Clinical signs may vary, with regurgitation and neurological symptoms being the most prominent in the early and later stages of its progression. In boa constrictors, the first signs may include off-and-on regurgitation, and some develop head tremors. Abnormal shedding may occur. Some develop chronic regurgitation and anorexia (lack of appetite or refusal to feed). However, not all infected snakes may regurgitate. Boas lose weight and may develop clogged nares (nostrils), stomatitis, or secondary pneumonia. The disease can rapidly progress to produce nervous-system disorders, such as disorientation, corkscrewing of the head and neck, holding the head in abnormal and unnatural positions, rolling onto the back, or stargazing. Stomatitis, pneumonia, undifferentiated cutaneous sarcomas, lymphoproliferative disorders, and leukemia have all been observed in affected specimens. Burmese pythons generally show signs of central nervous system disease without manifestation of other clinical signs and regurgitation is seen only in boas. These are symptoms similar to those seen in specimens infected by "Chlamydia"–specifically "Chlamydophila psittaci", the so-called parrot's disease.

Several snakes have been seen with proliferative pneumonia, while inclusions are commonly seen in the liver, kidney, and pancreas. Cases have also been observed where with only very few inclusions. In a few snakes with signs of central nervous system disease, and with a severe encephalitis, no inclusions have been seen in any cells. While the presence of characteristic inclusions is diagnostic for the disease, the absence of such inclusions does not necessarily indicate that the snake is not diseased or is free from the IBD virus. While cells having inclusions may show mild degenerative changes, inflammation is rarely seen in visceral tissues. In the brain, mild to severe encephalitis occurs, with lymphocytic perivascular cuffing. Several snakes with lymphoproliferative disorders have been identified with lymphoid infiltrates in multiple organs.

Clinical signs are normally only seen in either piglets less than 3 weeks old or pregnant sows.

Signs in piglets include rhinitis, pneumonia, anaemia, fever and sudden death. Black discoloration around the eyes is often seen and gastrointestinal and neurological signs are also reported.

Signs in pregnant sows include reproductive failure, genital ulceration and agalactia.

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.

Inclusion body disease (IBD) in the boid family of snakes, particularly "Boa constrictor", has been recognized since the mid-1970s. It is so named because of the characteristic intracytoplasmic inclusions which are observed in clinical examinations in epidermal cells, oral mucosal epithelial cells, visceral epithelial cells, and neurons. In the 1970s and 1980s, the disease was most commonly observed in Burmese pythons, "Python bivittatus". From the 1980s till the present day, it has been most commonly observed in boa constrictors from South America.

All boid snakes should be considered susceptible to the disease. Many zoos quarantine boas specifically as a result of this high risk before introducing them into their permanent collections and (breeding) programs. While the disease has not been identified in non-boid snakes, it is yet unknown whether non-boid snakes harbour the virus. The primary host of this virus has not yet been identified, but mites are thought to be primary hosts or at least a contributory factor.

Its distribution is worldwide, specifically in captive boid snakes. Its occurrence in the wild is unknown. Strangely enough, the disease has only been identified in adult and subadult specimens. Even so, all age groups are considered susceptible. Also, anecdotal reports of the infection in neonates have been made. A retro-like virus infection was suspected as the causative agent of IBD, but identification of highly divergent arenavirus sequences from boa constrictors with IBD suggested arenaviruses to be the etiological agent of IBD. Cell culture isolation of several arenaviruses from boid snakes with IBD further solidified, but did not yet confirm, the etiological relationship between IBD and arenaviruses.

The acute stage of the disease, occurring most often in the spring and summer, begins one to three weeks after infection and lasts for two to four weeks. Clinical signs include a fever, petechiae, bleeding disorders, vasculitis, lymphadenopathy, discharge from the nose and eyes, and edema of the legs and scrotum. There are no outward signs of the subclinical phase. Clinical signs of the chronic phase include weight loss, pale gums due to anemia, bleeding due to thrombocytopenia, vasculitis, lymphadenopathy, dyspnea, coughing, polyuria, polydipsia, lameness, ophthalmic diseases such as retinal hemorrhage and anterior uveitis, and neurological disease. Dogs that are severely affected can die from this disease.

Although people can get ehrlichiosis, dogs do not transmit the bacteria to humans; rather, ticks pass on the "ehrlichia" organism. Clinical signs of human ehrlichiosis include fever, headache, eye pain, and gastrointestinal upset. It is quite similar to Rocky Mountain spotted fever, but rash is not seen in patients.

