A number of vaccines against canine distemper exist for dogs (ATCvet code: and combinations) and domestic ferrets (), which in many jurisdictions are mandatory for pets. Infected animals should be quarantined from other dogs for several months owing to the length of time the animal may shed the virus. The virus is destroyed in the environment by routine cleaning with disinfectants, detergents, or drying. It does not survive in the environment for more than a few hours at room temperature (20–25 °C), but can survive for a few weeks in shady environments at temperatures slightly above freezing. It, along with other labile viruses, can also persist longer in serum and tissue debris.

Despite extensive vaccination in many regions, it remains a major disease of dogs.

To prevent canine distemper, puppies should begin vaccination at six to eight weeks of age and then continue getting the “booster shot” every two to four weeks until they are 16 weeks of age. Without the full series of shots, the vaccination will not provide protection against the virus. Since puppies are typically sold at the age of eight to ten weeks, they typically receive the first shot while still with their breeder, but the new owner often does not finish the series. These dogs are not protected against the virus and so are susceptible to canine distemper infection, continuing the downward spiral that leads to outbreaks throughout the country.

The above signs, especially fever, respiratory signs, neurological signs, and thickened footpads occurring in unvaccinated dogs strongly indicate canine distemper. However, several febrile diseases match many of the signs of the disease and only recently has distinguishing between canine hepatitis, herpes virus, parainfluenza and leptospirosis been possible. Thus, finding the virus by various methods in the dog's conjunctival cells or foot pads gives a definitive diagnosis. In older dogs that develop distemper encephalomyelitis, diagnosis may be more difficult, since many of these dogs have an adequate vaccination history.

An additional test to confirm distemper is a brush border slide of the bladder transitional epithelium of the inside lining from the bladder, stained with Dif-Quick. These infected cells have inclusions which stain a carmine red color, found in the paranuclear cytoplasm readability. About 90% of the bladder cells will be positive for inclusions in the early stages of distemper.

However, simple husbandry changes and practical midge control measures may help break the livestock infection cycle. Housing livestock during times of maximum midge activity (from dusk to dawn) may lead to significantly reduced biting rates. Similarly, protecting livestock shelters with fine mesh netting or coarser material impregnated with insecticide will reduce contact with the midges. The "Culicoides" midges that carry the virus usually breed on animal dung and moist soils, either bare or covered in short grass. Identifying breeding grounds and breaking the breeding cycle will significantly reduce the local midge population. Turning off taps, mending leaks and filling in or draining damp areas will also help dry up breeding sites. Control by trapping midges and removing their breeding grounds may reduce vector numbers. Dung heaps or slurry pits should be covered or removed, and their perimeters (where most larvae are found) regularly scraped.

Outbreaks in southern Europe have been caused by serotypes 2 and 4, and vaccines are available against these serotypes (ATCvet codes: for sheep, for cattle). However, the disease found in northern Europe (including the UK) in 2006 and 2007 has been caused by serotype 8. Vaccine companies Fort Dodge Animal Health (Wyeth), Merial and Intervet were developing vaccines against serotype 8 (Fort Dodge Animal Health has serotype 4 for sheep, serotype 1 for sheep and cattle and serotype 8 for sheep and cattle) and the associated production facilities. A vaccine for this is now available in the UK, produced by Intervet. Fort Dodge Animal Health has their vaccines available for multiple European Countries (vaccination will start in 2008 in Germany, Belgium, Switzerland, Spain and Italy). However, immunization with any of the available vaccines preclude later serological monitoring of affected cattle populations, a problem which could be resolved using next-generation subunit vaccines currently in development.

In January 2015, Indian researchers launched its vaccine. Named 'Raksha Blu', it will protect the animals against five strains of the ‘bluetongue’ virus prevalent in the country.

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.

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.

On post-mortem examination (necropsy), the most obvious gross lesion is subcutaneous oedema in the submandibular and pectoral (brisket) regions. Petechial haemorrhages are found subcutaneously and in the thoracic cavity. In addition, congestion and various degrees of consolidation of the lung may occur. Animals that die within 24–36 hours, have only few petechial haemorrhages on the heart and generalised congestion of the lung, while in animals that die after 72 hours, petechial and ecchymotic haemorrhages were more evident and lung consolidation are more extensive.

