The most common form of the disease is the head and eye form. Typical symptoms of this form include fever, depression, discharge from the eyes and nose, lesions of the buccal cavity and muzzle, swelling of the lymph nodes, opacity of the corneas leading to blindness, inappetance and diarrhea. Some animals have neurologic signs, such as ataxia, nystagmus, and head pressing. Peracute, alimentary and cutaneous clinical disease patterns have also been described. Death usually occurs within ten days. The mortality rate in symptomatic animals is 90 to 100 percent. Treatment is supportive only.

It develops 6 months to 4 years after the primary rubella infection, which in most cases is a congenital rubella.

In children with congenital rubella infection the deficits remain stable; neurological deterioration after the

first few years of life is not believed to occur.

Progression of the disease can be divided into two stages:

- 1st stage: Behavioural Changes

- insidious onset

- subtle changes in behaviour and declining school work

- 2nd stage: Neurological Changes

- seizures – sometimes myoclonic

- cerebellar ataxia

- spastic weakness

- retinopathy, optic atrophy

- frank dementia leading to coma

- spasticity and brainstem involvement with death in 2–5 years

The diagnosis is considered when a child with congenital rubella develops progressive spasticity, ataxia, mental deterioration, and seizures. Testing involves at least CSF examination and serology. Elevated CSF total protein and globulin and elevated rubella antibody titers in CSF and serum occur. CT may show ventricular enlargement due to cerebellar atrophy and white matter disease. Brain biopsy may be necessary to exclude other causes of encephalitis or encephalopathy. Rubella virus cannot usually be recovered by viral culture or immunohistologic testing.

Acute cerebellar ataxia usually follows 2–3 weeks after an infection. Onset is abrupt. Vomiting may be present at the onset but fever and nuchal rigidity characterestically are absent. Horizontal nystagmus is present is approximately 50% of cases.

- Truncal ataxia with deterioration of gait

- Slurred speech and nystagmus

- Afebrile

Bovine malignant catarrhal fever (BMCF) is a fatal lymphoproliferative disease caused by a group of ruminant gamma herpes viruses including Alcelaphine gammaherpesvirus 1 (AlHV-1) and Ovine gammaherpesvirus 2 (OvHV-2) These viruses cause unapparent infection in their reservoir hosts (sheep with OvHV-2 and wildebeest with AlHV-1), but are usually fatal in cattle and other ungulates such as deer, antelope, and buffalo.

BMCF is an important disease where reservoir and susceptible animals mix. There is a particular problem with Bali cattle in Indonesia, bison in the US and in pastoralist herds in Eastern and Southern Africa.

Disease outbreaks in cattle are usually sporadic although infection of up to 40% of a herd has been reported. The reasons for this are unknown. Some species appear to be particularly susceptible, for example Pére Davids deer, Bali cattle and bison, with many deer dying within 48 hours of the appearance of the first symptoms and bison within three days. In contrast, post infection cattle will usually survive a week or more.

About 70% of patients have prodromal symptoms consisting of headache, fever, nausea, vomiting, diarrhoea, or upper respiratory-tract symptoms.

Possible causes of acute cerebellar ataxia include varicella infection, as well as infection with influenza, Epstein-Barr virus, Coxsackie virus, Echo virus or mycoplasma.

Some children and adults with herpes simplex virus (HSV) encephalitis and subsequent relapses characterized by choreoathetosis in children and behavioral/psychiatric features in adults were found to have NMDAR Abs without HSV reactivation, they improved with immunotherapy.

HIV-associated neurocognitive disorders (HAND) are neurological disorders associated with HIV infection and AIDS. HAND may include neurological disorders of various severity. HIV-associated neurocognitive disorders are associated with a metabolic encephalopathy induced by HIV infection and fueled by immune activation of macrophages and microglia. These cells are actively infected with HIV and secrete neurotoxins of both host and viral origin. The essential features of ADC are disabling cognitive impairment accompanied by motor dysfunction, speech problems and behavioral change. Cognitive impairment is characterised by mental slowness, trouble with memory and poor concentration. Motor symptoms include a loss of fine motor control leading to clumsiness, poor balance and tremors. Behavioral changes may include apathy, lethargy and diminished emotional responses and spontaneity. Histopathologically, it is identified by the infiltration of monocytes and macrophages into the central nervous system (CNS), gliosis, pallor of myelin sheaths, abnormalities of dendritic processes and neuronal loss.

