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Onset of symptoms begins one to nine days following exposure (with an average of five). Initial symptoms include changes in taste and smell, headache, fever, nausea, vomiting, back pain, and a stiff neck. Secondary symptoms are also meningitis-like including confusion, hallucinations, lack of attention, ataxia, cramp and seizures. After the start of symptoms, the disease progresses rapidly over three to seven days, with death usually occurring anywhere from seven to fourteen days later, although it can take longer. In 2013, a man in Taiwan died twenty-five days after being infected by "Naegleria fowleri".
It affects healthy children or young adults who have recently been exposed to bodies of fresh water. Some people have presented with a clinical triad of edematous brain lesions, immune suppression, and fever.
Naegleriasis (also known as primary amoebic meningoencephalitis) is an infection of the brain by the free-living unicellular "Naegleria fowleri".
"N. fowleri" is typically found in warm bodies of fresh water, such as ponds, lakes, rivers, and hot springs. It is also found in soil, poorly maintained municipal water supplies, water heaters, near warm-water discharges of industrial plants, and in poorly chlorinated or unchlorinated swimming pools, in an amoeboid or temporary flagellate stage. There is no evidence of it living in salt water. As the disease is rare, it is often not considered. Symptoms are similar to those of meningitis.
Although infection occurs rarely, it nearly always results in death, with a case fatality rate greater than 95%.
GAE may present in numerous ways. There is no solid definition, as only a handful of patients have presented thus far with GAE. GAE can present with: focal paralysis, seizures, brainstem symptoms, and other neurological problems, some of which may mimic glioma (especially brainstem glioma), or other brain diseases, which may hamper timely diagnosis. These symptoms are caused by inflammatory necrosis of brain tissue brought on by amoebic infiltrates.
"Acanthamoeba spp." causes mostly subacute or chronic granulomatous amoebic encephalitis (GAE), with a clinical picture of headaches, altered mental status, and focal neurologic deficit, which progresses over several weeks to death. In addition, "Acanthamoeba spp." can cause granulomatous skin lesions and, more seriously, keratitis and corneal ulcers following corneal trauma or in association with contact lenses.
Granulomatous amoebic encephalitis (GAE) is a central nervous system disease caused by certain species of free-living amoebae, especially species of "Acanthamoeba" and "Balamuthia mandrillaris".
The term is most commonly used with "Acanthamoeba". In more modern references, the term "balamuthia amoebic encephalitis" (BAE) is commonly used when "Balamuthia mandrillaris" is the cause.
Meningoencephalitis (; from Greek μῆνιγξ "meninx", "membrane", ἐγκέφαλος, "enképhalos" "brain", and the medical suffix "-itis", "inflammation") is a medical condition that simultaneously resembles both meningitis, which is an infection or inflammation of the meninges, and encephalitis, which is an infection or inflammation of the brain.
Causative organisms include protozoans, viral and bacterial pathogens.
Specific types include:
Sappinia amoebic encephalitis (SAE) is the name for amoebic encephalitis caused by species of "Sappinia".
The causative organism was originally identified as "Sappinia diploidea", but is now considered to be "Sappinia pedata".
It has been treated with azithromycin, pentamidine, itraconazole, and flucytosine.
In "Acanthamoeba" infections, the diagnosis can be made from microscopic examination of stained smears of biopsy specimens (brain tissue, skin, cornea) or of corneal scrapings, which may detect trophozoites and cysts. Cultivation of the causal organism, and its identification by direct immunofluorescent antibody, may also prove useful. Laboratory workers and physicians often mistake the organisms on wet mount for monocytes and a diagnosis of viral meningitis is mistakenly given if the organisms are not motile. Heating a copper penny with an alcohol lamp and placing it on the wet mount slide will activate sluggish trophozoites and more rapidly make the diagnosis. If the person performing the spinal tap rapidly looks at the heated wet mount slide the trophozoites can be seen to swarm while monocytes do not.
Symptoms manifest within 7–10 days and include fever, headache, partial paralysis, confusion, nausea and even coma.
The virus can infect the brain (encephalitis), the meninges (meningitis) or both (meningoencephalitis).
In general, mortality is 1% to 2%, with deaths occurring 5 to 7 days after the onset of neurologic signs.
In dogs, the disease also manifests as a neurological disorder with signs varying from tremors to seizures and death.
