Both PMWS and porcine dermatitis and nephropathy syndrome (PDNS) are associated to PCV-2. Many pigs affected by the circovirus also seem to develop secondary bacterial infections, like Glässer disease ("Haemophilus parasuis"), pulmonary pasteurellosis, colibacilosis, salmonellosis and others. Postmortem lesions occur in multiple organs, especially in lymphoid tissues and lung, giving rise to the term "multisystemic". Lesions may also affect the skin, kidney, reproductive tissue, brain, or blood vessels.

Wasting pigs is the most common sign of PMWS infection, increasing the mortality rate significantly.

Postweaning multisystemic wasting syndrome ("PMWS") is the classic PCVD entity, caused by PCV-2. PCV-2 has a near universal distribution – present in most pig herds. In contrast, PMWS is more sporadic in its distribution. Experimental induction of PMWS has not been achieved by PCV-2 infection alone, using infectious DNA clones of the virus or a pure form of PCV-2 derived from infectious DNA clones. Therefore, it is assumed that PMWS is a multifactorial disease. PCV-2 is necessary but not sufficient for the development of PMWS. However, viral infection by itself tends to cause only mild disease, and co-factors such as other infections or immunostimulation seem necessary for development of severe disease.[1] For example, concurrent infection with porcine parvovirus or PRRS virus, or immunostimulation lead to increased replication of PCV-2 and more severe disease in PCV-2-infected pigs. There is no significant correlation of the disease with virus sequence variation with affected and control pigs.

Removing the pig from the stressful situation can prevent the episode.

Sedation and glucocorticoids may be beneficial.

Under anaesthesia, dantrolene sodium is a very effective treatment.

Genetic testing enables animals to be removed from the herd if they are positive for the gene. This means that the disorder is rare in the developed world these days.

Stress at slaughter should be minimised in all cases.

Porcine stress syndrome, also known as malignant hyperthermia or PSS, is a condition in pigs. It is characterised by hyperthermia triggered by stress, anaesthesia with halothane or intense exercise. PSS may appear as sudden death in pigs, often after transport. It is an inherited, autosomal recessive disorder due to a defective ryanodine receptor leading to huge calcium influx, muscle contracture and increase in metabolism.

PSS can manifest itself in the abattoir as the production of Pale, Soft and Exudative meat due to a rapid fall in muscle pH and degradation of muscle proteins and structure. This meat is usually rejected after inspection.

This disorder is most common in Landrace, Piétrain and crossbreeds of these breeds of pig. The genes may have been favoured in the past due to a larger muscle bulk in these breeds. However this is not standard protocol in developed countries these days.

Inclusion Body Rhinitis, also known as IBR or Cytomegalic Inclusion Disease, is a pig disease caused by porcine cytomegalovirus, which is a member of the herpesvirus family. It is a notifiable disease that is found worldwide. It is spread both vertically and horizontally and prevalence is high.

It is not a zoonosis but the risk to humans that receive pig organ transplants is currently under investigation.

There is no vaccine for SVD. Prevention measures are similar to those for foot-and-mouth disease: controlling animals imported from infected areas, and sanitary disposal of garbage from international aircraft and ships, and thorough cooking of garbage. Infected animals should be placed in strict quarantine. Eradication measures for the disease include quarantining infected areas, depopulation and disposal of infected and contact pigs, and cleaning and disinfecting

contaminated premises.

The illness is generally self-limiting. Management on the whole is preventative, by limiting exposure to mouldy environments with ventilation, or by wearing respiratory protection such as facemasks.

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.

Swine vesicular disease is most commonly brought into a herd by the introduction of a subclinically infected pig.

The disease can be transmitted in feed containing infected meat scraps, or by direct contact with infected feces (such as in an improperly cleaned truck).

An inflammatory reaction of the airways and alveoli, the mechanism of organic dust toxic syndrome is thought to be toxic rather than autoimmune in origin. The airways are exposed to high concentrations of organic dust created by some form of disturbance or mechanical process. They can be such materials such as grain kernel fragments, bits of insects, bacteria, fungal spores, molds or chemical residues, the individual particles 0.1 to 50 µm in size. A common scenario is exposure to moldy grain, hay or woodchips, with farmers and pig workers the most common occupations affected. Those who work with grain, poultry and mushrooms also frequently report symptoms.

