If a pregnant mother is identified as being infected with syphilis, treatment can effectively prevent congenital syphilis from developing in the fetus, especially if he or she is treated before the sixteenth week of pregnancy. The fetus is at greatest risk of contracting syphilis when the mother is in the early stages of infection, but the disease can be passed at any point during pregnancy, even during delivery (if the child had not already contracted it). A woman in the secondary stage of syphilis decreases her fetus's risk of developing congenital syphilis by 98% if she receives treatment before the last month of pregnancy. An afflicted child can be treated using antibiotics much like an adult; however, any developmental symptoms are likely to be permanent.

Kassowitz’s law is an empirical observation used in context of congenital syphilis stating that the greater the duration between the infection of the mother and conception, the better is the outcome for the infant. Features of a better outcome include less chance of stillbirth and of developing congenital syphilis.

The Centers for Disease Control and Prevention recommends treating symptomatic or babies born to infected mother with unknown treatment status with procaine penicillin G, 50,000 U/kg dose IM a day in a single dose for 10 days. Treatment for these babies can vary on a case by case basis. Treatment cannot reverse any deformities, brain, or permanent tissue damage that has already occurred.

Meningitis is a very common in children. Newborns can develop herpes virus infections through contact with infected secretions in the birth canal. Other viral infections are acquired by breathing air contaminated with virus-containing droplets exhaled by an infected person. Arbovirus infections are acquired from bites by infected insects (called epidemic encephalitis). Viral central nervous system infections in newborns and infants usually begin with fever. The inability of infants to communicate directly makes it difficult to understand their symptoms. Newborns may have no other symptoms and may initially not otherwise appear ill. Infants older than a month or so typically become irritable and fussy and refuse to eat. Vomiting is common. Sometimes the soft spot on top of a newborn's head (fontanelle) bulges, indicating an increase in pressure on the brain. Because irritation of the meninges is worsened by movement, an infant with meningitis may cry more, rather than calm down, when picked up and rocked. Some infants develop a strange, high-pitched cry. Infants with encephalitis often have seizures or other abnormal movements. Infants with severe encephalitis may become lethargic and comatose and then die. To make the diagnosis of meningitis or the diagnosis of encephalitis, doctors do a spinal tap (lumbar puncture) to obtain cerebrospinal fluid (CSF) for laboratory analysis in children.

Meningeal syphilis (as known as syphilitic aseptic meningitis or meningeal neurosyphilis) is a chronic form of syphilis infection that affects the central nervous system. Treponema pallidum, which is a spirochate bacterium, is the main cause of syphilis, which spreads drastically throughout the body and can infect all the systems of the body if not treated appropriately. The bacterium is the main cause of the onset of meningeal syphilis and other treponemal diseases, and it consists of a cytoplasmic and outer membrane that can cause a diverse array of diseases in the central nervous system and brain.

Early symptomatic neurosyphillis (or acute syphilitic meningitis or neurorecurrence) is the onset of meningeal syphilis. The symptoms arise as a result of inflamed meninges, which eventually lead up to signs of meningitis.

"Treponema pallidum" invades the nervous system within three to eighteen months after the primary infection. The initial series of events is asymptomatic meningitis, which can remain in the human body system and produce more damage within the body. Every form of neurosyphilis has meningitis as a component; however, every case differs in severity. The individual is infected with syphilis through a gram negative bacteria that only humans can obtain. Syphilis has four stages of infection, which are primary, secondary, latent, and tertiary. If syphilis is not treated, the disease can affect various other systems in the body, including the brain, heart, and vessels. The infection of the heart and vessels leads to meningovascular syphilis, which is usually presented during the secondary stage of syphilis. If syphilis is prolonged, it can affect the nervous system, which is known as neurosyphilis. Meningeal syphilis is a component of neurosyphilis, which usually occurs in the tertiary stage of syphilis.

Death from congenital syphilis is usually due to bleeding into the lungs.

