Timbrt/Liver-Text-OA huggingface dataset:
Question: What is (are) Generalized Gangliosidoses ?
Answer: The gangliosidoses are a group of inherited metabolic diseases caused by a deficiency of the different proteins needed to break down fatty substances called lipids. Excess buildup of these fatty materials (oils, waxes, steroids, and other compounds) can cause permanent damage in the cells and tissues in the brain and nervous systems, particularly in nerve cells. There are two distinct groups of the gangliosidoses, which affect males and females equally.
                
The GM1 gangliosidoses are caused by a deficiency of the enzyme beta-galactosidase. Signs of early infantile GM1 gangliodisosis (the most severe subtype, with onset shortly after birth) may include neurodegeneration, seizures, liver and spleen enlargement, coarsening of facial features, skeletal irregularities, joint stiffness, distended abdomen, muscle weakness, exaggerated startle response, and problems with gait. About half of affected persons develop cherry-red spots in the eye. Children may be deaf and blind by age 1.Onset of late infantile GM1 gangliosidosisis typically between ages 1 and 3 years. Signs include an inability to control movement, seizures, dementia, and difficulties with speech. Adult GM1 gangliosidosis strikes between ages 3 and 30, with symptoms that include the wasting away of muscles, cloudiness in the corneas, and dystonia (sustained moscle contractions that case twisting and repetitive movements or abnormal postures). Non-cancerous skin blemishes may develop on the lower part of the trunk of the body. Adult GM1 is usually less severe and progresses more slowly than other forms of the disorder.
                
The GM2 gangliosidoses include Tay-Sachs disease and its more severe form, called Sandhoff disease, both of whichresult from a deficiency of the enzyme beta-hexosaminidase. Symptoms begin by age 6 months and include progressive mental deterioration, cherry-red spots in the retina, marked startle reflex, and seizures. Children with Tay-Sachs may also have dementia, progressive loss of hearing, some paralysis, and difficulty in swallowing that may require a feeding tube. A rarer form of the disorder, which occurs in individuals in their twenties and early thirties, is characterized by an unsteady gait and progressive neurological deterioration. Additional signs of Sandhoff disease include weakness in nerve signaling that causes muscles to contract, early blindness, spasticity, muscle contractions, an abnormally enlarged head, and an enlarged liver and spleen.
Question: What is (are) Sjgren's Syndrome ?
Answer: Sjgren's syndrome is an autoimmune disorder in which immune cells attack and destroy the glands that produce tears and saliva. Sjgren's syndrome is also associated with rheumatic disorders such as rheumatoid arthritis. The hallmark symptoms of the disorder are dry mouth and dry eyes. In addition, Sjogren's syndrome may cause skin, nose, and vaginal dryness, and may affect other organs of the body including the kidneys, blood vessels, lungs, liver, pancreas, and brain.  Sjgren's syndrome affects 1-4 million people in the United States. Most people are more than 40 years old at the time of diagnosis. Women are 9 times more likely to have Sjgren's syndrome than men.
Question: What is (are) Mucopolysaccharidoses ?
Answer: The mucopolysaccharidoses are a group of inherited metabolic diseases in which a defective or missing enzyme causes large amounts of complex sugar molecules to accumulate in harmful amounts in the body's cells and tissues. This accumulation causes permanent, progressive cellular damage that affects appearance, physical abilities, organ and system functioning, and, in most cases, mental development.Depending on the type of mucopolysaccharidosis, affected individuals may have normal intellect or may be profoundly impaired, may experience developmental delay, or have severe behavioral problems. Physical symptoms generally include coarse or rough facial features, thick lips, an enlarged mouth and tongue, short stature with a disproportionately short trunk (dwarfism), abnormal bone size or shape (and other skeletal irregularities), thickened skin, enlarged organs such as the liver or spleen, hernias, and excessive body hair growth.
Question: What is (are) Zellweger Syndrome ?
Answer: Zellweger syndrome is one of a group of four related diseases called peroxisome biogenesis disorders (PBD). The diseases are caused by defects in any one of 13 genes, termed PEX genes, required for the normal formation and function of peroxisomes. The PBDs are divided into two groups: Zellweger spectrum disorders and Rhizomelic Chondrodysplasia Punctua spectrum. The Zellweger spectrum is comprised of three disorders that have considerable overlap of features. These include Zellweger syndrome (ZS, the most severe form), neonatal adrenoleukodystrophy (NALD), and Infantile Refsum disease (IRD, the least severe form).
                
