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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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Developing countries are more severely affected by TORCH syndrome.
TORCH syndrome can be prevented by treating an infected pregnant person, thereby preventing the infection from affecting the fetus.
At the October 23 meeting of the Child Neurology Society, it was a matter of debate whether acute flaccid myelitis would be likely to return the next year. Enteroviruses D68 and A71 tend to cause neurological symptoms more often than other enteroviruses, but have been infrequent causes of colds. It is possible that enteroviruses have been causing acute flaccid myelitis at a very low rate for many years, misdiagnosed as transverse myelitis, and enterovirus 68 simply happened to become more prevalent in the 2014 season.
The CDC had confirmed 538 cases of enterovirus 68 infection in 43 states. The CDC has determined and submitted to GenBank complete or nearly-complete genomic sequences for three known strains of the virus, which are "genetically related to strains of EV-D68 that were detected in previous years in the United States, Europe, and Asia."
While rates of paralytic symptoms appear to be correlated with the number of respiratory infections, in initial anecdotal reports the cases are not clustered within a family or school, suggesting that the paralysis "per se" is not directly contagious, but arises as a very rare complication of the common respiratory infection.
Efforts to develop a vaccine for the virus depend on whether multiple strains of enteroviruses actually cause acute flaccid myelitis, and if so, whether a vaccine can be designed to protect against them all.
Complications from the viral infections that cause HFMD are rare, but require immediate medical treatment if present. HFMD infections caused by Enterovirus 71 tend to be more severe and are more likely to have neurologic or cardiac complications including death than infections caused by Coxsackievirus A16. Viral or aseptic meningitis can occur with HFMD in rare cases and is characterized by fever, headache, stiff neck, or back pain. The condition is usually mild and clears without treatment; however, hospitalization for a short time may be needed. Other serious complications of HFMD include encephalitis (swelling of the brain), or flaccid paralysis in rare circumstances.
Fingernail and toenail loss have been reported in children 4–8 weeks after having HFMD. The relationship between HFMD and the reported nail loss is unclear; however, it is temporary and nail growth resumes without treatment.
Minor complications due to symptoms can occur such as dehydration, due to mouth sores causing discomfort with intake of foods and fluid.
This depends on the age of the animal affected and the efficiency of its immune system.
Colostral protection lasts up to 5 months of age, after which it decreases to an all-time low to increase yet again at about 12 months of age.
- Prenatal infection: virus travels from infected mother to fetus via the placenta. In this case, the time of gestation determines the result of the infection.
- If the fetus is infected in the first 30 days of fetal life, death and absorption of all, or some of the fetuses may occur. In this case, some immunotolerant healthy piglets may be born.
- If the infection happens at 40 days, death and mummification may occur. Also in this case, some or all the fetuses are involved, i.e. some of the fetuses can be born healthy and immunotolerant, or else carriers of the disease.
- If the viruses crosses the placenta in the last trimester, neonatal death may occur, or the birth of healthy piglets with a protective pre-colostral immunity.
- Postnatal infection (pigs up to 1 year of age): Infection occurs oro-nasally, followed by a viremic period associated with transitory leucopenia.
- Infection in adults (over 1 year of age): These subject would have an active, protective immune system which protects them from future exposures (e.g. mating with an infected male).
Therefore, it is important to note that the virus is particularly dangerous for the sow in her first gestation, which would be at 7–8 months of age, as she would have a particularly low antibody count at this age and could easily contract the virus via copulation.
Preventive measures include avoiding direct contact with infected individuals (including keeping infected children home from school), proper cleaning of shared utensils, disinfecting contaminated surfaces, and proper hand hygiene. These measures have been shown to be effective in decreasing the transmission of the viruses responsible for HFMD.
Protective habits include hand washing and disinfecting surfaces in play areas. Breast-feeding has also shown to decrease rates of severe HFMD, though does not reduce the risk for the infection of the disease.
Viral encephalitis is a type of encephalitis caused by a virus.
It is unclear if anticonvulsants used in people with viral encephalitis would prevent seizures.
SMEDI (an acronym of stillbirth, mummification, embryonic death, and infertility) is a reproductive disease of swine caused by "Porcine parvovirus" ("PPV") and "Porcine enterovirus". The term SMEDI usually indicates "Porcine enterovirus", but it also can indicate "Porcine parvovirus", which is a more important cause of the syndrome. SMEDI also causes abortion, neonatal death, and decreased male fertility.