Identification of poor prognostic factors include thrombocytopenia, cerebral edema, status epilepticus, and thrombocytopenia. In contrast, a normal encephalogram at the early stages of diagnosis is associated with high rates of survival.

Congenital syphilis is that which is transmitted during pregnancy or during birth. Two-thirds of syphilitic infants are born without symptoms. Common symptoms that develop over the first couple of years of life include enlargement of the liver and spleen (70%), rash (70%), fever (40%), neurosyphilis (20%), and lung inflammation (20%). If untreated, late congenital syphilis may occur in 40%, including saddle nose deformation, Higoumenakis sign, saber shin, or Clutton's joints among others. Infection during pregnancy is also associated with miscarriage.

The number of new cases a year of acute encephalitis in Western countries is 7.4 cases per 100,000 population per year. In tropical countries, the incidence is 6.34 per 100,000 per year. The incidence of Encephalitis has not changed much over time, with an incidence of encephalitis in the US of 250,000 from 2005 to 2015. Approximately seven per 100,000 patients were hospitalized for encephalitis in the US during this time. In 2015, encephalitis was estimated to have affected 4.3 million people and resulted in 150,000 deaths worldwide. Herpes simplex encephalitis has an incidence of 2–4 per million population per year.

Many viral infections of the central nervous system occur in seasonal peaks or as epidemics, whereas others, such as herpes simplex encephalitis, are sporadic. In endemic areas it is mostly a disease of children, but as the disease spreads to new regions, or nonimmune travelers visit endemic regions, nonimmune adults are also affected.

Herpesviral Encephalitis can be treated with high-dose intravenous acyclovir. Without treatment, HSE results in rapid death in approximately 70% of cases; survivors suffer severe neurological damage. When treated, HSE is still fatal in one-third of cases, and causes serious long-term neurological damage in over half of survivors. Twenty percent of treated patients recover with minor damage. Only a small population of survivors (2.5%) regain completely normal brain function. Indeed, many amnesic cases in the scientific literature have etiologies involving HSE. Earlier treatment (within 48 hours of symptom onset) improves the chances of a good recovery. Rarely, treated individuals can have relapse of infection weeks to months later. There is evidence that aberrant inflammation triggered by herpes simplex can result in granulomatous inflammation in the brain, which responds to steroids. While the herpes virus can be spread, encephalitis itself is not infectious. Other viruses can cause similar symptoms of encephalitis, though usually milder (Herpesvirus 6, varicella zoster virus, Epstein-Barr, cytomegalovirus, coxsackievirus, etc.).

, there is no vaccine effective for prevention. Several vaccines based on treponemal proteins reduce lesion development in an animal model, and research is ongoing.

There are many different forms on prevention of syphilis and other sexually transmitted diseases in general. Prevention of syphilis includes avoiding contact of bodily fluids with an infected person. This can be particularly difficult because syphilis is usually transmitted by people who are unaware that they have the disease because they do not have any visible sores or rashes that may denote having an infection in general. Being abstinent or having mutually monogamous sex with a person who is uninfected with any type of sexually transmitted disease is the greatest guarantee of not becoming infected with syphilis or any form of a sexually transmitted disease. Using latex condoms can however reduce the risk of obtaining syphilis. In order to prevent further contamination to other individuals, benzathine penicillin is given to any contacts. Washing, douching, or urinating cannot prevent the transmission of a sexually transmitted disease in general.

Individuals obtain syphilis through a variety of circumstances. In general, syphilis can be transmitted from individual to individual through direct contact with sores that are present on the external genitals, vagina, rectum, anus, lips, or mouth. Transmission can occur through any form of sexual contact, including vaginal, anal, and oral sex. In addition, women who are pregnant and infected with syphilis can transmit the disease onto their child as well. If transmission has occurred, it is important to check up immediately with a physician to avoid further damage.

The disease is associated with high rates of mortality and severe morbidity.

Herpesviral encephalitis is encephalitis due to herpes simplex virus.

