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Incubation period is usually two to three weeks. The most common manifestation is flu-like symptoms with abrupt onset of fever, malaise, profuse perspiration, severe headache, muscle pain, joint pain, loss of appetite, upper respiratory problems, dry cough, pleuritic pain, chills, confusion, and gastrointestinal symptoms, such as nausea, vomiting, and diarrhea. About half of infected individuals exhibit no symptoms.
During its course, the disease can progress to an atypical pneumonia, which can result in a life-threatening acute respiratory distress syndrome, whereby such symptoms usually occur during the first four to five days of infection.
Less often, Q fever causes (granulomatous) hepatitis, which may be asymptomatic or becomes symptomatic with malaise, fever, liver enlargement, and pain in the right upper quadrant of the abdomen. Whereas transaminase values are often elevated, jaundice is uncommon. Retinal vasculitis is a rare manifestation of Q fever.
The chronic form of Q fever is virtually identical to inflammation of the inner lining of the heart (endocarditis), which can occur months or decades following the infection. It is usually fatal if untreated. However, with appropriate treatment, the mortality falls to around 10%.
Lábrea fever has a sudden onset, with jaundice (yellowing of the skin), anorexia (lack of appetite), hematemesis (vomiting of blood), headache, fever and severe prostration. Death occurs by acute liver failure (ALF). In the last phase, neurological symptoms such as agitation, delirium, convulsions and hemorrhagic coma commonly appear.
Q fever is a disease caused by infection with "Coxiella burnetii", a bacterium that affects humans and other animals. This organism is uncommon, but may be found in cattle, sheep, goats, and other domestic mammals, including cats and dogs. The infection results from inhalation of a spore-like small-cell variant, and from contact with the milk, urine, feces, vaginal mucus, or semen of infected animals. Rarely, the disease is tick-borne. The incubation period is 9–40 days. Humans are vulnerable to Q fever, and infection can result from even a few organisms. The bacterium is an obligate intracellular pathogenic parasite.
Lábrea fever, also known as Lábrea's black fever and Lábrea hepatitis, is a lethal tropical viral infection discovered in the 1950s in the city of Lábrea, in the Brazilian Amazon basin, where it occurs mostly in the area south of the Amazon River, in the states of Acre, Amazonas and Rondônia
. The disease has also been diagnosed in Colombia and Peru. The similar form in Colombia has been named Santa Marta fever.
Its main manifestation is a fulminant hepatitis which may kill in less than a week, and which characteristically affects children and young adults, and more males than females. It is accompanied also by an encephalitis in many cases. The disease is highly lethal: in a study carried out in 1986 at Boca do Acre, also in the Amazon, 39 patients out of 44 died in the acute phase of the disease. Survivors may develop chronic disease.
Early symptoms of hepatitis A infection can be mistaken for influenza, but some sufferers, especially children, exhibit no symptoms at all. Symptoms typically appear 2 to 6 weeks (the incubation period) after the initial infection. About 90% of children do not have symptoms. The time between infection and symptoms, in those who develop them, is between 2 and 6 weeks with an average of 28 days.
The risk for symptomatic infection is directly related to age, with more than 80% of adults having symptoms compatible with acute viral hepatitis and the majority of children having either asymptomatic or unrecognized infections.
Symptoms usually last less than 2 months, although some people can be ill for as long as 6 months:
- Fatigue
- Fever
- Nausea
- Appetite loss
- Jaundice, a yellowing of the skin or the whites of the eyes owing to hyperbilirubinemia
- Bile is removed from the bloodstream and excreted in the urine, giving it a dark amber colour
- Diarrhea
- Light, or clay-coloured faeces (acholic faeces)
- Abdominal discomfort
There is a rapid onset of clinical signs over the period of 2–7 days, beginning with anorexia, lethargy, and hyperbilirubinemia (icterus and discolored urine). Signs of hepatic encephalopathy (ataxia, blindness, aggression, and coma) and fever can also occur. Other signs include photodermatitis, hemorrhagic diathesis, dependent edema, and colic. The reason for colic is unknown, but is thought to be due to rapid decrease in the size of the liver, and the increased risk of gastric impaction. Rarely, weight loss can occur.
