Risk factors independently associated with developing a clinical infection with WNV include a suppressed immune system and a patient history of organ transplantation. For neuroinvasive disease the additional risk factors include older age (>50+), male sex, hypertension, and diabetes mellitus.

A genetic factor also appears to increase susceptibility to West Nile disease. A mutation of the gene "CCR5" gives some protection against HIV but leads to more serious complications of WNV infection. Carriers of two mutated copies of "CCR5" made up 4.0 to 4.5% of a sample of West Nile disease sufferers, while the incidence of the gene in the general population is only 1.0%.

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

Vertical transmission, the transmission of a viral or bacterial disease from the female of the species to her offspring, has been observed in various West Nile virus studies, amongst different species of mosquitoes in both the laboratory and in nature. Mosquito progeny infected vertically in autumn, may potentially serve as a mechanism for WNV to overwinter and initiate enzootic horizontal transmission the following spring, although it likely plays little role in transmission in the summer and fall.

Cats with Avian Influenza exhibit symptoms that can result in death. They are one of the few species that can get Avian Influenza. The specific virus that they get is H5N1, which is a subtype of Avian Influenza. In order to get the virus, cats need to be in contact with waterfowl, poultry, or uncooked poultry that are infected. Two of the main organs that the virus affects are the lungs and liver.

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.

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.

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.

The study of RRF has been recently facilitated by the development of a mouse model. Mice infected with RRV develop hind-limb arthritis/arthralgia which is similar to human disease. The disease in mice is characterized by an inflammatory infiltrate including macrophages which are immunopathogenic and exacerbate disease. Furthermore, mice deficient in the C3 protein do not suffer from severe disease following infection. This indicates that an aberrant innate immune response is responsible for severe disease following RRV infection.

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.

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

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 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.

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.

West Nile virus (WNV) is a single-stranded RNA virus that causes West Nile fever. It is a member of the family Flaviviridae, specifically from the genus Flavivirus which also contain the Zika virus, dengue virus, and the yellow fever virus. The West Nile virus is primarily transmitted through mosquitoes, mostly by the Culex species. However, ticks have been found to carry the virus. The primary hosts of WNV are birds, so that the virus remains within a "bird-mosquito-bird" transmission cycle.

Rocio viral encephalitis is an epidemic flaviviral disease of humans first observed in São Paulo State, Brazil, in 1975. Low-level enzootic transmission is likely continuing in the epidemic zone, and with increased deforestation and population expansion, additional epidemics caused by Rocio virus are highly probable. If migratory species of birds are, or become involved in, the virus transmission cycle, the competency of a wide variety of mosquito species for transmitting Rocio virus experimentally suggest that the virus may become more widely distributed. The encephalitis outbreak in the western hemisphere caused by West Nile virus, a related flavivirus, highlights the potential for arboviruses to cause severe problems far from their source enzootic foci.

The causative Rocio virus belongs to the genus "Flavivirus" (the same genus as the Zika virus) in family Flaviviridae and is closely related serologically to Ilhéus, St. Louis encephalitis, Japanese encephalitis and Murray Valley encephalitis viruses.

There is currently no vaccine available. The primary method of disease prevention is minimizing mosquito bites, as the disease is only transmitted by mosquitoes. Typical advice includes use of mosquito repellent and mosquito screens, wearing light coloured clothing, and minimising standing water around homes (e.g. removing Bromeliads, plant pots, garden ponds). Staying indoors during dusk/dawn hours when mosquitos are most active may also be effective. Bush camping is a common precipitant of infection so particular care is required.

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.

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.

Japanese encephalitis (JE) is the leading cause of viral encephalitis in Asia, with up to 70,000 cases reported annually. Case-fatality rates range from 0.3% to 60% and depend on the population and age. Rare outbreaks in U.S. territories in the Western Pacific have also occurred. Residents of rural areas in endemic locations are at highest risk; Japanese encephalitis does not usually occur in urban areas.

Countries which have had major epidemics in the past, but which have controlled the disease primarily by vaccination, include China, South Korea, Japan, Taiwan and Thailand. Other countries that still have periodic epidemics include Vietnam, Cambodia, Myanmar, India, Nepal, and Malaysia. Japanese encephalitis has been reported in the Torres Strait Islands and two fatal cases were reported in mainland northern Australia in 1998. There were reported cases in Kachin State, Myanmar in 2013. The spread of the virus in Australia is of particular concern to Australian health officials due to the unplanned introduction of "Culex gelidus", a potential vector of the virus, from Asia. However, the current presence on mainland Australia is minimal. There had been 116 deaths reported in Odisha's backward Malkangiri district of India in 2016.