Ehrlichiosis (; also known as canine rickettsiosis, canine hemorrhagic fever, canine typhus, tracker dog disease, and tropical canine pancytopenia is a tick-borne disease of dogs usually caused by the organism "Ehrlichia canis". "Ehrlichia canis" is the pathogen of animals. Humans can become infected by "E. canis" and other species after tick exposure. German Shepherd Dogs are thought to be susceptible to a particularly severe form of the disease, other breeds generally have milder clinical signs. Cats can also be infected.

Subacute sclerosing panencephalitis (SSPE) is a rare and chronic form of progressive brain inflammation caused by a persistent infection with measles virus (which can be a result of a mutation of the virus itself). The condition primarily affects children and young adults. It has been estimated that about 1 in 10,000 people infected with measles will eventually develop SSPE. However, a 2016 study estimated that the rate for babies who contracted measles was as high as 1 in 609. No cure for SSPE exists and the condition is often fatal. However, SSPE can be managed by medication if treatment is started at an early stage. Much of the work on SSPE has been performed by the National Institute of Neurological Disorders and Stroke (NINDS).

SSPE should not be confused with acute disseminated encephalomyelitis which has a similar cause but very different timing and course.

Various systems are affected.

- CNS abnormalities – microcephaly, mental retardation, spasticity, epilepsy, periventricular calcification

- Eye – choroidoretinitis and optic atrophy

- Ear – sensorineural deafness

- Liver – hepatosplenomegaly and jaundice due to hepatitis

- Lung – pneumonitis (interstitial pneumonitis)

- Heart – myocarditis

- Thrombocytopenic purpura, haemolytic anaemia

- Late sequelae in individuals asymptomatic at birth – hearing defects and reduced intelligence

Cytomegalic inclusion body disease (CIBD) is a series of signs and symptoms caused by cytomegalovirus infection, toxoplasmosis or other rare infections such as herpes or rubella viruses. It can produce massive calcification of the central nervous system, and often the kidneys.

Cytomegalic inclusion body disease is the most common cause of congenital abnormalities in the United States. It can also cause pneumonia and other diseases in immunocompromised patients, such as those with HIV/AIDS or recipients of organ transplants.

Characterized by a history of primary measles infection usually before the age of 2 years, followed by several asymptomatic years (6–15 on average), and then gradual, progressive psychoneurological deterioration, consisting of personality change, seizures, myoclonus, ataxia, photosensitivity, ocular abnormalities, spasticity, and coma.

Feline viral rhinotracheitis (FVR) is an upper respiratory or pulmonary infection of cats caused by "feline herpesvirus 1", of the family "Herpesviridae". It is also commonly referred to as feline influenza, feline coryza, and feline pneumonia but, as these terms describe other very distinct collections of respiratory symptoms, they are misnomers for the condition. Viral respiratory diseases in cats can be serious, especially in catteries and kennels. Causing one-half of the respiratory diseases in cats, FVR is the most important of these diseases and is found worldwide. The other important cause of feline respiratory disease is "feline calicivirus".

FVR is very contagious and can cause severe disease, including death from pneumonia in young kittens. It can cause flat-chested kitten syndrome, but most evidence for this is anecdotal. All members of the "Felidae" family are susceptible to FVR; in fact, FHV-1 has caused a fatal encephalitis in lions in Germany.

Initial signs of FVR include coughing, sneezing, nasal discharge, conjunctivitis, and sometimes fever (up to 106) and loss of appetite. These usually resolve within four to seven days, but secondary bacterial infections can cause the persistence of clinical signs for weeks. Frontal sinusitis and empyema can also result.

FHV-1 also has a predilection for corneal epithelium, resulting in corneal ulcers, often pinpoint or dendritic in shape. Other ocular signs of FHV-1 infection include conjunctivitis, keratitis, keratoconjunctivitis sicca (decreased tear production), and corneal sequestra. Infection of the nasolacrimal duct can result in chronic epiphora (excess tearing). Ulcerative skin disease can also result from FHV-1 infection. FHV-1 can also cause abortion in pregnant queens, usually at the sixth week of gestation, although this may be due to systemic effects of the infection rather than the virus directly.

In chronic nasal and sinus disease of cats, FHV-1 may play more of an initiating role than an ongoing cause. Infection at an early age may permanently damage nasal and sinus tissue, causing a disruption of ciliary clearance of mucus and bacteria, and predispose these cats to chronic bacterial infections.

