime (Rose, 390).
Advanced sleep phase disorder (ASPD), also known as the advanced sleep-phase type (ASPT) of circadian rhythm sleep disorder or advanced sleep phase syndrome (ASPS), is a condition in which patients feel very sleepy and go to bed early in the evening (e.g. 6:00–8:00 p.m.) and wake up very early in the morning (e.g. around 3:00 a.m.).
Ehrlichiosis is a nationally notifiable disease in the United States. There have been cases reported in every month of the year, but most cases are reported during April–September. These months are also the peak months for tick activity in the United States.
From 2008-2012, the average yearly incidence of ehrlichiosis was 3.2 cases per million persons. This is more than twice the estimated incidence for the years 2000-2007. The incidence rate increases with age, with the ages of 60–69 years being the highest age-specific years. Children of less than 10 years and adults aged 70 years and older, have the highest case-fatality rates. There is a documented higher risk of death among persons who are immunosuppressed.
About 14 million people, mainly children, are treated annually for head lice in the United States alone. Only a small proportion of those treated, however, may have objective evidence of an extant infestation. High levels of louse infestations have also been reported from all over the world including Denmark, Sweden, U.K., France and Australia.
Normally head lice infest a new host only by close contact between individuals, making social contacts among children and parent child interactions more likely routes of infestation than shared combs, brushes, towels, clothing, beds or closets. Head-to-head contact is by far the most common route of lice transmission.
The United Kingdom's National Health Service, and many American health agencies, report that lice "prefer" clean hair, because it's easier to attach eggs and to cling to the strands.
Head lice ("Pediculus humanus capitis") are not known to be vectors of diseases, unlike body lice ("Pediculus humanus humanus"), which are known vectors of epidemic or louse-borne typhus ("Rickettsia prowazekii"), trench fever ("Rochalimaea quintana") and louse-borne relapsing fever ("Borrelia recurrentis").
Anecdotal data gathered from helminth self-treaters and their physicians and presented in socio-medical studies suggest that a much larger number of diseases may be amenable to helminthic therapy than are currently being investigated by formal clinical trials.
Many species of arthropods (insects, arachnids and others) regularly or occasionally bite or sting human beings. Insect saliva contains anticoagulants and enzymes that cause local irritation and allergic reactions. Insect venoms can be delivered by their stingers, which often are modified ovipositors, or by their mouthparts. Insect, spider and scorpion venom can cause serious injury or death. Dipterans account for the majority of insect bites, while hymenopterans account for the majority of stings. Among arachnids spider bites are the most common. Arthropods bite or sting humans for a number of reasons including feeding or defense. Arthropods are major vectors of human disease, with the pathogens typically transmitted by bites.
Contact with farm animals can lead to disease in farmers or others that come into contact with infected animals. Glanders primarily affects those who work closely with horses and donkeys. Close contact with cattle can lead to cutaneous anthrax infection, whereas inhalation anthrax infection is more common for workers in slaughterhouses, tanneries and wool mills. Close contact with sheep who have recently given birth can lead to clamydiosis, or enzootic abortion, in pregnant women, as well as an increased risk of Q fever, toxoplasmosis, and listeriosis in pregnant or the otherwise immunocompromised. Echinococcosis is caused by a tapeworm which can be spread from infected sheep by food or water contaminated with feces or wool. Bird flu is common in chickens. While rare in humans, the main public health worry is that a strain of bird flu will recombine with a human flu virus and cause a pandemic like the 1918 Spanish flu. In 2017, free range chickens in the UK were temporarily ordered to remain inside due to the threat of bird flu. Cattle are an important reservoir of cryptosporidiosis and mainly affects the immunocompromised.
In 1999, Louis Ptáček's and Ying-Hui Fu's research group at the University of California, San Francisco reported findings of a human circadian rhythm disorder showing a familial tendency. The disorder was characterized by a lifelong pattern of sleep onset around 7:30 p.m. and offset around 4:30 a.m. Among three lineages, 29 people were identified as affected with this familial advanced sleep-phase disorder (FASPD), and 46 were considered unaffected. The pedigrees demonstrated FASPD to be a highly penetrant, autosomal dominant trait.
Two years after reporting the finding of FASPD, Ptáček's and Fu's groups published results of genetic sequencing analysis on a family with FASPD. They genetically mapped the FASPD locus to chromosome 2q where very little human genome sequence was then available. Thus, they identified and sequenced all the genes in the critical interval. One of these was Period2 (Per2). Sequencing of the hPer2 gene revealed a serine-to-glycine point mutation in the CKI binding domain of the hPER2 protein that resulted in hypophosphorylation of Per2 in vitro.
