Hepatitis A can be prevented by vaccination, good hygiene, and sanitation.

It is believed that only 5–50% of those infected in the United States and Canada are aware of their status. Testing is recommended for those at high risk, which includes injection drug users, those who have received blood transfusions before 1992, those who have been in jail, those on long term hemodialysis, and those with tattoos. Screening is also recommended in those with elevated liver enzymes, as this is frequently the only sign of chronic hepatitis. Routine screening is not currently recommended in the United States. In 2012, the U.S. Centers for Disease Control and Prevention (CDC) added a recommendation for a single screening test for those born between 1945 and 1965.

At present this can only be made definitively by liver biopsy or post mortem examination. Given the isolation of a causative virus it should soon be possible to diagnose this by serology, polymerase chain reaction or viral culture. On necropsy, the liver will be small, flaccid, and "dish-rag" in appearance. It has a mottled and bile stained surface. On microscopy there is marked centrilobular to midzonal hepatocellular necrosis and a mild to moderate mononuclear infiltrate. Mild to moderate bile duct proliferation may also be present. On radiology, the liver may be shrunken and difficult to visualize on ultrasound. Ascites may be present.

Blood for blood transfusion is screened for many bloodborne diseases. Additionally, a technique that uses a combination of riboflavin and UV light to inhibit the replication of these pathogens by altering their nucleic acids can be used to treat blood components prior to their transfusion, and can reduce the risk of disease transmission.

A technology using the synthetic psoralen, amotosalen HCl, and UVA light (320–400 nm) has been implemented in European blood centers for the treatment of platelet and plasma components to prevent transmission of bloodborne diseases caused by bacteria, viruses and protozoa.

The CDC recommends the hepatitis A vaccine for all children beginning at age one, as well as for those who have not been previously immunized and are at high risk for contracting the disease.

For children 12 months of age or older, the vaccination is given as a shot into the muscle in two doses 6–18 months apart and should be started before the age 24 months. The dosing is slightly different for adults depending on the type of the vaccine. If the vaccine is for hepatitis A only, two doses are given 6–18 months apart depending on the manufacturer. If the vaccine is combined hepatitis A and hepatitis B, up to 4 doses may be required.

The most characteristic feature are elevated levels of gamma glutamyl transferase (100–300 IU/L), aspartate transaminase (>1000 IU/L) and sorbitol dehydrogenase, with AST levels > 4000 IU/L indicating a poor prognosis. High levels of unconjugated and total bilirubin, and serum bile acids, can be seen. Moderate to severe acidosis, leukocytosis, polycythaemia, increased creatine kinase and hyperammonemia may be present, and hemolysis can occur at the end stage. The prothrombin time (PT) and partial thromboplastin time (PTT) is often prolonged. Subclinical horses may only show elevated liver enzymes without any other clinical signs. Horses are rarely hypoglycemic, but blood glucose monitoring is ideal to indicate which horses may be benefited by glucose treatment.

Although HAV is excreted in the feces towards the end of the incubation period, specific diagnosis is made by the detection of HAV-specific IgM antibodies in the blood. IgM antibody is only present in the blood following an acute hepatitis A infection. It is detectable from 1-2 weeks after the initial infection and persists for up to 14 weeks. The presence of IgG antibodies in the blood means the acute stage of the illness has passed and the person is immune to further infection. IgG antibodies to HAV are also found in the blood following vaccination, and tests for immunity to the virus are based on the detection of this antibody.

During the acute stage of the infection, the liver enzyme alanine transferase (ALT) is present in the blood at levels much higher than is normal. The enzyme comes from the liver cells damaged by the virus.

Hepatovirus A is present in the blood (viremia) and feces of infected people up to 2 weeks before clinical illness develops.

The CDC recommends the routine vaccination of all children under the age of 19 with the hepatitis B vaccine. They also recommend it for those who desire it or are at high risk.

Routine vaccination for hepatitis B starts with the first dose administered as a shot into the muscle before the newborn is discharged from the hospital. An additional two doses should be administered before the child is 18 months.

For babies born to a mother with hepatitis B surface antigen positivity, the first dose is unique – in addition to the vaccine, the hepatitis immune globulin should also be administered, both within 12 hours of birth. These newborns should also be regularly tested for infection for at least the first year of life.

There is also a combination formulation that includes both hepatitis A and B vaccines.

There are a number of diagnostic tests for , including HCV antibody enzyme immunoassay or ELISA, recombinant immunoblot assay, and quantitative HCV RNA polymerase chain reaction (PCR). HCV RNA can be detected by PCR typically one to two weeks after infection, while antibodies can take substantially longer to form and thus be detected.

Chronic is defined as infection with the virus persisting for more than six months based on the presence of its RNA. Chronic infections are typically asymptomatic during the first few decades, and thus are most commonly discovered following the investigation of elevated liver enzyme levels or during a routine screening of high-risk individuals. Testing is not able to distinguish between acute and chronic infections. Diagnosis in the infant is difficult as maternal antibodies may persist for up to 18 months.