Herpes simplex encephalitis (HSE) is a viral infection of the human central nervous system. It is estimated to affect at least 1 in 500,000 individuals per year and some studies suggest an incidence rate of 5.9 cases per 100,000 live births. The majority of cases of herpes encephalitis are caused by herpes simplex virus-1 (HSV-1), the same virus that causes cold sores. 57% of American adults are infected with HSV-1, which is spread through droplets, casual contact, and sometimes sexual contact, though most infected people never have cold sores. About 10% of cases of herpes encephalitis are due to HSV-2, which is typically spread through sexual contact. About 1 in 3 cases of HSE result from primary HSV-1 infection, predominantly occurring in individuals under the age of 18; 2 in 3 cases occur in seropositive persons, few of whom have history of recurrent orofacial herpes. Approximately 50% of individuals who develop HSE are over 50 years of age.

Limbic encephalitis is associated with an autoimmune reaction. In non-paraneoplastic limbic enephalitis, this is typically due to infection (commonly herpes simplex virus) or as a systemic autoimmune disorder. Limbic encephalitis associated with cancer or tumors is called paraneoplastic limbic encephalitis.

Viral encephalitis is a type of encephalitis caused by a virus.

It is unclear if anticonvulsants used in people with viral encephalitis would prevent seizures.

PRP is very rare and similar to SSPE but without intracellular inclusion bodies.

Only 20 patients have been identified since first recognized in 1974.

Limbic encephalitis is broadly grouped into two types: paraneoplastic limbic encephalitis and non-paraneoplastic limbic encephalitis.

- Paraneoplastic limbic encephalitis (PNLE) is caused by cancer or tumor, and may be treated by removal of the tumor.

- Non-paraneoplastic limbic encephalitis (NPLE) is not associated with cancer. More common than PNLE, it is caused by am infection, autoimmune disorder, or other condition that may never be identified.

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

Arbovirus encephalitis refers to encephalitis that is caused by arbovirus infection.

There are many types of arboviral encephalitides found in the United States.

Examples include:

- California encephalitis

- Japanese encephalitis

- St. Louis encephalitis

- Tick-borne encephalitis

- West Nile fever

- Murray Valley encephalitis

Patients infected in solid organ transplants have developed a severe fatal illness, starting within weeks of the transplant. In all reported cases, the initial symptoms included fever, lethargy, anorexia and leukopenia, and quickly progressed to multisystem organ failure, hepatic insufficiency or severe hepatitis, dysfunction of the transplanted organ, coagulopathy, hypoxia, multiple bacteremias and shock. Localized rash and diarrhea were also seen in some patients. Nearly all cases have been fatal.

In May 2005, four solid-organ transplant recipients contracted an illness that was later diagnosed as lymphocytic choriomeningitis. All received organs from a common donor, and within a month of transplantation, three of the four recipients had died as a result of the viral infection. Epidemiologic investigation traced the source to a pet hamster that the organ donor had recently purchased from a Rhode Island pet store. Similar cases occurred in Massachusetts in 2008, and Australia in 2013. Currently, there is not a LCMV infection test that is approved by the Food and Drug Administration for organ donor screening. The "Morbidity and Mortality Weekly Report" advises health-care providers to "consider LCMV infection in patients with aseptic meningitis and encephalitis and in organ transplant recipients with unexplained fever, hepatitis, or multisystem organ failure."

The causes of encephalitis lethargica (EL) are uncertain.

Veins of modern research have explored its origins in an autoimmune response, and, separately or in relation to an immune response, links to pathologies of infectious disease (viral and bacterial, e.g., in the case of influenza, where a link with encephalitis is clear). Postencephalic Parkinsonism was clearly documented to have followed an outbreak of EL following 1918 influenza pandemic; evidence for viral causation of the Parkinson's symptoms is circumstantial (epidemiologic, and finding influenza antigens in EL patients), while evidence arguing against this cause is of the negative sort (e.g., lack of viral RNA in postencephalic parkinsonian brain material).

