Antibiotics are commonly used to prevent secondary bacterial infection. There are no specific antiviral drugs in common use at this time for FVR, although one study has shown that ganciclovir, PMEDAP, and cidofovir hold promise for treatment. More recent research has indicated that systemic famciclovir is effective at treating this infection in cats without the side effects reported with other anti-viral agents. More severe cases may require supportive care such as intravenous fluid therapy, oxygen therapy, or even a feeding tube. Conjunctivitis and corneal ulcers are treated with topical antibiotics for secondary bacterial infection.

Lysine is commonly used as a treatment, however in a 2015 systematic review, where the authors investigated all clinical trials with cats as well as "in vitro" studies, concluded that lysine supplementation is not effective for the treatment or prevention of feline herpesvirus 1 infection.

The infection is treated with antibiotics. Tetracyclines and chloramphenicol are the drugs of choice for treating patients with psittacosis. Most persons respond to oral therapy doxycycline, tetracycline hydrochloride, or chloramphenicol palmitate. For initial treatment of severely ill patients, doxycycline hyclate may be administered intravenously. Remission of symptoms usually is evident within 48–72 hours. However, relapse can occur, and treatment must continue for at least 10–14 days after fever abates.

There is a vaccine for FHV-1 available (ATCvet code: , plus various combination vaccines), but although it limits or weakens the severity of the disease and may reduce viral shedding, it does not prevent infection with FVR. Studies have shown a duration of immunity of this vaccine to be at least three years. The use of serology to demonstrate circulating antibodies to FHV-1 has been shown to have a positive predictive value for indicating protection from this disease.

Most cases of HHV-6 infection get better on their own. If encephalitis occurs ganciclovir or foscarnet may be useful.

Although no specific treatment for acute infection with SuHV1 is available, vaccination can alleviate clinical signs in pigs of certain ages. Typically, mass vaccination of all pigs on the farm with a modified live virus vaccine is recommended. Intranasal vaccination of sows and neonatal piglets one to seven days old, followed by intramuscular (IM) vaccination of all other swine on the premises, helps reduce viral shedding and improve survival. The modified live virus replicates at the site of injection and in regional lymph nodes. Vaccine virus is shed in such low levels, mucous transmission to other animals is minimal. In gene-deleted vaccines, the thymidine kinase gene has also been deleted; thus, the virus cannot infect and replicate in neurons. Breeding herds are recommended to be vaccinated quarterly, and finisher pigs should be vaccinated after levels of maternal antibody decrease. Regular vaccination results in excellent control of the disease. Concurrent antibiotic therapy via feed and IM injection is recommended for controlling secondary bacterial pathogens.

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.

As the infection is usually transmitted into humans through animal bites, antibiotics usually treat the infection, but medical attention should be sought if the wound is severely swelling. Pasteurellosis is usually treated with high-dose penicillin if severe. Either tetracycline or chloramphenicol provides an alternative in beta-lactam-intolerant patients. However, it is most important to treat the wound.

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

Most people recover from West Nile virus without treatment. No specific treatment is available for WNV infection. In mild cases over the counter pain relievers can help ease mild headaches and muscle aches in adults. In severe cases treatment consists of supportive care that often involves hospitalization, intravenous fluids, pain medication, respiratory support, and prevention of secondary infections.

The current medical treatments for aggressive invasive aspergillosis include voriconazole and liposomal amphotericin B in combination with surgical debridement.

For the less aggressive allergic bronchopulmonary aspergillosis findings suggest the use of oral steroids for a prolonged period of time, preferably for 6–9 months in allergic aspergillosis of the lungs. Itraconazole is given with the steroids, as it is considered to have a "steroid sparing" effect, causing the steroids to be more effective, allowing a lower dose.,

Other drugs used, such as amphotericin B, caspofungin (in combination therapy only), flucytosine (in combination therapy only), or itraconazole,

are used to treat this fungal infection. However, a growing proportion of infections are resistant to the triazoles. "A. fumigatus", the most commonly infecting species, is intrinsically resistant to fluconazole.

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.

Treatment depends on the type of opportunistic infection, but usually involves different antibiotics.

Prevention of aspergillosis involves a reduction of mold exposure via environmental infection-control. Anti-fungal prophylaxis can be given to high-risk patients. Posaconazole is often given as prophylaxis in severely immunocompromised patients.

There is no specific vaccine against or treatment for exanthema subitum, and most children with the disease are not seriously ill.

SuHV1 can be used to analyze neural circuits in the central nervous system (CNS). For this purpose the attenuated (less virulent) Bartha SuHV1 strain is commonly used and is employed as a retrograde and anterograde transneuronal tracer. In the retrograde direction, SuHV1-Bartha is transported to a neuronal cell body via its axon, where it is replicated and dispersed throughout the cytoplasm and the dendritic tree. SuHV1-Bartha released at the synapse is able to cross the synapse to infect the axon terminals of synaptically connected neurons, thereby propagating the virus; however, the extent to which non-synaptic transneuronal transport may also occur is uncertain. Using temporal studies and/or genetically engineered strains of SuHV1-Bartha, second, third, and higher order neurons may be identified in the neural network of interest.