Peroxisomes are cell structures that break down toxic substances and synthesize lipids (fatty acids. oils, and waxes) that are necessary for cell function. Peroxisomes are required for normal brain development and function and the formation of myelin, the whitish substance that coats nerve fibers. They are also required for normal eye, liver, kidney, and bone functions. Zellweger spectrum disorders result from dysfunctional lipid metabolism, including the over-accumulation of very long-chain fatty acids and phytanic acid, and defects of bile acids and plasmalogens--specialized lipids found in cell membranes and myelin sheaths of nerve fibers. Symptoms of these disorders include an enlarged liver; characteristic facial features such as a high forehead, underdeveloped eyebrow ridges, and wide-set eyes; and neurological abnormalities such as cognitive impairment and seizures. Infants will Zellweger syndrome also lack muscle tone, sometimes to the point of being unable to move, and may not be able to suck or swallow. Some babies will be born with glaucoma, retinal degeneration, and impaired hearing. Jaundice and gastrointestinal bleeding also may occur.
Question: What is the outlook for Zellweger Syndrome ?
Answer: The prognosis for infants with Zellweger syndrome is poor. Most infants do not survive past the first 6 months, and usually succumb to respiratory distress, gastrointestinal bleeding, or liver failure.
Question: What is (are) Acid Lipase Disease ?
Answer: Acid lipase disease or deficiency occurs when the enzyme needed to break down certain fats that are normally digested by the body is lacking or missing, resulting in the toxic buildup of these fats in the bodys cells and tissues. These fatty substances, called lipids, include fatty acids, oils, and cholesterol. Two rare lipid storage diseases are caused by the deficiency of the enzyme lysosomal acid lipase:
                
Wolmans disease (also known as acid lipase deficiency) is an autosomal recessive disorder marked by the buildup of cholesteryl esters (normally a tranport form of cholesterol that brings nutrients into the cells and carries out waste) and triglycerides (a chemical form in which fats exist in the body). Infants with the disorder appear normal at birth but quickly develop progressive mental deterioration, low muscle tone,enlarged liver and grossly enlarged spleen, gastrointestinal problems including an excessive amount of fats in the stools, jaundice, anemia, vomiting, and calcium deposits in the adrenal glands, which causes them to harden. Both male and female infants are affected by the disorder.
                
Cholesteryl ester storage disease (CESD) is an extremely rare disorder that results from storage of cholesteryl esters and triglycerides in cells in the blood and lymph and lymphoid tissue. Children develop an enlarged liver, leading to cirrhosis and chronic liver failure before adulthood. Children may also develop calcium deposits in the adrenal glands and jaundice. Onset varies, and the disorder may not be diagnosed until adulthood.
Question: How to diagnose Parasites - Baylisascaris infection ?
Answer: If you suspect you have been infected, consult your health care provider immediately. Be sure to tell your health care provider if you have recently been exposed to raccoons or their feces.
    
Diagnosis is difficult because symptoms depend on the number of infecting larvae and location in the body. Ocular larva migrans, when the larvae migrate to the eye, can cause sensitivity to light, inflammation of the eye, and blindness. Symptoms of visceral larva migrans, when the larvae travel to organs, depend on which organs are affected. For example, an invasion of the liver may cause hepatomegaly (inflammation and enlargement of the liver), while an invasion of the lung may cause pulmonary symptoms such as cough or chest pain. Larvae rarely end up in the nervous system but the most severe cases are neural larva migrans, when the larvae migrate into the brain and cause it to swell (encephalitis). There is no commercially available test for Baylisascaris infection. A health care provider may test blood, cerebrospinal fluid (CSF), and tissue to determine if an individual is infected. Eye examinations may reveal a migrating larva or lesions and are often the most significant clue to infection with Baylisascaris.
    