Diagnosis is based on "post mortem" examination (necropsy) and testing; examination of the dead body is not definitive as many animals die early in the course of the disease and conditions found are non-specific; general signs of poor health and Aspiration pneumonia, which may be the actual cause of death, are common. On microscopic examination, lesions of CWD in the central nervous system resemble those of other TSEs. In addition, scientists use immunohistochemistry to test brain, lymph, and neuroendocrine tissues for the presence of the abnormal prion protein to diagnose CWD; positive IHC findings in the obex is considered the gold standard.

As of 2015 there were no commercially feasible diagnostic tests that could be used on live animals. It is possible to run a bioassay, taking fluids from cervids suspected of infection and incubating them in transgenic mice that express the cervid prion protein, to determine if the cervid is infected, but there are ethical issues with this and it is not scalable.

A wide variety of clinical signs have been described for HS in cattle and buffaloes. The incubation periods (the time between exposure and observable disease) for buffalo calves 4–10 months of age varies according to the route of infection. The incubation period is 12–14 hours, approximately 30 hours and 46–80 hours for subcutaneous infection, oral infection and natural exposure, respectively.

There is variability in the duration of the clinical course of the disease. In the case of experimental subcutaneous infection, the clinical course lasted only a few hours, while it persisted for 2–5 days following oral infection and in buffaloes and cattle that had been exposed to naturally-infected animals. It has also been recorded from field observations that the clinical courses of per-acute and acute cases were 4–12 hours and 2–3 days, respectively.

Generally, progression of the disease in buffaloes and cattle is divided into three phases. Phase one is characterised by fever, with a rectal temperature of , loss of appetite and depression. Phase two is typified by increased respiration rate (40–50/minute), laboured breathing, clear nasal discharge (turns opaque and mucopurulent as the disease progresses), salivation and submandibular oedema spreading to the pectoral (brisket) region and even to the forelegs. Finally, in phase three, there is typically recumbency, continued acute respiratory distress and terminal septicaemia. The three phases overlap when the disease course is short. In general, buffaloes have a more acute onset of disease than cattle, with a shorter duration.

The origin and mode of transmission of the prions causing CWD is unknown, but recent research indicates that prions can be excreted by deer and elk, and are transmitted by eating grass growing in contaminated soil. Animals born in captivity and those born in the wild have been affected with the disease. Based on epidemiology, transmission of CWD is thought to be lateral (from animal to animal). Maternal transmission may occur, although it appears to be relatively unimportant in maintaining epidemics. An infected deer's saliva is able to spread the CWD prions. Exposure between animals is associated with sharing food and water sources contaminated with CWD prions shed by diseased deer.

The disease was first identified in 1967 in a closed herd of captive mule deer in contiguous portions of northeastern Colorado. In 1980, the disease was determined to be a TSE. It was first identified in wild elk and mules in 1981 in Colorado and Wyoming, and in farmed elk in 1997.

In May 2001, CWD was also found in free-ranging deer in the southwestern corner of Nebraska (adjacent to Colorado and Wyoming) and later in additional areas in western Nebraska. The limited area of northern Colorado, southern Wyoming, and western Nebraska in which free-ranging deer, moose, and/or elk positive for CWD have been found is referred to as the endemic area. The area in 2006 has expanded to six states, including parts of eastern Utah, southwestern South Dakota, and northwestern Kansas. Also, areas not contiguous (to the endemic area) areas in central Utah and central Nebraska have been found. The limits of the affected areas are not well defined, since the disease is at a low incidence and the amount of sampling may not be adequate to detect it. In 2002, CWD was detected in wild deer in south-central Wisconsin and northern Illinois and in an isolated area of southern New Mexico. In 2005, it was found in wild white-tailed deer in New York and in Hampshire County, West Virginia. In 2008, the first confirmed case of CWD in Michigan was discovered in an infected deer on an enclosed deer-breeding facility. It is also found in the Canadian provinces of Alberta and Saskatchewan. In February 2011, the Maryland Department of Natural Resources reported the first confirmed case of the disease in that state. The affected animal was a white-tailed deer killed by a hunter.

