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Cerebrospinal Fluid and Central Nervous System Infections CSF Description
A watery fluid that fills the ventricles and bathes the internal brain surface
Clear, colorless liquid containing small amounts of CHON, glucose and potassium
There is no cellular component (up to 1-5 cells/mm3), high Na, Cl, and Mg concentrations, and low glucose concentrations
The ventricles and subarachnoid space contain approximately 125 ml of CSF (25 ml in the ventricles and 100 ml in the subarachnoid space)
70% - choroid plexus; 30% -capillary bed + metabolic water production (capillary ultrafiltrate)
Net production: 0.35-0.37 ml per minute (400ml/day)
CSF turnover rate of 0.25% per minute
CSF Functions
It provides physical support and cushion for the brain which floats within the liquid
It serves an excretory function and regulates the chemical environment of the central nervous system
It acts as a channel for chemical communication within the central nervous system
Removes waste products of neuronal metabolism, drugs and other substances which diffuse into the brain from the blood
Integrates brain and peripheral endocrine functions (hormone-releasing factors)
Influences microenvironment of neurons and glial cells (via pia-glial membrane)
CSF Production
Total cerebrospinal fluid production is approximately 500 ml per day (450-600ml/day)
70% of the CSF is produced by the choroid plexus and the remaining 30% is derived from metabolic water production
Of the 30%, 12% is produced by way of oxidation, 18% is capillary ultrafiltrate
Net production in man is about 0.35 ml/min
INFECTIONS OF THE NERVOUS SYSTEM (CHAPTERS 32 & 33) Bacterial Infections
Acute meningitis
Acute encephalitis
Subdural empyema
Epidural abscess
Intracranial septic thrombophlebitis
Brain abscess
Subacute and chronic meningitis
Pathways of Spread
Bacterial infections reach the intracranial structures by:
Hematogenous spread (emboli of bacteria or infected thrombi)
Extension from cranial structures (ears, sinuses)
Iatrogenic
Hematogenous Spread
In most cases of bacteremia, the CNS seems spared
Direct injection of virulent bacteria into the brain seldom results in abscess
Cranial epidural and subdural spaces are practically never the sites of blood-borne infections
In humans, infarction of brain tissue by arterial or venous occlusion appears to be common and perhaps a necessary antecedent
Extension From Cranial Structures
Infected thrombi may form in the diploic veins and spread along to the dural sinuses meningeal veins brain
An osteomyelitic focus may form with erosion of the inner table of the skull and invasion of the dura, subdural space, pia-arachnoid layer and brain
Etiology
Most common organisms in adults: o Streptococcus pneumoniae
o Neisseria meningitidis
o H. influenzae
o Listeria monocytogenes Most common organisms in neonates:
o E. coli
o Group B Streptococcus
Most common organism in children: o H. influenzae – controlled
When septic embolus comes from lungs, congenital heart lesions, ears and sinuses: Mixed flora
Iatrogenic infections: Staphylococcal
ACUTE BACTERIAL MENINGITIS Acute Bacterial Meningitis
Inflammatory reaction in the pia, arachnoid and the CSF of the brain and spinal cord
Initial hyperemia and permeability of vessels exudation of protein and migration of neutrophils.