Diagnosis often is made by ruling out other infections that cause similar symptoms. Information on diagnosis and testing can be obtained through your local or state health department or CDC.
    
More on: Resources for Health Professionals: Diagnosis
Question: What is (are) Parasites - Leishmaniasis ?
Answer: Leishmaniasis is a parasitic disease that is found in parts of the tropics, subtropics, and southern Europe. Leishmaniasis is caused by infection with Leishmania parasites, which are spread by the bite of infected sand flies. There are several different forms of leishmaniasis in people. The most common forms are cutaneous leishmaniasis, which causes skin sores, and visceral leishmaniasis, which affects several internal organs (usually spleen, liver, and bone marrow).
Question: What are the symptoms of Crimean-Congo Hemorrhagic Fever (CCHF) ?
Answer: The onset of CCHF is sudden, with initial signs and symptoms including headache, high fever, back pain, joint pain, stomach pain, and vomiting. Red eyes, a flushed face, a red throat, and petechiae (red spots) on the palate are common. Symptoms may also include jaundice, and in severe cases, changes in mood and sensory perception. 
                
As the illness progresses, large areas of severe bruising, severe nosebleeds, and uncontrolled bleeding at injection sites can be seen, beginning on about the fourth day of illness and lasting for about two weeks. In documented outbreaks of CCHF, fatality rates in hospitalized patients have ranged from 9% to as high as 50%. 
                
The long-term effects of CCHF infection have not been studied well enough in survivors to determine whether or not specific complications exist. However, recovery is slow.
Question: What are the symptoms of Lujo Hemorrhagic Fever (LUHF) ?
Answer: The symptoms of Lujo hemorrhagic fever, as described in the five patients in the original cluster outbreak, resemble those of severe Lassa Fever. After an incubation period of 7 to 13 days, the clinical course started by a non-specific febrile illness accompanied by headache and muscle pain. 
                
The disease increases in severity, with: 
 
 - a morbilliform rash of the face and trunk 
 - face and neck swelling 
 - pharyngitis (sore throat) 
 - diarrhea 
 
                
Bleeding was not a prominent feature during the illness. 
                
In the fatal cases (4/5 patients), a transient improvement was followed by: 
 
 - rapid deterioration with respiratory distress 
 - neurological signs and circulatory collapse 
 
                
Death occurred 10 to 13 days after onset. 
                
Low blood platelets, low white blood cell count (at the onset, rising later on) and elevated liver function values were present in all patients. 
                
Since Arenaviruses may enter the fetus through infection of the mother, and anectodal evidence suggests that infected pregnant women may suffer miscarriages, it is reasonable to assume that both infection of the fetus and miscarriage may be associated with Lujo infection in the mother.
Question: How to diagnose Lujo Hemorrhagic Fever (LUHF) ?
Answer: During the acute febrile phase, Lujo virus was isolated from blood from days 2 to 13 after onset. Virus was also isolated from liver tissue obtained post-mortem. A subsequent complete genomic analysis of Lujo virus facilitated the development of specific molecular detection (RT-PCR) assays. 
   
Serologic diagnosis of Lujo hemorrhagic fever can be made by indirect immunofluorescent assay and ELISA. However, individuals from endemic areas displaying fever, rash, pharyngitis, accompanied by laboratory findings of low platelet counts and elevated liver enzymes, should be suspected of having a hemorrhagic fever virus infection. Clinical specimens should be tested using specific assays.
Question: Who is at risk for Parasites - Toxocariasis (also known as Roundworm Infection)? ?
Answer: Infected dogs and cats shed Toxocara eggs in their feces into the environment. Once in the environment, it takes 2 to 4 weeks for Toxocara larvae to develop and for the eggs to become infectious. Humans or other animals can be infected by accidentally ingesting Toxocara eggs. For example, humans can become infected if they work with dirt and accidentally ingest dirt containing Toxocara eggs. Although rare, people can be infected by eating undercooked or raw meat from an infected animal such as a lamb or rabbit. Because dogs and cats are frequently found where people live, there may be large numbers of infected eggs in the environment. Once in the body, the Toxocara eggs hatch and roundworm larvae can travel in the bloodstream to different parts of the body, including the liver, heart, lungs, brain, muscles, or eyes. Most infected people do not have any symptoms. However, in some people, the Toxocara larvae can cause damage to these tissues and organs. The symptoms of toxocariasis, the disease caused by these migrating larvae, include fever, coughing, inflammation of the liver, or eye problems.
    