In 2005, Fu's and Ptáček's labs reported discovery of a different mutation causing FASPD. This time, CKIδ was implicated, demonstrating an A-to-G missense mutation that resulted in a threonine-to-alanine alteration in the protein. The evidence for both of these reported causes of FASPD is strengthened by the absence of said mutations in all tested control subjects and by demonstration of functional consequences of the respective mutations in vitro. Fruit flies and mice engineered to carry the human mutation also demonstrated abnormal circadian phenotypes although the mutant flies had a long circadian period while the mutant mice had a shorter period. The differences between flies and mammals that account for this difference are not known. Most recently, Ptáček and Fu reported additional studies of the human Per2 S662G mutation and generation of mice carrying the human mutation. These mice had a circadian period almost 2 hours shorter than wild-type animals. Genetic dosage studies of CKIδ on the Per2 S662G mutation revealed that CKIδ is having opposite effects on Per2 levels depending on the sites on Per2 that CKIδ is phosphorylating.
The U.S. Centers for Disease Control and Prevention (CDC) publishes a journal "Emerging Infectious Diseases" that identifies the following factors contributing to disease emergence:
- Microbial adaption; e.g. genetic drift and genetic shift in Influenza A
- Changing human susceptibility; e.g. mass immunocompromisation with HIV/AIDS
- Climate and weather; e.g. diseases with zoonotic vectors such as West Nile Disease (transmitted by mosquitoes) are moving further from the tropics as the climate warms
- Change in human demographics and trade; e.g. rapid travel enabled SARS to rapidly propagate around the globe
- Economic development; e.g. use of antibiotics to increase meat yield of farmed cows leads to antibiotic resistance
- Breakdown of public health; e.g. the current situation in Zimbabwe
- Poverty and social inequality; e.g. tuberculosis is primarily a problem in low-income areas
- War and famine
- Bioterrorism; e.g. 2001 Anthrax attacks
- Dam and irrigation system construction; e.g. malaria and other mosquito borne diseases
Fasciolosis is caused by two digenetic trematodes "F. hepatica" and "F. gigantica". Adult flukes of both species are localized in the bile ducts of the liver or gallbladder. "F. hepatica" measures 2 to 3 cm and has a cosmopolitan distribution. "F. gigantica" measures 4 to 10 cm in length and the distribution of the species is limited to the tropics and has been recorded in Africa, the Middle East, Eastern Europe and south and eastern Asia. In domestic livestock in Japan, diploid (2n = 20), triploid (3n = 30) and chimeric flukes (2n/3n) have been described, many of which reproduce parthenogenetically. As a result of this unclear classification, flukes in Japan are normally referred to as "Fasciola" spp. Recent reports based on mitochondrial genes analysis has shown that Japanese "Fasciola" spp. is more closely related to "F. gigantica" than to "F. hepatica". In India, a species called "F. jacksoni" was described in elephants.
"Y. enterocolitica" infections are sometimes followed by chronic inflammatory diseases such as arthritis, erythema nodosum, and reactive arthritis. This is most likely because of some immune-mediated mechanism.
"Y. enterocolitica" seems to be associated with autoimmune Graves-Basedow thyroiditis.
Whilst indirect evidence exists, direct causative evidence is limited,
and "Y. enterocolitica" is probably not a major cause of this disease, but may contribute to the development of thyroid autoimmunity arising for other reasons in genetically susceptible individuals.
"Y. enterocolitica" infection has also been suggested to not be the cause of autoimmune thyroid disease, but rather is only an associated condition, with both having a shared inherited susceptibility.
More recently, the role for "Y. enterocolitica" has been disputed.
The most common symptoms include headache, muscle aches, and fatigue. A rash may occur, but is uncommon. Ehrlichiosis can also blunt the immune system by suppressing production of TNF-alpha, which may lead to opportunistic infections such as candidiasis.
Most of the signs and symptoms of ehrlichiosis can likely be ascribed to the immune dysregulation that it causes. A "toxic shock-like" syndrome is seen in some severe cases of ehrlichiosis. Some cases can present with purpura and in one such case the organisms were present in such overwhelming numbers that in 1991 Dr. Aileen Marty of the AFIP was able to demonstrate the bacteria in human tissues using standard stains, and later proved that the organisms were indeed Ehrlichia using immunoperoxidase stains.
Experiments in mouse models further supports this hypothesis, as mice lacking TNF-alpha I/II receptors are resistant to liver injury caused by ehrlichia infection.
3% of human monocytic ehrlichiosis cases result in death; however, these deaths occur "most commonly in immunosuppressed individuals who develop respiratory distress syndrome, hepatitis, or opportunistic nosocomial infections."