CWD has also been diagnosed in farmed elk and deer herds in a number of states and in two Canadian provinces. The first positive farmed elk herd in the United States was detected in 1997 in South Dakota.

Since then, additional positive elk herds and farmed white-tailed deer herds have been found in South Dakota (7), Nebraska (4), Colorado (10), Oklahoma (1), Kansas (1), Minnesota (3), Montana (1), Wisconsin (6) and New York (2). As of fall of 2006, four positive elk herds in Colorado and a positive white-tailed deer herd in Wisconsin remain under state quarantine. All of the other herds have been depopulated or have been slaughtered and tested, and the quarantine has been lifted from one herd that underwent rigorous surveillance with no further evidence of disease. CWD also has been found in farmed elk in the Canadian provinces of Saskatchewan and Alberta. A retrospective study also showed mule deer exported from Denver to the Toronto Zoo in the 1980s were affected. In June 2015, the disease was detected in a male white-tailed deer on a breeding ranch in Medina County, Texas. State officials euthanized 34 deer in an effort to contain a possible outbreak.

Species that have been affected with CWD include elk, mule deer, white-tailed deer, black-tailed deer, and moose. Other ruminant species, including wild ruminants and domestic cattle, sheep, and goats, have been housed in wildlife facilities in direct or indirect contact with CWD-affected deer and elk, with no evidence of disease transmission. However, experimental transmission of CWD into other ruminants by intracranial inoculation does result in disease, suggesting only a weak molecular species barrier exists. Research is ongoing to further explore the possibility of transmission of CWD to other species.

By April 2016 CWD had been found in captive animals in South Korea; the disease arrived there with live elk that were imported for farming in the late 1990s.

Human milk sickness is uncommon today in the United States. Current practices of animal husbandry generally control the pastures and feed of cattle, and the pooling of milk from many producers lowers the risk of tremetol present in dangerous amounts. The poison tremetol is not inactivated by pasteurization. Although extremely rare, milk sickness can occur if a person drinks contaminated milk or eats dairy products gathered from a single cow or from a smaller herd that has fed on the white snakeroot plant. There is no cure, but treatment is available.

Milk sickness, also known as tremetol vomiting or, in animals, as trembles, is a kind of poisoning, characterized by trembling, vomiting, and severe intestinal pain, that affects individuals who ingest milk, other dairy products, or meat from a cow that has fed on white snakeroot plant, which contains the poison tremetol.

Although very rare today, milk sickness claimed thousands of lives among migrants to the Midwest in the early 19th century in the United States, especially in frontier areas along the Ohio River Valley and its tributaries where white snakeroot was prevalent. New settlers were unfamiliar with the plant and its properties. A notable victim was Nancy Hanks Lincoln, the mother of Abraham Lincoln, who died in 1818. Nursing calves and lambs may have died from their mothers' milk contaminated with snakeroot, although the adult cows and sheep showed no signs of poisoning. Cattle, horses, and sheep are the animals most often poisoned.

Anna Pierce Hobbs Bixby, called Dr. Anna on the frontier, is credited today by the American medical community with having identified white snakeroot as the cause of the illness. Told about the plant's properties by an elderly Shawnee woman she befriended, Bixby did testing to observe and document evidence. She wrote up her findings to share the discovery in the medical world. The Shawnee woman's name has been lost to history.

Pulicosis (also known as "flea bites") is a skin condition caused by several species of fleas, including the cat flea ("Ctenocephalides felis") and dog flea ("Ctenocephalides canis"). This condition can range from mild irritation to severe irritation. In some cases, 48 to 72 hours after being bitten, a more severe rash-like irritation may begin to spread across the body. Symptoms include swelling of the bitten area, erythema, ulcers of the mouth and throat, restlessness, and soreness of the areolae. In extreme cases, within 1 week after being bitten, the condition may spread through the lymph nodes and begin affecting the central nervous system. Permanent nerve damage can occur.

If they receive an excessive number of bites, pets can also develop flea allergy dermatitis, which can potentially be fatal if no actions are taken. However, dogs and cats are not the only ones that are at risk. Humans can suffer from flea bites and, depending on a variety of factors, the bites can cause much pain and discomfort.

