Postencephalitic trophic ulcer is an ulceration of the nose similar to trigeminal trophic lesions, and has been reported following epidemic encephalitis and herpes zoster of the trigeminal nerve.

The syndrome typically presents as a progressive flaccid symmetric paralysis with areflexia, often causing respiratory failure. Electromyographic studies and nerve conduction studies show normal motor conduction velocity and latency with decreased amplitude of compound muscle action potentials. F wave and sensory nerve action potentials are often normal in this illness. Pathologically, it is a noninflammatory axonopathy without demyelination. Antibodies attack the coating of the motor neurons without causing inflammation or loss of myelin. It does not affect sensory neurons, so sensation remains intact despite loss of movement.

Symptoms may include fever and headache, but the distinguishing characteristic of this disease is attacks of severe pain in the lower chest, often on one side. The slightest movement of the rib cage causes a sharp increase of pain, which makes it very difficult to breathe, and an attack is therefore quite a frightening experience, although it generally passes off before any actual harm occurs. The attacks are unpredictable and strike "out of the blue" with a feeling like an iron grip around the rib cage. The colloquial names for the disease, such as 'The Devil's grip' (see also "other names" below) reflect this symptom.

The course of encephalitis lethargica can vary significantly between individuals, particularly when accompanied by preexisting or simultaneous diseases and disorders. It is characterized by high fever, sore throat, headache, lethargy, double vision, delayed physical and mental response, sleep inversion and catatonia. In severe cases, patients may enter a coma-like state (akinetic mutism). Patients may also experience abnormal eye movements ("oculogyric crises"), parkinsonism, upper body weakness, muscular pains, tremors, neck rigidity, and behavioral changes including psychosis. Klazomania (a vocal tic) is sometimes present.

Acute motor axonal neuropathy (AMAN) is a variant of Guillain–Barré syndrome. It is characterized by acute paralysis and loss of reflexes without sensory loss. Pathologically, there is motor axonal degeneration with antibody-mediated attacks of motor nerves and nodes of Ranvier.

Keratoconjunctivitis is inflammation ("-itis") of the cornea and conjunctiva.

When only the cornea is inflamed, it is called "keratitis"; when only the conjunctiva is inflamed, it is called "conjunctivitis".

There are several potential causes of the inflammation:

- Keratoconjunctivitis sicca is used when the inflammation is due to dryness. ("Sicca" means "dryness" in medical contexts.) It occurs with 20% of rheumatoid arthritis patients.

- The term "Vernal keratoconjunctivitis" (VKC) is used to refer to keratoconjunctivitis occurring in spring, and is usually considered to be due to allergens.

- "Atopic keratoconjunctivitis" is one manifestation of atopy.

- "Epidemic keratoconjunctivitis" is caused by an adenovirus infection.

- "Infectious bovine keratoconjunctivitis" (IBK) is a disease affecting cattle caused by the bacteria "Moraxella bovis".

- "Pink eye in sheep and goat" is another infectious keratoconjunctivitis of veterinary concern, mostly caused by "Chlamydophila pecorum"

- "Superior limbic keratoconjunctivitis" is thought to be caused by mechanical trauma.

- "Keratoconjunctivitis photoelectrica" (arc eye) means inflammation caused by photoelectric UV light. It is a type of ultraviolet keratitis. Such UV exposure can be caused by arc welding without wearing protective eye glass, or by high altitude exposure from sunlight reflected from snow ("snow blindness"). The inflammation will only appear after about 6 to 12 hours. It can be treated by rest, as the inflammation usually heals after 24–48 hours. Proper eye protection should be worn to prevent keratoconjunctivitis photoelectrica.

Inoculation of throat washings taken from people with pleurodynia into the brains of newborn mice revealed that enteroviruses in the Coxsackie B virus group were likely to be the cause of pleurodynia, and those findings were supported by subsequent studies of IgM antibody responses measured in serum from people with pleurodynia. Other viruses in the enterovirus family, including echovirus and Coxsackie A virus, are infrequently associated with pleurodynia.

