In dogs, signs of distemper vary widely from no signs, to mild respiratory signs indistinguishable from kennel cough, to severe pneumonia with vomiting, bloody diarrhea and death.

Commonly observed signs are a runny nose, vomiting and diarrhea, dehydration, excessive salivation, coughing and/or labored breathing, loss of appetite, and weight loss. If neurological signs develop, incontinence may ensue. Central nervous system signs include a localized involuntary twitching of muscles or groups of muscles, seizures with salivation and jaw movements commonly described as "chewing gum fits", or more appropriately as "distemper myoclonus". As the condition progresses, the seizures worsen and advance to grand mal convulsions followed by death of the animal. The animal may also show signs of sensitivity to light, incoordination, circling, increased sensitivity to sensory stimuli such as pain or touch, and deterioration of motor capabilities. Less commonly, they may lead to blindness and paralysis. The length of the systemic disease may be as short as 10 days, or the start of neurological signs may not come until several weeks or months later. Those few that survive usually have a small tic or twitch of varying levels of severity. With time, this tic will usually diminish somewhat in its severity.

A dog that survives distemper will continue to have both nonlife-threatening and life-threatening signs throughout its lifespan. The most prevalent nonlife-threatening symptom is hard pad disease. This occurs when a dog experiences the thickening of the skin on the pads of its paws as well as on the end of its nose. Another lasting symptom commonly is enamel hypoplasia. Puppies, especially, will have damage to the enamel of teeth that are not completely formed or those that have not yet grown through the gums. This is a result of the virus's killing the cells responsible for manufacturing the tooth enamel. These affected teeth tend to erode quickly.

Life-threatening signs usually include those due to the degeneration of the nervous system. Dogs that have been infected with distemper tend to suffer a progressive deterioration of mental abilities and motor skills. With time, the dog can acquire more severe seizures, paralysis, reduction in sight and incoordination. These dogs are usually humanely euthanized because of the immense pain and suffering they face.

In sheep, BTV causes an acute disease with high morbidity and mortality. BTV also infects goats, cattle and other domestic animals as well as wild ruminants (for example, blesbuck, white-tailed deer, elk, and pronghorn antelope).

Major signs are high fever, excessive salivation, swelling of the face and tongue and cyanosis of the tongue. Swelling of the lips and tongue gives the tongue its typical blue appearance, though this sign is confined to a minority of the animals. Nasal signs may be prominent, with nasal discharge and stertorous respiration.

Some animals also develop foot lesions, beginning with coronitis, with consequent lameness. In sheep, this can lead to knee-walking. In cattle, constant changing of position of the feet gives bluetongue the nickname The Dancing Disease. Torsion of the neck (opisthotonos or torticollis) is observed in severely affected animals.

Not all animals develop signs, but all those that do lose condition rapidly, and the sickest die within a week. For affected animals which do not die, recovery is very slow, lasting several months.

The incubation period is 5–20 days, and all signs usually develop within a month. The mortality rate is normally low, but it is high in susceptible breeds of sheep. In Africa, local breeds of sheep may have no mortality, but in imported breeds it may be up to 90 percent.

In cattle, goats and wild ruminants infection is usually asymptomatic despite high virus levels in blood. Red deer are an exception, and in them the disease may be as acute as in sheep.

Bluetongue disease is a non-contagious, insect-borne, viral disease of ruminants, mainly sheep and less frequently cattle, goats, buffalo, deer, dromedaries, and antelope. It is caused by the Bluetongue virus (BTV). The virus is transmitted by the midge "Culicoides imicola", "Culicoides variipennis", and other culicoids.

Respiratory infection is usually asymptomatic in pigs more than 2 months old, but it can cause abortion, high mortality in piglets, and coughing, sneezing, fever, constipation, depression, seizures, ataxia, circling, and excess salivation in piglets and mature pigs. Mortality in piglets less than one month of age is close to 100%, but it is less than 10% in pigs between one and six months of age. Pregnant swine can reabsorb their litters or deliver mummified, stillborn, or weakened piglets. In cattle (see next section), symptoms include intense itching followed by neurological signs and death. In dogs, symptoms include intense itching, jaw and pharyngeal paralysis, howling, and death Any infected secondary host generally only lives two to three days.

Genital infection appears to have been common in a great part of the 20th century in many European countries in swine herds, where boars from boar centres were used for natural service of sows or gilts. This disease manifestation has always been asymptomatic in affected pigs, and presence of the infection on a farm was detected only because of cases in cattle showing pruritus on the hindquarters (vaginal infection, see below).

In susceptible animals other than swine, infection is usually fatal, and the affected animals most often show intense pruritus in a skin area.

Pruritus in Aujeszky's disease is considered a phantom sensation, and virus has never been found at the site of pruritus.