As in humans, the sensitivity of testing methods for rodents contributes to the accuracy of diagnosis. LCMV is typically identified through serology. However, in an endemically infected colony, more practical methods include MAP (mouse antibody production) and PCR testing. Another means of diagnosis is introducing a known naïve adult mouse to the suspect rodent colony. The introduced mouse will seroconvert, allowing use of immunofluorescence antibody (IFA), MFIA or ELISA to detect antibodies.

A number of different tests are available to determine the degree of cirrhosis present. Transient elastography (FibroScan) is the test of choice, but it is expensive. Aspartate aminotransferase to platelet ratio index may be used when cost is an issue.

The tests, called assays, for detection of virus infection involve serum or blood tests that detect either viral antigens (proteins produced by the virus) or antibodies produced by the host. Interpretation of these assays is complex.

The surface antigen (HBsAg) is most frequently used to screen for the presence of this infection. It is the first detectable viral antigen to appear during infection. However, early in an infection, this antigen may not be present and it may be undetectable later in the infection as it is being cleared by the host. The infectious virion contains an inner "core particle" enclosing viral genome. The icosahedral core particle is made of 180 or 240 copies of the core protein, alternatively known as core antigen, or HBcAg. During this 'window' in which the host remains infected but is successfully clearing the virus, IgM antibodies specific to the core antigen ("anti-HBc IgM") may be the only serological evidence of disease. Therefore, most diagnostic panels contain HBsAg and total anti-HBc (both IgM and IgG).

Shortly after the appearance of the HBsAg, another antigen called e antigen (HBeAg) will appear. Traditionally, the presence of HBeAg in a host's serum is associated with much higher rates of viral replication and enhanced infectivity; however, variants of the virus do not produce the 'e' antigen, so this rule does not always hold true. During the natural course of an infection, the HBeAg may be cleared, and antibodies to the 'e' antigen ("anti-HBe") will arise immediately afterwards. This conversion is usually associated with a dramatic decline in viral replication.

If the host is able to clear the infection, eventually the HBsAg will become undetectable and will be followed by IgG antibodies to the surface antigen and core antigen ("anti-HBs" and "anti HBc IgG"). The time between the removal of the HBsAg and the appearance of anti-HBs is called the window period. A person negative for HBsAg but positive for anti-HBs either has cleared an infection or has been vaccinated previously.

Individuals who remain HBsAg positive for at least six months are considered to be carriers. Carriers of the virus may have chronic hepatitis B, which would be reflected by elevated serum alanine aminotransferase (ALT) levels and inflammation of the liver, if they are in the immune clearance phase of chronic infection. Carriers who have seroconverted to HBeAg negative status, in particular those who acquired the infection as adults, have very little viral multiplication and hence may be at little risk of long-term complications or of transmitting infection to others.

PCR tests have been developed to detect and measure the amount of HBV DNA, called the viral load, in clinical specimens. These tests are used to assess a person's infection status and to monitor treatment. Individuals with high viral loads, characteristically have ground glass hepatocytes on biopsy.

Immunosuppressive therapy has been effective in halting the disease for laboratory animals.

Needle exchange programs (NEPs) are an attempt to reduce the spread of bloodborne diseases between intravenous drug users. They often also provide addiction counseling services, infectious disease testing, and in some cases mental health care and/or other case management. NEPs acquired their name as they were initially places where intravenous (IV) illicit substance users were provided with clean, unused needles in exchange for their used needles. This allows for proper disposal of the needles. Empirical studies confirm the benefits of NEPs. NEPs can affect behaviors that result in the transmission of HIV. These behaviors include decreased sharing of used syringes, which reduces contaminated syringes from circulation and replaces them with sterile ones, among other risk reductions.

There is no specific treatment for the condition.

Control may rely on boosting bird immunity, preventing group mixing and faecal spreading.

A vaccine based on recombinant viral proteins was developed in the 1990s and tested in a high-risk population (in Nepal) in 2001. The vaccine appeared to be effective and safe, but development was stopped for lack of profitability, since hepatitis E is rare in developed countries. No hepatitis E vaccine is licensed for use in the United States.

Although other HEV vaccine trials have been successful, these vaccines have not yet been produced or made available to susceptible populations. The exception is China; after more than a year of scrutiny and inspection by China's State Food and Drug Administration (SFDA), a hepatitis E vaccine developed by Chinese scientists was available at the end of 2012. The vaccine—called HEV 239 by its developer Xiamen Innovax Biotech—was approved for prevention of hepatitis E in 2012 by the Chinese Ministry of Science and Technology, following a controlled trial on 100,000+ people from Jiangsu Province where none of those vaccinated became infected during a 12-month period, compared to 15 in the group given placebo. The first vaccine batches came out of Innovax' factory in late October 2012, to be sold to Chinese distributors.