From an economic standpoint SMEDI is an important disease because of the loss of productivity from fetal death in affected herds. Initial infection of a herd causes the greatest effect, but losses slow over time. The disease is spread most commonly by ingestion of food and water contaminated with infected feces and occasionally through sexual contact and contact with aborted tissue. A vaccine is available (ATCvet code: ).
Enterovirus 70 is a member of the genus of viruses called Enterovirus and family of the viruses Picornaviridae. Usually very small (about 30 nm in diameter), it is non-enveloped (meaning it only has a nucleic acid core and protein capsid) and has a single-stranded positive-sense RNA genome; the protein capsid the virus itself is surrounded by is icosahedral. It is known as one of the more new enteroviruses within this category. It spreads easily from one person’s eyes to another’s through contact with infected objects, like fingers, or through the eye secretion itself. Enterovirus 70 infrequently causes polio-like permanent paralysis.
There are three main viruses that have been studied and confirmed as the agents responsible for AHC, including enterovirus 70, coxsakievirus A24 variant (CA24v) and adenovirus 11.
AHC can only exist in a human host and is transmitted through human contact with an infected individual or object, such as a towel used by an infected person. It is also easily communicable through fecal-oral pathways, thus allowing for its abundance in areas of the world with low levels of hygiene. Within one to two days of infection, symptoms will begin to become apparent.
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
Types of encephalitis in humans include:
- Arbovirus encephalitis
- La Crosse encephalitis
- Enterovirus
- California encephalitis virus
- Japanese encephalitis
- St. Louis encephalitis
- Eastern equine encephalitis virus
- Western equine encephalitis virus
- Venezuelan equine encephalitis virus
- Murray Valley encephalitis virus
- Tick-borne meningoencephalitis
- Powassan encephalitis
- West Nile virus
- Herpes simplex
- Human herpesvirus 6
- Varicella zoster virus
- Rabies
- HIV
- H5N1 encephalitis
- Nipah virus encephalitis
- Lymphocytic choriomeningitis, which also causes encephalitis
Coxsackie B virus is spread by contact and epidemics usually occur during warm weather in temperate regions and at any time in the tropics.
Microchimerism has been implicated in autoimmune diseases. Independent studies repeatedly suggested that microchimeric cells of fetal origin may be involved in the pathogenesis of systemic sclerosis. Moreover, microchimeric cells of maternal origin may be involved in the pathogenesis of a group of autoimmune diseases found in children, i.e. juvenile idiopathic inflammatory myopathies (one example would be juvenile dermatomyositis). Microchimerism has now been further implicated in other autoimmune diseases, including systemic lupus erythematosus. Contrarily, an alternative hypothesis on the role of microchimeric cells in lesions is that they may be facilitating tissue repair of the damaged organ.
Moreover, fetal immune cells have also been frequently found in breast cancer stroma as compared to samples taken from healthy women. It is not clear, however, whether fetal cell lines promote the development of tumors or, contrarily, protect women from developing breast carcinoma.
Microchimerism occurs in most pairs of twins in cattle. In cattle (and other bovines), the placentae of fraternal twins usually fuse and the twins share blood circulation, resulting in exchange of cell lines. If the twins are a male-female pair, the male hormones from the bull calf have the effect of partially masculinising the heifer (female), creating a "martin heifer" or "freemartin". Freemartins appear female, but are infertile and so cannot be used for breeding or dairy production. Microchimerism provides a method of diagnosing the condition, because male genetic material can be detected in a blood sample.
An emerging infectious disease (EID) is an infectious disease whose incidence has increased in the past 20 years and could increase in the near future. Emerging infections account for at least 12% of all human pathogens. EIDs are caused by newly identified species or strains (e.g. Severe acute respiratory syndrome, HIV/AIDS) that may have evolved from a known infection (e.g. influenza) or spread to a new population (e.g. West Nile fever) or to an area undergoing ecologic transformation (e.g. Lyme disease), or be "reemerging" infections, like drug resistant tuberculosis. Nosocomial (hospital-acquired) infections, such as methicillin-resistant Staphylococcus aureus are emerging in hospitals, and extremely problematic in that they are resistant to many antibiotics. Of growing concern are adverse synergistic interactions between emerging diseases and other infectious and non-infectious conditions leading to the development of novel syndemics. Many emerging diseases are zoonotic - an animal reservoir incubates the organism, with only occasional transmission into human populations.
The illness lasts about a week and is rarely fatal. Treatment includes the administration of nonsteroidal anti-inflammatory agents or the application of heat to the affected muscles. Relapses during the weeks following the initial episode are a characteristic feature of this disease.
