Antibiotics are given to treat any bacterial infection present. Cough suppressants are used if the cough is not productive. NSAIDs are often given to reduce fever and upper respiratory inflammation. Prevention is by vaccinating for canine adenovirus, distemper, parainfluenza, and "Bordetella". In kennels, the best prevention is to keep all the cages disinfected. In some cases, such as "doggie daycares" or nontraditional playcare-type boarding environments, it is usually not a cleaning or disinfecting issue, but rather an airborne issue, as the dogs are in contact with each other's saliva and breath. Although most kennels require proof of vaccination, the vaccination is not a fail-safe preventative. Just like human influenza, even after receiving the vaccination, a dog can still contract mutated strains or less severe cases.

To increase their effectiveness, vaccines should be administered as soon as possible after a dog enters a high-risk area, such as a shelter. 10 to 14 days are required for partial immunity to develop. Administration of B. bronchiseptica and canine-parainfluenza vaccines may then be continued routinely, especially during outbreaks of kennel cough. There are several methods of administration, including parenteral and intranasal. However, the intranasal method has been recommended when exposure is imminent, due to a more rapid and localized protection. Several intranasal vaccines have been developed that contain canine adenovirus in addition to B bronchiseptica and canine-parainfluenza virus antigens. Studies have thus far not been able to determine which formula of vaccination is the most efficient. Adverse effects of vaccinations are mild, but the most common effect observed up to 30 days after administration is nasal discharge. Vaccinations are not always effective. In one study it was found that 43.3% of all dogs in the study population with respiratory disease had in fact been vaccinated.

The best prevention against viral pneumonia is vaccination against influenza, adenovirus, chickenpox, herpes zoster, measles, and rubella.

No specific treatment is available, but antibiotics can be used to prevent secondary infections.

Vaccines are available (ATCvet codes: for the inactivated vaccine, for the live vaccine; plus various combinations).

Biosecurity protocols including adequate isolation, disinfection are important in controlling the spread of the disease.

There is no vaccine for SARS to date. Isolation and quarantine remain the most effective means to prevent the spread of SARS. Other preventative measures include:

- Handwashing

- Disinfection of surfaces for fomites

- Wearing a surgical mask

- Avoiding contact with bodily fluids

- Washing the personal items of someone with SARS in hot, soapy water (eating utensils, dishes, bedding, etc.)

- Keeping children with symptoms home from school

Many public health interventions were taken to help control the spread of the disease; which is mainly spread through respiratory droplets in the air. These interventions included earlier detection of the disease, isolation of people who are infected, droplet and contact precautions, and the use of personal protective equipment (PPE); including masks and isolation gowns. A screening process was also put in place at airports to monitor air travel to and from affected countries. Although no cases have been identified since 2004, the CDC is still working to make federal and local rapid response guidelines and recommendations in the event of a reappearance of the virus.

Human-to-human transmission of SARS-CoV-2 has been confirmed during the 2019–20 coronavirus pandemic. Transmission occurs primarily via respiratory droplets from coughs and sneezes within a range of about 1.8 metres (6 ft). Indirect contact via contaminated surfaces is another possible cause of infection. Preliminary research indicates that the virus may remain viable on plastic and steel for up to three days, but does not survive on cardboard for more than one day or on copper for more than four hours; the virus is inactivated by soap, which destabilises its lipid bilayer. Viral RNA has also been found in stool samples from infected individuals.

The degree to which the virus is infectious during the incubation period is uncertain, but research has indicated that the pharynx reaches peak viral load approximately four days after infection. On 1 February 2020, the World Health Organization (WHO) indicated that "transmission from asymptomatic cases is likely not a major driver of transmission". However, an epidemiological model of the beginning of the outbreak in China suggested that "pre-symptomatic shedding may be typical among documented infections" and that subclinical infections may have been the source of a majority of infections.

There is some evidence of human-to-animal transmission of SARS-CoV-2, including examples in felids. Some institutions have advised those infected with SARS-CoV-2 to restrict contact with animals.