Rabies is a viral disease that exists in Haiti and throughout the world. It often causes fatal inflammation of the brain in humans and other mammals, such as dogs and mongooses in Haiti. The term "rabies" is derived from a Latin word that means "to rage"; rabid animals sometimes appear to be angry. Early symptoms can include fever and tingling at the site of exposure, followed by one or more of the following symptoms: violent movements, uncontrolled excitement, fear of water, an inability to move parts of the body, confusion, and loss of consciousness. Once symptoms appear, death is nearly always the outcome. The time period between contracting the disease and showing symptoms is usually one to three months; however, this time period can vary from less than a week to more than a year. The time between contraction and the onset of symptoms is dependent on the distance the virus must travel to reach the central nervous system.
Haiti is one of five remaining countries in the Americas where canine rabies is still a problem. It has the highest rate of human rabies deaths in the western hemisphere with an estimated two deaths each week. Only about seven deaths are reported to health authorities each year due to poor surveillance, limitations in diagnostic capacity, and lack of awareness and education about the disease among Haitians.
Clinical signs of fasciolosis are always closely associated with infectious dose (amount of ingested metacercariae). In sheep, as the most common definitive host, clinical presentation is divided into 4 types:
- Acute Type I Fasciolosis: infectious dose is more than 5000 ingested metacercariae. Sheep suddenly die without any previous clinical signs. Ascites, abdominal haemorrhage, icterus, pallor of membranes, weakness may be observed in sheep.
- Acute Type II Fasciolosis: infectious dose is 1000-5,000 ingested metacercariae. As above, sheep die but briefly show pallor, loss of condition and ascites.
- Subacute Fasciolosis: infectious dose is 800-1000 ingested metacercariae. Sheep are lethargic, anemic and may die. Weight loss is dominant feature.
- Chronic Fasciolosis: infectious dose is 200-800 ingested metacercariae. Asymptomatic or gradual development of bottle jaw and ascites (ventral edema), emaciation, weight loss.
In blood, anemia, hypoalbuminemia, and eosinophilia may be observed in all types of fasciolosis. Elevation of liver enzyme activities, such a glutamate dehydrogenase (GLDH), gamma-glutamyl transferase (GGT), and lactate dehydrogenase (LDH), is detected in subacute or chronic fasciolosis from 12 to 15 weeks after ingestion of metacercariae. Economical effect of fasciolosis in sheep consists in sudden deaths of animals as well as in reduction of weight gain and wool production. In goats and cattle, the clinical manifestation is similar to sheep. However, acquired resistance to "F. hepatica" infection is well known in adult cattle. Calves are susceptible to disease but in excess of 1000 metacercariae are usually required to cause clinical fasciolosis. In this case the disease is similar to sheep and is characterized by weight loss, anemia, hypoalbuminemia and (after infection with 10,000 metacercariae) death. Importance of cattle fasciolosis consist in economic losses caused by condemnation of livers at slaughter and production losses especially due to reduced weight gain.
In sheep and sometimes cattle, the damaged liver tissue may become infected by the "Clostridium" bacteria "C. novyi" type B. The bacteria will release toxins into the bloodstream resulting in what is known as black disease. There is no cure and death follows quickly. As "C. novyi" is common in the environment, black disease is found wherever populations of liver flukes and sheep overlap.
The most significant zoonotic pathogens causing foodborne diseases are , "Campylobacter", "Caliciviridae", and "Salmonella".
In 2006, a conference held in Berlin was focusing on the issue of zoonotic pathogen effects on food safety, urging governments to intervene, and the public to be vigilant towards the risks of catching food-borne diseases from farm-to-dining table.
Many food outbreaks can be linked to zoonotic pathogens. Many different types of food can be contaminated that have an animal origin. Some common foods linked to zoonotic contaminations include eggs, seafood, meat, dairy, and even some vegetables. Food outbreaks should be handled in preparedness plans to prevent widespread outbreaks and to efficiently and effectively contain outbreaks.
Many human diseases can be transmitted to other primates, due to their extensive biological similarities. As a result, centers that hold, treat, or involve close proximity to primates and some other kinds of animals (for example zoos, researchers, and animal hospitals), often take steps to ensure animals are not exposed to human diseases they can catch. In some cases animals are routinely immunized with the same vaccines given to humans.
- Leishmaniasis - Both zoonotic and anthroponotic.
- Influenza, Measles, pneumonia and various other pathogens - Many primates.
- Tuberculosis - Both zoonotic and anthroponotic, with birds, cows, elephants, meerkats, mongooses, monkeys, and pigs known to have been affected.
Yersiniosis is usually self-limiting and does not require treatment. For severe infections (sepsis, focal infection) especially if associated with immunosuppression, the recommended regimen includes doxycycline in combination with an aminoglycoside. Other antibiotics active against "Y. enterocolitica" include trimethoprim-sulfamethoxasole, fluoroquinolones, ceftriaxone, and chloramphenicol. "Y. enterocolitica" is usually resistant to penicillin G, ampicillin, and cephalotin due to beta-lactamase production.