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.

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.

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

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.

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.

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.

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.

When physical examination of the newborn shows signs of a vertically transmitted infection, the examiner may test blood, urine, and spinal fluid for evidence of the infections listed above. Diagnosis can be confirmed by culture of one of the specific pathogens or by increased levels of IgM against the pathogen.

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.

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.

Some vertically transmitted infections, such as toxoplasmosis and syphilis, can be effectively treated with antibiotics if the mother is diagnosed early in her pregnancy. Many viral vertically transmitted infections have no effective treatment, but some, notably rubella and varicella-zoster, can be prevented by vaccinating the mother prior to pregnancy.

If the mother has active herpes simplex (as may be suggested by a pap test), delivery by Caesarean section can prevent the newborn from contact, and consequent infection, with this virus.

IgG antibody may play crucial role in prevention of intrauterine infections and extensive research is going on for developing IgG-based therapies for treatment and vaccination.

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.

Acute disease leads to death in most birds between the ages of 7–10 days. Clinical signs are quite limited in those cases. Older animals tend to show severe systemic and neurological signs and diarrhoea.

Adults do not show any clinical signs.

Viral isolation should be attempted for diagnosis, and immunofluorescence and electron microscopy can confirm the viral infection. Pathological changes may also help the diagnosis.

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.

There is currently no known treatment for Aleutian virus. When evidence of ADV shows in a ferret, it is strongly recommended that a CEP (counterimmunoelectrophoresis) blood test or an IFA (immunoflourescent antibody) test be done. The CEP test is usually faster and less expensive than the IFA test, but the IFA test is more sensitive and can detect the disease in borderline cases.

Additionally modern methods such as Real-Time PCR allow for rapid and accurate detection as well as determination of the amount of viron present.

Prevention is best accomplished by stopping the spread of ADV. Any new ferret, or those who have been confirmed as serum positive for the virus should be perpetually isolated from other ferrets. All items that may have come into contact with the infected ferret should be cleaned with a 10% bleach solution.

This is a growing concern within mink producers as it is the most crucial infectious disease which affects farmed mink worldwide.

PBFD is usually acquired by nestlings from their parents (vertical transmission) or from other members of the flock (horizontal transmission). The immature immune system of young birds makes them susceptible to the PBFDV. The virus may be transferred in crop secretions, in fresh or dried feces, and in feather and skin particles.

Adult birds coming into contact with the virus usually (but not always) develop resistance to it, but the virus is retained in their body and, in most cases, is excreted in feces and feather debris for the rest of their lives.

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.

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

Developing countries are more severely affected by TORCH syndrome.

In addition to the drop in peak production figures, earlier detection can be achieved. Sentinel birds can be placed in the flock and tested for haemagglutination.

TORCH syndrome can be prevented by treating an infected pregnant person, thereby preventing the infection from affecting the fetus.

During 1975 and 1976, Rocio virus was responsible for several epidemics of meningoencephalitis in coastal communities in southern São Paulo, Brazil. The outbreaks affected over 1,000 people and killed about 10% of those infected, but apparently responded well to treatment for viral encephalitides. The disease progresses rapidly after onset, with patients dying within 5 days of symptoms first appearing. The disease first presents with fever, headache, vomiting, and conjunctivitis, then progresses to neurological symptoms (confusion, disorientation, etc.) and muscle weakness; about one-third of cases enter a coma, and a third of those patients die, although supportive care such as intensive nursing and symptomatic treatment might reduce the case fatality rate to 4%. Survivors show neurological and psychological after-effects (sequelae) in about 20% of cases.