Antibiotics are ineffective, as SARS is a viral disease. Treatment of SARS is largely supportive with antipyretics, supplemental oxygen and mechanical ventilation as needed.

People with SARS must be isolated, preferably in negative pressure rooms, with complete barrier nursing precautions taken for any necessary contact with these patients.

Some of the more serious damage caused by SARS may be due to the body's own immune system reacting in what is known as cytokine storm.

As of 2017, there is no cure or protective vaccine for SARS that has been shown to be both safe and effective in humans. The identification and development of novel vaccines and medicines to treat SARS is a priority for governments and public health agencies around the world. MassBiologics, a non-profit organization engaged in the discovery, development and manufacturing of biologic therapies, is cooperating with researchers at NIH and the CDC developed a monoclonal antibody therapy that demonstrated efficacy in animal models.

In cases of viral pneumonia where influenza A or B are thought to be causative agents, patients who are seen within 48 hours of symptom onset may benefit from treatment with oseltamivir or zanamivir. Respiratory syncytial virus (RSV) has no direct acting treatments, but ribavirin in indicated for severe cases. Herpes simplex virus and varicella-zoster virus infections are usually treated with aciclovir, whilst ganciclovir is used to treat cytomegalovirus. There is no known efficacious treatment for pneumonia caused by SARS coronavirus, MERS coronavirus, adenovirus, hantavirus, or parainfluenza. Care is largely supportive.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the virus strain that causes coronavirus disease 2019 (COVID-19), a respiratory illness. It is colloquially known as the coronavirus, and was previously referred to by its provisional name 2019 novel coronavirus (2019-nCoV). SARS-CoV-2 is a positive-sense single-stranded RNA virus. It is contagious in humans, and the World Health Organization (WHO) has designated the ongoing pandemic of COVID-19 a Public Health Emergency of International Concern. Because the strain was first discovered in Wuhan, China, it is sometimes referred to as "Wuhan virus" or "Wuhan coronavirus". Since the WHO discourages the use of names based on locations such as MERS, and to avoid confusion with the disease SARS, it sometimes refers to SARS-CoV-2 as "the COVID-19 virus" in public health communications. The general public frequently calls both SARS-CoV-2 and the disease it causes "coronavirus", but scientists typically use more precise terminology.

Taxonomically, SARS-CoV-2 is a strain of Severe acute respiratory syndrome-related coronavirus (SARSr-CoV). It is believed to have zoonotic origins and has close genetic similarity to bat coronaviruses, suggesting it emerged from a bat-borne virus. An intermediate animal reservoir such as a pangolin is also thought to be involved in its introduction to humans. The virus shows little genetic diversity, indicating that the spillover event introducing SARS-CoV-2 to humans is likely to have occurred in late 2019.

Epidemiological studies estimate each infection results in 1.4 to 3.9 new ones when no members of the community are immune and no preventive measures taken. The virus is primarily spread between people through close contact and via respiratory droplets produced from coughs or sneezes. It mainly enters human cells by binding to the receptor angiotensin converting enzyme 2 (ACE2).

Avian infectious bronchitis (IB) is an acute and highly contagious respiratory disease of chickens. The disease is caused by avian infectious bronchitis virus (IBV), a coronavirus, and characterized by respiratory signs including gasping, coughing, sneezing, tracheal rales, and nasal discharge. In young chickens, severe respiratory distress may occur. In layers, respiratory distress, nephritis, decrease in egg production, and loss of internal (watery egg white) and external (fragile, soft, irregular or rough shells, shell-less) egg quality are reported.

The mainstay of eradication is the identification and removal of persistently infected animals. Re-infection is then prevented by vaccination and high levels of biosecurity, supported by continuing surveillance. PIs act as viral reservoirs and are the principal source of viral infection but transiently infected animals and contaminated fomites also play a significant role in transmission.

