The Central Nervous Syste1
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Transcript of The Central Nervous Syste1
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The Central Nervous System: II. Infections: Introduction
Infections of the nervous system are classified according to the infected tissue into
(1) meningeal infections (meningitis), which may involve the dura primarily (pachymeningitis) or the pia-arachnoid (leptomeningitis);
and
(2) infections of the cerebral and spinal parenchyma (encephalitis or myelitis).
In many cases, both the meninges and the brain parenchyma are affected to varying degrees (meningoencephalitis).
Meningeal Infections
Acute Leptomeningitis
Acute leptomeningitis is an acute inflammation of the pia mater and arachnoid.
Most cases are caused by infectious agents; rarely, release of keratinaceous contents from an intradural epidermoid cyst or
teratoma causes a chemical meningitis. When the term meningitis is used without qualification, it means leptomeningitis.
Classification
Acute meningitis may be classified according to etiology.
Acute Bacterial Meningitis
Etiologic Agents in Bacterial Meningitis.
Organism Patient Profile
Streptococcus pneumoniae Most common agent in patients over age 40 years
3050% of cases in adults
1020% of cases in children
5% of cases in infants
Neisseria meningitidis Most common agent in patients aged 540 years
2549% of cases in children aged 515 years
1035% of cases in adults
Haemophilus influenzae Most common agent in patients aged 15 years
4060% of cases in children aged 15 years
2% of cases in adults
Listeria monocytogenes 1% of all cases of bacterial meningitis. Common in infants, elderly, or immunosuppressed
patients
Streptococcus agalactiae (group B) 40% of cases in neonates
Escherichia coli 40% of cases in neonates
Gramnegative bacilli (other than E
coli)
Posttraumatic postneurosurgical; 20% of cases in patients over age 50 years and in
debilitated patients
Staphylococcus aureus Postneurosurgical posttraumatic
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Staphylococcus epidermidis 75% of cases of meningitis complicating shunts
Neonatal meningitis is acquired during passage of the fetus through the birth canal. Organisms found in the maternal vagina,
commonly Escherichia coliand Streptococcus agalactiae (a group B streptococcus), are responsible.
In children up to 5 years of age, the most common pathogen causing meningitis is Haemophilus influenzae.
In adolescents, Neisseria meningitidis (meningococcus) is the most common cause.
Streptococcus pneumoniae (pneumococcus) causes meningitis in all age groups.
Listeria monocytogenes and gram-negative bacilli are important causes in older, debilitated, and immunosuppressed patients.
Acute Viral Meningitis
90% of these occur in patients under 30 years of age.
This is a mild, benign illness, which rarely causes death.
It is caused most commonly by enteroviruses, mumps virus, and lymphocytic choriomeningitis (LCM) virus.
An acute meningitis occurs in 10% of patients with human immunodeficiency virus (HIV) infection, most commonly at the time of
seroconversion.
Tuberculous Meningitis
Tuberculous meningitis is typically chronic; however, in the early stages there may be an exudative phase that resembles acute
meningitis.
Other Causes
The fungi Cryptococcus neoformans, Histoplasma, Blastomyces, and Candida albicans may cause meningitis in immunocompromised
patients. Free-living amebas belonging to the genera Naegleria andAcanthamoeba are rare causes of pyogenic meningitis.
Routes of Infection of the Meninges
Bloodstream spread accounts for the majority of cases; the primary entry site of the organism may be the respiratory tract (N
meningitidis, H influenzae, S pneumoniae, C neoformans, many viruses), skin (bacteria causing neonatal meningitis), or intestine
(enteroviruses).
Meningitis may also result from direct spread of organisms from an infected middle ear or paranasal sinus, especially in childhood.
Meningitis may be associated with skull fractures, especially those at the base of the skull causing free communication between the
subarachnoid space and the upper respiratory tract; brain surgery; or lumbar puncture.
Organisms may also gain entry through the intact nasal cribriform plate (eg, free-living soil amebas in stagnant swimming pools).
Tuberculous meningitis may occur during severe tuberculous bacteremia (miliary tuberculosis) or as a result of reactivation of a
meningeal focus, in which case the patient may have no evidence of tuberculosis elsewhere.
