Signs and symptoms of PHF include acute-onset fever, depression (sometimes profound), inappetance, mild colic-like symptoms, decreased manure production, profuse watery non-fetid diarrhea endotoxemia, edema due to protein imbalances, abortion by pregnant mares, and acute laminitis (20 to 40 percent of cases). Infected horses founder usually within three days of the initial symptoms, thought to be secondary to endotoxemia. Death may occur and is usually due to severe laminitis leading to founder.

Horses may not always display any other symptoms beyond a fever.

Potomac Horse Fever (PHF) is a potentially-fatal febrile illness affecting horses caused by the intracellular bacterium "Neorickettsia risticii". PHF is also known as Shasta River Crud and Equine Monocytic Ehrlichiosis. It was first described in areas surrounding the Potomac River northwest of Washington, D.C., in the 1980s, but cases have been described in many other parts of the United States, such as Minnesota, California, and Pennsylvania. Currently, it is found in more than 40 U.S. states and Canada.

Acute: The acute form is a sudden onset of the disease at full-force. Symptoms include high fever, anemia (due to the breakdown of red blood cells), weakness, swelling of the lower abdomen and legs, weak pulse, and irregular heartbeat. The horse may die suddenly.

Subacute: A slower, less severe progression of the disease. Symptoms include recurrent fever, weight loss, an enlarged spleen (felt during a rectal examination), anemia, and swelling of the lower chest, abdominal wall, penile sheath, scrotum, and legs.

Chronic: The horse tires easily and is unsuitable for work. The horse may have a recurrent fever and anemia, and may relapse to the subacute or acute form even several years after the original attack.

A horse may also not appear to have any symptoms, yet still tests positive for EIA antibodies. Such a horse can still pass on the disease. According to most veterinarians, horses diagnosed EIA positive usually do not show any sign of sickness or disease.

EIA may cause abortion in pregnant mares. This may occur at any time during the pregnancy if there is a relapse when the virus enters the blood. Most infected mares will abort, however some give birth to healthy foals. Foals are not necessarily infected.

Studies indicate that there are breeds with a tolerance to EIA.

Recent studies in Brazil on living wild horses have shown that in the Pantanal, about 30% of domesticated and about 5.5% of the wild horses are chronically infected with EIA.

Pacheco's disease is an acute and often lethal infectious disease in psittacine birds. The disease is caused by a group of herpesviruses, "Psittacid herpesvirus 1" (PsHV-1), which consists of four genotypes. Birds which do not succumb to Pacheco's disease after infection with the virus become asymptomatic carriers that act as reservoirs of the infection. These persistently infected birds, often Macaws, Amazon parrots and some species of conures, shed the virus in feces and in respiratory and oral secretions. Outbreaks can occur when stress causes healthy birds who carry the virus to shed it. Birds generally become infected after ingesting the virus in contaminated material, and show signs of the disease within several weeks.

The main sign of Pacheco's disease is sudden death, sometimes preceded by a short, severe illness. If a bird survives Pacheco's disease following infection with PsHV-1 genotypes 1, 2 or 3, it may later develop internal papilloma disease in the gastrointestinal tract.

Susceptible parrot species include the African gray parrot, and cockatoo. Native Australian birds, such as the eclectus parrot, Bourke's parrot, and budgerigar are susceptible to Pacheco's disease, although the disease itself has not been found in Australia.

Equine infectious anemia or equine infectious anaemia (EIA), also known by horsemen as swamp fever, is a horse disease caused by a retrovirus and transmitted by bloodsucking insects. The virus ("EIAV") is endemic in the Americas, parts of Europe, the Middle and Far East, Russia, and South Africa. The virus is a lentivirus, like human immunodeficiency virus (HIV). Like HIV, EIA can be transmitted through blood, milk, and body secretions.

Transmission is primarily through biting flies, such as the horse-fly and deer-fly. The virus survives up to 4 hours in the vector (epidemiology). Contaminated surgical equipment and recycled needles and syringes, and bits can transmit the disease. Mares can transmit the disease to their foals via the placenta.

The risk of transmitting the disease is greatest when an infected horse is ill, as the blood levels of the virus are then highest.

There are two ways in which the virus can progress, systematic and encephalitic, depending on the person's age. Encephalitic involves swelling of the brain and can be asymptomatic while the systemic illness occurs very abruptly. Those with the systemic illness usually recover within one to two weeks. While the encephalitis is more common among infants in adults and children it usually manifests after experiencing the systemic illness. Symptoms include high fever, muscle pain, altered mental status, headache, meningeal irritation, photophobia, and seizures, which occur three to 10 days after the bite of an infected mosquito. Due to the virus's effect on the brain, patients who survive can be left with mental and physical impairments such as personality disorders, paralysis, seizures, and intellectual impairment

Eastern equine encephalitis (EEE), commonly called Triple E or, sleeping sickness (not to be confused with "Trypanosomiasis") is a zoonotic alphavirus and arbovirus present in North, Central and South America and the Caribbean. EEE was first recognized in Massachusetts, United States in 1831 when 75 horses died mysteriously of viral encephalitis.