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.

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.

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.

Most cases of CWD occur in adult animals; the youngest animal diagnosed with natural CWD was 17 months. The disease is progressive and always fatal. The first signs are difficulties in movement. The most obvious and consistent clinical sign of CWD is weight loss over time. Behavioral changes also occur in the majority of cases, including decreased interactions with other animals, listlessness, lowering of the head, tremors, repetitive walking in set patterns, and nervousness. Excessive salivation and grinding of the teeth also are observed. Most deer show increased drinking and urination; the increased drinking and salivation may contribute to the spread of the disease.

Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy (TSE) of mule deer, white-tailed deer, elk (or "wapiti"), moose, and reindeer. As of 2016, CWD had only been found in members of the deer family. First recognized as a clinical "wasting" syndrome in 1967 in mule deer in a wildlife research facility in northern Colorado, USA, it was identified as a TSE in 1978 and has spread to free-ranging and captive populations in 23 US states and two Canadian provinces. CWD is typified by chronic weight loss leading to death. No relationship is known between CWD and any other TSE of animals or people.

Although reports in the popular press have been made of humans being affected by CWD, a study by the Centers for Disease Control and Prevention suggests, "[m]ore epidemiologic and laboratory studies are needed to monitor the possibility of such transmissions".

The epidemiological study further concluded, "[a]s a precaution, hunters should avoid eating deer and elk tissues known to harbor the CWD agent (e.g., brain, spinal cord, eyes, spleen, tonsils, lymph nodes) from areas where CWD has been identified".

An early sign in several animals including cattle, sheep, and guinea pigs is listlessness, which is commonly followed by significant loss of weight and pronounced trembling in the legs and muzzle. These signs often appear several hours after ingestion of white snakeroot. Signs of abdominal pain, polydipsia, and vomiting may be noted. As the effects of the poison progress, signs of constipation, appetite loss, weakness, and difficulty standing and/or walking are usually observed. Complete loss of muscle coordination, stupor, and/or coma precede death. Death usually occurs within 2-10 days of symptom onset. Signs unique to cattle and sheep include peculiar odors found in the breath and urine, breathing difficulties, and over-salivation. Symptoms unique to horses include depression, bloody urine, and choking. In addition to increased heart rate and jugular pulse, swelling around the thoracic inlet in also observed. Horses may also stand with their hind legs wide apart. Symptoms unique to guinea pigs include crouching with half-closed eyes and roughening of the hair. Treatment for milk sickness is typically symptom amelioration, as well as administration of laxatives, sodium lactate, glucose, or hypotonic Ringer’s solution.

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.

As with bodig, the symptoms and forms of lytico present themselves differently from patient to patient.

Patient presentations include muscle atrophy, maxillofacial paralysis, inability to speak or swallow and subsequent choking. Some patients retain mental lucidity throughout the illness until death, much like ALS patients.

Diaphragm and respiratory accessory muscles can become paralyzed necessitating mechanical ventilation to facilitate breathing. Saliva must be suctioned from the mouth to prevent aspiration. This form of lytico-bodig is fatal in all cases.

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.

Geniculate ganglionitis or geniculate neuralgia (GN), also called nervus intermedius neuralgia, Ramsay Hunt syndrome, or Hunt's neuralgia, is a rare disorder characterized by severe paroxysmal neuralgic pain deep in the ear, that may spread to the ear canal, outer ear, mastoid or eye regions. GN may also occur in combination with trigeminal or glossopharyngeal neuralgia.

The pain of GN is sharp, shooting or burning and can last for hours. Painful attacks can be triggered by cold, noise, swallowing or touch, but triggers are usually unique to the sufferer. Other related symptoms that may be experienced include increased salivation, bitter taste, tinnitus and vertigo.

GN is rare, and only limited data is available regarding the incidence, prevalence, and risk factors associated with this condition. Middle-aged adults, however, seem to be predominantly affected, women more than men.

GN may be caused by compression of somatic sensory branch of cranial nerve VII which goes through the nervus intermedius. In sufferers of GN, signals sent along these nerves are altered and interpreted by the geniculate ganglion (a structure in the brain) as GN pain. GN may also develop following herpes zoster oticus (Ramsay Hunt syndrome), where cold sores occur on the ear drum or ear. This may also be associated with facial paresis (weakness), tinnitus, vertigo and deafness. Disorders of lacrimation, salivation and/or taste sometimes accompany the pain. There is a common association with herpes zoster.

Lytico-bodig disease presents itself in two ways:

- lytico is a progressive paralysis that resembles ALS (amyotrophic lateral sclerosis)

- bodig is a condition resembling parkinsonism with occasional dementia.

