bowang0911/MedQuAD huggingface dataset:
Transmission to humans may occur after a tick bite or contact with an infected animal, most importantly a sick or recently dead monkey. No person-to-person transmission has been described. 
 
Large animals such as goats, cows, and sheep may become infected with KFD but play a limited role in the transmission of the disease. These animals provide the blood meals for ticks and it is possible for infected animals with viremia to infect other ticks, but transmission of KFDV to humans from these larger animals is extremely rare. Furthermore, there is no evidence of disease transmission via the unpasteurized milk of any of these animals.
After an incubation period of 3-8 days, the symptoms of KFD begin suddenly with chills, fever, and headache. Severe muscle pain with vomiting, gastrointestinal symptoms and bleeding problems may occur 3-4 days after initial symptom onset. Patients may experience abnormally low blood pressure, and low platelet, red blood cell, and white blood cell counts. 
                
After 1-2 weeks of symptoms, some patients recover without complication. However, the illness is biphasic for a subset of patients (10-20%) who experience a second wave of symptoms at the beginning of the third week. These symptoms include fever and signs of neurological manifestations, such as severe headache, mental disturbances, tremors, and vision deficits. 
                
The estimated case-fatality rate is from 3 to 5% for KFD.
KFD has historically been limited to the western and central districts of Karnataka State, India. However, in November 2012, samples from humans and monkeys tested positive for KFDV in the southernmost district of the State which neighbors Tamil Nadu State and Kerala State, indicating the possibility of wider distribution of KFDV. Additionally, a virus very similar to KFD virus (Alkhurma hemorrhagic fever virus) has been described in Saudi Arabia. 
                
People with recreational or occupational exposure to rural or outdoor settings (e.g., hunters, herders, forest workers, farmers) within Karnataka State are potentially at risk for infection by contact with infected ticks. Seasonality is another important risk factor as more cases are reported during the dry season, from November through June.
People become infected with Cyclospora by ingesting sporulated oocysts, which are the infective form of the parasite. This most commonly occurs when food or water contaminated with feces is consumed. An infected person sheds unsporulated (immature, non-infective) Cyclospora oocysts in the feces. The oocysts are thought to require days to weeks in favorable environmental conditions to sporulate (become infective). Therefore, direct person-to-person transmission is unlikely, as is transmission via ingestion of newly contaminated food or water.
    
More on: Cyclospora Biology
    Geographic Distribution
    
Cyclosporiasis occurs in many countries, but it seems to be most common in tropical and subtropical regions. In areas where cyclosporiasis has been studied, the risk for infection is seasonal. However, no consistent pattern has been identified regarding the time of year or the environmental conditions, such as temperature or rainfall.
    
In the United States, foodborne outbreaks of cyclosporiasis since the mid-1990s have been linked to various types of imported fresh produce, including raspberries, basil, snow peas, and mesclun lettuce; no commercially frozen or canned produce has been implicated.
    
U.S. cases of infection also have occurred in persons who traveled to Cyclospora-endemic areas. To reduce the risk for infection, travelers should take precautions, such as those recommended in CDC's Health Information for International Travel (Yellow Book). Travelers also should be aware that treatment of water or food with chlorine or iodine is unlikely to kill Cyclospora oocysts.
Clinical Diagnosis
    
Health care providers should consider Cyclospora as a potential cause of prolonged diarrheal illness, particularly in patients with a history of recent travel to Cyclospora-endemic areas. Testing for Cyclospora is not routinely done in most U.S. laboratories, even when stool is tested for parasites. Therefore, if indicated, health care providers should specifically request testing for Cyclospora.
    
More on: Resources for Health Professionals: Diagnosis
    Laboratory Diagnosis
    
Cyclospora infection is diagnosed by examining stool specimens. Diagnosis can be difficult in part because even persons who are symptomatic might not shed enough oocysts in their stool to be readily detectable by laboratory examinations. Therefore, patients might need to submit several specimens collected on different days.
    