The incubation period of hepatitis E varies from 3 to 8 weeks. After a short prodromal phase symptoms lasting from days to weeks follow. They may include jaundice, fatigue, and nausea. The symptomatic phase coincides with elevated hepatic aminotransferase levels.
Viral RNA becomes detectable in stool and blood serum during incubation period. Serum IgM and IgG antibodies against HEV appear just before onset of clinical symptoms. Recovery leads to virus clearance from the blood, while the virus may persist in stool for much longer. Recovery is also marked by disappearance of IgM antibodies and increase of levels of IgG antibodies.
While usually an acute disease, in immunocompromised subjects—particularly in solid organ transplant patients—hepatitis E may cause a chronic infection. Occasionally this may cause liver fibrosis and cirrhosis.
Theiler's disease, also known as idiopathic acute hepatitis disease (IAHD), serum-associated hepatitis, serum sickness, and postvaccinal hepatitis, is a viral hepatitis that affects horses. It is one of the most common cause of acute hepatitis and liver failure in the horse.
Hepatitis A is an infectious disease of the liver caused by the hepatitis A virus (HAV). Many cases have few or no symptoms, especially in the young. The time between infection and symptoms, in those who develop them, is between two and six weeks. When symptoms occur, they typically last eight weeks and may include nausea, vomiting, diarrhea, jaundice, fever, and abdominal pain. Around 10–15% of people experience a recurrence of symptoms during the six months after the initial infection. Acute liver failure may rarely occur, with this being more common in the elderly.
It is usually spread by eating food or drinking water contaminated with infected feces. Shellfish which have not been sufficiently cooked are a relatively common source. It may also be spread through close contact with an infectious person. While children often do not have symptoms when infected, they are still able to infect others. After a single infection, a person is immune for the rest of his or her life. Diagnosis requires blood testing, as the symptoms are similar to those of a number of other diseases. It is one of five known hepatitis viruses: A, B, C, D, and E.
The hepatitis A vaccine is effective for prevention. Some countries recommend it routinely for children and those at higher risk who have not previously been vaccinated. It appears to be effective for life. Other preventive measures include hand washing and properly cooking food. No specific treatment is available, with rest and medications for nausea or diarrhea recommended on an as-needed basis. Infections usually resolve completely and without ongoing liver disease. Treatment of acute liver failure, if it occurs, is with liver transplantation.
Globally, around 1.4 million symptomatic cases occur each year and about 114 million infections (symptomatic and asymptomatic). It is more common in regions of the world with poor sanitation and not enough safe water. In the developing world, about 90% of children have been infected by age 10, thus are immune by adulthood. It often occurs in outbreaks in moderately developed countries where children are not exposed when young and vaccination is not widespread. Acute hepatitis A resulted in 11,200 deaths in 2015. World Hepatitis Day occurs each year on July 28 to bring awareness to viral hepatitis.
Viral cardiomyopathy occurs when viral infections cause myocarditis with a resulting thickening of the myocardium and dilation of the ventricles. These viruses include Coxsackie B and adenovirus, echoviruses, influenza H1N1, Epstein-Barr virus, rubella (German measles virus), varicella (chickenpox virus), mumps, measles, parvoviruses, yellow fever, dengue fever, polio, rabies and the viruses that cause hepatitis A and C.
A "vaccine-preventable disease" is an infectious disease for which an effective preventive vaccine exists. If a person acquires a vaccine-preventable disease and dies from it, the death is considered a vaccine-preventable death.
The most common and serious vaccine-preventable diseases tracked by the World Health Organization (WHO) are: diphtheria, "Haemophilus influenzae" serotype b infection, hepatitis B, measles, meningitis, mumps, pertussis, poliomyelitis, rubella, tetanus, tuberculosis, and yellow fever. The WHO reports licensed vaccines being available to prevent, or contribute to the prevention and control of, 25 vaccine-preventable infections.