Diagnostic criteria:

A. Pain paroxysms of intermittent occurrence, lasting for seconds or minutes, in the depth of the ear

B. Presence of a trigger area in the posterior wall of the auditory canal

C. Not attributed to another disorder

A variety of surgeries have been performed including microvascular decompression (MVD) of the fifth, ninth, and tenth nerves; as well as partial cutting of the nervus intermedius, geniculate ganglion, chorda tympani and/or the ninth and tenth cranial nerves.

A thorough medical history and physical examination, including a neurological examination, are the first steps in making a diagnosis. This alone may be sufficient to diagnose Bell's Palsy, in the absence of other findings. Additional investigations may be pursued, including blood tests such as ESR for inflammation, and blood sugar levels for diabetes. If other specific causes, such as sarcoidosis or Lyme disease are suspected, specific tests such as angiotensin converting enzyme levels, chest x-ray or Lyme titer may be pursued. If there is a history of trauma, or a tumour is suspected, a CT scan may be used.

Routine vaccination against meningococcus is recommended by the Centers for Disease Control and Prevention for all 11- to 18-year-olds and people who have poor splenic function (who, for example, have had their spleen removed or who have sickle-cell disease which damages the spleen), or who have certain immune disorders, such as a complement deficiency.

A number of measurements exist to assess exposure and early biological effects for organophosphate poisoning. Measurements of OP metabolites in both the blood and urine can be used to determine if a person has been exposed to organophosphates. Specifically in the blood, metabolites of cholinesterases, such as butyrylcholinesterase (BuChE) activity in plasma, neuropathy target esterase (NTE) in lymphocytes, and of acetylcholinesterase (AChE) activity in red blood cells. Due to both AChE and BuChE being the main targets of organophosphates, their measurement is widely used as an indication of an exposure to an OP. The main restriction on this type of diagnosis is that depending on the OP the degree to which either AChE or BuChE are inhibited differs; therefore, measure of metabolites in blood and urine do not specify for a certain OP. However, for fast initial screening, determining AChE and BuChE activity in the blood are the most widely used procedures for confirming a diagnosis of OP poisoning. The most widely used portable testing device is the Test-mate ChE field test, which can be used to determine levels of Red Blood Cells (RBC), AChE and plasma (pseudo) cholinesterase (PChE) in the blood in about four minutes. This test has been shown to be just as effective as a regular laboratory test and because of this, the portable ChE field test is frequently used by people who work with pesticides on a daily basis.

Fear of needles, especially in its more severe forms, is often comorbid with other phobias and psychological ailments; for example, iatrophobia, or an irrational fear of doctors, is often seen in needle phobic patients.

A needle phobic patient does not need to physically be in a doctor's office to experience panic attacks or anxiety brought on by needle phobia. There are many triggers in the outside world that can bring on an attack through association. Some of these are blood, injuries, the sight of the needle physically or on a screen, paper pins, examination rooms, hospitals, white lab coats, hospital gowns, doctors, dentists, nurses, the antiseptic smell associated with offices and hospitals, the sight of a person who physically resembles the patient's regular health care provider, or even reading about the fear.

The diagnosis can be confirmed when the characteristic centrotemporal spikes are seen on electroencephalography (EEG). Typically, high-voltage spikes followed by slow waves are seen. Given the nocturnal activity, a sleep EEG can often be helpful. Technically, the label "benign" can only be confirmed if the child's development continues to be normal during follow-up. Neuroimaging, usually with an MRI scan, is only advised for cases with atypical presentation or atypical findings on clinical examination or EEG.

The disorder should be differentiated from several other conditions, especially centrotemporal spikes without seizures, centrotemporal spikes with local brain pathology, central spikes in Rett syndrome and fragile X syndrome, malignant Rolandic epilepsy, temporal lobe epilepsy and Landau-Kleffner syndrome.

The medical literature suggests a number of treatments that have been proven effective for specific cases of needle phobia, but provides very little guidance to predict which treatment may be effective for any specific case. The following are some of the treatments that have been shown to be effective in some specific cases.

- Ethyl Chloride Spray (and other freezing agents). Easily administered, but provides only superficial pain control.