Special techniques, such as acid-fast staining, are often used to make Cyclospora oocysts more visible under the microscope. In addition, Cyclospora oocysts are autofluorescent, meaning that when stool containing the parasite is viewed under an ultraviolet (UV) fluorescence microscope the parasite appears blue or green against a black background. Molecular diagnostic methods, such as polymerase chain reaction (PCR) analysis, are used to look for the parasite's DNA in the stool.
    
More on: Key points for the laboratory diagnosis of cyclosporiasis
Trimethoprim/sulfamethoxazole (TMP/SMX), sold under the trade names Bactrim*, Septra*, and Cotrim*, is the usual therapy for Cyclospora infection. No highly effective alternative antibiotic regimen has been identified yet for patients who do not respond to the standard treatment or have a sulfa allergy.
    
More on: Resources for Health Professionals: Treatment
    
Most people who have healthy immune systems will recover without treatment. If not treated, the illness may last for a few days to a month or longer. Symptoms may seem to go away and then return one or more times (relapse). Anti-diarrheal medicine may help reduce diarrhea, but a health care provider should be consulted before such medicine is taken. People who are in poor health or who have weakened immune systems may be at higher risk for severe or prolonged illness.
    
More on: Resources for Health Professionals FAQs
    
* Use of trade names is for identification only and does not imply endorsement by the Public Health Service or by the U.S. Department of Health and Human Services.
On the basis of the currently available information, avoiding food or water that may have been contaminated with feces is the best way to prevent cyclosporiasis. Treatment with chlorine or iodine is unlikely to kill Cyclospora oocysts. No vaccine for cyclosporiasis is available.
    
The U.S. Food and Drug Administration's (FDA) Center for Food Safety and Applied Nutrition (CFSAN) publishes detailed food safety recommendations for growers and suppliers. In its Guide to Minimize Microbial Food Safety Hazards for Fresh Fruits and Vegetables, CFSAN describes good agricultural practices (GAPs) and good manufacturing practices (GMPs) for fresh fruits and vegetables. The guidelines address the growing, harvesting, sorting, packaging, and storage processes; following the guidelines can help reduce the overall risk for microbial contamination during these processes. The precise ways that food and water become contaminated with Cyclospora oocysts are not fully understood.
    
CDC monitors the occurrence of cyclosporiasis in the United States and helps state health departments identify and investigate cyclosporiasis outbreaks to prevent additional cases of illness.
    
More on: Surveillance and Outbreak Response
People acquire trichinellosis by consuming raw or undercooked meat infected with the Trichinella parasite, particularly wild game meat or pork. Even tasting very small amounts of undercooked meat during preparation or cooking puts you at risk for infection. Outbreaks occur in settings where multiple people consume the same Trichinella-infected meat.
Worldwide, an estimated 10,000 cases of trichinellosis occur every year. Several different species of Trichinella can cause human disease; the most common species is Trichinella spiralis, which has a global distribution and is the species most commonly found in pigs. Other Trichinella species are less commonly reported as the cause of human disease and may be found in different parts of the world, usually infecting wild animals.
In the United States, trichinellosis cases are reported to CDC much less commonly now than in the past (Figure 1). During the late 1940s, when the U.S. Public Health Service began counting cases of trichinellosis, 400 cases in the United States were recorded each year on average. During 2008-2010, 20 cases were reported to CDC each year on average. The overall number of cases reported has decreased because of improved pig-raising practices in the pork industry, commercial and home freezing of pork, and public awareness of the danger of eating raw or undercooked meat products. The number of cases associated with raw or undercooked wild game meats has remained relatively constant over time (Figure 2). Over the past 40 years, few cases of trichinellosis have been reported in the United States, and the risk of trichinellosis from commercially raised and properly prepared pork is very low. However, eating undercooked wild game, particularly bear meat, puts one at risk for acquiring this disease.
A diagnosis of trichinellosis is made in patients whose signs and symptoms are compatible with trichinellosis, have a positive laboratory test for Trichinella, and who can recall eating raw or undercooked pork or wild game meat.
    