Aujeszky's disease, usually called pseudorabies in the United States, is a viral disease in swine that has been endemic in most parts of the world. It is caused by "Suid herpesvirus 1" (SuHV1). Aujeszky's disease is considered to be the most economically important viral disease of swine in areas where hog cholera has been eradicated. Other mammals, such as humans, cattle, sheep, goats, cats, dogs, and raccoons, are also susceptible. The disease is usually fatal in these animal species bar humans.

The term "pseudorabies" is found inappropriate by many people, as SuHV1 is a herpesvirus and not related to the rabies virus.

Research on SuHV1 in pigs has pioneered animal disease control with genetically modified vaccines. SuHV1 is now used in model studies of basic processes during lytic herpesvirus infection, and for unravelling molecular mechanisms of herpesvirus neurotropism.

Foot-and-mouth disease or hoof-and-mouth disease (Aphthae epizooticae) is an infectious and sometimes fatal viral disease that affects cloven-hoofed animals, including domestic and wild bovids. The virus causes a high fever for approximately two to six days, followed by blisters inside the mouth and on the feet that may rupture and cause lameness.

Foot-and-mouth disease (FMD) has very severe implications for animal farming, since it is highly infectious and can be spread by infected animals comparatively easily through contact with contaminated farming equipment, vehicles, clothing, feed and by domestic and wild predators. Its containment demands considerable efforts in vaccination, strict monitoring, trade restrictions, quarantines and occasionally the culling of animals.

Susceptible animals include cattle, water buffalo, sheep, goats, pigs, antelope, deer, and bison. It has also been known to infect hedgehogs and elephants; llamas and alpacas may develop mild symptoms, but are resistant to the disease and do not pass it on to others of the same species. In laboratory experiments, mice, rats, and chickens have been successfully infected by artificial means, but they are not believed to contract the disease under natural conditions. Humans are very rarely infected.

The virus responsible for the disease is a picornavirus, the prototypic member of the genus "Aphthovirus". Infection occurs when the virus particle is taken into a cell of the host. The cell is then forced to manufacture thousands of copies of the virus, and eventually bursts, releasing the new particles in the blood. The virus is genetically highly variable, which limits the effectiveness of vaccination.

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.

Necrotising hepatopancreatitis (NHP), is also known as Texas necrotizing hepatopancreatitis (TNHP), Texas Pond Mortality Syndrome (TPMS) and Peru necrotizing hepatopancreatitis (PNHP), is a lethal epizootic disease of farmed shrimp. It is not very well researched yet, but generally assumed to be caused by a bacterial infection.

NHP mainly affects the farmed shrimp species "Litopenaeus vannamei" (Pacific white shrimp) and "Litopenaeus stylirostris" (Western blue shrimp), but has also been reported in three other American species, namely "Farfantepenaeus aztecus", "Farfantepenaeus californiensis", and "Litopenaeus setiferus". The highest mortality rates occur in "L. vannamei", which is one of the two most frequently farmed species of shrimp. Untreated, the disease causes mortality rates of up to 90 percent within 30 days. A first outbreak of NHP had been reported in Texas in 1985; the disease then spread to shrimp aquacultures in South America, in 2009 to China and subsequently Southeast Asia, followed by massive outbreaks in that region in 2012-2013.

NHP is associated with a small, gram-negative, and highly pleomorphic "Rickettsia"-like bacterium that belongs to its own, new genus in the alpha proteobacteria. However, in early-2013 a novel strain of "Vibrio parahaemolyticus" was identified as a more likely causative agent, though involvement of a virus cannot be definitely ruled out yet.

The aetiological agent is the pathogenic agent Candidatus "Hepatobacter penaei", an obligate intracellular bacterium of the Order α-Proteobacteria.

Infected shrimps show gross signs including soft shells and flaccid bodies, black or darkened gills, dark edges of the pleopods, and uropods, and an atrophied hepatopancreas that is whitish instead of orange or tan as is usual.

Whichever of the two bacteria associated with NHP actually causes it, the pathogen seems to prefer high water temperatures (above ) and elevated levels of salinity (more than 20–38 ppt). Avoiding such conditions in shrimp ponds is thus an important disease control measure.

Porcine enzootic pneumonia is caused by "Mycoplasma hyopneumoniae" and describes an important respiratory disease of pigs.