ADC typically occurs after years of HIV infection and is associated with low CD4+ T cell levels and high plasma viral loads. It is sometimes seen as the first sign of the onset of AIDS. Prevalence is between 10–24% in Western countries and has only been seen in 1–2% of India-based infections. With the advent of highly active antiretroviral therapy (HAART), the incidence of ADC has declined in developed countries, although its prevalence is increasing. HAART may prevent or delay the onset of ADC in people with HIV infection, and may also improve mental function in people who already have ADC.

Dementia only exists when neurocognitive impairment in the patient is severe enough to interfere markedly with day-to-day function. That is, the patient is typically unable to work and may not be able to take care of him or herself. Before this, the patient is said to have a mild neurocognitive disorder.

While the progression of dysfunction is variable, it is regarded as a serious complication and untreated can progress to a fatal outcome. Diagnosis is made by neurologists who carefully rule out alternative diagnoses. This routinely requires a careful neurological examination, brain scans (MRI or CT scan) and a lumbar puncture to evaluate the cerebrospinal fluid. No single test is available to confirm the diagnosis, but the constellation of history, laboratory findings and examination can reliably establish the diagnosis when performed by experienced clinicians. The amount of virus in the brain does not correlate well with the degree of dementia, suggesting that secondary mechanisms are also important in the manifestation of ADC.

"B. henselae" is the etiologic agent for peliosis hepatis, which is defined as a vascular proliferation of sinusoid hepatic capillaries resulting in blood-filled spaces in the liver in HIV patients and organ transplant recipients. Peliosis hepatis can be associated with peliosis of the spleen, as well as bacillary angiomatosis of the skin in HIV patients.

"B. henselae" and "B. quintana" can cause bacillary angiomatosis, a vascular proliferative disease involving mainly the skin, and other organs. The disease was first described in human immunodificiency virus (HIV) patients and organ transplant recipients. Severe, progressive and disseminated disease may occur in HIV patients. Differential diagnoses include Kaposi´s sarcoma, pyogenic granuloma, hemangioma, "verruga Peruana", and subcutanous tumors. Lesions can affect bone marrow, liver, spleen, or lymph nodes.

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.

In most cases OMS starts with an acute flare-up of physical symptoms within days or weeks, but some less obvious symptoms such as irritability and malaise may begin weeks or months earlier.

This depends on the degree of hepatocellular necrosis that has occurred. Decreases in the SDH and prothrombin time along with improvement in appetite are the best positive predictive indicators of recovery. GGT may remain elevated for weeks even if the horse is recovering. Horses that survive for greater than one week and that continue to eat usually recover. Cases with rapid progression of clinical signs, uncontrollable encephalopathy, haemorrhage or haemolysis have a poor prognosis. Horses that display clinical signs have a mortality rate of 50–90%.

Symptoms include:

- opsoclonus (rapid, involuntary, multivectorial (horizontal and vertical), unpredictable, conjugate fast eye movements without intersaccadic [quick rotation of the eyes] intervals)

- myoclonus (brief, involuntary twitching of a muscle or a group of muscles)

- cerebellar ataxia, both truncal and appendicular

- aphasia (a language disorder in which there is an impairment of speech and of comprehension of speech, caused by brain damage)

- mutism (a language disorder in which a person does not speak despite evidence of speech ability in the past, often part of a larger neurological or psychiatric disorder)

- lethargy

- irritability or malaise

- drooling

- strabismus (a condition in which the eyes are not properly aligned with each other)

- vomiting

- sleep disturbances

About half of all OMS cases occur in association with neuroblastoma (a cancer of the sympathetic nervous system usually occurring in infants and children).

Coxsackieviruses-induced cardiomyopathy are positive-stranded RNA viruses in picornavirus family and the genus enterovirus, acute enterovirus infections such as Coxsackievirus B3 have been identified as the cause of virally induced acute myocarditis, resulting in dilated cardiomyopathy. Dilated cardiomyopathy in humans can be caused by multiple factors including hereditary defects in the cytoskeletal protein dystrophin in Duchenne muscular dystrophy (DMD) patients). A heart that undergoes dilated cardiomyopathy shows unique enlargement of ventricles, and thinning of the ventricular wall that may lead to heart failure. In addition to the genetic defects in dystrophin or other cytoskeletal proteins, a subset of dilated cardiomyopathy is linked to enteroviral infection in the heart, especially coxsackievirus B. Enterovirus infections are responsible for about 30% of the cases of acquired dilated cardiomyopathy in humans.