Leading the way in BVD eradication, almost 20 years ago, were the Scandinavian countries. Despite different conditions at the start of the projects in terms of legal support, and regardless of initial prevalence of herds with PI animals, it took all countries approximately 10 years to reach their final stages.

Once proven that BVD eradication could be achieved in a cost efficient way, a number of regional programmes followed in Europe, some of which have developed into national schemes.

Vaccination is an essential part of both control and eradication. While BVD virus is still circulating within the national herd, breeding cattle are at risk of producing PI neonates and the economic consequences of BVD are still relevant. Once eradication has been achieved, unvaccinated animals will represent a naïve and susceptible herd. Infection from imported animals or contaminated fomites brought into the farm, or via transiently infected in-contacts will have devastating consequences.

Lesions of paravaccinia virus will clear up with little to no scaring after 4 to 8 weeks. An antibiotic may be prescribed by a physician to help prevent bacterial infection of the lesion area. In rare cases, surgical removal of the lesions can be done to help increase rate of healing, and help minimize risk of bacterial or fungal infection. Upon healing, no long term side effects have been reported.

Paravaccinia virus originates from livestock infected with bovine papular stomatitis. When a human makes physical contact with the livestock's muzzle, udders, or an infected area, the area of contact will become infected. Livestock may not show symptoms of bovine papular stomatitis and still be infected and contagious. Paravaccinia can enter the body though all pathways including: skin contact by mechanical means, through the respiratory tract, or orally. Oral or respiratory contraction may be more likely to cause systemic symptoms such as lesions across the whole body

A person who has not previously been infected with paravaccinia virus should avoid contact with infected livestock to prevent contraction of disease. There is no commercially available vaccination for cattle or humans against paravaccinia. However, following infection, immunization has been noted in humans, making re-infection difficult. Unlike other pox viruses, there is no record of contracting paravaccinia virus from another human. Further, cattle only show a short immunization after initial infection, providing opportunity to continue to infect more livestock and new human hosts.

Modern vaccination programmes aim not only to provide a high level of protection from clinical disease for the dam, but, crucially, to protect against viraemia and prevent the production of PIs. While the immune mechanisms involved are the same, the level of immune protection required for foetal protection is much higher than for prevention of clinical disease.

While challenge studies indicate that killed, as well as live, vaccines prevent foetal infection under experimental conditions, the efficacy of vaccines under field conditions has been questioned. The birth of PI calves into vaccinated herds suggests that killed vaccines do not stand up to the challenge presented by the viral load excreted by a PI in the field.

Neither the combination of antivirals and interferons (ribavirin + interferon alfa-2a or interferon alfa-2b) nor corticosteroids improved outcomes.

When rhesus macaques were given interferon-α2b and ribavirin and exposed to MERS, they developed less pneumonia than control animals. Five critically ill people with MERS in Saudi Arabia with ARDS and on ventilators were given interferon-α2b and ribavirin but all ended up dying of the disease. The treatment was started late in their disease (a mean of 19 days after hospital admission) and they had already failed trials of steroids so it remains to be seen whether it may have benefit earlier in the course of disease. Another proposed therapy is inhibition of viral protease or kinase enzymes. Researchers are investigating a number of ways to combat the outbreak of Middle East respiratory syndrome coronavirus, including using interferon, chloroquine, chlorpromazine, loperamide, and lopinavir, as well as other agents such as mycophenolic acid and camostat.

Vaccination helps prevent bronchopneumonia, mostly against influenza viruses, adenoviruses, measles, rubella, streptococcus pneumoniae, haemophilus influenzae, diphtheria, bacillus anthracis, chickenpox, and bordetella pertussis.

Recent work has been done by virologists to learn more about the interference in infection of host cells and how DI genomes could potentially work as antiviral agents. The Dimmock & Easton, 2014 article explains that pre-clinical work is being done to test their effectiveness against influenza viruses. DI-RNAs have also been found to aid in the infection of fungi via viruses of the family "Partitiviridae" for the first time, which makes room for more interdisciplinary work.