Pathology
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Grossly, the leptomeninges are congested and opaque and contain an exudate.
Microscopically, acute meningitis is characterized by hyperemia, fibrin formation, and inflammatory cells.
In bacterial meningitis, neutrophils dominate
in acute viral meningitis, neutrophils are rare and lymphocytes dominate . In acute tuberculous meningitis, there is an inflammatory
exudate that contains increased numbers of both neutrophils and lymphocytes.
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Clinical Features
Acute meningitis presents with fever and symptoms of meningeal irritation, which include headache, neck pain, and vomiting.
Physical examination reveals neck stiffness and a positive Kernig sign (inability to straighten the raised leg because of pain), both of
which are due to reflex spasm of spinal muscles, a consequence of irritation of nerves passing across the inflamed meninges.
In general, bacterial meningitis is a serious disease with considerable risk of death while viral meningitis is usually a mild, self-limited
infection. Tuberculous meningitis has an insidious onset and a slow rate of progression but is frequently a severe illness with a fataloutcome if not treated.
Diagnosis
The diagnosis is made by examination of the cerebrospinal fluid (CSF), a sample of which is obtained by lumbar puncture. The
leptomeningeal exudate becomes admixed with the CSF, which reflects the type of inflammatory response and contains the
infectious agent
Cerebrospinal Fluid Changes in Infections of the Central Nervous System.
Encephalitis Bacterial
Meningitis1
Viral
Meningitis
Tuberculous (Chronic)
Meningitis
Brain Abscess
Pressure Raised Raised Raised Raised May be very high
Gross appearance Clear Turbid Clear Clear; may clot Clear
Protein Slightly elevated High Slightly
elevated
Very high Elevated
Glucose Normal Very low Normal Low Normal
Chloride Normal Low Normal Very low Normal or low
Cells Lymphocytes ornormal
Neutrophils Lymphocytes Pleocytosis2
Pleocytosis
Gram stain Negative Positive in 90% Negative Negative Occasionally
positive
Acidfast stain Negative Negative Negative Rarely positive Negative
Bacterial culture Negative Positive in 90% Negative Negative Occasionally
positive
Mycobacterial
culture
Negative Negative Negative Positive Negative
Viral culture Positive in 30% or
less
Negative Positive in 70% Negative Negative
1Amebic and cryptococcal meningitis are diagnosed by the finding of these organisms in the smear.
2Pleocytosis is the presence of both neutrophils and lymphocytes in cerebrospinal fluid.
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Chronic Meningitis
Chronic meningitis is caused by facultative intracellular organisms such as Mycobacterium tuberculosis, fungi, and Treponema
pallidum.
Pathology & Clinical Features
Chronic tuberculous and fungal meningitis are characterized by caseous granulomatous inflammation with fibrosis.
Marked fibrous thickening of the meninges is the dominant pathologic feature. The entire brain surface is involved, with the basal
meninges more severely affected in cases of tuberculosis. The causative agent may be identified in tissue sections specially stained
for acid-fast bacilli and fungi.
The meningovascular phase of syphilis also causes a basal chronic inflammation with marked fibrosis and obliterative vasculitis,
with large numbers of plasma cells infiltrating the meninges; granulomas are not present.
Complications of chronic meningitis include
(1) obliterative vasculitis (endarteritis obliterans), which may produce focal ischemia with microinfarcts in the brain and brain stem;
(2) entrapment of cranial nerves in the fibrosis as they traverse the meninges, resulting in cranial nerve palsies; and
(3) fibrosis around the fourth ventricular foramina, causing obstructive hydrocephalus.
Clinically, chronic meningitis is characterized by an insidious onset with symptoms of diffuse neurologic involvement, including
apathy, somnolence, personality change, and poor concentration. These symptoms are thought to stem from a concomitant diffuse
encephalopathy.
Headache and vomiting are less severe than in acute meningitis, and fever is often low-grade. Focal neurologic signs and epileptic
seizures result from ischemia, cranial nerve palsies, or hydrocephalus.
Infections of the Brain Parenchyma
Cerebral Abscess
Cerebral abscess is a localized area of suppurative inflammation in the brain substance. The cavity contains thick pus formed from
necrotic, liquefied brain tissue and large numbers of neutrophils and is surrounded by a fibrogliotic wall.