Physical symptoms include dry mouth, tremors, tightening in the chest, rapid breathing, sweating of the palms, nausea and irregular heart beat.

The symptoms of Ablutophobia as well as many specific phobias are as follows:

- Feelings of panic, dread, horror, or terror

- Recognition that the fear goes beyond normal boundaries and the actual threat of danger

- Reactions that are automatic and uncontrollable, practically taking over the person’s thoughts

- Rapid heartbeat, shortness of breath, trembling, and an overwhelming desire to flee the situation—all the physical reactions associated with extreme fear

- Extreme measures taken to avoid the feared object or situation.

Feelings of shame are also not uncommon. Many cultures place a heavy value on cleanliness, and refusing to bathe can make someone the target of mockery or teasing, which can increase the severity of the phobia. It may also cause the sufferer to not seek treatment.

Phobophobia is mainly linked with internal predispositions. It is developed by the unconscious mind which is linked to an event in which phobia was experienced with emotional trauma and stress, which are closely linked to anxiety disorders and by forgetting and recalling the initiating trauma. Phobophobia might develop from other phobias, in which the intense anxiety and panic caused by the phobia might lead to fearing the phobia itself, which triggers phobophobia before actually experiencing the other phobia. The extreme fear towards the other phobia can lead the patient to believe that their condition may develop into something worse, intensifying the effects of the other phobia by fearing it. Also, phobophobia can be developed when anxiety disorders are not treated, creating an extreme predisposition to other phobias. The development of phobophobia can also be attributed to characteristics of the patient itself, such as phylogenetic influence, the prepotency of certain stimuli, individual genetic inheritance, age incidence, sex incidence, personality background, cultural influence inside and outside the family, physiological variables and biochemical factors.

Phobophobia shares the symptoms of many other anxiety disorders, more specifically panic attacks and generalized anxiety disorder:

1. Dizziness

2. Heart pounding

3. An excess of perspiration

4. Slight paresthesia

5. Tension

6. Hyperventilation

7. Angst

8. Faintness

9. Avoidance

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

Hyperalgesic fear of needles is another form that does not have as much to do with fear of the actual needle. Patients with this form have an inherited hypersensitivity to pain, or hyperalgesia. To them, the pain of an injection is unbearably great and many cannot understand how anyone can tolerate such procedures.

This form of fear of needles affects around 10% of needle phobes. The symptoms include extreme explained anxiety, and elevated blood pressure and heart rate at the immediate point of needle penetration or seconds before. The recommended forms of treatment include some form of anesthesia, either topical or general.

The level of fear as well as other symptoms will vary between individuals. There are four general types of symptoms: psychological, physical, mental and emotional.

Symptoms can range from mild to extreme—often described as extreme flu-like symptoms. Many symptoms may be associated with fungemia, including pain, acute confusion, chronic fatigue, and infections. Skin infections can include persistent or non-healing wounds and lesions, sweating, itching, and unusual discharge or drainage.

Whilst witnessing procedures involving needles it is possible for the phobic present to suffer the symptoms of a needle phobic attack without actually being injected. Prompted by the sight of the injection the phobic may exhibit the normal symptoms of vasovagal syncope and fainting or collapse is common. While the cause of this is not known, it may be due to the phobic imagining the procedure being performed on themselves. Recent neuroscience research shows that feeling a pin prick sensation and watching someone else's hand get pricked by a pin activate the same part of the brain.

Waterhouse-Friderichsen Syndrome can be caused by a number of different organisms (see below). When caused by Neisseria meningitidis, WFS is considered the most severe form of meningococcal sepsis. The onset of the illness is nonspecific with fever, rigors, vomiting, and headache. Soon a rash appears; first macular, not much different from the rose spots of typhoid, and rapidly becoming petechial and purpuric with a dusky gray color. Low blood pressure (hypotension) develops and rapidly leads to septic shock. The cyanosis of extremities can be extreme and the patient is very prostrated or comatose. In this form of meningococcal disease, meningitis generally does not occur. Low levels of blood glucose and sodium, high levels of potassium in the blood, and the ACTH stimulation test demonstrate the acute adrenal failure. Leukocytosis need not be extreme and in fact leukopenia may be seen and it is a very poor prognostic sign. C-reactive protein levels can be elevated or almost normal. Thrombocytopenia is sometimes extreme, with alteration in prothrombin time (PT) and partial thromboplastin time (PTT) suggestive of disseminated intravascular coagulation (DIC). Acidosis and acute kidney failure can be seen as in any severe sepsis. Meningococci can be readily cultured from blood or cerebrospinal fluid, and can sometimes be seen in smears of cutaneous lesions. Difficulty swallowing, atrophy of the tongue, and cracks at the corners of the mouth are also characteristic features.