Vaccination

There is one intra-nasal FIP vaccine available: its use is controversial but in an independent study the authors concluded that vaccination can protect cats with no or low FCoV antibody titres and that in some cats vaccine failure was probably due to pre-existing infection.

Prevention of FCoV infection, and therefore FIP, in kittens

Kittens are protected from infection by maternally derived antibody until it wanes, usually around 5–7 weeks of age, therefore it is possible to prevent infection of kittens by removing them from sources of infection. However, FCoV is a very contagious virus and such prevention does require rigorous hygiene.

Antivirals have been tested for effectiveness in the common cold; as of 2009, none had been both found effective and licensed for use. There are ongoing trials of the anti-viral drug pleconaril which shows promise against picornaviruses as well as trials of BTA-798. The oral form of pleconaril had safety issues and an aerosol form is being studied. DRACO, a broad-spectrum antiviral therapy, has shown preliminary effectiveness in treating rhinovirus, as well as other infectious viruses.

The genomes for all known human rhinovirus strains have been sequenced.

Antibiotics do not help the many lower respiratory infections which are caused by parasites or viruses. While acute bronchitis often does not require antibiotic therapy, antibiotics can be given to patients with acute exacerbations of chronic bronchitis. The indications for treatment are increased dyspnoea, and an increase in the volume or purulence of the sputum. The treatment of bacterial pneumonia is selected by considering the age of the patient, the severity of the illness and the presence of underlying disease. Amoxicillin and doxycycline are suitable for many of the lower respiratory tract infections seen in general practice.

While the mechanism of spread of MERS-CoV is currently not known, based on experience with prior coronaviruses, such as SARS, the WHO currently recommends that all individuals coming into contact with MERS suspects should (in addition to standard precautions):

- Wear a medical mask

- Wear eye protection (i.e. goggles or a face shield)

- Wear a clean, non sterile, long sleeved gown; and gloves (some procedures may require sterile gloves)

- Perform hand hygiene before and after contact with the person and his or her surroundings and immediately after removal of personal protective equipment (PPE)

For procedures which carry a risk of aerosolization, such as intubation, the WHO recommends that care providers also:

- Wear a particulate respirator and, when putting on a disposable particulate respirator, always check the seal

- Wear eye protection (i.e. goggles or a face shield)

- Wear a clean, non-sterile, long-sleeved gown and gloves (some of these procedures require sterile gloves)

- Wear an impermeable apron for some procedures with expected high fluid volumes that might penetrate the gown

- Perform procedures in an adequately ventilated room; i.e. minimum of 6 to 12 air changes per hour in facilities with a mechanically ventilated room and at least 60 liters/second/patient in facilities with natural ventilation

- Limit the number of persons present in the room to the absolute minimum required for the person’s care and support

- Perform hand hygiene before and after contact with the person and his or her surroundings and after PPE removal.

The duration of infectivity is also unknown so it is unclear how long people must be isolated, but current recommendations are for 24 hours after resolution of symptoms. In the SARS outbreak the virus was not cultured from people after the resolution of their symptoms.

It is believed that the existing SARS research may provide a useful template for developing vaccines and therapeutics against a MERS-CoV infection. Vaccine candidates are currently awaiting clinical trials.

The go-to immunosuppressive drug in FIP is prednisolone.

An experimental polyprenyl immunostimulant (PI) is manufactured by Sass and Sass and tested by Dr. Al Legendre, who described survival over 1 year in three cats diagnosed with FIP and treated with the medicine. In a subsequent field study of 60 cats with non-effusive FIP treated with PI, 52 cats (87%) died before 200 days, but eight cats survived over 200 days from the start of PI treatment for and four of those survived beyond 300 days. There are anecdotal reports on the internet of cats surviving even longer.