Encephalitis lethargica or Nellysa disease is an atypical form of encephalitis. Also known as "sleeping sickness" or "sleepy sickness" (distinct from tsetse fly-transmitted sleeping sickness), it was first described in 1917 by the neurologist Constantin von Economo and the pathologist Jean-René Cruchet.

The disease attacks the brain, leaving some victims in a statue-like condition, speechless and motionless. Between 1915 and 1926, an epidemic of encephalitis lethargica spread around the world. Nearly five million people were affected, a third of whom died in the acute stages. Many of those who survived never returned to their pre-existing "aliveness".They would be conscious and aware – yet not fully awake; they would sit motionless and speechless all day in their chairs, totally lacking energy, impetus, initiative, motive, appetite, affect or desire; they registered what went on about them without active attention, and with profound indifference. They neither conveyed nor felt the feeling of life; they were as insubstantial as ghosts, and as passive as zombies.No recurrence of the epidemic has since been reported, though isolated cases continue to occur.

The patient with meningococcal meningitis typically presents with high fever, nuchal rigidity (stiff neck), Kernig's sign, severe headache, vomiting, purpura, photophobia, and sometimes chills, altered mental status, or seizures. Diarrhea or respiratory symptoms are less common. Petechiae are often also present, but do not always occur, so their absence should not be used against the diagnosis of meningococcal disease. Anyone with symptoms of meningococcal meningitis should receive intravenous antibiotics before the results of lumbar puncture, as delay in treatment worsens the prognosis.

Symptoms of meningococcemia are, at least initially, similar to those of influenza. Typically, the first symptoms include fever, nausea, myalgia, headache, arthralgia, chills, diarrhea, stiff neck, and malaise. Later symptoms include septic shock, purpura, hypotension, cyanosis, petechiae, seizures, anxiety, and multiple organ dysfunction syndrome. Acute respiratory distress syndrome and altered mental status may also occur. The petichial rash appear with the 'star-like' shape. Meningococcal sepsis has a greater mortality rate than meningococcal meningitis, but the risk of neurologic sequelae is much lower.

Nephropathia epidemica ("NE" or epidemic nephropathy) is a type of viral haemorrhagic fever with renal syndrome (HFRS) caused by the Puumala virus. The incubation period is three weeks. Nephropathia epidemica has a sudden onset with fever, abdominal pain, headache, back pain and gastrointestinal symptoms. More severe symptoms include internal hemorrhaging. Although fatal in a small percentage of cases, nephropathia epidemica is generally milder than the HFRS that is caused by hantaviruses in other parts of the world. The bank vole is the reservoir for the virus, which humans contract through inhalation of aerosolised vole droppings.

The majority of infected individuals are asymptomatic or develop only mild symptoms, and the disease is not known to spread from human to human.

This infection is known as "sorkfeber" in Swedish and "myyräkuume" in Finnish (vole fever). In Norway, it is called "musepest" (mouse plague).

"Pharyngoconjunctival fever" is a specific presentation of adenovirus infection, manifested as:

- high fever that lasts 4–5 days

- pharyngitis (sore throat)

- conjunctivitis (inflamed eyes, usually without pus formation like pink eye)

- enlargement of the lymph nodes of the neck

- headache, malaise, and weakness

- Incubation period of 5–9 days

It usually occurs in the age group 5–18. It is often found in summer camps and during the spring and fall in schools. In Japan, the illness is commonly referred to as "pool fever" as it is often spread via public swimming pools.