People with CHS have light skin and silvery hair (albinism) and frequently complain of solar sensitivity and photophobia. Other signs and symptoms vary considerably, but frequent infections and neuropathy are common. The infections involve mucous membranes, skin, and the respiratory tract. Affected children are susceptible to infection by Gram-positive and gram-negative bacteria and fungi, with "Staphylococcus aureus" being the most common infection cause. Infections in CHS patients tend to be very serious and even life-threatening. Neuropathy often begins in the teenage years and becomes the most prominent problem. Few patients with this condition live to adulthood.

Most children with Chédiak–Higashi syndrome ultimately reach a stage known as the "accelerated phase", or the "lymphoma-like syndrome", in which defective white blood cells divide uncontrollably and invade many of the body's organs. The accelerated phase is associated with fever, episodes of abnormal bleeding, overwhelming infections, and organ failure. These medical problems are usually life-threatening in childhood.

In the leukocytes, the presence of very small rods (around 3 micrometers), or Döhle-like bodies can be seen in the cytoplasm.

Microvillus inclusion disease, also known as Davidson's disease, congenital microvillus atrophy and, less specifically, microvillus atrophy (note: microvillus is often misspelled as microvillous), is a rare genetic disorder of the small intestine that is inherited in an autosomal recessive pattern.

How sIBM affects individuals is quite variable as is the age of onset (which generally varies from the forties upwards). Because sIBM affects different people in different ways and at different rates, there is no "textbook case."

Eventually, sIBM results in general, progressive muscle weakness. The muscles in the thighs called the quadriceps and the muscles in the arms that control finger flexion—making a fist—are usually affected early on. Common early symptoms include frequent tripping and falling, weakness going up stairs and trouble manipulating the fingers (including difficulty with tasks such as turning doorknobs or gripping keys). Foot drop in one or both feet has been a symptom of IBM and advanced stages of polymyositis (PM).

During the course of the illness, the patient's mobility is progressively restricted as it becomes hard for him or her to bend down, reach for things, walk quickly and so on. Many patients say they have balance problems and fall easily, as the muscles cannot compensate for an off-balanced posture. Because sIBM makes the leg muscles weak and unstable, patients are very vulnerable to serious injury from tripping or falling down. Although pain has not been traditionally part of the "textbook" description, many patients report severe muscle pain, especially in the thighs.

When present, difficulty swallowing (dysphagia) is a progressive condition in those with inclusion body myositis and often leads to death from aspiration pneumonia. Dysphagia is present in 40 to 85% of IBM cases.

IBM can also result in diminished capacity for aerobic exercise. This decline is most likely a consequence of the sedentary lifestyle that is often associated with the symptoms of IBM (i.e. progressive muscle weakness, decreased mobility, and increased level of fatigue). Therefore, one focus of treatment should be the improvement of aerobic capacity.

Patients with sIBM usually eventually need to resort to a cane or a walker and in most cases, a wheelchair eventually becomes a necessity.

"The progressive course of s-IBM leads slowly to severe disability. Finger functions can become very impaired, such as for manipulating pens, keys, buttons, and zippers, pulling handles, and firmly grasping handshakes. Arising from a chair becomes difficult. Walking becomes more precarious. Sudden falls, sometimes resulting in major injury to the skull or other bones, can occur, even from walking on minimally-irregular ground or from other minor imbalances outside or in the home, due to weakness of quadriceps and gluteus muscles depriving the patient of automatic posture maintenance. A foot-drop can increase the likelihood of tripping. Dysphagia can occur, usually caused by upper esophageal constriction that often can be symptomatically improved, for several months to years, by bougie dilation per a GI or ENT physician. Respiratory muscle weakness can sometimes eventuate."

It is characterized by chronic, intractable diarrhea in new-born infants, starting in the first few days of life.

This results in metabolic acidosis and severe dehydration. Pregnancy and birth are usually normal.