In ruminants, neurological disease is also present, and animals may refuse to eat, appear lethargic, and also develop respiratory signs.
Adult patients with encephalitis present with acute onset of fever, headache, confusion, and sometimes seizures. Younger children or infants may present irritability, poor appetite and fever.
Neurological examinations usually reveal a drowsy or confused patient. Stiff neck, due to the irritation of the meninges covering the brain, indicates that the patient has either meningitis or meningoencephalitis.
It takes 5 to 15 days after the bite of an infected mosquito to develop symptoms of LACV disease. Symptoms include nausea, headache, vomiting in milder cases and seizures, coma, paralysis and permanent brain damage in severe cases.
LAC encephalitis initially presents as a nonspecific summertime illness with fever, headache, nausea, vomiting and lethargy. Severe disease occurs most commonly in children under the age of 16 and is characterized by seizures, coma, paralysis, and a variety of neurological sequelae after recovery. Death from LAC encephalitis occurs in less than 1% of clinical cases. In many clinical settings, pediatric cases presenting with CNS involvement are routinely screened for herpes or enteroviral causes. Since there is no specific treatment for LAC encephalitis, physicians often do not request the tests required to specifically identify LAC virus, and the cases are reported as aseptic meningitis or viral encephalitis of unknown cause.
As with many infections, the very young, the very old and the immunocompromised are at a higher risk of developing severe symptoms.
The incubation period for WNV—the amount of time from infection to symptom onset—is typically from between 2 and 15 days. Headache can be a prominent symptom of WNV fever, meningitis, encephalitis, meningoencephalitis, and it may or may not be present in poliomyelitis-like syndrome. Thus, headache is not a useful indicator of neuroinvasive disease.
- West Nile fever (WNF), which occurs in 20 percent of cases, is a febrile syndrome that causes flu-like symptoms. Most characterizations of WNF generally describe it as a mild, acute syndrome lasting 3 to 6 days after symptom onset. Systematic follow-up studies of patients with WNF have not been done, so this information is largely anecdotal. In addition to a high fever, headache, chills, excessive sweating, weakness, fatigue, swollen lymph nodes, drowsiness, pain in the joints and flu-like symptoms. Gastrointestinal symptoms that may occur include nausea, vomiting, loss of appetite, and diarrhea. Fewer than one-third of patients develop a rash.
- West Nile neuroinvasive disease (WNND), which occurs in less than 1 percent of cases, is when the virus infects the central nervous system resulting in meningitis, encephalitis, meningoencephalitis or a poliomyelitis-like syndrome. Many patients with WNND have normal neuroimaging studies, although abnormalities may be present in various cerebral areas including the basal ganglia, thalamus, cerebellum, and brainstem.
- West Nile virus encephalitis (WNE) is the most common neuroinvasive manifestation of WNND. WNE presents with similar symptoms to other viral encephalitis with fever, headaches, and altered mental status. A prominent finding in WNE is muscular weakness (30 to 50 percent of patients with encephalitis), often with lower motor neuron symptoms, flaccid paralysis, and hyporeflexia with no sensory abnormalities.
- West Nile meningitis (WNM) usually involves fever, headache, and stiff neck. Pleocytosis, an increase of white blood cells in cerebrospinal fluid, is also present. Changes in consciousness are not usually seen and are mild when present.
- West Nile meningoencephalitis is inflammation of both the brain (encephalitis) and meninges (meningitis).
- West Nile poliomyelitis (WNP), an acute flaccid paralysis syndrome associated with WNV infection, is less common than WNM or WNE. This syndrome is generally characterized by the acute onset of asymmetric limb weakness or paralysis in the absence of sensory loss. Pain sometimes precedes the paralysis. The paralysis can occur in the absence of fever, headache, or other common symptoms associated with WNV infection. Involvement of respiratory muscles, leading to acute respiratory failure, can sometimes occur.
- West-Nile reversible paralysis, Like WNP, the weakness or paralysis is asymmetric. Reported cases have been noted to have an initial preservation of deep tendon reflexes, which is not expected for a pure anterior horn involvement. Disconnect of upper motor neuron influences on the anterior horn cells possibly by myelitis or glutamate excitotoxicity have been suggested as mechanisms. The prognosis for recovery is excellent.