Symptoms are different for every person depending on the type of rat-bite fever with which the person is infected. Both spirillary and streptobacillary rat-bite fever have a few individual symptoms, although most symptoms are shared. Streptobacillosis is most commonly found in the United States and spirillary rat-bite fever is generally diagnosed in patients in Africa. Rat-bite symptoms are visually seen in most cases and include inflammation around the open sore. A rash can also spread around the area and appear red or purple. Other symptoms associated with streptobacillary rat-bite fever include chills, fever, vomiting, headaches, and muscle aches. Joints can also become painfully swollen and pain can be experienced in the back. Skin irritations such as ulcers or inflammation can develop on the hands and feet. Wounds heal slowly, so symptoms possibly come and go over the course of a few months.

Symptoms associated with spirillary rat-bite fever include issues with the lymph nodes, which often swell or become inflamed as a reaction to the infection. The most common locations of lymph node swelling are in the neck, groin, and underarm. Symptoms generally appear within 2 to 10 days of exposure to the infected animal. It begins with the fever and progresses to the rash on the hands and feet within 2 to 4 days. Rash appears all over the body with this form, but rarely causes joint pain.

Apart from respiratory involvement, illnesses and presentations of adenovirus include gastroenteritis, conjunctivitis, cystitis, and rash illness. Symptoms of respiratory illness caused by adenovirus infection range from the common cold syndrome to pneumonia, croup, and bronchitis. Patients with compromised immune systems are especially susceptible to severe complications of adenovirus infection. Acute respiratory disease (ARD), first recognized among military recruits during World War II, can be caused by adenovirus infections during conditions of crowding and stress.

The streptobacillosis form of rat-bite fever is known by the alternative names Haverhill fever and epidemic arthritic erythema. It is a severe disease caused by "Streptobacillus moniliformis", transmitted either by rat bite or ingestion of contaminated products (Haverhill fever). After an incubation period of 2–10 days, Haverhill fever begins with high prostrating fevers, rigors (shivering), headache, and polyarthralgia (joint pain). Soon, an exanthem (widespread rash) appears, either maculopapular (flat red with bumps) or petechial (red or purple spots) and arthritis of large joints can be seen. The organism can be cultivated in blood or articular fluid. The disease can be fatal if untreated in 20% of cases due to malignant endocarditis, meningoencephalitis, or septic shock. Treatment is with penicillin, tetracycline, or doxycycline.

Haverhill fever (or epidemic arthritic erythema) is a form of "rat-bite fever" caused by the bacterium "Streptobacillus moniliformis", an organism common in rats and mice. Symptoms begin to appear two to ten days after a rat bite injury. The illness resembles a severe influenza, with a moderate fever (38-40 °C, or 101-104 °F), chills, joint pain, and a diffuse red rash, located mostly on the hands and feet. The causative organism can be isolated by blood culture, and penicillin is the most common treatment. Treatment is usually quite successful, although the body can clear the infection by itself in most cases. Complications are rare, but can include endocarditis and meningitis.

Despite its name, it can present without being bitten by a rat.

The disease was recognized from an outbreak which occurred in Haverhill, Massachusetts in January, 1926. The organism "S. moniliformis" was isolated from the patients. Epidemiology implicated infection via consumption of milk from one particular dairy.

The symptoms of diphtheria usually begin two to seven days after infection. Symptoms of diphtheria include fever of 38 °C (100.4 °F) or above, chills, fatigue, bluish skin coloration (cyanosis), sore throat, hoarseness, cough, headache, difficulty swallowing, painful swallowing, difficulty breathing, rapid breathing, foul-smelling and bloodstained nasal discharge, and lymphadenopathy. Within two to three days, diphtheria may destroy healthy tissues in the respiratory system. The dead tissue forms a thick, gray coating that can build up in the throat or nose. This thick gray coating is called a “pseudomembrane.” It can cover tissues in the nose, tonsils, voice box, and throat, making it very hard to breathe and swallow. Symptoms can also include cardiac arrhythmias, myocarditis, and cranial and peripheral nerve palsies.