Etiology
Cerebral abscesses are caused by a large variety of bacteria; several organisms may occur in a single abscess, and anaerobic bacteriasuch as Bacteroides and anaerobic streptococci are common. Nocardia, Staphylococcus aureus, and gram-negative enteric bacteria
may also be isolated.
Cerebral abscesses occur as complications of other diseases
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Cerebral abscesscommon sites and routes of infection.
(1) Chronic suppurative infections of the middle ear and mastoid air spaces and of the paranasal sinuses. The middle ear is
separated from the middle and posterior cranial fossas by thin bony plates that may be eroded by infection. The temporal lobeand the cerebellum are usually involved. Infections of the paranasal sinuses are occasionally associated with frontal lobe
abscesses.
(2) Infective endocarditis with embolization to brain. These patients commonly develop parietal lobe abscesses, which are often
small and multiple.
(3) Right-to-left shunts (eg, in patients with congenital cyanotic heart disease) may divert infected systemic emboli to the brain.
(4) Suppurative lung diseases such as chronic lung abscess and bronchiectasis are rarely complicated by embolization of infected
material to the brain, leading to parietal lobe abscesses.
Pathology
Grossly, a cerebral abscess appears as a mass lesion in the brain. It has a liquefied center filled with pus and a fibrogliotic wall whosethickness depends on the duration of the abscess. The surrounding brain tissue frequently shows vasogenic edema.
Clinical Features & Diagnosis
Cerebral abscess presents with
(1) features of a space-occupying lesion, including evidence of increased intracranial pressure (headache, vomiting, papilledema) and
focal neurologic
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(2) features relating to the source of infection, such as chronic otitis media, suppurative lung disease, and endocarditis; and
(3) general evidence of infection, such as fever, rapid (elevated) erythrocyte sedimentation rate, and weight loss in chronic cases.
In untreated cases, the abscess progressively enlarges and may cause death from increased intracranial pressure or rupture into the
ventricular system.
Diagnosis
The diagnosis of cerebral abscess is made clinically and confirmed by computed tomography (CT) scan or magnetic resonance
imaging (MRI). Lumbar puncture is dangerous because of the risk of precipitating tonsillar herniation.
Treatment
Surgical evacuation of the abscess followed by antibiotic therapy is effective treatment and has reduced the previously high
mortality rate of cerebral abscess to about 510%.
Viral Encephalitis
The frequency of viral encephalitis is difficult to estimate.
Most of these are presumptive diagnosesthe etiologic virus is identified in only about 30% of cases.
Causes of Viral Encephalitis.
Diffuse encephalitis
Epidemic (arbovirus) encephalitis
Eastern equine encephalitis
Western equine encephalitis
Venezuelan equine encephalitis
St. Louis encephalitis
California encephalitis
Japanese B encephalitis
Sporadic encephalitis
Herpes simplex encephalitis
Enterovirus encephalitis
Measles encephalitis
Varicella (chickenpox) encephalitis
Encephalitis in the immunocompromised patient
Herpes simplex encephalitis
Progessive multifocal leukoencephalopathy (PML)
Cytomegalovirus
HIV (AIDS) encephalitis
Specific types of encephalitis
Poliomyelitis
Rabies
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Subacute sclerosing panencephalitis (SSPE)
Prion (slow virus) infections
Pathology
The virus usually reaches the brain via the bloodstream. It infects brain cells, causing neuronal necrosis and marked cerebral edema,
which in turn leads to acute cerebral dysfunction and increased intracranial pressure.
Perivascular lymphocytic infiltration (perivascular cuffing) is characteristic.
Viral encephalitis, showing perivascular lymphocytic cuffing.
Clinical Features
Viral encephalitis has an acute onset with fever, headache, and signs of brain dysfunction, the nature of which depend on the areas
of brain involved.
Convulsions may occur. There may be papilledema if cerebral edema is severe. In many cases of viral encephalitis, there isconcomitant meningeal inflammation causing neck stiffness and CSF abnormalities typical of viral meningitis.
The diagnosis is based on the clinical picture. Lumbar puncture with examination and culture of CSF may provide an etiologic
diagnosis.