Epizootics in horses have continued to occur regularly in the United States. It can also be identified in asses and zebras. Due to the rarity of the disease its occurrence can cause economic impact in relation to the loss of horses and poultry. EEE is found today in the eastern part of the country and is often associated with coastal plains. It can most commonly be found in east and gulf coast states. In Florida about one to two human cases are reported a year although over sixty cases of equine encephalitis are reported. Some years in which there are favorable conditions for the disease there number of equine cases are over two-hundred. Diagnosing equine encephalitis is challenging because many of the symptoms are shared with other illnesses and patients can be asymptomatic. Confirmations may require a sample of cerebral spinal fluid or brain tissue although CT scans and MRI scans are used to detect encephalitis. This could be an indication that the need to test for Eastern Equine Encephalitis is necessary. If a biopsy of the cerebral spinal fluid is taken it is sent to a specialized laboratory for testing.

EEEV is closely related to Venezuelan equine encephalitis virus and Western equine encephalitis virus.

Common clinical signs of Tyzzer’s Disease include watery diarrhea, depression, emaciation, and a ruffled coat. Other observed clinical signs include melena, depression, lethargy, and decreased temperature. In muskrats, this disease is characterized by extensive hemorrhaging within the lower intestine and abdomen. Due to the fast-acting nature of this disease, infected individuals often do not live long enough to exhibit symptoms. It is not uncommon for an infected animal to die within 1-10 days of disease contraction.

During necropsy, inflammation of the ileum, cecum, and colon are commonly present. Perhaps the most distinctive trait of this disease, however, is the grayish yellow necrotic lesions found on the liver of diseased animals. The number of these spots present can range from one to countless. Occasionally, lesions are discovered in the lower intestinal tract and heart as well. Even with physical signs and symptoms present, a conclusive diagnosis is dependent upon the presence of "C. piliforme" within the liver of the infected animal.

Clinical appearance of the disease includes depression, a serous nasal discharge, and sporadically minor facial inflammation in mild form of the disease. In severe form, there is severe inflammation of one or both infraorbital sinuses with edema of the surrounding tissue. The swelling can cause closure of one eye or both of them. Intermandibular space and wattles of corks do swell as a course of the disease .

The signs shown depend on the horse's age, the strain of the infecting virus, the condition of the horse and the route by which it was infected. Most horses with EVA infection don't show any signs; if a horse does show symptoms, these can vary greatly in severity. Following infection, the first sign is fever, peaking at , followed by various signs such as depression, nasal discharge, "pink eye" (conjunctivitis), swelling over the eye (supraorbital edema), urticaria, and swelling of the limbs and under the belly (the ventral abdomen) which may extend to the udder in mares or the scrotum of male horses. More unusual signs include abortion in pregnant mares, and, most likely in foals, severe respiratory distress and death.

This is the least common form of pigeon fever seen in horses. It is characterized by severe limb swelling and cellulitis in one or both hind limbs and can lead to lameness, fever, lethargy and loss of appetite. Antimicrobial and anti-inflammatory treatments are required to prevent further complications such as limb edema, prolonged or recurrent infection, lameness, weakness and weight loss.

Covering sickness, or dourine (French, from the Arabic "darina", meaning mangy (said of a female camel), feminine of "darin", meaning dirty), is a disease of horses and other members of the family Equidae. The disease is caused by "Trypanosoma equiperdum", which belongs to an important genus of parasitic protozoa, and is the only member of the genus that is spread through sexual intercourse. The occurrence of dourine is notifiable in the European Union under legislation from the OIE. There currently is no vaccine and although clinical signs can be treated, there is no cure.

External abscesses are the most common form of pigeon fever seen in horses. Abscesses develop on the body, usually in the pectoral region and along the ventral midline of the abdomen. However, abscesses can also develop on other areas of the body such as the prepuce, mammary gland, triceps, limbs and head. The fatality rate for this form infection is very low. The abscess is often drained once it has matured.