A U.S. study in 1996 showed that 30% of dogs younger than 6 months deposit Toxocara eggs in their feces; other studies have shown that almost all puppies are born already infected with Toxocara canis. Research also suggests that 25% of all cats are infected with Toxocara cati. Infection rates are higher for dogs and cats that are left outside for more time and allowed to eat other animals. In humans, it has been found that almost 14% of the U.S. population has been infected with Toxocara. Globally, toxocariasis is found in many countries, and prevalence rates can reach as high as 40% or more in parts of the world. There are several factors that have been associated with higher rates of infection with Toxocara. People are more likely to be infected with Toxocara if they own a dog. Children and adolescents under the age of 20 are more likely to test positive for Toxocara infection. This may be because children are more likely to eat dirt and play in outdoor environments, such as sandboxes, where dog and cat feces can be found. This infection is more common in people living in poverty. Geographic location plays a role as well, because Toxocara is more prevalent in hot, humid regions where eggs are kept viable in the soil.
Question: What are the symptoms of Marburg hemorrhagic fever (Marburg HF) ?
Answer: After an incubation period of 5-10 days, symptom onset is sudden and marked by fever, chills, headache, and myalgia. Around the fifth day after the onset of symptoms, a maculopapular rash, most prominent on the trunk (chest, back, stomach), may occur. Nausea, vomiting, chest pain, a sore throat, abdominal pain, and diarrhea may then appear. Symptoms become increasingly severe and can include jaundice, inflammation of the pancreas, severe weight loss, delirium, shock, liver failure, massive hemorrhaging, and multi-organ dysfunction. 
 
Because many of the signs and symptoms of Marburg hemorrhagic fever are similar to those of other infectious diseases such as malaria or typhoid fever, clinical diagnosis of the disease can be difficult, especially if only a single case is involved. 
 
The case-fatality rate for Marburg hemorrhagic fever is between 23-90%. For a complete listing of the case fatality rates for previous outbreaks, please see the History of Outbreaks table
Question: What are the symptoms of Alkhurma Hemorrhagic Fever (AHF) ?
Answer: Based on limited information, after an incubation period that could be as short as 2-4 days, the disease presents initially with non-specific flu-like symptoms, including fever, anorexia (loss of appetite), general malaise, diarrhea, and vomiting; a second phase has appeared in some patients, and includes neurologic and hemorrhagic symptoms in severe form. Multi-organ failure precedes fatal outcomes. No repeated or chronic symptoms have been reported following recovery. Evidence suggests that a milder form may exist, where hospitalization is not required. 
                
Thrombocytopenia, leukopenia, and elevated liver enzymes are nearly always observed in patients who have been hospitalized.
Question: what diseases are vaccine preventable
Answer: List of Vaccine-Preventable Diseases The following links will lead you to the main page that describes both the disease and the vaccine(s). Vaccines are available for all of the following vaccine-preventable diseases (unless otherwise noted): Anthrax Cervical Cancer (Human Papillomavirus) Diphtheria Hepatitis A Hepatitis B Haemophilus influenzae type b (Hib) Human Papillomavirus (HPV) Influenza (Flu) Japanese encephalitis (JE) Measles Meningococcal Mumps Pertussis Pneumococcal Polio Rabies Rotavirus Rubella Shingles (Herpes Zoster) Smallpox Tetanus Typhoid Tuberculosis (TB) Varicella (Chickenpox) Yellow Fever Related Pages For Parents: What You Need to Know List of Vaccines Used in U.S. Photos of diseases Top of Page   Images and logos on this website which are trademarked/copyrighted or used with permission of the trademark/copyright or logo holder are not in the public domain. These images and logos have been licensed for or used with permission in the materials provided on this website. The materials in the form presented on this website may be used without seeking further permission. Any other use of trademarked/copyrighted images or logos requires permission from the trademark/copyright holder...more This graphic notice means that you are leaving an HHS Web site. For more information, please see the Exit Notification and Disclaimer policy.
Question: Who is at risk for Acanthamoeba - Granulomatous Amebic Encephalitis (GAE); Keratitis? ?
Answer: Acanthamoeba keratitis
  
