The types of neurosyphilis include asymptomatic, acute syphilitic meningitis, meningovascular syphilis, parenchymatous syphilis (which includes general paresis and tabes dorsalis), and optic atrophy.

The secondary stages of syphilis persists to be more dangerous to the systems of the human body. The disseminated disease can cause constitutional symptoms and condylomata lata. Many treponemes are present in chancres in the primary stage; however, condylomata lata is usually present in the secondary stage. The pathogen can spread through blood, which can infect the vessels in the body. The infection of the heart, muscles, and vessels in the body can lead to meningovascular syphilis. Generally, rashes may start developing on the hands and soles of the feet, and it can spread to various parts of skin on the body. Other symptoms may include sore throat, headache, joint pain, fever, and patches of hair loss. As in stage one, lesions may start to form on the body, but in this stage in particular, lesions are found in mucous membranes of the mouth, throat, bones, and internal organs. Also common with stage one, the symptoms and signs of secondary syphilis will go away with or without treatment and medication. The diagnosis includes serology nonspecific and specific, both positive. The secondary stage is however highly infectious because the bacteria is spreading drastically throughout the body.

Secondary syphilis occurs approximately four to ten weeks after the primary infection. While secondary disease is known for the many different ways it can manifest, symptoms most commonly involve the skin, mucous membranes, and lymph nodes. There may be a symmetrical, reddish-pink, non-itchy rash on the trunk and extremities, including the palms and soles. The rash may become maculopapular or pustular. It may form flat, broad, whitish, wart-like lesions known as condyloma latum on mucous membranes. All of these lesions harbor bacteria and are infectious. Other symptoms may include fever, sore throat, malaise, weight loss, hair loss, and headache. Rare manifestations include liver inflammation, kidney disease, joint inflammation, periostitis, inflammation of the optic nerve, uveitis, and interstitial keratitis. The acute symptoms usually resolve after three to six weeks; about 25% of people may present with a recurrence of secondary symptoms. Many people who present with secondary syphilis (40–85% of women, 20–65% of men) do not report previously having had the classic chancre of primary syphilis.

Tertiary syphilis may occur approximately 3 to 15 years after the initial infection, and may be divided into three different forms: gummatous syphilis (15%), late neurosyphilis (6.5%), and cardiovascular syphilis (10%). Without treatment, a third of infected people develop tertiary disease. People with tertiary syphilis are not infectious.

Gummatous syphilis or late benign syphilis usually occurs 1 to 46 years after the initial infection, with an average of 15 years. This stage is characterized by the formation of chronic gummas, which are soft, tumor-like balls of inflammation which may vary considerably in size. They typically affect the skin, bone, and liver, but can occur anywhere.

Neurosyphilis refers to an infection involving the central nervous system. It may occur early, being either asymptomatic or in the form of syphilitic meningitis, or late as meningovascular syphilis, general paresis, or tabes dorsalis, which is associated with poor balance and lightning pains in the lower extremities. Late neurosyphilis typically occurs 4 to 25 years after the initial infection. Meningovascular syphilis typically presents with apathy and seizure, and general paresis with dementia and tabes dorsalis. Also, there may be Argyll Robertson pupils, which are bilateral small pupils that constrict when the person focuses on near objects but do not constrict when exposed to bright light.

Cardiovascular syphilis usually occurs 10–30 years after the initial infection. The most common complication is syphilitic aortitis, which may result in aneurysm formation.

Characteristics of a viral infection can include pain, swelling, redness, impaired function, fever, drowsiness, confusion and convulsions.

Fungal meningitis refers to meningitis caused by a fungal infection.

Symptoms of fungal meningitis are generally similar to those of other types of meningitis, and include: a fever, stiff neck, severe headache, photophobia (sensitivity to light), nausea and vomiting, and altered mental status (drowsiness or confusion).

The following is a list of common signs and symptoms found with neonatal meningitis.

- Fever

- poor appetite

- anterior fontanelle bulging

- seizure

- jitteriness

- dyspnea

- irritability

- anorexia

- vomiting

- diarrhea

- abdominal distention (increase in abdominal size)

- neck rigidity

- cyanosis

- jaundice

- and sunset eyes (downward gaze of the eyes)

- abnormal body temperature (hypo-or hyperthermia)

- change of activity (lethargy or irritability)

Unfortunately these symptoms are unspecific and may point to many different conditions.

The most common diseases caused by chronic viral infections are subacute-sclerosing panencephalitis, progressive multifocal leukoencephalopathy, retrovirus disease and spongiform encephalopathies.

In adolescence and young adulthood, the disease presents with a characteristic triad:

- Fever – usually lasting 14 days; often mild

- Sore throat – usually severe for 3–5 days, before resolving in the next 7–10 days.

- Swollen glands – mobile; usually located around the back of the neck (posterior cervical lymph nodes) and sometimes throughout the body.

Another major symptom is feeling tired. Headaches are common, and abdominal pains with nausea or vomiting sometimes also occur. Symptoms most often disappear after about 2–4 weeks. However, fatigue and a general feeling of being unwell (malaise) may sometimes last for months. Fatigue lasts more than one month in an estimated 28% of cases. Mild fever, swollen neck glands and body aches may also persist beyond 4 weeks. Most people are able to resume their usual activities within 2–3 months.