Individuals at higher risk are often prescribed prophylactic medication to prevent an infection from occurring. A patient's risk level for developing an opportunistic infection is approximated using the patient's CD4 T-cell count and sometimes other markers of susceptibility. Common prophylaxis treatments include the following:

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.

Methicillin-resistant Staphylococcus aureus (MRSA) evolved from Methicillin-susceptible Staphylococcus aureus (MSSA) otherwise known as common "S. aureus". Many people are natural carriers of "S. aureus", without being affected in any way. MSSA was treatable with the antibiotic methicillin until it acquired the gene for antibiotic resistance. Though genetic mapping of various strains of MRSA, scientists have found that MSSA acquired the mecA gene in the 1960s, which accounts for its pathogenicity, before this it had a predominantly commensal relationship with humans. It is theorized that when this "S. aureus" strain that had acquired the mecA gene was introduced into hospitals, it came into contact with other hospital bacteria that had already been exposed to high levels of antibiotics. When exposed to such high levels of antibiotics, the hospital bacteria suddenly found themselves in an environment that had a high level of selection for antibiotic resistance, and thus resistance to multiple antibiotics formed within these hospital populations. When "S. aureus" came into contact with these populations, the multiple genes that code for antibiotic resistance to different drugs were then acquired by MRSA, making it nearly impossible to control. It is thought that MSSA acquired the resistance gene through the horizontal gene transfer, a method in which genetic information can be passed within a generation, and spread rapidly through its own population as was illustrated in multiple studies. Horizontal gene transfer speeds the process of genetic transfer since there is no need to wait an entire generation time for gene to be passed on. Since most antibiotics do not work on MRSA, physicians have to turn to alternative methods based in Darwinian medicine. However prevention is the most preferred method of avoiding antibiotic resistance. By reducing unnecessary antibiotic use in human and animal populations, antibiotics resistance can be slowed.

Often no treatment is required. However, as porcine cytomegalovirus is a herpes virus it remains latent and sheds at times of stress. Therefore husbandry measures to minimise stress levels should be in place.

Antibiotic treatment only has a marginal effect on the duration of symptoms, and its use is not recommended except in high-risk patients with clinical complications.

Erythromycin can be used in children, and tetracycline in adults. Some studies show, however, that erythromycin rapidly eliminates "Campylobacter" from the stool without affecting the duration of illness. Nevertheless, children with dysentery due to "C. jejuni" benefit from early treatment with erythromycin. Treatment with antibiotics, therefore, depends on the severity of symptoms. Quinolones are effective if the organism is sensitive, but high rates of quinolone use in livestock means that quinolones are now largely ineffective.

Antimotility agents, such as loperamide, can lead to prolonged illness or intestinal perforation in any invasive diarrhea, and should be avoided. Trimethoprim/sulfamethoxazole and ampicillin are ineffective against "Campylobacter".

The infection is usually self-limiting, and in most cases, symptomatic treatment by liquid and electrolyte replacement is enough in human infections.

Vaccination is the only known method to prevent the development of tumors when chickens are infected with the virus. However, administration of vaccines does not prevent transmission of the virus, i.e., the vaccine is not sterilizing. However, it does reduce the amount of virus shed in the dander, hence reduces horizontal spread of the disease. Marek's disease does not spread vertically. The vaccine was introduced in 1970 and the scientist credited with its development is Dr. Ben Roy Burmester and Dr. Frank J Siccardi. Before that, Marek's disease caused substantial revenue loss in the poultry industries of the United States and the United Kingdom. The vaccine can be administered to one-day-old chicks through subcutaneous inoculation or by "in ovo" vaccination when the eggs are transferred from the incubator to the hatcher. "In ovo" vaccination is the preferred method, as it does not require handling of the chicks and can be done rapidly by automated methods. Immunity develops within two weeks.

The vaccine originally contained the antigenically similar turkey herpesvirus, which is serotype 3 of MDV. However, because vaccination does not prevent infection with the virus, the Marek's disease virus has evolved increased virulence and resistance to this vaccine. As a result, current vaccines use a combination of vaccines consisting of HVT and gallid herpesvirus type 3 or an attenuated MDV strain, CVI988-Rispens (ATCvet code: ).

The two classes of antiviral drugs used against influenza are neuraminidase inhibitors (oseltamivir and zanamivir) and M2 protein inhibitors (adamantane derivatives).

While the general prognosis is favorable, current studies indicate that West Nile Fever can often be more severe than previously recognized, with studies of various recent outbreaks indicating that it may take as long as 60–90 days to recover. People with milder WNF are just as likely as those with more severe manifestations of neuroinvasive disease to experience multiple long term (>1+ years) somatic complaints such as tremor, and dysfunction in motor skills and executive functions. People with milder illness are just as likely as people with more severe illness to experience adverse outcomes. Recovery is marked by a long convalescence with fatigue. One study found that neuroinvasive WNV infection was associated with an increased risk for subsequent kidney disease.