- Jet Injectors. Jet Injectors work by introducing substances into the body through a jet of high pressure gas as opposed to by a needle. Though these eliminate the needle, some people report that they cause more pain. Also, they are only helpful in a very limited number of situations involving needles i.e. insulin and some inoculations.

- Iontophoresis. Iontophoresis drives anesthetic through the skin by using an electric current. It provides effective anesthesia, but is generally unavailable to consumers on the commercial market and some regard it as inconvenient to use.

- EMLA. EMLA is a topical anesthetic cream that is a eutectic mixture of lidocaine and prilocaine. It is a prescription cream in the United States, and is available without prescription in some other countries. Although not as effective as iontophoresis, since EMLA does not penetrate as deeply as iontophoresis-driven anesthetics, EMLA provides a simpler application than iontophoresis. EMLA penetrates much more deeply than ordinary topical anesthetics, and it works adequately for many individuals.

- Ametop. Ametop gel appears to be more effective than EMLA for eliminating pain during venepuncture.

- Lidocaine/tetracaine patch. A self-heating patch containing a eutectic mixture of lidocaine and tetracaine is available in several countries, and has been specifically approved by government agencies for use in needle procedures. The patch is sold under the trade name "Synera" in the United States and "Rapydan" in European Union. Each patch is packaged in an air-tight pouch. It begins to heat up slightly when the patch is removed from the packaging and exposed to the air. The patch requires 20 to 30 minutes to achieve full anesthetic effect. The Synera patch was approved by the United States Food and Drug Administration on 23 June 2005.

- Behavioral therapy. Effectiveness of this varies greatly depending on the person and the severity of the condition. There is some debate as to the effectiveness of behavioral treatments for specific phobias (like blood, injection, injury type phobias), though some data are available to support the efficacy of approaches like exposure therapy. Any therapy that endorses relaxation methods may be contraindicated for the treatment of fear of needles as this approach encourages a drop in blood pressure that only enhances the vasovagal reflex. In response to this, graded exposure approaches can include a coping component relying on applied tension as a way to prevent complications associated with the vasovagal response to specific blood, injury, injection type stimulus.

- Nitrous Oxide (Laughing Gas). This will provide sedation and reduce anxiety for the patient, along with some mild analgesic effects.

- Inhalation General Anesthesia. This will eliminate all pain and also all memory of any needle procedure. On the other hand, it is often regarded as a very extreme solution. It is not covered by insurance in most cases, and most physicians will not order it. It can be risky and expensive and may require a hospital stay.

- Benzodiazepines, such as diazepam (Valium) or lorazepam, may help alleviate the anxiety of needle phobics, according to Dr. James Hamilton. These medications have an onset of action within 5 to 15 minutes from ingestion. A relatively large oral dose may be necessary.

There are also many options for treatment of Ablutophobia. Generally seeking professional help from a person with a background in psychology is the best option. A sufferer of Ablutophobia can also undergo Exposure-Based Cognitive Behavioral Therapy in which the person is allowed to confront the feared object (in this case, water) in controlled situations.

There are anxiety medications that medical professionals can prescribe as well, however these medications have yet to show much promise in the treatments of specific phobias such as Ablutophobia. The use of d-cycloserine (DCS) in conjunction with Exposure therapy is the only drug to show developments in alleviating the phobia-related symptoms even after a 3-month period.

Scientists have developed medications that can be taken to reduce patients' fears. This medication is known as anti-anxiety medication. However, medications may have side-effects or withdrawal symptoms that can be severe. The most popular form of treatment is visiting a cognitive behavioral therapist, psychologist, psychiatrist, hypnotherapist, or hypnotist. These therapies are also used to help patients forget what they are afraid of. Some basic therapy sessions involve making the patient stand in front of a fan, or making the patient face their fears in a safe environment. With the use of hypnotherapy, the subconscious mind of a person can be reached, potentially eliminating those fears.

Facial nerve paralysis may be divided into supranuclear and infranuclear lesions.

Helminthophobia, scoleciphobia or vermiphobia is a specific phobia, the fear of worms, especially parasitic worms. The sight of a worm, or anything that looks like a worm, may cause someone with this phobia to have extreme anxiety or even panic attacks.