The key symptom of RCVS is recurrent thunderclap headaches, which over 95% of patients experience. In two-thirds of cases, it is the only symptom. These headaches are typically bilateral, very severe and peak in intensity within a minute. They may last from minutes to days, and may be accompanied by nausea, photophobia, phonophobia or vomiting. Some patients experience only one headache, but on average there are four attacks over a period of one to four weeks. A milder, residual headache persists between severe attacks for half of patients.

1–17% of patients experience seizures. 8–43% of patients show neurologic problems, especially visual disturbances, but also hemiplegia, ataxia, dysarthria, aphasia, and numbness. These neurologic issues typically disappear within minutes or a few hours; more persistent symptoms may indicate a stroke. Posterior reversible encephalopathy syndrome is present in a small minority of patients.

This condition features the unique property that the patient's cerebral arteries can spontaneously constrict and relax back and forth over a period of time without intervention and without clinical findings. Vasospasm is common post subarachnoid hemorrhage and cerebral aneurysm, but in RCVS only 25% of patients have symptoms post subarachnoid hemorrhage.

Acute, tender, erythematous plaques, nodes, pseudovesicles and, occasionally, blisters with an annular or arciform pattern occur on the head, neck, legs, and arms, particularly the back of the hands and fingers. The trunk is rarely involved. Fever (50%); arthralgia or arthritis (62%); eye involvement, most frequently conjunctivitis or iridocyclitis (38%); and oral aphthae (13%) are associated features.

Progressive inflammatory neuropathy (PIN) is a disease that was identified in a report, released on January 31, 2008, by the Centers for Disease Control and Prevention. The first known outbreak of this neuropathy occurred in southeastern Minnesota in the United States. The disease was reported among pig slaughterhouse workers who appeared at various care facilities in the area reporting similar neurological symptoms. The disease was later identified at pork processing plants in Indiana and Nebraska as well. The condition is characterized by acute paralysis, pain, fatigue, numbness, and weakness, especially in extremities. It was initially believed that workers might have contracted the disease through inhaling aerosols from pig brains blown through a compressed-air hose and that this exposure to pig neural tissue induced an autoimmune response that might have produced their mysterious peripheral neuropathy. These suspicions were confirmed in reports and investigations conducted at the Mayo Clinic in Rochester, Minnesota.

Reversible cerebral vasoconstriction syndrome (RCVS, sometimes called Call-Fleming syndrome) is a disease characterized by a weeks-long course of thunderclap headaches, sometimes focal neurologic signs, and occasionally seizures. Symptoms are thought to arise from transient abnormalities in the blood vessels of the brain. In some cases, it may be associated with childbirth, vasoactive or illicit drug use, or complications of pregnancy.

For the vast majority of patients, all symptoms disappear on their own within three weeks. Deficits persist in a small minority of patients, with severe complications or death being very rare. Because symptoms resemble a variety of life-threatening conditions, differential diagnosis is necessary.

Over 40 laboratory tests were initially conducted to rule out various pathogens and environmental toxins. These tests were used to try to identify potential viruses carried by humans, pigs, or both, including rotoviruses, adenoviruses, hepatitis A, and hepatitis E. They also tried to identify bacteria such as salmonella and escherichia coli (e. coli), and parasites such as Giardia and cryptosporidium that could be causing the symptoms. All were ruled out.

Neurodegenerative diseases were considered specifically because of the similarity of symptoms and animal involvement thus included investigation of prion associated diseases such as bovine spongiform encephalopathy (BSE), chronic wasting disease (CWD), and variant Creutzfeldt–Jakob disease (vCJD). These all have highly transmissible pathogenic agents that induce brain damage. Since no pathogenic agent had been found, these diseases were ruled out as being related.

Next two very similar neuropathies were ruled out. Guillain–Barré syndrome (GBS) induces an acute autoimmune response which affects the Schwann cells in the peripheral nervous system. GBS is usually triggered by an infection that causes weakness and tingling that may lead to muscle loss. This condition may be life-threatening if muscle atrophy ascends to affect the pulmonary or cardiac systems. So far, no infectious agents have been found that relate to the current disease, progressive infammatory neuropathy. They looked at chronic inflammatory demyelinating polyneuropathy (CIDP) which is characterized by progressive weakness and sensory impairment in the arms and legs. Damage occurs to the myelin sheath in the peripheral nervous system. As doctors at the Mayo Clinic were beginning to note, the problem they were seeing in progressive inflammatory neuropathy was occurring in the spinal nerve roots.