The majority of infections result in mild illness, including fever and headache. When infection is more severe the person may experience headache, high fever, neck stiffness, stupor, disorientation, coma, tremors, occasional convulsions and spastic paralysis. Fatality ranges from . Aged people are more likely to have a fatal infection.

Laryngeal diphtheria can lead to a characteristic swollen neck and throat, or "bull neck". The swollen throat is often accompanied by a serious respiratory condition, characterized by a brassy or "barking" cough, stridor, hoarseness, and difficulty breathing, and historically referred to variously as "diphtheritic croup", "true croup", or sometimes simply as "croup". Diphtheritic croup is extremely rare in countries where diphtheria vaccination is customary. As a result, the term "croup" nowadays most often refers to an unrelated viral illness that produces similar but milder respiratory symptoms.

Post-encephalitic Parkinsonism is a disease believed to be caused by a viral illness that triggers degeneration of the nerve cells in the substantia nigra. Overall, this degeneration leads to clinical parkinsonism.

Historically, starting in 1917 an epidemic of encephalitis lethargica, also called von Economo’s encephalitis or "sleepy-disease" occurred, possibly related to the 1918 Spanish flu pandemic; however, even with the use of modern molecular diagnostic tests on appropriate corpses no firm link between encephalitis lethargica with influenza has been made. Although parkinsonism was occasionally seen during the acute

encephalitic phase of encephalitis lethargica, it was often encountered in the post-encephalitic phase. The onset of post encephalitic

parkinsonism can be delayed by several years from the resolution of encephalitis lethargica.

The brain regions affected contain neurofibrillary tangles, similar to those seen in Alzheimer's disease. Nevertheless, the senile plaques common in Alzheimer's disease are not found.

A rickettsiosis is a disease caused by intracellular bacteria. It has been predicted that global warming may lead to greater incidence.

Saint Louis encephalitis is a disease caused by the mosquito borne Saint Louis encephalitis virus. Saint Louis encephalitis virus is related to Japanese encephalitis virus and is a member of the Flaviviridae subgroup. This disease mainly affects the United States. Occasional cases have been reported from Canada and Mexico.

Murray Valley encephalitis virus (MVEV) is a zoonotic flavivirus endemic to northern Australia and Papua New Guinea. It is the causal agent of Murray Valley encephalitis (previously known as Australian encephalitis or Australian X disease). In humans it can cause permanent neurological disease or death. MVEV is related to Kunjin virus which has a similar ecology but a lower morbidity rate. Although the arbovirus is endemic to Northern Australia, it has occasionally spread to the southern states during times of heavy rainfall during the summer monsoon season via seasonal flooding of the Murray-Darling river system. These outbreaks can be "...decades apart, with no or very few cases identified in between".

Symptoms of endemic typhus include headache, fever, muscle pain, joint pain, nausea and vomiting. 40–50% of patients will develop a discrete rash six days after the onset of signs. Up to 45% will develop neurological signs such as confusion, stupor, seizures or imbalance.

Symptoms may resemble those of measles, rubella, or possibly Rocky Mountain spotted fever. These symptoms are likely caused by a vasculitis caused by the rickettsia.

Rocio viral encephalitis is an epidemic flaviviral disease of humans first observed in São Paulo State, Brazil, in 1975. Low-level enzootic transmission is likely continuing in the epidemic zone, and with increased deforestation and population expansion, additional epidemics caused by Rocio virus are highly probable. If migratory species of birds are, or become involved in, the virus transmission cycle, the competency of a wide variety of mosquito species for transmitting Rocio virus experimentally suggest that the virus may become more widely distributed. The encephalitis outbreak in the western hemisphere caused by West Nile virus, a related flavivirus, highlights the potential for arboviruses to cause severe problems far from their source enzootic foci.

The causative Rocio virus belongs to the genus "Flavivirus" (the same genus as the Zika virus) in family Flaviviridae and is closely related serologically to Ilhéus, St. Louis encephalitis, Japanese encephalitis and Murray Valley encephalitis viruses.