The most prominent sign of the disease is often the pharyngitis, which is frequently accompanied by enlarged tonsils with pus—an exudate similar to that seen in cases of strep throat. In about 50% of cases, small reddish-purple spots called petechiae can be seen on the roof of the mouth. Palatal enanthem can also occur, but is relatively uncommon.

Spleen enlargement is common in the second and third weeks, although this may not be apparent on physical examination. Rarely the spleen may rupture. There may also be some enlargement of the liver. Jaundice occurs only occasionally.

A small minority of people spontaneously present a rash, usually on the arms or trunk, which can be macular (morbilliform) or papular. Almost all people given amoxicillin or ampicillin eventually develop a generalized, itchy maculopapular rash, which however does not imply that the person will have adverse reactions to penicillins again in the future. Occasional cases of erythema nodosum and erythema multiforme have been reported.

Before puberty, the disease typically only produces flu-like symptoms, if any at all. When found, symptoms tend to be similar to those of common throat infections (mild pharyngitis, with or without tonsillitis).

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

Late congenital syphilis is a subset of cases of congenital syphilis. By definition, it occurs in children at or greater than 2 years of age who acquired the infection trans-placentally.

Symptoms include

- blunted upper incisor teeth known as Hutchinson's teeth

- inflammation of the cornea known as interstitial keratitis

- deafness from auditory nerve disease

- frontal bossing (prominence of the brow ridge)

- saddle nose (collapse of the bony part of nose)

- hard palate defect

- swollen knees

- saber shins

- short maxillae

- protruding mandible

A frequently-found group of symptoms is Hutchinson's triad, which consists of Hutchinson's teeth (notched incisors), keratitis and deafness and occurs in 63% of cases.

Treatment (with penicillin) before the development of late symptoms is essential.

Tuberculous meningitis is also known as TB meningitis or tubercular meningitis. Tuberculous meningitis is "Mycobacterium tuberculosis" infection of the meninges—the system of membranes which envelop the central nervous system.

Fever and headache are the cardinal features, confusion is a late feature and coma bears a poor prognosis. Meningism is absent in a fifth of patients with TB meningitis. Patients may also have focal neurological deficits.

Laboratory features that are characteristic of neonatal bacterial meningitis include:

- Isolation of a bacterial pathogen from the cerebrospinal fluid (CSF) by culture and/or visualization by Gram stain

- Increased CSF white blood cell (WBC) count (typically >1000 WBC/mL, but may be lower, especially with gram-positive organisms) with a predominance of neutrophils

- Elevated CSF protein concentration (>150 mg/dL in preterm (premature birth) and >100 mg/dL in term (on time) infants)

- Decreased CSF glucose concentration (<20 mg/dL [1.1 mmol/L] in preterm (premature birth) and <30 mg/dL [1.7 mmol/L] in term (on time) infants)

Cryptococcosis, also known as cryptococcal disease, is a potentially fatal fungal disease. It is caused by one of two species; "Cryptococcus neoformans" and "Cryptococcus gattii". These were all previously thought to be subspecies of "C. neoformans" but have now been identified as distinct species.

Cryptococcosis is believed to be acquired by inhalation of the infectious propagule from the environment. Although the exact nature of the infectious propagule is unknown, the leading hypothesis is the basidiospore created through sexual or asexual reproduction.

Leptospiral infection in humans causes a range of symptoms, and some infected persons may have no symptoms at all. Leptospirosis is a biphasic disease that begins suddenly with fever accompanied by chills, intense headache, severe myalgia (muscle ache), abdominal pain, conjunctival suffusion (red eye), and occasionally a skin rash. The symptoms appear after an incubation period of 7–12 days. The first phase (acute or septic phase) ends after 3–7 days of illness. The disappearance of symptoms coincides with the appearance of antibodies against "Leptospira" and the disappearance of all the bacteria from the bloodstream. The patient is asymptomatic for 3–4 days until the second phase begins with another episode of fever. The hallmark of the second phase is meningitis (inflammation of the membranes covering the brain).

Ninety percent of cases of the disease are mild leptospirosis. The rest experience severe disease, which develops during the second stage or occurs as a single progressive illness. The classic form of severe leptospirosis is known as Weil's disease, which is characterized by liver damage (causing jaundice), kidney failure, and bleeding. Additionally, the heart and brain can be affected, meningitis of the outer layer of the brain, encephalitis of brain tissue with same signs and symptoms; and lung affected as the most serious and life-threatening of all leptospirosis complications. The infection is often incorrectly diagnosed due to the nonspecific symptoms.

Other severe manifestations include extreme fatigue, hearing loss, respiratory distress, and azotemia.

Aseptic meningitis, or sterile meningitis, is a condition in which the layers lining the brain, the meninges, become inflamed and a pyogenic bacterial source is not to blame. Meningitis is diagnosed on a history of characteristic symptoms and certain examination findings (e.g., Kernig's sign). Investigations should show an increase in the number of leukocytes present in the cerebrospinal fluid (CSF) obtained via lumbar puncture (normally being fewer than five visible leukocytes per microscopic high-power field).