   
Acanthamoeba keratitis is a rare disease that can affect anyone, but is most common in individuals who wear contact lenses. In the United States, an estimated 85% of cases occur in contact lens users. The incidence of the disease in developed countries is approximately one to 33 cases per million contact lens wearers.
   
For people who wear contact lenses, certain practices can increase the risk of getting Acanthamoeba keratitis:
   
    - Storing and handling lenses improperly
    - Disinfecting lenses improperly (such as using tap water or topping off solutions when cleaning the lenses or lens case)
    - Swimming, using a hot tub, or showering while wearing lenses
    - Coming into contact with contaminated water
    - Having a history of trauma to the cornea
   
   
Contact lens wearers who practice proper lens care and non-contact lens wearers can still develop the infection. For additional information on contact lens care and prevention of Acanthamoeba keratitis visit CDC’s web page on Prevention and Control.
   
There have been no reports of Acanthamoeba keratitis being spread from one person to another.
   Granulomatous Amebic Encephalitis (GAE)
   
Granulomatous Amebic Encephalitis (GAE) and disseminated infection are very rare forms of Acanthamoeba infection and primarily affect people with compromised immune systems. While unusual, disseminated infection can also affect healthy children and adults. Conditions that may increase a patient’s risk for GAE and disseminated infection include:
   
    - AIDS
    - Organ/Tissue transplant
    - Steroids or excessive use of antibiotics
    - Diabetes Mellitus
    - Cancer
    - Disorders in which white blood cells in the lymphatic tissue are over-produced or abnormal
    - Disorders in which blood cells or blood clotting mechanisms do not function properly or are abnormal
    - Liver cirrhosis
    - Lupus
Question: How to diagnose Lymphocytic Choriomeningitis (LCM) ?
Answer: During the first phase of the disease, the most common laboratory abnormalities are a low white blood cell count (leukopenia) and a low platelet count (thrombocytopenia). Liver enzymes in the serum may also be mildly elevated. After the onset of neurological disease during the second phase, an increase in protein levels, an increase in the number of white blood cells or a decrease in the glucose levels in the cerebrospinal fluid (CSF) is usually found. 
   
Laboratory diagnosis is usually made by detecting IgM and IgG antibodies in the CSF and serum. Virus can be detected by PCR or virus isolation in the CSF at during the acute stage of illness.
Question: What is (are) Parasites - Echinococcosis ?
Answer: Frequently Asked Questions (FAQs)
    
Cystic echinococcosis (CE) disease results from being infected with the larval stage of Echinococcus granulosus, a tiny tapeworm (~2-7 millimeters in length) found in dogs (definitive host), sheep, cattle, goats, foxes, and pigs, amongst others (intermediate hosts). Most infections in humans are asymptomatic, but CE, also known as hydatid disease, causes slowly enlarging masses, most commonly in the liver and the lungs. Treatment can involve both medication and surgery.
    
More on: Cystic Echinococcosis (CE) FAQs
    
Alveolar echinococcosis (AE) disease results from being infected with the larval stage of Echinococcus multilocularis, a tiny tapeworm (~1-4 millimeters in length) found in foxes, coyotes, dogs, and cats (definitive hosts). Although human cases are rare, infection in humans causes parasitic tumors to form in the liver, and, less commonly, the lungs, brain, and other organs. If left untreated, infection with AE can be fatal.
    
More on: Alveolar Echinococcosis (AE) FAQs