Laboratory diagnosis of Trichinella infection is most often made by a Trichinella antibody test. In some cases a muscle biopsy may be performed.
    
More on: Resources for Health Professionals: Diagnosis
- Wash your hands with warm water and soap after handling raw meat.
    - Curing (salting), drying, smoking, or microwaving meat alone does not consistently kill infective worms; homemade jerky and sausage were the cause of many cases of trichinellosis reported to CDC in recent years.
    - Freeze pork less than 6 inches thick for 20 days at 5°F (-15°C) to kill any worms.
    - Freezing wild game meats, unlike freezing pork products, may not effectively kill all worms because some worm species that infect wild game animals are freeze-resistant.
    - Clean meat grinders thoroughly after each use.
   
   
To help prevent Trichinella infection in animal populations, do not allow pigs or wild animals to eat uncooked meat, scraps, or carcasses of any animals, including rats, which may be infected with Trichinella.
Striatonigral degeneration is a neurological disorder caused by a disruption in the connection between two areas of the brain-the striatum and the substantia nigra. These two areas work together to enable balance and movement. Striatonigral degeneration is a type of multiple system atrophy (MSA). Symptoms of the disorder resemble some of those seen in Parkinson's disease, including rigidity, instability, impaired speech, and slow movements.
Empty Sella Syndrome (ESS) is a disorder that involves the sella turcica, a bony structure at the base of the brain that surrounds and protects the pituitary gland. ESS is often discovered during radiological imaging tests for pituitary disorders. ESS occurs n up to 25 percent of the population.An individual with ESS may have no symptoms or may have symptoms resulting from partial or complete loss of pituitary function (including headaches, low sex drive, and impotence).There are two types of ESS: primary and secondary. Primary ESS happens when a small anatomical defect above the pituitary gland allows spinal fluid to partially or completely fill the sella turcica. This causes the gland to flatten out along the interior walls of the sella turcica cavity. Individuals with primary ESS may have high levels of the hormone prolactin, which can interfere with the normal function of the testicles and ovaries. Primary ESS is most common in adults and women, and is often associated with obesity and high blood pressure. In some instances the pituitary gland may be smaller than usual; this may be due to a condition called pseudotumor cerebri (which means "false brain tumor," brought on by high pressure within the skull), In rare instances this high fluid pressure can be associated with drainage of spinal fluid through the nose. Secondary ESS is the result of the pituitary gland regressing within the cavity after an injury, surgery, or radiation therapy. Individuals with secondary ESS can sometimes have symptoms that reflect the loss of pituitary functions, such as the ceasing of menstrual periods, infertility, fatigue, and intolerance to stress and infection. In children, ESS may be associated with early onset of puberty, growth hormone deficiency, pituitary tumors, or pituitary gland dysfunction. Magnetic resonance imaging (MRI) scans are useful in evaluating ESS and for identifying underlying disorders that may be the cause of high fluid pressure.
The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system, and to use that knowledge to reduce the burden of neurological disease. The NINDS supports and conducts fundamental studies that explore the complex mechanisms of normal brain development and to better understand neurological conditions such as ESS. The knowledge gained from these fundamental studies helps researchers understand neurodevelopment and provides opportunities to more effectively treat and perhaps even prevent, such disorders.
Primary lateral sclerosis (PLS) is a rare neuromuscular disease with slowly progressive weakness in voluntary muscle movement. PLS belongs to a group of disorders known as motor neuron diseases. PLS affects the upper motor neurons (also called corticospinal neurons) in the arms, legs, and face. It occurs when nerve cells in the motor regions of the cerebral cortex (the thin layer of cells covering the brain which is responsible for most higher level mental functions) gradually degenerate, causing movements to be slow and effortful. The disorder often affects the legs first, followed by the body, trunk, arms and hands, and, finally the bulbar muscles (muscles that control speech, swallowing, and chewing). Symptoms include weakness, muscle stiffness and spasticity, clumsiness, slowing of movement, and problems with balance and speech. PLS is more common in men than in women, with a varied gradual onset that generally occurs between ages 40 and 60. PLS progresses gradually over a number of years, or even decades. Scientists do not believe PLS has a simple hereditary cause. The diagnosis of PLS requires extensive testing to exclude other diseases. When symptoms begin, PLS may be mistaken for amyotrophic lateral sclerosis (ALS) or spastic paraplegia. Most neurologists follow an affected individual's clinical course for at least 3 to 4 years before making a diagnosis of PLS..