The term "aseptic" is frequently a misnomer, implying a lack of infection. On the contrary, many cases of aseptic meningitis represent infection with viruses or mycobacteria that cannot be detected with routine methods. While the advent of polymerase chain reaction has increased the ability of clinicians to detect viruses such as enterovirus, cytomegalovirus, and herpes virus in the CSF, many viruses can still escape detection. Additionally, mycobacteria frequently require special stains and culture methods that make their detection difficult. When CSF findings are consistent with meningitis, and microbiologic testing is unrevealing, clinicians typically assign the diagnosis of aseptic meningitis—making it a relative diagnosis of exclusion.

Aseptic meningitis can result from non-infectious causes as well. it can be a relatively infrequent side effect of medications, or be a result of an autoimmune disease. There is no formal classification system of aseptic meningitis except to state the underlying cause, if known. The absence of bacteria found in the spinal fluid upon spinal tap, either through microscopic examination or by culture, usually differentiates aseptic meningitis from its pyogenic counterpart.

"Aseptic meningitis", like non-gonococcal urethritis, non-Hodgkin lymphoma and atypical pneumonia, merely states what the condition is not, rather than what it is. Terms such as viral meningitis, bacterial meningitis, fungal meningitis, neoplastic meningitis and drug-induced aseptic meningitis can provide more information about the condition, and without using one of these more specific terms, it is difficult to describe treatment options or prognosis.

Dependent on the infectious syndrome, symptoms include fever, fatigue, dry cough, headache, blurred vision, and confusion. Symptom onset is often subacute, progressively worsened over several weeks. The two most common presentations are meningitis (an infection in and around the brain) and pulmonary (lung) infection.

Detection of cryptococcal antigen (capsular material) by culture of CSF, sputum and urine provides definitive diagnosis. Blood cultures may be positive in heavy infections. India ink of the CSF is a traditional microscopic method of diagnosis, although the sensitivity is poor in early infection, and may miss 15-20% of patients with culture-positive cryptococcal meningitis. Unusual morphological forms are rarely seen. Cryptococcal antigen from cerebrospinal fluid is the best test for diagnosis of cryptococcal meningitis in terms of sensitivity. Apart from conventional methods of detection like direct microscopy and culture, rapid diagnostic methods to detect cryptococcal antigen by latex agglutination test, lateral flow immunochromatographic assay (LFA), or enzyme immunoassay (EIA). A new cryptococcal antigen LFA was FDA approved in July 2011. Polymerase chain reaction (PCR) has been used on tissue specimens.

Cryptococcosis can rarely occur in the non-immunosuppressed people, particularly with "Cryptococcus gattii".

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.

The several forms of the infection are:

- Skin/subcutaneous tissue disease is a septic phlegmon that develops classically in the hand and forearm after a cat bite. Inflammatory signs are very rapid to develop; in 1 or 2 hours, edema, severe pain, and serosanguineous exudate appear. Fever, moderate or very high, can be seen, along with vomiting, headache, and diarrhea. Lymphangitis is common. Complications are possible, in the form of septic arthritis, osteitis, or evolution to chronicity.

- Sepsis is very rare, but can be as fulminant as septicaemic plague, with high fever, rigors, and vomiting, followed by shock and coagulopathy.

- Pneumonia disease is also rare and appears in patients with some chronic pulmonary pathology. It usually presents as bilateral consolidating pneumonia, sometimes very severe.

- Zoonosis, pasteurellosis can be transmitted to humans through cats.

Other locations are possible, such as septic arthritis, meningitis, and acute endocarditis, but are very rare.

Neuroborreliosis is often preceded by the typical symptoms of Lyme disease, which include erythema migrans and flu-like symptoms such as fever and muscle aches. Neurologic symptoms of neuroborreliosis include the meningoradiculitis (which is more common in European patients), cranial nerve abnormalities, and altered mental status. Sensory findings may also be present. Rarely, a progressive form of encephalomyelitis may occur. In children, symptoms of neuroborreliosis include headache, sleep disturbance, and symptoms associated with increased intracranial pressure, such as papilledema, can occur. Less common childhood symptoms can include meningitis, myelitis, ataxia, and chorea. Ocular Lyme disease has also been reported, as has neuroborreliosis affecting the spinal cord, but neither of these findings are common.

LCMV causes callitrichid hepatitis in New World primates. The onset of the infection is nonspecific and may include fever, anorexia, dyspnea, weakness and lethargy. Jaundice is characteristic and petechial hemorrhages may develop. Prostration and death usually follow.

Necropsy lesions in primates with callitrichid hepatitis show signs of jaundice, hepatomegaly, splenomegaly, and subcutaneous and intramuscular hemorrhages. Pleural and pericardial effusion, sometimes sanguineous, has also been reported. On histology, multifocal necrosis with acidophilic bodies and mild inflammatory infiltrates are typically found in the liver.