Acute infection with virus is associated with acute viral hepatitis, an illness that begins with general ill-health, loss of appetite, nausea, vomiting, body aches, mild fever, and dark urine, and then progresses to development of jaundice. It has been noted that itchy skin has been an indication as a possible symptom of all hepatitis virus types. The illness lasts for a few weeks and then gradually improves in most affected people. A few people may have a more severe form of liver disease known as (fulminant hepatic failure) and may die as a result. The infection may be entirely asymptomatic and may go unrecognized.
Chronic infection with virus either may be asymptomatic or may be associated with a chronic inflammation of the liver (chronic hepatitis), leading to cirrhosis over a period of several years. This type of infection dramatically increases the incidence of hepatocellular carcinoma (HCC; liver cancer). Across Europe, hepatitis B and C cause approximately 50% of hepatocellular carcinomas. Chronic carriers are encouraged to avoid consuming alcohol as it increases their risk for cirrhosis and liver cancer. virus has been linked to the development of membranous glomerulonephritis (MGN).
Symptoms outside of the liver are present in 1–10% of HBV-infected people and include serum-sickness–like syndrome, acute necrotizing vasculitis (polyarteritis nodosa), membranous glomerulonephritis, and papular acrodermatitis of childhood (Gianotti–Crosti syndrome). The serum-sickness–like syndrome occurs in the setting of acute , often preceding the onset of jaundice. The clinical features are fever, skin rash, and polyarteritis. The symptoms often subside shortly after the onset of jaundice but can persist throughout the duration of acute . About 30–50% of people with acute necrotizing vasculitis (polyarteritis nodosa) are HBV carriers. HBV-associated nephropathy has been described in adults but is more common in children. Membranous glomerulonephritis is the most common form. Other immune-mediated hematological disorders, such as essential mixed cryoglobulinemia and aplastic anemia have been described as part of the extrahepatic manifestations of HBV infection, but their association is not as well-defined; therefore, they probably should not be considered etiologically linked to HBV.
Affected turkeys may show systemic signs such as anorexia, lethargy and death. Hepatic encephalopathy occurs secondary to liver involvement.
Egg hatching and production can be affected.
Diagnosis relies on isolation of the virus from samples of internal organs or the faeces inoculated into embryonated chicken eggs.
The main necropsy findings are multiple necrotic lesions on the liver and sometimes the spleen.
infection causes acute symptoms in 15% of cases. Symptoms are generally mild and vague, including a decreased appetite, fatigue, nausea, muscle or joint pains, and weight loss and rarely does acute liver failure result. Most cases of acute infection are not associated with jaundice. The infection resolves spontaneously in 10–50% of cases, which occurs more frequently in individuals who are young and female.
The aetiological agent of turkey viral hepatitis is a virus from the Picornaviridae family.
The disease is restricted to turkeys and is highly contagious but usually subclinical. It usually present in young birds under the age of 6 weeks.
It has been seen in Canada, Italy, the US and the UK.
Transmission is thought to be via the faeces and vertical transmission may also occur.
Hepatitis D (hepatitis delta) is a disease caused by the "hepatitis D virus" ("HDV"), a small spherical enveloped virusoid. This is one of five known hepatitis viruses: A, B, C, D, and E. HDV is considered to be a subviral satellite because it can propagate only in the presence of the hepatitis B virus (HBV). Transmission of HDV can occur either via simultaneous infection with HBV (coinfection) or superimposed on chronic hepatitis B or hepatitis B carrier state (superinfection).
Both superinfection and coinfection with HDV results in more severe complications compared to infection with HBV alone. These complications include a greater likelihood of experiencing liver failure in acute infections and a rapid progression to liver cirrhosis, with an increased risk of developing liver cancer in chronic infections. In combination with hepatitis B virus, hepatitis D has the highest fatality rate of all the hepatitis infections, at 20%.