The hallmark of encephalopathy is an altered mental state. Characteristic of the altered mental state is impairment of the cognition, attention, orientation, sleep–wake cycle and consciousness. An altered state of consciousness may range from failure of selective attention to drowsiness. Hypervigilance may be present; with or without: congnitive deficits, headache, epileptic seizures, myoclonus (involuntary twitching of a muscle or group of muscles) or asterixis ("flapping tremor" of the hand when wrist is extended).

Depending on the type and severity of encephalopathy, common neurological symptoms are loss of cognitive function, subtle personality changes, inability to concentrate. Other neurological signs may include dysarthria, hypomimia, problems with movements (they can be clumsy or slow), ataxia, tremor. Another neurological signs may include involuntary grasping and sucking motions, nystagmus (rapid, involuntary eye movement), jactitation (restless picking at things characteristic of severe infection), and respiratory abnormalities such as Cheyne-Stokes respiration (cyclic waxing and waning of tidal volume), apneustic respirations and post-hypercapnic apnea. Focal neurological deficits are less common.

Encephalopathies exhibits both neurologic and psychopathologic symptoms.

Sweet described a disease with four features: fever; leukocytosis; acute, tender, red plaques; and a dermal infiltrate of neutrophils. This led to the name acute febrile neutrophilic dermatosis. Larger series of patients showed that fever and neutrophilia are not consistently present. The diagnosis is based on the two constant features, a typical eruption and the characteristic histologic features; thus the eponym "Sweet's syndrome" is used.

Transmissible spongiform encephalopathies (TSEs), also known as prion diseases, are a group of progressive, invariably fatal, conditions that affect the brain (encephalopathies) and nervous system of many animals, including humans. According to the most widespread hypothesis, they are transmitted by prions, though some other data suggest an involvement of a "Spiroplasma" infection. Mental and physical abilities deteriorate and myriad tiny holes appear in the cortex causing it to appear like a sponge (hence spongiform) when brain tissue obtained at autopsy is examined under a microscope. The disorders cause impairment of brain function, including memory changes, personality changes and problems with movement that worsen chronically.

Prion diseases of humans include Creutzfeldt–Jakob disease—which has four main forms, the sporadic (sCJD), the hereditary/familiar (fCJD), the iatrogenic (iCJD) and the variant form (vCJD)—Gerstmann–Sträussler–Scheinker syndrome, fatal familial insomnia, kuru, and the recently discovered variably protease-sensitive prionopathy. These conditions form a spectrum of diseases with overlapping signs and symptoms. TSEs in non-human mammals include scrapie in sheep, bovine spongiform encephalopathy (BSE)—popularly known as 'mad cow's disease'—in cattle and chronic wasting disease (CWD) in deer and elk. The variant form of Creutzfeldt–Jakob disease is caused by exposure to bovine spongiform encephalopathy prions.

Unlike other kinds of infectious disease, which are spread by agents with a DNA or RNA genome (such as virus or bacteria), the infectious agent in TSEs is believed to be a prion, thus being composed solely of protein material. Misshapen prion proteins carry the disease between individuals and cause deterioration of the brain. TSEs are unique diseases in that their aetiology may be genetic, sporadic, or infectious via ingestion of infected foodstuffs and via iatrogenic means (e.g., blood transfusion). Most TSEs are sporadic and occur in an animal with no prion protein mutation. Inherited TSE occurs in animals carrying a rare mutant prion allele, which expresses prion proteins that contort by themselves into the disease-causing conformation. Transmission occurs when healthy animals consume tainted tissues from others with the disease. In the 1980s and 1990s, bovine spongiform encephalopathy (BSE) spread in cattle in an epidemic fashion. This occurred because cattle were fed the processed remains of other cattle, a practice now banned in many countries. In turn, consumption (by humans) of bovine-derived foodstuff which contained prion-contaminated tissues resulted in an outbreak of the variant form of Creutzfeldt–Jakob disease in the 1990s and 2000s.

Prions cannot be transmitted through the air or through touching or most other forms of casual contact. However, they may be transmitted through contact with infected tissue, body fluids, or contaminated medical instruments. Normal sterilization procedures such as boiling or irradiating materials fail to render prions non-infective.