Treatment
Therapy is supportive. Control of cerebral edema with high doses of corticosteroids is important in preventing death in the acute
phase from increased intracranial pressure. The mortality rate from severe viral encephalitis is high, and patients who recover are
frequently left with permanent neurologic deficits due to irreversible neuronal necrosis.
Herpes Simplex Encephalitis
Incidence & Etiology
Herpes simplex encephalitis occurs in 3 classes of patients:
Neonates are infected during delivery to a woman with active genital herpes. The presence of herpes genitalis in the mother is an
absolute indication for cesarian section. Herpes simplex type 2 is responsible for most cases.
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Adults are infected through the bloodstream from a minor focus of viral replication, usually in the mouth. Herpes simplex type 1 is
commonly involved.
Immunocompromised persons, particularly patients undergoing chemotherapy for the treatment of cancer, have an increased
susceptibility not only to become infected by herpes simplex virus but also to develop viremia and encephalitis.
Pathology
Herpes simplex encephalitis affects the temporal and inferior frontal lobes selectively, producing a necrotizing, hemorrhagic acute
encephalitis that may rapidly cause death. Patients who survive frequently suffer permanent neurologic defects, the nature of which
depends on the neuronal loss.
Diagnosis
The diagnosis may be made by brain biopsy, which shows cerebral edema, necrosis, lymphocytic infiltration, and the presence of
intranuclear Cowdry A inclusions in infected cells. Electron microscopy or, preferably, immunohistochemical or in situ hybridization
tests demonstrate the virus in the majority of cases.
Herpes simplex encephalitis. This section has been stained for herpes simplex viral antigens by the immunoperoxidase technique. The
darkly staining (positive) cells are infected with the virus.
Treatment
Treatment of herpes simplex encephalitis with antiviral agents such as vidarabine improves prognosis if undertaken early.
HIV Encephalitis
HIV is a neurotrophic virus that causes subacute encephalitis characterized pathologically by small nodules composed of
demyelination, reactive astroglial proliferation, and infiltration by lymphocytes and microglial cells.
These microglial nodules occur in about 30% of patients with acquired immunodeficiency disease (AIDS). Their relationship to the
occurrence of dementia in AIDS patients is uncertain.
Poliomyelitis
Poliomyelitis is caused by the poliovirus, an enterovirus transmitted by the fecaloral route.
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The virus enters the body through the intestine and infects the brain and spinal cord via the bloodstream.
The poliovirus selectively infects
(1) the meninges, producing acute lymphocytic meningitis; and
(2) the lower motor neurons in the anterior horn of the spinal cord and medulla oblongata. Loss of motor neurons causes acute
paralysis of affected muscles. The paralysis is typically asymmetric and flaccid, with muscle atrophy and loss of deep tendon reflexes
With time, the atrophic muscles may undergo fibrous contracture.
Poliomyelitis is a very serious disease associated with a significant mortality rate in the acute phase, when paralysis of respiratory
muscle results in failure of ventilation. Patients who survive are commonly left with permanent muscle paralysis.
Poliomyelitis, showing the phases of infection. Patients who recover show a permanent neurologic deficit that corresponds to theneuronal necrosis in the acute phase.
Rabies
Rabies is rare in humans but occurs in a variety of wild animals and domestic pets, including dogs and cats, in whom it causes a fatal
illness called hydrophobia characterized by abnormal behavior, difficulty in swallowing, and convulsions.
Humans are infected when bitten by an infected animal.
The rabies virus enters the cutaneous nerve radicles at the site of inoculation and passes proximally to the central nervous system.
The incubation period is 13 months and is shortest in facial bites.
Rabies virus causes a severe necrotizing encephalitis that maximally affects the basal ganglia, hippocampus, and brain stem. Infected
neurons show diagnostic eosinophilic intracytoplasmic inclusion bodies (Negri bodies). The virus can also be identified in the
infected cells by electron microscopy and immunoperoxidase techniques.
Clinically, rabies presents with fever and generalized convulsions that are precipitated by the slightest of sensory stimulations such
as a gust of wind, a faint noise, or the sight of water. Death is inevitable.