Mucolipidosis II (ML II) is a particularly severe form of ML that has a significant resemblance to another mucopolysaccharidoses called Hurler syndrome. Generally only laboratory testing can distinguish the two as the presentation is so similar. There are high plasma levels of lysosomal enzymes and are often fatal in childhood. Typically, by the age of 6 months, failure to thrive and developmental delays are obvious symptoms of this disorder. Some physical signs, such as abnormal skeletal development, coarse facial features, and restricted joint movement, may be present at birth. Children with ML II usually have enlargement of certain organs, such as the liver (hepatomegaly) or spleen (splenomegaly), and sometimes even the heart valves. Affected children often have stiff claw-shaped hands and fail to grow and develop in the first months of life. Delays in the development of their motor skills are usually more pronounced than delays in their cognitive (mental processing) skills. Children with ML II eventually develop a clouding on the cornea of their eyes and, because of their lack of growth, develop short-trunk dwarfism (underdeveloped trunk). These young patients are often plagued by recurrent respiratory tract infections, including pneumonia, otitis media (middle ear infections), bronchitis and carpal tunnel syndrome. Children with ML II generally die before their seventh year of life, often as a result of congestive heart failure or recurrent respiratory tract infections.

May–Hegglin anomaly (MHA), also known as Döhle leukocyte inclusions with giant platelets and macrothrombocytopenia with leukocyte inclusions, is a rare genetic disorder of the blood platelets that causes them to be abnormally large.

Neonatal conjunctivitis by definition presents during the first month of life. It may be infectious or non infectious. In infectious conjunctivitis, the organism is transmitted from the genital tract of an infected mother during birth or by infected hands.

- Pain and tenderness in the eyeball.

- Conjunctival discharge: purulent, mucoid or mucopurulent depending on the cause.

- Conjunctiva shows hyperaemia and chemosis. Eyelids are usually swollen.

- Corneal involvement (rare) may occur in herpes simplex ophthalmia neonatorum.

Chédiak–Higashi syndrome is a rare autosomal recessive disorder that arises from a mutation of a lysosomal trafficking regulator protein, which leads to a decrease in phagocytosis. The decrease in phagocytosis results in recurrent pyogenic infections, albinism and peripheral neuropathy. It occurs in humans, cattle, blue Persian cats, Australian blue rats, mice, mink, foxes, and the only known captive white orca.

Symptoms of Lafora disease begin to develop during early adolescent years and symptoms progress to worsen as time passes. The first ten years of life there is generally no indication of the presence of the disease. The most common feature of Lafora disease is seizures that have been reported mainly as occipital seizures and myoclonic seizures with some cases of generalized tonic-clonic seizures, atypical absence seizures, and atonic and complex partial seizures. Other symptoms common with the seizures are drop attacks, ataxia, temporary blindness, visual hallucinations, and a quickly-developing and dramatic dementia.

Other common signs and symptoms associated with Lafora disease are behavioral changes because of the frequency of seizures. Over time those affected with Lafora disease have brain changes that cause things such as confusion, speech difficulties, depression, decline in intellectual function, and impaired judgement and memory. If area's of the cerebellum are affected by seizures then it is common to see issues with speech, coordination, and balance in Lafora patients.

For dogs that are affected with Lafora disease, common symptoms are rapid shuddering, shaking, or jerking of the canine's head backwards, high pitched vocalizations that could indicate the dog is panicking, seizures, and as the disease progresses dementia, blindness, and loss of balance.

Neonatal conjunctivitis, also known as ophthalmia neonatorum, is a form of conjunctivitis and a type of neonatal infection contracted by newborns during delivery. The baby's eyes are contaminated during passage through the birth canal from a mother infected with either "Neisseria gonorrhoeae" or "Chlamydia trachomatis". Antibiotic ointment is typically applied to the newborn's eyes within 1 hour of birth as prevention against gonococcal ophthalmia. Most hospitals in the United States are required by state law to apply eye drops or ointment soon after birth to prevent the disease. If left untreated it can cause blindness.

Congenital tufting enteropathy is an inherited disorder of the small intestine that presents with intractable diarrhea in young children.

Inclusion-cell (I-cell) disease, also referred to as mucolipidosis II (ML II), is part of the lysosomal storage disease family and results from a defective phosphotransferase (an enzyme of the Golgi apparatus). This enzyme transfers phosphate to mannose residues on specific proteins. Mannose 6 phosphate serves as a marker for them to be targeted to lysosomes within the cell. Without this marker, the proteins are instead excreted outside the cell—the default pathway for proteins moving through the Golgi apparatus. Lysosomes cannot function without these proteins, which function as catabolic enzymes for the normal breakdown of substances (e.g. oligosaccharides, lipids, and glycosaminoglycans) in various tissues throughout the body (i.e. fibroblasts). As a result, a buildup of these substances occurs within lysosomes because they cannot be degraded, resulting in the characteristic I-cells, or "inclusion cells". These cells can be identified under the microscope. In addition, the defective lysosomal enzymes normally found only within lysosomes are instead found in high concentrations in the blood.