Previous methods of diagnosis included HI, complement fixation, neutralization tests, and injecting the serum of infected individuals into mice. However, new research has introduced more efficient methods to diagnose KFDV. These methods include: nested RT-PCR, TaqMan-based real-time RT-PCR, and immunoglobin M antibodies detection by ELISA. The two methods involving PCR are able to function by attaching a primer to the NS-5 gene which is highly conserved among the genus to which KFDV belongs. The last method allows for the detections of anti-KFDV antibodies in patients.

A number of various diseases may present with symptoms similar to those caused by a clinical West Nile virus infection. Those causing neuroinvasive disease symptoms include the enterovirus infection and bacterial meningitis. Accounting for differential diagnoses is a crucial step in the definitive diagnosis of WNV infection. Consideration of a differential diagnosis is required when a patient presents with unexplained febrile illness, extreme headache, encephalitis or meningitis. Diagnostic and serologic laboratory testing using polymerase chain reaction (PCR) testing and viral culture of CSF to identify the specific pathogen causing the symptoms, is the only currently available means of differentiating between causes of encephalitis and meningitis.

Cats can be protected from H5N1 if they are given a vaccination, as mentioned above. However, it was also found that cats can still shed some of the virus but in low numbers.

If a cat is exhibiting symptoms, they should be put into isolation and kept indoors. Then they should be taken to a vet to get tested for the presence of H5N1. If there is a possibility that the cat has Avian Influenza, then there should be extra care when handling the cat. Some of the precautions include avoiding all direct contact with the cat by wearing gloves, masks, and goggles. Whatever surfaces the cat comes in contact with should be disinfected with standard household cleaners.

They have given tigers an antiviral treatment of Oseltamivir with a dose of 75 mg/60 kg two times a day. The specific dosage was extrapolated from human data, but there hasn't been any data to suggest protection. As with many antiviral treatments, the dosage depends on the species.

Preliminary diagnosis is often based on the patient's clinical symptoms, places and dates of travel (if patient is from a nonendemic country or area), activities, and epidemiologic history of the location where infection occurred. A recent history of mosquito bites and an acute febrile illness associated with neurologic signs and symptoms should cause clinical suspicion of WNV.

Diagnosis of West Nile virus infections is generally accomplished by serologic testing of blood serum or cerebrospinal fluid (CSF), which is obtained via a lumbar puncture. Initial screening could be done using the ELISA technique detecting immunoglobulins in the sera of the tested individuals.

Typical findings of WNV infection include lymphocytic pleocytosis, elevated protein level, reference glucose and lactic acid levels, and no erythrocytes.

Definitive diagnosis of WNV is obtained through detection of virus-specific antibody IgM and neutralizing antibodies. Cases of West Nile virus meningitis and encephalitis that have been serologically confirmed produce similar degrees of CSF pleocytosis and are often associated with substantial CSF neutrophilia.

Specimens collected within eight days following onset of illness may not test positive for West Nile IgM, and testing should be repeated. A positive test for West Nile IgG in the absence of a positive West Nile IgM is indicative of a previous flavavirus infection and is not by itself evidence of an acute West Nile virus infection.

If cases of suspected West Nile virus infection, sera should be collected on both the acute and

convalescent phases of the illness. Convalescent specimens should be collected 2–3 weeks after acute specimens.

It is common in serologic testing for cross-reactions to occur among flaviviruses such as dengue virus (DENV) and tick-borne encephalitis virus; this necessitates caution when evaluating serologic results of flaviviral infections.

Four FDA-cleared WNV IgM ELISA kits are commercially available from different manufacturers in the U.S., each of these kits is indicated for use on serum to aid in the presumptive laboratory diagnosis of WNV infection in patients with clinical symptoms of meningitis or encephalitis. Positive WNV test results obtained via use of these kits should be confirmed by additional testing at a state health department laboratory or CDC.

In fatal cases, nucleic acid amplification, histopathology with immunohistochemistry, and virus culture of autopsy tissues can also be useful. Only a few state laboratories or other specialized laboratories, including those at CDC, are capable of doing this specialized testing.

Japanese encephalitis is diagnosed by commercially available tests detecting JE virus-specific IgM antibodies in serum and /or cerebrospinal fluid, for example by IgM capture ELISA.