Hepatitis B is an infectious disease caused by the hepatitis B virus (HBV) that affects the liver. It can cause both acute and chronic infections. Many people have no symptoms during the initial infection. Some develop a rapid onset of sickness with vomiting, yellowish skin, tiredness, dark urine and abdominal pain. Often these symptoms last a few weeks and rarely does the initial infection result in death. It may take 30 to 180 days for symptoms to begin. In those who get infected around the time of birth 90% develop chronic while less than 10% of those infected after the age of five do. Most of those with chronic disease have no symptoms; however, cirrhosis and liver cancer may eventually develop. These complications result in the death of 15 to 25% of those with chronic disease.
The virus is transmitted by exposure to infectious blood or body fluids. Infection around the time of birth or from contact with other people's blood during childhood is the most frequent method by which hepatitis B is acquired in areas where the disease is common. In areas where the disease is rare, intravenous drug use and sexual intercourse are the most frequent routes of infection. Other risk factors include working in healthcare, blood transfusions, dialysis, living with an infected person, travel in countries where the infection rate is high, and living in an institution. Tattooing and acupuncture led to a significant number of cases in the 1980s; however, this has become less common with improved sterility. The viruses cannot be spread by holding hands, sharing eating utensils, kissing, hugging, coughing, sneezing, or breastfeeding. The infection can be diagnosed 30 to 60 days after exposure. The diagnosis is usually confirmed by testing the blood for parts of the virus and for antibodies against the virus. It is one of five known hepatitis viruses: A, B, C, D, and E.
The infection has been preventable by vaccination since 1982. Vaccination is recommended by the World Health Organization in the first day of life if possible. Two or three more doses are required at a later time for full effect. This vaccine works about 95% of the time. About 180 countries gave the vaccine as part of national programs as of 2006. It is also recommended that all blood be tested for hepatitis B before transfusion and condoms be used to prevent infection. During an initial infection, care is based on the symptoms that a person has. In those who develop chronic disease, antiviral medication such as tenofovir or interferon may be useful; however, these drugs are expensive. Liver transplantation is sometimes used for cirrhosis.
About a third of the world population has been infected at one point in their lives, including 343 million who have chronic infections. Another 129 million new infections occurred in 2013. Over 750,000 people die of hepatitis B each year. About 300,000 of these are due to liver cancer. The disease is now only common in East Asia and sub-Saharan Africa where between 5 and 10% of adults are chronically infected. Rates in Europe and North America are less than 1%. It was originally known as "serum hepatitis". Research is looking to create foods that contain HBV vaccine. The disease may affect other great apes as well.
Acute viral hepatitis follows a pattern of infection that involves three distinct phases:
1. The initial prodromal phase (preceding symptoms) involves non-specific and flu-like symptoms common to many acute viral infections. These include fatigue, nausea, vomiting, poor appetite, joint pain, and headaches. Fever, when present, is most common in cases of hepatitis A and E. Late in this phase, people can experience liver-specific symptoms, including choluria (dark urine) and clay-colored stools.
2. Yellowing of the skin and whites of the eyes follow the prodrome after about 1–2 weeks and can last for up to 4 weeks. The non-specific symptoms seen in the prodromal typically resolve by this time, but people will develop an enlarged liver and right upper abdominal pain or discomfort. 10–20% of people will also experience an enlarged spleen, while some people will also experience a mild unintentional weight loss.
3. The recovery phase is characterized by resolution of the clinical symptoms of hepatitis with persistent elevations in liver lab values and potentially a persistently enlarged liver. All cases of hepatitis A and E are expected to fully resolve after 1–2 months. Most hepatitis B cases are also self-limiting and will resolve in 3–4 months. Few cases of hepatitis C will resolve completely.
Both drug-induced hepatitis and autoimmune hepatitis can present very similarly to acute viral hepatitis, with slight variations in symptoms depending on the cause. Cases of drug-induced hepatitis can manifest with systemic signs of an allergic reaction including rash, fever, serositis (inflammation of membranes lining certain organs), elevated eosinophils (a type of white blood cell), and suppression of bone marrow activity.