- Nonneurologic complications of WNV infection that may rarely occur include fulminant hepatitis, pancreatitis, myocarditis, rhabdomyolysis, orchitis, nephritis, optic neuritis and cardiac dysrhythmias and hemorrhagic fever with coagulopathy. Chorioretinitis may also be more common than previously thought.
- Cutaneous manifestations specifically rashes, are not uncommon in WNV-infected patients; however, there is a paucity of detailed descriptions in case reports and there are few clinical images widely available. Punctate erythematous, macular, and papular eruptions, most pronounced on the extremities have been observed in WNV cases and in some cases histopathologic findings have shown a sparse superficial perivascular lymphocytic infiltrate, a manifestation commonly seen in viral exanthems. A literature review provides support that this punctate rash is a common cutaneous presentation of WNV infection.
Encephalitis is inflammation of the brain. Severity is variable. Symptoms may include headache, fever, confusion, a stiff neck, and vomiting. Complications may include seizures, hallucinations, trouble speaking, memory problems, and problems with hearing.
Causes of encephalitis include viruses such as herpes simplex virus or rabies, bacteria, fungus, or parasites. Other causes include autoimmune diseases and certain medication. In many cases the cause remains unknown. Risk factors include a weak immune system. Diagnosis is typically based on symptoms and supported by blood tests, medical imaging, and analysis of cerebrospinal fluid.
Certain types are preventable with vaccines. Treatment may include, antiviral medication (such as acyclovir), anticonvulsants, and corticosteroids. Treatment generally takes place in hospital. Some people require artificial respiration. Once the immediate problem is under control, rehabilitation may be required. In 2015, encephalitis was estimated to have affected 4.3 million people and resulted in 150,000 deaths worldwide.
An emerging infectious disease (EID) is an infectious disease whose incidence has increased in the past 20 years and could increase in the near future. Emerging infections account for at least 12% of all human pathogens. EIDs are caused by newly identified species or strains (e.g. Severe acute respiratory syndrome, HIV/AIDS) that may have evolved from a known infection (e.g. influenza) or spread to a new population (e.g. West Nile fever) or to an area undergoing ecologic transformation (e.g. Lyme disease), or be "reemerging" infections, like drug resistant tuberculosis. Nosocomial (hospital-acquired) infections, such as methicillin-resistant Staphylococcus aureus are emerging in hospitals, and extremely problematic in that they are resistant to many antibiotics. Of growing concern are adverse synergistic interactions between emerging diseases and other infectious and non-infectious conditions leading to the development of novel syndemics. Many emerging diseases are zoonotic - an animal reservoir incubates the organism, with only occasional transmission into human populations.
Japanese encephalitis (JE) is an infection of the brain caused by the Japanese encephalitis virus (JEV). While most infections result in little or no symptoms, occasional inflammation of the brain occurs. In these cases symptoms may include headache, vomiting, fever, confusion, and seizures. This occurs about 5 to 15 days after infection.
JEV is generally spread by mosquitoes, specifically those of the "Culex" type. Pigs and wild birds serve as a reservoir for the virus. The disease mostly occurs outside of cities. Diagnosis is based on blood or cerebrospinal fluid testing.
Prevention is generally with the Japanese encephalitis vaccine, which is both safe and effective. Other measures include avoiding mosquito bites. Once infected there is no specific treatment, with care being supportive. This is generally carried out in hospital. Permanent problems occur in up to half of people who recover from encephalopathy.
The disease occurs in Southeast Asia and the Western Pacific. About 3 billion people live in areas where the disease occurs. About 68,000 symptomatic cases occur a year with about 17,000 deaths. Often cases occur in outbreaks. The disease was first described in 1871.
Viral meningitis characteristically presents with fever, headache and neck stiffness. Fever is the result of cytokines released that affect the thermoregulatory neurons of the hypothalamus. Cytokines and increased intracranial pressure stimulate nociceptors in the brain that lead to headaches. Neck stiffness is the result of inflamed meninges stretching due to flexion of the spine. In contrast to bacterial meningitis, symptoms are often less severe and do not progress as quickly. Nausea, vomiting and photophobia (light sensitivity) also commonly occur, as do general signs of a viral infection, such as muscle aches and malaise. Increased cranial pressure from viral meningitis stimulates the area postrema, which causes nausea and vomiting. Photophobia is due to meningeal irritation. In severe cases, people may experience concomitant encephalitis (meningoencephalitis), which is suggested by symptoms such as altered mental status, seizures or focal neurologic deficits.