Tyzzer’s disease is an acute epizootic bacterial disease found in rodents, rabbits, dogs, cats, birds, pandas, deer, foals, cattle, and other mammals including gerbils. It is caused by the spore-forming bacterium "Clostridium piliforme", formerly known as "Bacillus piliformis". It is an infectious disease characterized by necrotic lesions on the liver, is usually fatal, and is present worldwide. Animals with the disease become infected through oral ingestion of the bacterial spores and usually die within a matter of days. Animals most commonly affected include young, stressed animals in laboratory environments, such as immature rodents and rabbits. Most commonly affected wild animals include muskrats "(Ondatra zibethicus)" and occasionally cottontail rabbits "(Lepus sylvaticus)". Even today, much remains unknown about Tyzzer’s disease, including how and why it occurs.

Equine viral arteritis (EVA) is a disease of horses caused by equine arteritis virus, an RNA virus of the genus "Arterivirus". The virus which causes EVA was first isolated in 1953, but the disease has afflicted equine animals worldwide for centuries. It has been more common in some breeds of horses in the United States, but there is no breed "immunity". In the UK, it is a notifiable disease. There is no known human hazard.

Infectious coryza is a serious bacterial disease of chickens which affects respiratory system and it is manifested by inflammation of the area below the eye, nasal discharge and sneezing...The disease is found all over the world causing high economic losses. Economic loss is due to stumping off and reduction of egg production in case of laying chickens. The disease was discovered early 1930s by considering clinical signs

This disease affects the external genitalia, and is caused by equine herpesvirus 3. This disease remains with the horse for all its life. Equine coital exanthema is believed to only be transmitted during the acute phase of the disease through serous fluid from the blisters during sexual intercourse, and via breeding tools, handlers, etc.

Clinical signs include cute small lesions, no bigger than 2 mm in diameter around the vulva in mares, and on the sheath in stallions. The small bumps blister and then rupture, leaving raw, ulcerated, painful sores. While the majority of the symptoms are external, the presence of the virus can cause small and large plaque variants in tissues.

There is a rapid onset of clinical signs over the period of 2–7 days, beginning with anorexia, lethargy, and hyperbilirubinemia (icterus and discolored urine). Signs of hepatic encephalopathy (ataxia, blindness, aggression, and coma) and fever can also occur. Other signs include photodermatitis, hemorrhagic diathesis, dependent edema, and colic. The reason for colic is unknown, but is thought to be due to rapid decrease in the size of the liver, and the increased risk of gastric impaction. Rarely, weight loss can occur.

The most detailed study on the frequency, onset, and duration of MVD clinical signs and symptoms was performed during the 1998–2000 mixed MARV/RAVV disease outbreak. A maculopapular rash, petechiae, purpura, ecchymoses, and hematomas (especially around needle injection sites) are typical hemorrhagic manifestations. However, contrary to popular belief, hemorrhage does not lead to hypovolemia and is not the cause of death (total blood loss is minimal except during labor). Instead, death occurs due to multiple organ dysfunction syndrome (MODS) due to fluid redistribution, hypotension, disseminated intravascular coagulation, and focal tissue necroses.

Clinical phases of Marburg Hemorrhagic Fever's presentation are described below. Note that phases overlap due to variability between cases.

1. Incubation: 2–21 days, averaging 5–9 days.

2. Generalization Phase: Day 1 up to Day 5 from onset of clinical symptoms. MHF presents with a high fever (~40˚C) and a sudden, severe headache, with accompanying chills, fatigue, nausea, vomiting, diarrhea, pharyngitis, maculopapular rash, abdominal pain, conjunctivitis, & malaise.

3. Early Organ Phase: Day 5 up to Day 13. Symptoms include prostration, dyspnea, edema, conjunctival injection, viral exanthema, and CNS symptoms, including encephalitis, confusion, delirium, apathy, and aggression. Hemorrhagic symptoms typically occur late and herald the end of the early organ phase, leading either to eventual recovery or worsening & death. Symptoms include bloody stools, ecchymoses, blood leakage from venipuncture sites, mucosal & visceral hemorrhaging, and possibly hematemesis.

4. Late Organ Phase: Day 13 up to Day 21+. Symptoms bifurcate into two constellations for survivors & fatal cases. Survivors will enter a convalescence phase, experiencing myalgia, fibromyalgia, hepatitis, asthenia, ocular symptoms, & psychosis. Fatal cases continue to deteriorate, experiencing continued fever, obtundation, coma, convulsions, diffuse coagulopathy, metabolic disturbances, shock and death, with death typically occurring between Days 8 and 16.

Infants with Krabbe disease are normal at birth. Symptoms begin between the ages of 3 and 6 months with irritability, fevers, limb stiffness, seizures, feeding difficulties, vomiting, and slowing of mental and motor development. In the first stages of the disease, doctors often mistake the symptoms for those of cerebral palsy. Other symptoms include muscle weakness, spasticity, deafness, optic atrophy, optic nerve enlargement, blindness, paralysis, and difficulty when swallowing. Prolonged weight loss may also occur. Juvenile- and adult-onset cases of Krabbe disease also occur, which have similar symptoms but slower progression.