Due to the lack of evidence, WHO did not make a recommendation regarding routine use of the HEV 239 vaccine. National authorities may however, decide to use the vaccine based on the local epidemiology.

Sanitation is the most important measure in prevention of hepatitis E; this consists of proper treatment and disposal of human waste, higher standards for public water supplies, improved personal hygiene procedures, and sanitary food preparation. Thus, prevention strategies of this disease are similar to those of many others that plague developing nations.

Neonatal sepsis of the newborn is an infection that has spread through the entire body. The inflammatory response to this systematic infection can be as serious as the infection itself. In infants that weigh under 1500 g, sepsis is the most common cause of death. Three to four percent of infants per 1000 births contract sepsis. The mortality rate from sepsis is near 25%. Infected sepsis in an infant can be identified by culturing the blood and spinal fluid and if suspected, intravenous antibiotics are usually started. Lumbar puncture is controversial because in some cases it has found not to be necessary while concurrently, without it estimates of missing up to one third of infants with meningitis is predicted.

The Centers for Disease Control and Prevention (CDC) recommends HIV testing for all pregnant women as a part of routine prenatal care. The test is usually performed in the first trimester of pregnancy with other routine laboratory tests. HIV testing is recommended because HIV-infected women who do not receive testing are more likely to transmit the infection to their children.

HIV testing may be offered to pregnant women on an "opt-in" or an "opt-out" basis. In the "opt-in" model, women are counseled on HIV testing and elect to receive the test by signing a consent form. In the "opt-out" model, the HIV test is automatically performed with other routine prenatal tests. If a woman does not want to be tested for HIV, she must specifically refuse the test and sign a form declining testing. The CDC recommends "opt-out" testing for all pregnant women because it improves disease detection and treatment and helps reduce transmission to children.

If a woman chooses to decline testing, she will not receive the test. However, she will continue to receive HIV counseling throughout the pregnancy so that she may be as informed as possible about the disease and its impact. She will be offered HIV testing at all stages of her pregnancy in case she changes her mind.

HIV testing begins with a screening test. The most common screening test is the rapid HIV antibody test which tests for HIV antibodies in blood, urine, or oral fluid. HIV antibodies are only produced if an individual is infected with the disease. Therefore, presence of the antibodies is indicative of an HIV infection. Sometimes, however, a person may be infected with HIV but the body has not produced enough antibodies to be detected by the test. If a woman has risk factors for HIV infection but tests negative on the initial screening test, she should be retested in 3 months to confirm that she does not have HIV. Another screening test that is more specific is the HIV antigen/antibody test. This is a newer blood test that can detect HIV infection quicker than the antibody test because it detects both virus particles and antibodies in the blood.

Any woman who has a positive HIV screening test must receive follow-up testing to confirm the diagnosis. The follow-up test can differentiate HIV-1 from HIV-2 and is a more specific antibody test. It may also detect the virus directly in the bloodstream.

Treatment is similar to hepatitis B, but due to its high lethality, more aggressive therapeutic approaches are recommended in the acute phase. In absence of a specific vaccine against delta virus, the vaccine against HBV must be given soon after birth in risk groups.

The vaccine for hepatitis B protects against hepatitis D virus because of the latter's dependence on the presence of hepatitis B virus for it to replicate.

Latest evidence suggests that Pegylated interferon alpha is effective in reducing the viral load and the effect of the disease during the time the drug is given, but the benefit generally stops if the drug is discontinued. The efficiency of the pegylated interferon treatment does not usually exceed ~20%.

The drug myrcludex B, which inhibits virus entry into hepatocytes, is in clinical trials .

Viral disease is usually detected by clinical presentation, for instance severe muscle and joint pains preceding fever, or skin rash and swollen lymph glands.

Laboratory investigation is not directly effective in detecting viral infections, because they do not themselves increase the white blood cell count. Laboratory investigation may be useful in diagnosing associated bacterial infections, however.

Viral infections are commonly of limited duration, so treatment usually consists in reducing the symptoms; antipyretic and analgesic drugs are commonly prescribed.

Symptoms and the isolation of the virus pathogen the upper respiratory tract is diagnostic. Virus identification is specific immunologic methods and PCR. The presence of the virus can be rapidly confirmed by the detection of the virus antigen. The methods and materials used for identifying the RSV virus has a specificity and sensitivity approaching 85% to 95%. Not all studies confirm this sensitivity. Antigen detection has comparatively lower sensitivity rates that approach 65% to 75%.

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.

The symptoms of neonatal hepatitis are similar to another infant liver disease, biliary atresia, in which the bile ducts are destroyed for reasons that are not understood. The infant with biliary atresia is also jaundiced and has an enlarged liver, but is growing well and does not have an enlarged spleen. These symptoms, along with a liver biopsy and blood tests, are needed to distinguish biliary atresia from neonatal hepatitis.