JE virus IgM antibodies are usually detectable 3 to 8 days after onset of illness and persist for 30 to 90 days, but longer persistence has been documented. Therefore, positive IgM antibodies occasionally may reflect a past infection or vaccination. Serum collected within 10 days of illness onset may not have detectable IgM, and the test should be repeated on a convalescent sample. For patients with JE virus IgM antibodies, confirmatory neutralizing antibody testing should be performed.

Confirmatory testing in the US is only available at CDC and a few specialized reference laboratories. In fatal cases, nucleic acid amplification, and virus culture of autopsy tissues can be useful. Viral antigen can be shown in tissues by indirect fluorescent antibody staining.

The presence of avian botulism is extremely hard to detect before an outbreak. Frequent surveillance of sites at risk is needed for early detection of the disease in order to take action and remove carcasses. Vaccines are also developed, but they are expected to have limited effectiveness in stemming outbreaks in wild waterbird populations. However may be effective in reducing mortality for endangered island waterfowl and small non-migratory wild populations. Field tests are needed.

The disease can be prevented in horses with the use of vaccinations. These vaccinations are usually given together with vaccinations for other diseases, most commonly WEE, VEE, and tetanus. Most vaccinations for EEE consist of the killed virus. For humans there is no vaccine for EEE so prevention involves reducing the risk of exposure. Using repellent, wearing protective clothing, and reducing the amount of standing water is the best means for prevention

Prophylaxis by vaccination, as well as preventive measures like protective clothing, tick control, and mosquito control are advised. The vaccine for KFDV consists of formalin-inactivated KFDV. The vaccine has a 62.4% effectiveness rate for individuals who receive two doses. For individuals who receive an additional dose, the effectiveness increases to 82.9%. Specific treatments are not available.

The CDC recommends real-time PCR as the method of choice for diagnosing H1N1. The oral or nasal fluid collection and RNA virus preserving filter paper card is commercially available. This method allows a specific diagnosis of novel influenza (H1N1) as opposed to seasonal influenza. Near-patient point-of-care tests are in development.

Infection with Japanese encephalitis confers lifelong immunity. There are currently three vaccines available: SA14-14-2, IC51 (marketed in Australia and New Zealand as JESPECT and elsewhere as IXIARO) and ChimeriVax-JE (marketed as IMOJEV). All current vaccines are based on the genotype III virus.

A formalin-inactivated mouse-brain derived vaccine was first produced in Japan in the 1930s and was validated for use in Taiwan in the 1960s and in Thailand in the 1980s. The widespread use of vaccine and urbanization has led to control of the disease in Japan, Korea, Taiwan, and Singapore. The high cost of this vaccine, which is grown in live mice, means that poorer countries have not been able to afford to give it as part of a routine immunization program.

The most common adverse effects are redness and pain at the injection site. Uncommonly, an urticarial reaction can develop about four days after injection. Vaccines produced from mouse brain have a risk of autoimmune neurological complications of around 1 per million vaccinations. However where the vaccine is not produced in mouse brains but in vitro using cell culture there is little adverse effects compared to placebo, the main side effects are headache and myalgia.

The neutralizing antibody persists in the circulation for at least two to three years, and perhaps longer. The total duration of protection is unknown, but because there is no firm evidence for protection beyond three years, boosters are recommended every three years for people who remain at risk. Furthermore, there is also no data available regarding the interchangeability of other JE vaccines and IXIARO.

In September 2012 the Indian firm Biological E. Limited has launched an inactivated cell culture derived vaccine based on SA 14-14-2 strain which was developed in a technology transfer agreement with Intercell and is a thiomersal-free vaccine.

A cat that is infected with a high dose of the virus can show signs of fever, lethargy, and dyspnea. There have even been recorded cases where a cat has neurological symptoms such as circling or ataxia.

In a case in February 2004, a 2-year-old male cat was panting and convulsing on top of having a fever two days prior to death. This cat also had lesions that were identified as renal congestion, pulmonary congestion, edema, and pneumonia. Upon inspection, the cat also had cerebral congestion, conjunctivitis, and hemorrhaging in the serosae of the intestines.

However, a cat that is infected with a low dose of the virus may not necessarily show symptoms. Though they may be asymptomatic, they can still transfer small amounts of the virus.

Prevention of swine influenza has three components: prevention in pigs, prevention of transmission to humans, and prevention of its spread among humans.

There is no cure for EEE. Treatment consists of corticosteroids, anticonvulsants, and supportive measures (treating symptoms) such as intravenous fluids, tracheal intubation, and antipyretics. About four percent of humans known to be infected develop symptoms, with a total of about six cases per year in the US. A third of these cases die, and many survivors suffer permanent brain damage.