No medications or vaccine is approved to treat the disease. International research on vaccines and medicines in COVID-19 are underway by government organisations, academic groups and industry researchers. In March, the World Health Organization initiated the "SOLIDARITY Trial" to assess treatment effects of four existing antiviral compounds with the most promise of efficacy.

There is no available vaccine, but various agencies are actively developing vaccine candidates. Previous work on SARS-CoV is being utilised because SARS-CoV and SARS-CoV-2 both use the ACE2 receptor to enter human cells. There are three vaccination strategies being investigated. First, researchers aim to build a whole virus vaccine. The use of such a virus, be it inactive or dead, aims to elicit a prompt immune response of the human body to a new infection with COVID-19. A second strategy, subunit vaccines, aims to create a vaccine that sensitises the immune system to certain subunits of the virus. In the case of SARS-CoV-2, such research focuses on the S-spike protein that helps the virus intrude the ACE2 enzyme receptor. A third strategy is that of the nucleic acid vaccines (DNA or RNA vaccines, a novel technique for creating a vaccination). Experimental vaccines from any of these strategies would have to be tested for safety and efficacy.

On 16 March 2020, the first clinical trial of a vaccine started with four volunteers in Seattle. The vaccine contains a harmless genetic code copied from the virus that causes the disease.

Antibody dependent enhancement has been suggested as a potential challenge for vaccine development for SARS-COV-2, but this is controversial.

The term "bovine malignant catarrhal fever" has been applied to three different patterns of disease:

- In Africa, wildebeests carry a lifelong infection of AlHV-1 but are not affected by the disease. The virus is passed from mother to offspring and shed mostly in the nasal secretions of wildebeest calves under one year old. Wildebeest associated MCF is transmitted from wildebeest to cattle normally following the wildebeest calving period. Cattle of all ages are susceptible to the disease, with a higher infection rate in adults, particularly in peripartuent females. Cattle are infected by contact with the secretions, but do not spread the disease to other cattle. Because no commercial treatment or vaccine is available for this disease, livestock management is the only method of control. This involves keeping cattle away from wildebeest during the critical calving period. This results in Massai pastoralists in Tanzania and Kenya being excluded from prime pasture grazing land during the wet season leading to a loss in productivity. In Eastern and Southern Africa MCF is classed as one of the five most important problems affecting pastoralists along with East coast fever, contagious bovine pleuropneumonia, foot and mouth disease and anthrax.Hartebeests and topi also may carry the disease. However, hartebeests and other antelopes are infected by a variant, Alcelaphine herpesvirus 2.

- Throughout the rest of the world, cattle and deer contract BMCF by close contact with sheep or goats during lambing. The natural host reservoir for Ovine herpesvirus 2 is the subfamily Caprinae (sheep and goats) whilst MCF affected animals are from the families Bovidae, Cervidae and suidae. Susceptibility to OHV-2 varies by species, with domestic cattle and zebus somewhat resistant, water buffalo and most deer somewhat susceptible, and bison, Bali cattle, and Pere David's deer very susceptible. OHV-2 viral DNA has been detected in the alimentary, respiratory and urino-genital tracts of sheep all of which could be possible transmission routes. Antibody from sheep and from cattle with BMCF is cross reactive with AlHV-1.

- AHV-1/OHV-2 can also cause problems in zoological collections, where inapparently infected hosts (wildebeest and sheep) and susceptible hosts are often kept in close proximity.

- Feedlot bison in North America not in contact with sheep have also been diagnosed with a form of BMCF. OHV-2 has been recently documented to infect herds of up to 5 km away from the nearest lambs, with the levels of infected animals proportional to the distance away from the closest herds of sheep.

The incubation period of BMCF is not known, however intranasal challenge with AHV-1 induced MCF in one hundred percent of challenged cattle between 2.5 and 6 weeks.

Shedding of the virus is greater from 6–9 month old lambs than from adults. After experimental infection of sheep, there is limited viral replication in nasal cavity in the first 24 hours after infection, followed by later viral replication in other tissues.