Treatment for individuals with PLS is symptomatic. Muscle relaxants such as baclofen, tizanidine, and the benzodiazepines may reduce spasticity. Other drugs may relieve pain and antidepressants can help treat depression. Physical therapy, occupational therapy, and rehabilitation may prevent joint immobility and slow muscle weakness and atrophy. Assistive devices such as supports or braces, speech synthesizers, and wheelchairs ma help some people retain independence.. Speech therapy may be useful for those with involvement of the facial muscles.
The dystonias are movement disorders in which sustained muscle contractions cause twisting and repetitive movements or abnormal postures. The movements, which are involuntary and sometimes painful, may affect a single muscle; a group of muscles such as those in the arms, legs, or neck; or the entire body. Early symptoms may include deterioration in handwriting, foot cramps, or a dragging foot after running or walking some distance. Other possible symptoms are tremor and voice or speech difficulties. About half the cases of dystonia have no connection to disease or injury and are called primary or idiopathic dystonia. Of the primary dystonias, many cases appear to be inherited. Dystonias can also be symptoms of other diseases, some of which may be hereditary. Dystonia can occur at any age, but is often described as either early, or childhood, onset versus adult onset.
The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to dystonia in its laboratories at the National Institutes of Health (NIH) and also supports additional dystonia research through grants to major research institutions across the country. Scientists at other NIH Institutes (National institute on Deafness and Other Communications Disorders, National Eye Institute, and Eunice Kennnedy Shriver National Institute on Child Health and Human Development) also support research that may benefit individuals with dystonia. Investigators believe that the dystonias result from an abnormality in an area of the brain called the basal ganglia, where some of the messages that initiate muscle contractions are processed. Scientists at the NINDS laboratories have conducted detailed investigations of the pattern of muscle activity in persons with dystonias. Studies using EEG analysis and neuroimaging are probing brain activity. The search for the gene or genes responsible for some forms of dominantly inherited dystonias continues.
Farbers disease, also known as Farber's lipogranulomatosis, describes a group of inherited metabolic disorders called lipid storage diseases, in which excess amounts of lipids (oils, fatty acids, and related compounds) build up to harmful levels in the joints, tissues, and central nervous system. The liver, heart, and kidneys may also be affected. Disease onset is typically seen in early infancy but may occur later in life. Symptoms of the classic form may have moderately impaired mental ability and difficulty with swallowing. Other symptoms may include chronic shortening of muscles or tendons around joints. arthritis, swollen lymph nodes and joints, hoarseness, nodules under the skin (and sometimes in the lungs and other parts of the body), and vomiting. Affected persons may require the insertion of a breathing tube. In severe cases, the liver and spleen are enlarged. Farber's disease is caused by a deficiency of the enzyme ceramidase. The disease occurs when both parents carry and pass on the defective gene that regulates the protein sphingomyelin. Children born to these parents have a 25 percent chance of inheriting the disorder and a 50 percent chance of carrying the faulty gene. The disorder affects both males and females.
The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. Research funded by the NINDS focuses on better understanding of how neurological deficits arise in lipid storage diseases and on the development of new treatments targeting disease mechanisms, including gene therapies, cell-based therapies and pharmacological approaches. The NINDS, along with other Institutes and Centers at the National Institutes of Health, supports the Lysosomal Disease network of centers that addresses some of the major challenges in the diagnosis, management, and therapy of rare diseases, including the lipid storage diseases.Research on lipid storage diseases within the Network includes longitudinal studies of the natural history and/or treatment of these disorders. Additional studies will emphasize the quantitative analysis of the central nervous system structure and function, and develop biomarkers (signs that can indicate the diagnosis or progression of a disease) for these disorders.
Familial periodic paralyses are a group of inherited neurological disorders caused by mutations in genes that regulate sodium and calcium channels in nerve cells. They are characterized by episodes in which the affected muscles become slack, weak, and unable to contract. Between attacks, the affected muscles usually work as normal.
                