Because there is no treatment, prevention is essential and consists of controlling the disease in wild animals, rabies immunization of
domestic pets, and administration of antirabies vaccine to humans immediately after viral exposure.
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Cytomegalovirus Encephalitis
Cytomegalovirus infection of the brain occurs in the fetus during the last trimester of pregnancy as a result of transplacental
infection.
Periventricular necrosis and calcification lead to microcephaly and mental retardation; chorioretinitis is common.
Cytomegalovirus encephalitis also occurs in immunocompromised persons, particularly patients with AIDS.
Progressive Multifocal Leukoencephalopathy (PML)
PML is caused by Jamestown Canyon (JC) virus, a specific serologic type of human papovavirus, and occurs particularly in patients
with AIDS and those undergoing chemotherapy for cancer.
PML is characterized pathologically by widespread focal demyelination of cerebral white matter.
Giant atypical astrocytes and intranuclear inclusions in oligodendroglial cells are typically present, along with a lymphocytic infiltrate
The JC virus can be identified by immunohistochemical techniques.
Clinically, PML presents as an acute, rapidly progressive illness associated with multifocal cerebral dysfunction. The diagnosis can be
established by brain biopsy. The mortality rate is high.
Subacute Sclerosing Panencephalitis (SSPE)
SSPE is an uncommon disease that affects children several years after a known attack of measles. Boys are five times more
commonly affected than girls.
The measles virus, which has been demonstrated in the cerebral lesions of SSPE, is the causal agent, and SSPE is therefore regarded
as a chronic measles virus infection.
The exact mechanism by which the virus causes encephalitis is unknown. Immunologic factors may play a role, or there may be some
alteration of the measles virus itself. The incidence has declined following measles vaccination.
Pathologically, SSPE is characterized by degeneration of neurons in the cerebral gray matter and basal ganglia. Intranuclear
inclusions are present in infected cells, and measles virus particles are present on electron microscopy. The white matter shows
demyelination, reactive astrocytic proliferation, and perivascular lymphocytic infiltration.
Clinically, patients present with personality changes and involuntary myoclonic-type movements. The disease is relentlessly
progressive, causing extensive brain damage and leading to death, usually within 12 years after onset.
Prion (Slow Virus) Infections
Creutzfeldt-Jakob disease and kuru are infections of the human brain that are characterized by a long latent period after infectionfollowed by a slowly progressive disease ending in death. Scrapie, an encephalopathy in sheep and goats, and bovine spongiform
encephalopathy (BSE), or mad cow disease) in cattle are apparently animal counterparts.
Kuru has occurred mainly among cannibalistic tribes in Papua New Guinea, where the disease is believed to be transmitted by the
ritualistic practice of eating brain tissue from deceased persons. The incidence of kuru is rapidly decreasing.
caused by an agent consisting solely of protein, a prion (forproteinaceous infectious particle). The mode of transmission and
whether or not activation of host genes is involved in pathogenesis remain unclear. About 10% of cases of Creutzfeldt-Jakob disease
may be inherited as a dominant trait; a gene responsible for production of prion proteins has been located in chromosome 20.
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Creutzfeldt-Jakob disease has occurred in patients who had received transplants of infected tissue (eg, corneal and dural
transplants). It is also important medically because the infectious agent is resistant to inactivation by formalin; this imposes a great
risk of infection on pathologists and other medical personnel who handle infected tissues.
Clinically, patients present with confusion and dementia followed by ataxia. Symptoms progress slowly but relentlessly to a fatal
outcome. There is no treatment.
Pathologically, both Creutzfeldt-Jakob disease and kuru are characterized by slowly progressive degeneration of the brain, with
neuronal loss, demyelination, and spongiform change in the cerebral white matter. There is no inflammatory cell infiltration.
Kuru tends to affect the cerebellum and is characterized microscopically by the presence of kuru plaques, which are amyloid bodies
with radially arranged spicules. The plaques appear to consist of filaments of prion protein.
Neurosyphilis
Congenital syphilis and adult syphilis in its late tertiary phase may involve the nervous system in many ways ; it has, however,
become relatively rare following the use of penicillin in the treatment of early syphilis.
Neurosyphilis: Pathologic and Clinical Features.