It is part of the Porcine Respiratory Disease Complex along with Swine Influenza, PRRS and Porcine circovirus 2, and even though on its own it is quite a mild disease, it predisposes to secondary infections with organisms such as "Pasteurella multocida".

Clinical signs are most commonly seen in pigs over 8 weeks of age, and the disease occurs worldwide. Transmission is horizontal and vertical from sows.

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.

Prognosis is poor if this condition is not aggressively treated. In the 1970s, mortality was greater than 80%; with the current management, however, mortality is now less than 5%.

It occurs in between 1:5,000 and 1:100,000 in procedures involving general anaesthesia. This disorder occurs worldwide and affects all racial groups. Most cases, however, occur in children and young adults, which might be related to the fact many older people will have already had surgeries and thus would know about and be able to avoid this condition.

Humans can be infected with foot-and-mouth disease through contact with infected animals, but this is extremely rare. Some cases were caused by laboratory accidents. Because the virus that causes FMD is sensitive to stomach acid, it cannot spread to humans via consumption of infected meat, except in the mouth before the meat is swallowed. In the UK, the last confirmed human case occurred in 1966, and only a few other cases have been recorded in countries of continental Europe, Africa, and South America. Symptoms of FMD in humans include malaise, fever, vomiting, red ulcerative lesions (surface-eroding damaged spots) of the oral tissues, and sometimes vesicular lesions (small blisters) of the skin. According to a newspaper report, FMD killed two children in England in 1884, supposedly due to infected milk.

Another viral disease with similar symptoms, hand, foot and mouth disease, occurs more frequently in humans, especially in young children; the cause, Coxsackie A virus, is different from FMDV. Coxsackie viruses belong to the "Enteroviruses" within the Picornaviridae.

Because FMD rarely infects humans, but spreads rapidly among animals, it is a much greater threat to the agriculture industry than to human health. Farmers around the world can lose enormous amounts of money during a foot-and-mouth epizootic, when large numbers of animals are destroyed, and revenues from milk and meat production go down.

Cerebellar abiotrophy (CA) is best known as a condition affecting Arabian horses. It has also been observed in the Curly horse, Miniature horse, the Gotland Pony, one Eriskay Pony, and possibly the Oldenburg. Most foals appear normal at birth, with symptoms noticeable at an average age of four months, though there have been cases where the condition is first seen shortly after birth and other cases where symptoms are first recognized in horses over one year of age.

Breeds DNA tested that reveal some carrier lines, but to date no affected animals, include the Welsh pony and the Trakehner. However, other breeds heavily influenced by Arabian breeding, such as the Thoroughbred and the American Saddlebred, do not appear to carry the mutation.

In horses, CA is believed to be linked to an autosomal recessive gene. This means it is not sex-linked, and the allele has to be carried and passed on by both parents in order for an affected animal to be born. Horses that only carry one copy of the gene may pass it on to their offspring, but themselves are perfectly healthy—without symptoms of the disease. Because it is recessive, the allele for CA may pass through multiple generations before it is expressed.

CA is sometimes misdiagnosed. Though the symptoms are quite distinguishable from other neurological conditions, it has been confused with Wobbler's syndrome, Equine Protozoal Myeloencephalitis (EPM), and injury-related problems such as a concussion.

A DNA test which identifies markers associated with cerebellar abiotrophy became available in 2008. The test was refined to identify the most likely mutations, and retesting of earlier samples based on an earlier indirect marker test developed by UCD, indicated a 97% accuracy rate for the old test relative to the newer version, with no false negatives. The causative mutation was identified in 2011. Research on CA and the DNA test was led by the Veterinary Genetics Laboratory at the UC Davis School of Veterinary Medicine. Researchers working on this problem include Dr. Cecilia Penedo, PhD, and Leah Brault, PhD. The late Dr. Ann T. Bowling made significant early contributions to the genetics research on CA.

It is expected that there will be no new cases of progressive inflammatory neuropathy since the process of aerosolizing the pig brains has been discontinued at all pork processing facilities.