A blood test is the only way to confirm a case of Ross River Fever. Several types of blood tests may be used to examine antibody levels in the blood. Tests may either look for simply elevated antibodies (which indicate some sort of infection), or specific antibodies to the virus.

Antiviral drugs, that target infections with RRV. Patients are usually managed with simple analgesics, anti-inflammatories, anti-pyretics and rest while the illness runs its course.

There is currently no specific treatment for the virus. A vaccine is available, but only experimentally. It has not been released to the public due to the risk it poses to already exposed birds.

Therapeutic intervention is limited to treating secondary infections. The individual bird can sometimes recover, but this is rare. If only the feathers are affected and the bird suffers no other symptoms, it can usually experience an acceptable quality of life. But if the bird's beak or nails are affected, veterinarians will recommend euthanasia.

The management of the disease lies thus mostly in prevention. Every new bird that enters a pen with other birds should be quarantined first and be tested for BFDV. Birds which are known carriers should not be introduced into new pens, especially not if those contain young birds.

Blood analysis shows leukopenia, thrombocytopenia and moderately elevated liver enzymes. Differential diagnosis must be made with typhus, typhoid and atypical pneumonia by Mycoplasma, Legionella or Q fever. Exposure history is paramount to diagnosis.

Diagnosis involves microbiological cultures from respiratory secretions of patients or serologically with a fourfold or greater increase in antibody titers against "C. psittaci" in blood samples combined with the probable course of the disease. Typical inclusions called "Leventhal-Cole-Lillie bodies" can be seen within macrophages in BAL (bronchoalveolar lavage) fluid. Culture of "C. psittaci" is hazardous and should only be carried out in biosafety laboratories.

The majority of MVEV infections are sub-clinical, i.e. do not produce disease symptoms, although some people may experience a mild form of the disease with symptoms such as fever, headaches, nausea and vomiting and only a very small number of these cases go on to develop MVE. In fact, serological surveys which measure the level of anti-MVEV antibodies within the population estimate that only 1 in 800-1000 of all infections result in clinical disease.

The incubation period following exposure to the virus is around 1 to 4 weeks. Following infection, a person will have lifelong immunity to the virus. When a patient appears to show MVE symptoms and has been in an MVE-endemic area during the wet season, when outbreaks usually occur, MVE infection must be confirmed by laboratory diagnosis, usually by detection of a significant rise of MVE-specific antibodies in the patient's serum.

Of those who contract MVE, one-quarter die from the disease.

There are no vaccines or any other treatments specifically for Saint Louis encephalitis virus, although one study showed that early use of interferon-alpha2b may decrease the severity of complications.

The scientific study of the genetics of MVEV has been facilitated by the construction and manipulation of an infectious cDNA clone of the virus.

The botulinum neurotoxin is lethal because it causes paralysis. Field identification involves locating birds showing flaccidity in the legs, wings and neck, as well as the presence of protuberant nictitating membrane. The presence of several dozen, or even hundreds, of fresh waterbird carcasses is the stereotypical sign an outbreak has occurred. In this case the specimens need to be taken to disease laboratory to determine the cause of mortality. Most commonly, detection of "C. botulinum" in carcasses during lab work is accomplished through analysis of polymerase chain reactions (PCR) and is often the most successful method.

Initial diagnosis may be via symptoms, but is usually confirmed via an antigen and antibody test. A PCR-based test is also available. Although any of these tests can confirm psittacosis, false negatives are possible and so a combination of clinical and lab tests is recommended before giving the bird a clean bill of health. It may die within three weeks.

In the United States an average of 128 cases of Saint Louis encephalitis are recorded annually. In temperate areas of the United States, Saint Louis encephalitis cases occur primarily in the late summer or early fall. In the southern United States where the climate is milder Saint Louis encephalitis can occur year-round.

Tiamulin, chlortetracycline or tilmicosin may be used to treat and prevent the spread of the disease.

Vaccination is a very effective method of control, and also has an effect on pig productivity.

Eradication of the disease is possible but the organism commonly reinfects herds.

No treatment exists for the viral infection. Antibiotics may help prevent secondary infections.

Vaccination is available in different forms, usually for naive flocks.

Good biosecurity measures should be maintained including adequate quarantine, isolation, separation of different age groups and disinfection.