Type of
Disease
Time Elapsed
After Primary
Infection
Principal Pathologic Features CSF Clinical Features
Asymptomatic 23 years Mild lymphocytic meningeal
infiltrate
Positive VDRL1
Very common; discovered by
routine lumbar puncture in patients
with secondary syphilis; penicillin is
curative
Meningovascular syphilis
Diffuse 3+ years Chronic inflammation of
meninges with fibrosis and
endarteritis
Increased protein; mild
lymphocytosis; positive
VDRL
Meningeal symptoms; cranial nerve
palsies; penicillin may be effective
in early stage
Focal 3+ years Gumma formation Positive VDRL; increased
protein, lymphocytosis
Very rare; acts as a space
occupying lesion
Parenchymatous syphilis
General
paresis
10+ years Diffuse cerebral cortical neuronal
loss; chronic encephalitis;
spirochetes present
Positive VDRL; mild
lymphocytosis
Progressive dementia and
psychosis; cerebral atrophy with
ventricle dilatation; penicillin not
effective
Tabesdorsalis
10+ years Demyelination of spinal cord(posterior columns) and sensory
nerve root; spirochetes absent
Positive VDRL; mildlymphocytosis
Lightning pains, sensory loss,hypotonia, areflexia; penicillin not
effective
1VDRL = Veneral Disease Research Laboratory serologic test for syphilis. This is positive in about 50% of all cases of neurosyphilis. The
more sensitive FTAABS (fluorescent treponemal antibody test) is positive in over 90%.
The parenchymatous and meningovascular lesions of late syphilis may occur together in a given patient or separately.
Parenchymatous disease may affect the cerebral cortex (general paresis) and the spinal cord (tabes dorsalis). Spirochetes are
present in the brain in general paresis but not in the spinal cord in tabes dorsalis. Penicillin may prevent progression of neurosyphilis
but will not reverse deficits already present
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Parasitic Infections
Toxoplasmosis
Toxoplasma gondiiis a protozoal parasite that has its definitive cycle in the intestine of cats. Humans become infected through
contact with cat feces containing infective forms of the parasite. Cerebral toxoplasmosis occurs in two distinct forms, congenital and
acquired.
Congenital Toxoplasmosis
Fetal infection with T gondiioccurs transplacentally in the third trimester of pregnancy. The organism infects the fetal brain and the
retina, leading to extensive necrosis, calcification, and gliosis. Many infants die soon after birth, and those who survive have a variety
of defects such as microcephaly, hydrocephalus, mental retardation, and visual disturbances. Toxoplasma pseudocysts can be
identified in the brain and retinal lesions.
Acquired Toxoplasmosis
Acquired toxoplasmosis rarely causes cerebral lesions in normal individuals. It may, however, occur as an opportunistic infection in
patients with AIDS and in other patients with deficient cell-mediated immunity.
Cerebral toxoplasmosis in AIDS is characterized by the presence of multiple necrotic lesions ranging in size from 0.5 to 3 cm.
Toxoplasma pseudocysts and tachyzoites may be seen in biopsies of lesions. Diagnosis in tissues is aided by staining for Toxoplasma
antigens by immunoperoxidase techniques.
Clinically, patients present with fever and symptoms of acute cerebral dysfunction. Computerized tomography shows ring-enhancing
mass lesions that are often multiple. Treatment with anti-Toxoplasma agents is effective.
Other Parasitic Diseases
Other parasitic diseases rarely involve the brain in the United States. In other countries, the following parasitic diseases occur
commonly:
(1) Cerebral malaria, due to Plasmodium falciparum.
(2) African trypanosomiasis (sleeping sickness). This is caused by Trypanosoma rhodesiense in East Africa and Trypanosoma
gambiense in West Africa.
(3) Cysticercosis, due to the larval form ofTaenia solium, the pork tapeworm.
(4) Hydatid cyst, due to the larval form ofEchinococcus granulosus.
(5) Trichinosis, due to Trichinella spiralis.
(6) Schistosomiasis, due to Schistosoma haematobium and Schistosoma mansoni(in the Middle East).
(7) Amebiasis, due to Entamoeba histolytica, which causes brain abscesses. Free-living amebae of the generaAcanthamoeba and
Naegleria are rare causes of meningoencephalitis.
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