Fulminant hepatitis, or massive hepatic cell death, is a rare and life-threatening complication of acute hepatitis that can occur in cases of hepatitis B, D, and E, in addition to drug-induced and autoimmune hepatitis. The complication more frequently occurs in instances of hepatitis B and D co-infection at a rate of 2–20% and in pregnant women with hepatitis E at rate of 15–20% of cases. In addition to the signs of acute hepatitis, people can also demonstrate signs of coagulopathy (abnormal coagulation studies with easy bruising and bleeding) and encephalopathy (confusion, disorientation, and sleepiness). Mortality due to fulminant hepatitis is typically the result of various complications including cerebral edema, gastrointestinal bleeding, sepsis, respiratory failure, or kidney failure.
Viral hepatitis is liver inflammation due to a viral infection. It may present in acute (recent infection, relatively rapid onset) or chronic forms.
The most common causes of viral hepatitis are the five unrelated hepatotropic viruses hepatitis A, hepatitis B, hepatitis C, hepatitis D, and hepatitis E. In addition to the nominal hepatitis viruses, other viruses that can also cause liver inflammation include cytomegalovirus, Epstein–Barr virus, and yellow fever. Up to 1997 there has been also 52 cases of viral hepatitis caused by herpes simplex virus.
There is the opportunity to prevent or treat the most common types. Hepatitis A and hepatitis B can be prevented by vaccination. Effective treatments for hepatitis C are available but expensive.
In 2013 about 1.5 million people died from viral hepatitis. Most deaths are due to hepatitis B and hepatitis C. East Asia is the region of the world most affected.
About 80% of those exposed to the virus develop a chronic infection. This is defined as the presence of detectable viral replication for at least six months. Most experience minimal or no symptoms during the initial few decades of the infection. Chronic can be associated with fatigue and mild cognitive problems. Chronic infection after several years may cause cirrhosis or liver cancer. The liver enzymes are normal in 7–53%. Late relapses after apparent cure have been reported, but these can be difficult to distinguish from reinfection.
Fatty changes to the liver occur in about half of those infected and are usually present before cirrhosis develops. Usually (80% of the time) this change affects less than a third of the liver. Worldwide hepatitis C is the cause of 27% of cirrhosis cases and 25% of hepatocellular carcinoma. About 10–30% of those infected develop cirrhosis over 30 years. Cirrhosis is more common in those also infected with hepatitis B, schistosoma, or HIV, in alcoholics and in those of male gender. In those with hepatitis C, excess alcohol increases the risk of developing cirrhosis 100-fold. Those who develop cirrhosis have a 20-fold greater risk of hepatocellular carcinoma. This transformation occurs at a rate of 1–3% per year. Being infected with hepatitis B in addition to hepatitis C increases this risk further.
Liver cirrhosis may lead to portal hypertension, ascites (accumulation of fluid in the abdomen), easy bruising or bleeding, varices (enlarged veins, especially in the stomach and esophagus), jaundice, and a syndrome of cognitive impairment known as hepatic encephalopathy. Ascites occurs at some stage in more than half of those who have a chronic infection.
Sodoku (鼠毒) is a bacterial zoonotic disease. It is caused by the Gram-negative rod "Spirillum minus" (also known as "Spirillium minor"). It is a form of rat-bite fever (RBF).
The initial scratch or wound caused by a bite from a carrier rodent results in mild inflammatory reactions and ulcerations. The wounds may heal initially, but reappear with the onset of symptoms. The symptoms include recurring fever, with body temperature 101–104°F (38–40°C). The fever lasts for 2–4 days, but recurs generally at 4–8 weeks. This cycle may continue for months or years. The other symptoms include regional lymphadenitis, malaise, and headache. The complications include myocarditis, endocarditis, hepatitis, splenomegaly, and meningitis.
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.