In 2003, the incidence of Rh(D) sensitization in the United States was 6.8 per 1000 live births; 0.27% of women with an Rh incompatible fetus experience alloimmunization.
In most cases Ballantyne syndrome causes fetal or neonatal death and in contrast, maternal involvement is limited at the most to preeclampsia.
Aseptic meningitis, or sterile meningitis, is a condition in which the layers lining the brain, the meninges, become inflamed and a pyogenic bacterial source is not to blame. Meningitis is diagnosed on a history of characteristic symptoms and certain examination findings (e.g., Kernig's sign). Investigations should show an increase in the number of leukocytes present in the cerebrospinal fluid (CSF) obtained via lumbar puncture (normally being fewer than five visible leukocytes per microscopic high-power field).
The term "aseptic" is frequently a misnomer, implying a lack of infection. On the contrary, many cases of aseptic meningitis represent infection with viruses or mycobacteria that cannot be detected with routine methods. While the advent of polymerase chain reaction has increased the ability of clinicians to detect viruses such as enterovirus, cytomegalovirus, and herpes virus in the CSF, many viruses can still escape detection. Additionally, mycobacteria frequently require special stains and culture methods that make their detection difficult. When CSF findings are consistent with meningitis, and microbiologic testing is unrevealing, clinicians typically assign the diagnosis of aseptic meningitis—making it a relative diagnosis of exclusion.
Aseptic meningitis can result from non-infectious causes as well. it can be a relatively infrequent side effect of medications, or be a result of an autoimmune disease. There is no formal classification system of aseptic meningitis except to state the underlying cause, if known. The absence of bacteria found in the spinal fluid upon spinal tap, either through microscopic examination or by culture, usually differentiates aseptic meningitis from its pyogenic counterpart.
"Aseptic meningitis", like non-gonococcal urethritis, non-Hodgkin lymphoma and atypical pneumonia, merely states what the condition is not, rather than what it is. Terms such as viral meningitis, bacterial meningitis, fungal meningitis, neoplastic meningitis and drug-induced aseptic meningitis can provide more information about the condition, and without using one of these more specific terms, it is difficult to describe treatment options or prognosis.
There is no vaccine for SVD. Prevention measures are similar to those for foot-and-mouth disease: controlling animals imported from infected areas, and sanitary disposal of garbage from international aircraft and ships, and thorough cooking of garbage. Infected animals should be placed in strict quarantine. Eradication measures for the disease include quarantining infected areas, depopulation and disposal of infected and contact pigs, and cleaning and disinfecting
contaminated premises.
Complications of HDN could include kernicterus, hepatosplenomegaly, inspissated (thickened or dried) bile syndrome and/or greenish staining of the teeth, hemolytic anemia and damage to the liver due to excess bilirubin. Similar conditions include acquired hemolytic anemia, congenital toxoplasma and syphilis infection, congenital obstruction of the bile duct and cytomegalovirus infection.
- High at birth or rapidly rising bilirubin
- Prolonged hyperbilirubinemia
- Bilirubin Induced Neuorlogical Dysfunction
- Cerebral Palsy
- Kernicterus
- Neutropenia
- Thrombocytopenia
- Hemolytic Anemia - MUST NOT be treated with iron
- Late onset anemia - Must NOT be treated with iron. Can persist up to 12 weeks after birth.
Some doctors recommend complete bed-rest for the mother coupled with massive intakes of protein as a therapy to try to counteract the syndrome. Research completed shows these nutritional supplements do work. Diet supplementation was associated with lower overall incidence of TTTS (20/52 versus 8/51, P = 0.02) and with lower prevalence of TTTS at delivery (18/52 versus 6/51, P = 0.012) when compared with no supplementation. Nutritional intervention also significantly prolonged the time between the diagnosis of TTTS and delivery (9.4 ± 3.7 weeks versus 4.6 ± 6.5 weeks; P = 0.014). The earlier nutritional regimen was introduced, the lesser chance of detecting TTTS ( P = 0.001). Although not statistically significant, dietary intervention was also associated with lower Quintero stage, fewer invasive treatments, and lower twin birth weight discordance. Diet supplementation appears to counter maternal metabolic abnormalities in monochorionic twin pregnancies and improve perinatal outcomes in TTTS when combined with the standard therapeutic options. Nutritional therapy appears to be most effective in mitigating cases that are caught in Quintero Stage I, little effect has been observed in those that are beyond Stage I.
Swine vesicular disease is most commonly brought into a herd by the introduction of a subclinically infected pig.
The disease can be transmitted in feed containing infected meat scraps, or by direct contact with infected feces (such as in an improperly cleaned truck).