Babies with viral meningitis may only appear irritable, sleepy or have trouble eating. In severe cases, people may experience concomitant encephalitis (meningoencephalitis), which is suggested by symptoms such as altered mental status, seizures or focal neurologic deficits. The pediatric population may show some additional signs and symptoms that include jaundice and bulging fontanelles.
Tick-borne encephalitis (TBE) is a viral infectious disease involving the central nervous system. The disease most often manifests as meningitis, encephalitis, or meningoencephalitis. Although TBE is most commonly recognized as a neurological disorder, mild fever can also occur. Long-lasting or permanent neuropsychiatric consequences are observed in 10 to 20% of infected patients.
The number of reported cases has been increasing in most countries.
The tick-borne encephalitis virus is known to infect a range of hosts including ruminants, birds, rodents, carnivores, horses, and humans. The disease can also be spread from animals to humans, with ruminants and dogs providing the principal source of infection for humans.
TBE, like Lyme disease, is one of the many tick-borne diseases.
Powassan encephalitis, caused by the Powassan virus (POWV), as flavivirus also known as the deer tick virus, is a form of arbovirus infection that results from tick bites. It can occur as a co-infection with Lyme disease since both are transmitted to humans by the same species of tick. There has been a surge in the number of cases and geographic range in the last decade. In the United States, cases have been recorded in the northeast. The disease was first isolated from the brain of a boy who died of encephalitis in Powassan, Ontario, in 1958. The disease is a zoonosis, an animal disease, usually found in rodents and ticks, with spillover transmission to humans. The virus is antigenically related to the Far Eastern tick-borne encephalitis viruses.
La Crosse encephalitis is an encephalitis caused by an arbovirus (the La Crosse virus) which has a mosquito vector ("Ochlerotatus triseriatus" synonym "Aedes" "triseriatus").
La Crosse encephalitis virus (LACV) is one of a group of mosquito-transmitted viruses that can cause encephalitis, or inflammation of the brain. LAC encephalitis is rare; in the United States, about 80–100 LACV disease cases are reported each year, although it is believed to be under-reported due to minimal symptoms experienced by many of those affected.
"Balamuthia" infection is a cutaneous condition resulting from "Balamuthia" that may result in various skin lesions.
"Balamuthia mandrillarisis" a free-living amoeba (a single-celled living organism) found in the environment. It is one of the causes of granulomatous amoebic encephalitis (GAE), a serious infection of the brain and spinal cord. "Balamuthia" is thought to enter the body when soil containing it comes in contact with skin wounds and cuts, or when dust containing it is breathed in or gets in the mouth. The "Balamuthia" amoebae can then travel to the brain through the blood stream and cause GAE. GAE is a very rare disease that is usually fatal.
Scientists at the Centers for Disease Control and Prevention (CDC) first discovered "Balamuthia mandrillaris" in 1986. The amoeba was found in the brain of a dead mandrill. After extensive research, "B. mandrillaris" was declared a new species in 1993. Since then, more than 200 cases of "Balamuthia" infection have been diagnosed worldwide, with at least 70 cases reported in the United States. Little is known at this time about how a person becomes infected.
An amoebic brain abscess is a brain abscess caused by amoebas. It is particularly serious in patients with immunodeficiency. It is very rare; the first case was reported in 1849.
It may be caused by "Entamoeba histolytica".
Most people infected with the West Nile virus usually do not develop symptoms. However, some individuals can develop cases of severe fatigue, weakness, headaches, body aches, joint and muscle pain, vomiting, diarrhea, and rash, which can last for weeks or months. More serious symptoms have a greater risk of appearing in people over 60 years of age, or those suffering from cancer, diabetes, hypertension, and kidney disease.
Dengue fever is mostly characterized by high fever, headaches, joint pain, and rash. However, more severe instances can lead to hemorrhagic fever, internal bleeding, and breathing difficulty, which can be fatal.
Symptoms vary on severity, from mild unnoticeable symptoms to more common symptoms like fever, rash, headache, achy muscle and joints, and conjunctivitis. Symptoms can last several days to weeks, but death resulting from this infection is rare.