Human, cattle, and horses are dead-end hosts as the disease manifests as fatal encephalitis. Swine acts as an amplifying host and has a very important role in the epidemiology of the disease. Infection in swine is asymptomatic, except in pregnant sows, when abortion and fetal abnormalities are common sequelae. The most important vector is "Culex tritaeniorhynchus", which feeds on cattle in preference to humans. It has been proposed that moving swine away from human habitation can divert the mosquito away from humans and swine. The natural hosts of the Japanese encephalitis virus are birds, not humans, and many believe the virus will therefore never be completely eliminated. In November 2011, the Japanese encephalitis virus was reported in "Culex bitaeniorhynchus" in South Korea.

Recently whole genome microarray research of neurons infected with the Japanese Encephalitis virus has shown that neurons play an important role in their own defense against Japanese Encephalitis infection. Although this challenges the long-held belief that neurons are immunologically quiescent, an improved understanding of the proinflammatory effects responsible for immune-mediated control of viral infection and neuronal injury during Japanese Encephalitis infection is an essential step for developing strategies for limiting the severity of CNS disease.

A number of drugs have been investigated to either reduce viral replication or provide neuroprotection in cell lines or studies upon mice. None are currently advocated in treating human patients.

- The use of rosmarinic acid, arctigenin, and oligosaccharides with degree of polymerization 6 from "Gracilaria" sp. or "Monostroma" "nitidum" have been shown to be effective in a mouse model of Japanese encephalitis.

- Curcumin has been shown to impart neuroprotection against Japanese Encephalitis infection in an in vitro study. Curcumin possibly acts by decreasing cellular reactive oxygen species level, restoration of cellular membrane integrity, decreasing pro-apoptotic signaling molecules, and modulating cellular levels of stress-related proteins. It has also been shown that the production of infective viral particles from previously infected neuroblastoma cells are reduced, which is achieved by the inhibition of ubiquitin-proteasome system.

- Minocycline in mice resulted in marked decreases in the levels of several markers, viral titer, and the level of proinflammatory mediators and also prevents blood brain barrier damage.

Hand, foot and mouth disease most commonly occurs in children under the age of 10. It tends to occur in outbreaks during the spring, summer, and autumn seasons. This is believed to be due to heat and humidity improving spread. HFMD is more common in rural areas than urban areas, however, socioeconomic status and hygiene levels need to considered. Poor hygiene is a risk factor for HFMD.

Outbreaks have relatively recently in China, Japan, Hong Kong, the Republic of Korea, Malaysia, Singapore, Thailand, Taiwan and Vietnam. HFMD most commonly affects young children under the age of 10 and more often under the age of 5, but can also affect adults with varying symptoms.

Since 1997 there have been 71 large enterovirus outbreaks reported, mostly in East and South East Asia, primarily affecting children. From the years 2008 to 2014, more than 1 million HFMD cases have been reported in China each year.

Avian Botulism is a strain of botulism that affects wild and captive bird populations, most notably waterfowl. This is a paralytic disease brought on by the Botulinum neurotoxin (BoNt) of the bacterium "Clostridium botulinum". "C. botulinum" can fall into one of 7 different types which are strains A through G. Type C BoNt is most frequently associated with waterfowl mortality. The Type E strain is also commonly associated with avian outbreaks and is frequently found in fish species which is why most outbreaks occur in piscivorous birds.

Avian Botulism occurs all over the world and its understanding is important for wildlife managers, hunters, bird watchers, and anyone who owns wetland property as this disease can account for over 1,000,000 waterbird deaths in a year.

Preventive measures include avoiding direct contact with infected individuals (including keeping infected children home from school), proper cleaning of shared utensils, disinfecting contaminated surfaces, and proper hand hygiene. These measures have been shown to be effective in decreasing the transmission of the viruses responsible for HFMD.

Protective habits include hand washing and disinfecting surfaces in play areas. Breast-feeding has also shown to decrease rates of severe HFMD, though does not reduce the risk for the infection of the disease.

Psittacine beak and feather disease (PBFD) is a viral disease affecting all Old World and New World parrots. The causative virus–beak and feather disease virus (BFDV)—belongs to the taxonomic genus Circovirus, family Circoviridae. It attacks the feather follicles and the beak and claw matrices of the bird, causing progressive feather, claw and beak malformation and necrosis. In later stages of the disease, feather shaft constriction occurs, hampering development until eventually all feather growth stops. It occurs in an acutely fatal form and a chronic form.

Cracking and peeling of the outer layers of the claws and beak make tissues vulnerable to . Because the virus also affects the thymus and Bursa of Fabricius, slowing lymphocyte production, immunosuppression occurs and the bird becomes more vulnerable to secondary infections. Beak fractures and necrosis of the hard palate can prevent the bird from eating.

There is no specific treatment for the condition.

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