The two most common types of periodic paralyses are: Hypokalemic periodic paralysis is characterized by a fall in potassium levels in the blood. In individuals with this mutation attacks often begin in adolescence and are triggered by strenuous exercise, high carbohydrate meals, or by injection of insulin, glucose, or epinephrine. Weakness may be mild and limited to certain muscle groups, or more severe and affect the arms and legs. Attacks may last for a few hours or persist for several days. Some patients may develop chronic muscle weakness later in life. Hyperkalemic periodic paralysis is characterized by a rise in potassium levels in the blood. Attacks often begin in infancy or early childhood and are precipitated by rest after exercise or by fasting. Attacks are usually shorter, more frequent, and less severe than the hypokalemic form. Muscle spasms are common.
Treatment of the periodic paralyses focuses on preventing further attacks and relieving acute symptoms. Avoiding carbohydrate-rich meals and strenuous exercise, and taking acetazolamide daily may prevent hypokalemic attacks. Attacks can be managed by drinking a potassium chloride oral solution. Eating carbohydrate-rich, low-potassium foods, and avoiding strenuous exercise and fasting, can help prevent hyperkalemic attacks. Dichorphenamide may prevent attacks.
A spinal cord injury usually begins with a sudden, traumatic blow to the spine that fractures or dislocates vertebrae. The damage begins at the moment of injury when displaced bone fragments, disc material, or ligaments bruise or tear into spinal cord tissue. Most injuries to the spinal cord don't completely sever it. Instead, an injury is more likely to cause fractures and compression of the vertebrae, which then crush and destroy axons -- extensions of nerve cells that carry signals up and down the spinal cord between the brain and the rest of the body. An injury to the spinal cord can damage a few, many, or almost all of these axons. Some injuries will allow almost complete recovery. Others will result in complete paralysis.
Improved emergency care for people with spinal cord injuries and aggressive treatment and rehabilitation can minimize damage to the nervous system and even restore limited abilities. Respiratory complications are often an indication of the severity of spinal cord injury About one-third of those with injury to the neck area will need help with breathing and require respiratory support. The steroid drug methylprednisolone appears to reduce the damage to nerve cells if it is given within the first 8 hours after injury. Rehabilitation programs combine physical therapies with skill-building activities and counseling to provide social and emotional support.Electrical simulation of nerves by neural prosthetic devices may restore specific functions, including bladder, breathing, cough, and arm or leg movements, though eligibility for use of these devices depends on the level and type of the spinal cord injury.
Spinal cord injuries are classified as either complete or incomplete. An incomplete injury means that the ability of the spinal cord to convey messages to or from the brain is not completely lost. People with incomplete injuries retain some motor or sensory function below the injury. A complete injury is indicated by a total lack of sensory and motor function below the level of injury. People who survive a spinal cord injury will most likely have medical complications such as chronic pain and bladder and bowel dysfunction, along with an increased susceptibility to respiratory and heart problems. Successful recovery depends upon how well these chronic conditions are handled day to day.
                
Surgery to relieve compression of the spinal tissue by surrounding bones broken or dislocated by the injury is often necessary, through timing of such surgery may vary widely. A recent prospective multicenter trial called STASCIS is exploring whether performing decompression surgery early (less than 24 hours following injury) can improve outcomes for patients with bone fragments or other tissues pressing on the spinal cord.