In reviewing the relationship between influenza and EL, McCall and coworkers conclude, as of 2008, that while "the case against influenza [is] less decisive than currently perceived… there is little direct evidence supporting influenza in the etiology of EL," and that "[a]lmost 100 years after the EL epidemic, its etiology remains enigmatic." Hence, while opinions on the relationship of EL to influenza remain divided, the preponderance of literature appears skeptical.

In 2010, in a substantial Oxford University Press compendium reviewing the historic and contemporary views on EL, its editor, Joel VIlensky of the Indiana University School of Medicine, quotes Pool, writing in 1930, who states, "we must confess that etiology is still obscure, the causative agent still unknown, the pathological riddle still unsolved…", and goes on to offer the following conclusion, as of that publication date:Subsequent to publication of this compendium, an enterovirus was discovered in EL cases from the epidemic.

Diplococcus has been implicated as a cause of EL.

Lymphocytic choriomeningitis is not a commonly reported infection in humans, though most infections are mild and are often never diagnosed. Serological surveys suggest that approximately 1–5% of the population in the U.S. and Europe has antibodies to LCMV. The prevalence varies with the living conditions and exposure to mice, and it has been higher in the past due to lower standards of living. The island of Vir in Croatia is one of the biggest described endemic places of origin of LCMV in the world, with IFA testing having found LCMV antibodies in 36% of the population. Individuals with the highest risk of infection are laboratory personnel who handle rodents or infected cells. Temperature and time of year is also a critical factor that contributes to the number of LCMV infections, particularly during fall and winter when mice tend to move indoors. Approximately 10–20% of the cases in immunocompetent individuals are thought to progress to neurological disease, mainly as aseptic meningitis. The overall case fatality rate is less than 1% and people with complications, including meningitis, almost always recover completely. Rare cases of meningoencephalitis have also been reported. More severe disease is likely to occur in people who are immunosuppressed.

More than 50 infants with congenital LCMV infection have been reported worldwide. The probability that a woman will become infected after being exposed to rodents, the frequency with which LCMV crosses the placenta, and the likelihood of clinical signs among these infants are still poorly understood. In one study, antibodies to LCMV were detected in 0.8% of normal infants, 2.7% of infants with neurological signs and 30% of infants with hydrocephalus. In Argentina, no congenital LCMV infections were reported among 288 healthy mothers and their infants. However, one study found that two of 95 children in a home for people with severe mental disabilities had been infected with this virus. The prognosis for severely affected infants appears to be poor. In one series, 35% of infants diagnosed with congenital infections had died by the age of 21 months.

Transplant-acquired lymphocytic choriomeningitis proves to have a very high morbidity and mortality rate. In the three clusters reported in the U.S. from 2005 to 2010, nine of the ten infected recipients died. One donor had been infected from a recently acquired pet hamster while the sources of the virus in the other cases were unknown.

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.

The disease is most common in Central and Eastern Europe, and Northern Asia. About ten to twelve thousand cases are documented a year but the rates vary widely from one region to another. Most of the variation is the result of variation in host population, particularly that of deer. In Austria, an extensive free vaccination program since the 1960s has reduced incidence by roughly 85%. In Sweden, most cases of TBE occur in a band running from Stockholm to the west, especially around lakes and the nearby region of the Baltic sea. This reflects the greater population involved in outdoor activities in these areas. Although in some regions of Russia and Slovenia the prevalence of cases can be as high as 70 cases per 100,000 people per year, in most regions it is far lower, and overall, for Europe the estimated risk is roughly 1 case per 10,000 human-months of woodland activity. Travelers to endemic regions do not experience many cases, with only 5 cases reported among U.S. travelers returning from Eurasia between 2000 and 2011, a rate so low that the U.S. Centers for Disease Control and Prevention recommend vaccination only for those who will be extensively exposed in high risk areas.

Even with treatment, the condition is often fatal, and there are very few recorded survivors, almost all of whom suffered permanent neurocognitive deficits. Antifungal drugs including ketoconazole, miconazole, 5-flucytosine and pentamidine have been shown to be effective against GAE-causing organisms in laboratory tests.