An initial comprehensive study of 24 known cases was conducted by multiple doctors from various disciplines at the Mayo Clinic. They identified the cause of this neurological disease to be occupational exposure to aerosolized pig neural tissue. Investigators from the Minnesota Department of Health (MDH) simultaneously determined that the 70 ppsi pressure used to liquefy and extract the pig brains caused the aerosolization of the pig neural tissue, sending it into the air in a fine mist. The workers closest in proximity to the "head" table, the area in the plant where high pressured air was used to evacuate the brain tissue from the pig's skull, were the most likely to be affected. The aerosolized mist was inhaled and readily absorbed into the workers' mucus membranes. The pig neural tissue was recognized by their systems as foreign and an immune response was initiated. The pig antigen was found most prominently in the nerve roots of the spine which were also swollen. Researchers determined that the irritation was due to the voltage-gated potassium channels being blocked. They identified 125 1-α-dendrotoxin as the antagonist that binds to and blocks the channels, causing an intracellular build-up of potassium ions which causes inflammation and irritation, and consequently, hyper-excitability in the peripheral nervous system. It is this hyper-excitability that leads to the tingling, numbness, pain, and weakness.

Researchers from the Mayo Clinic developed a mouse model that received twice daily liquefied pig neural tissue intranasally to replicate the symptoms that the workers were experiencing. Physiological testing indicated signature antibodies in the mouse model at 100% in potassium channel antibodies and myelin basic antibodies, and 91% in calcium channel antibodies. This model allowed the researchers to decipher what was causing these neurological symptoms. It was found that the potassium channels were being blocked so that inflammation was occurring at the nerve root and causing hyper-excitability down the peripheral nerves.

Cerebellar abiotrophy (CA), also referred to as the cerebellar cortical abiotrophy (CCA), is a genetic neurological disease in animals best known to affect certain breeds of horses, dogs and cats. It can also develop in humans. It develops when the neurons known as Purkinje cells, located in the cerebellum of the brain, begin to die off. These cells affect balance and coordination. They have a critical role to play in the brain. The Purkinje layer allows communication between the granular and molecular cortical layers in the cerebellum. Put simply, without Purkinje cells, an animal loses its sense of space and distance, making balance and coordination difficult. People with damage to the cerebellum can experience symptoms like unsteady gait, poor muscle control, and trouble speaking or swallowing.

"Abiotrophy" means the loss of a vital nutritive factor. The exact cause of cerebellar abiotrophy is not known, but it is thought to be due to an intrinsic metabolic defect.

In most cases, the Purkinje neurons begin to die off shortly after the animal is born and the condition is noticeable when the animal is less than six months old, though sometimes the onset of symptoms is gradual and the animal is much older before the owner or caretaker notices a problem.

CA cannot be prevented, other than by selective breeding to avoid the gene, and it cannot be cured. Genetic testing can detect carriers. In addition to dogs and horses, there also have been cases of cerebellar abiotrophy in Siamese and Domestic shorthair cats; in Angus, Polled Hereford, Charolais and Holstein Friesian cattle; Merino and Wiltshire sheep; and Yorkshire pigs.

Barcoo fever is an illness once common in the Australian outback that is now virtually unknown. It was characterised by nausea and vomiting exacerbated by the sight or smell of food and, unlike the usual gastro-intestinal infections, by constipation rather than diarrhoea. Fever and myalgia were also symptoms. Severe cases developed inanition and even death. It was seen in travelers in the outback rather than in cities or towns, but occasionally entire settlements were affected, such as occurred in Toowoomba in 1903. The aboriginal population knew to avoid the ailment by not drinking from certain water sources and by taking water from soaks or pits dug in the dry sandy bed of a stream.

It is postulated that the disease may be due to ingestion of cyanobacterial (blue-green algal) toxins, in particular cylindrospermopsin, a toxin from "Cylindrospermopsis raciborskii" and other cyanobacteria, which is a hepatotoxin. The symptoms of the disease are consistent with a hepatitis or liver disorder, and "Cylindrospermopsis" is known to be widespread in inland Australian water sources. The toxin is not destroyed by boiling and, although it would flavor water, this flavor would be masked by tea, the common beverage in the Australian bush. Provision of safe drinking water sources in Australia, with the development of bores and covered tanks to collect rainwater, explain the demise of a once-common illness.

Cows and horses as well as pet animals are also susceptible to the effects of lead toxicity. Sources of lead exposure in pets can be the same as those that present health threats to humans sharing the environment, such as paint and blinds, and there is sometimes lead in toys made for pets. Lead poisoning in a pet dog may indicate that children in the same household are at increased risk for elevated lead levels.