Half of all children and a quarter of previously healthy adults are asymptomatic with "Babesia" infection. When people do develop symptoms, the most common are fever and hemolytic anemia, symptoms that are similar to those of malaria. People with symptoms usually become ill 1 to 4 weeks after the bite, or 1 to 9 weeks after transfusion of contaminated blood products. A person infected with babesiosis gradually develops malaise and fatigue, followed by a fever. Hemolytic anemia, in which red blood cells are destroyed and removed from the blood, also develops. Chills, sweats, and thrombocytopenia are also common symptoms. Symptoms may last from several days to several months.

Less common symptoms and physical exam findings of mild-to-moderate babesiosis:

In more severe cases, symptoms similar to malaria occur, with fevers up to 40.5 °C (105 °F), shaking chills, and severe anemia (hemolytic anemia). Organ failure may follow, including adult respiratory distress syndrome. Severe cases occur mostly in people who have had a splenectomy. Severe cases are also more likely to occur in the very young, very old, and persons with immunodeficiency, such as HIV/AIDS patients.

A reported increase in human babesiosis diagnoses in the 2000s is thought to be caused by more widespread testing and higher numbers of people with immunodeficiencies coming in contact with ticks, the disease vector. Little is known about the occurrence of "Babesia" species in malaria-endemic areas, where "Babesia" can easily be misdiagnosed as "Plasmodium". Human patients with repeat babesiosis infection may exhibit premunity.

Symptoms of cerebellar abiotrophy include ataxia or lack of balance, an awkward wide-legged stance, a head tremor (intention tremor) (in dogs, body tremors also occur), hyperreactivity, lack of menace reflex, stiff or high-stepping gait, coarse or jerky head bob when in motion (or in very young animals, when attempting to nurse), apparent lack of awareness of where the feet are (sometimes standing or trying to walk with a foot knuckled over), poor depth perception, and a general inability to determine space and distance. The symptoms, when taken as a group, are distinctive and not easily mimicked by other illnesses, though certain types of neurological injury and infection need to be ruled out. Verifying the diagnosis in a laboratory setting is possible only by examining the brain post-mortem to determine if there has been a loss of Purkinje cells.

Most affected animals have normal intelligence and mildly affected animals can, in theory, live out a normal lifespan. However, affected animals are quite accident-prone, and for this reason many animals that develop CA, particularly horses, are euthanized for humane reasons. Horses may experience difficulty stepping up and over objects, run into fences, fall easily, and even if allowed to mature to full growth, are generally considered unsafe to ride. Dogs may need lifetime assistance with tasks such as climbing stairs.

In horses, the symptoms may worsen from the time of onset for six to 12 months, but if not severe enough to mandate euthansia, they stabilize over time. In some dog breeds, symptoms appear to progressively worsen, but research is not consistent on this point. There also is some evidence that affected animals partially compensate for the condition by cognitively learning alternative methods for moving or to determine distance, and thus appear to improve because they become less accident-prone.

Marburg virus disease (MVD; formerly Marburg hemorrhagic fever) is a severe illness of humans and non-human primates caused by either of the two marburgviruses, Marburg virus (MARV) and Ravn virus (RAVV). MVD is a viral hemorrhagic fever (VHF), and the clinical symptoms are indistinguishable from Ebola virus disease (EVD).

Equine venereal diseases are sexually transmitted infections in horses. They include contagious equine metritis (CEM) (caused by "Taylorella equigenitalis") and equine coital exanthema (caused by equine herpesvirus 3).

Horses with Type 1 PSSM usually appear normal at rest, but show signs of exertional rhabdomyolysis ("tying up") such as shortened stride, stiffness, firm musculature, sweating, pain or reluctance to exercise, when asked to perform light work. While episodes of exertional rhabdomyolysis is one of the most frequent signs associated with affected horses (reported in ~37% of affected animals), other common signs include gait abnormalities, shifting lameness, muscle weakness that may result in an inability to rise, colic-like pain, and muscle fasciculation, atrophy, and/or stiffness (most commonly seen in the semimembranosis, semitendinosis, and longissimus muscles).

These clinical signs usually first become apparent when the horse is placed into training as a young animal; however, affected horses will show histological changes consistent with muscle damage at one month of age, and may also show elevations in creatine kinase (CK), an enzyme that elevates with muscle damage. Concurrent illness, such as respiratory or gastrointestinal infection, can lead to elevations in CK and potentially life-threatening rhabdomyolysis, even without exercise. Horses with PSSM often have a persistently elevated CK at rest, which differentiates the disease from recurrent exertional rhabdomyolysis, in which horses have normal CK concentrations between episodes.