Neutrophils disintegrate replaced by lymphocytes, histiocytes and plasma cells
Cellular exudate forms and organizes resulting in fibrosis of the arachnoid and loculation of pockets of exudates
Epidemiology
75% of sporadic cases worldwide are due to:
o H. influenzae, Streptococcus pneumoniae, N. meningitidis
o Predominating slightly in males 3:1
4th most common is L. monocytogenes
H. influenzae – getting less common in infants and children and
getting more frequent in adults
Meningococcal – more common in children and adolescents; low incidence after age of 50
Pneumococcal – predominates in the very young and the old
Pathogenesis
The most common pathogens are all normal flora of the nasopharynx and depend on their antiphagocytic capsules for survival
Postulated factors that predispose to disruption of the blood-CSF barrier and invasion of the bloodstream and meninges include:
o Precedent viral infection, Trauma, Endotoxins
Blood > systemiccirc > aorta (innominate, l common carotid, l subclavian | r subclavian, r common carotid art > post anterior > internal carotid (anterior) > circle of willis, vertebral art > basilar art (post) Drainage - veins/sinuses
> 3rd ventricle > 4th ventricle (magendie, luschka) > subarachnoid space > arachnoid granulations (absorbs) > sinuses
Communicating type hydrocephalus - rounding of lateral ventricles border Obstructive type
StrepNeiHiLi
EG
Hi
Skin
Dura & particularly subarachnoid
StrepNeiHi
Fatal > immediate prophylaxis
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Clinical Features
Adults and children
o Fever, severe headaches, stiff neck, sometimes with generalized convulsions and altered sensorium o Nuchal rigidity, Kernig and Brudzinski signs
1. Meningococcal
o Extremely rapid evolution (hours), petechial and large ecchymoses, circulatory shock, epidemic setting
2. Pneumococcal
o Follows infection of lung, ears, sinuses, heart valves o Alcoholics, splenectomized, very elderly, sickle cell
disease, recurrent bacterial meningitis
3. H. influenzae
o Follows ears and URT infections in children o Early focal cerebral signs
4. Staphylococcal
o Follows neurosurgical procedures, furunculosis, ventricular shunts
5. Enterobacteriaceae, Pseudomonas, Listeria, Acinetobacter calcoaceticus
o Immunosuppressed
Infants and Newborns
o Fever, irritability, drowsiness, vomiting, convulsions and bulging fontanel
o More common in males (3:1)
o Maternal infection is the most significant factor
CSF Examination
INDISPENSABLE part of the examination of patients suspected with meningitis
Elevated pressure
Pleocytosis 250-100,000/mm³
Neutrophils predominate (85-95%)
Protein is higher than 45mg/dl
Glucose is usually 40mg/dl or 40% of RBS
Gram stain and cultures
High LDH particularly fractions 4 and 5
Other Tests
Blood culture
Chest x-ray
Serum Na - SIADH
CT scan – lesions that erode the skull or spine, brain abscess, empyema
MRI with gadolinium – meningeal exudate and cortical reaction, venous occlusions and adjacent infarctions
Treatment
Medical emergency
Sustain blood pressure and treat septic shock
Choose an antibiotic that is bactericidal and can penetrate the CSF in effective amounts
Antibiotics for 10-14 days except when there is persistent parameningeal focus, preferably intravenously
Corticosteroids: before antibiotics
o In children- dexamethasone 0.15mg/kg QID X 4days o In adults- only in pneumococcal
Prophylaxis
All household contacts of patients with meningococcal meningitis
Highest for those younger than 5yrs old, 2-4%
Single dose of ciprofloxacin
Rifampicin 600mg every 12hrs for 2 days
Vaccination vs. H. influenza, N. meningitidis
Prognosis and Sequelae
Untreated, usually fatal
Mortality rate:
o Uncomplicated meningococcal and H. influenzae, 5% o Streptococcal, 15%
o Highest in the neonates, elderly, fulminant
meningococcemia, with concomittant alcoholism, DM, MM, head trauma, Osler triad
Mechanism of death:
o Bacteremia and hypotension, brain swelling, aspiration pneumonia
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Residual neurologic deficits are found in 25% of H. influenzae, and30% with pneumococcal meningitis
Cranial nerve palsies tend to resolve after a few weeks or months
Only half with deafness resolves
Hydrocephalus
BACTERIAL ENCEPHALITIS
Mycoplasma pneumoniae – associated with neuritis, myositis,
meningitis, encephalitis
Listeria monocytogenes – focal, rhombencephalitis Legionella – often fatal, cerebellar and brainstem Catscratch
Anthrax
Brucellosis
Whipple
SUBDURAL EMPYEMA
An intracranial suppurative process between the inner surface of the dura and the subarachnoid
Usually originates from the frontal or ethmoid sinuses, less frequently from the sphenoid and middle ear
Most common in adolescent and young adult men
Streptococci (nonhemolytic and viridans) are most frequent followed by Bacteroides and anaerobic streptococci
Symptoms and signs: local pain and tenderness related to the origin of the infection and its intracranial extension
o Chills, fever, severe headaches, stiff neck, sensorial change, focal seizures, neurologic deficits o Intracranial hypertension and papilledema
Diagnosis: should be considered whenever a patient with a suppurative process in the sinuses or other cranial structures, develops meningeal symptoms or focal neurologic signs o CT scan: may show mastoiditis or osteomyelitis and crescent
shaped area of hypodensity in subdural space o MRI: more dependable visualization
o CSF examination is not helpful and may be dangerous
Treatment: most would require drainage coupled with antibiotic therapy
o Untreated – death within 6 days
o Treated – mortality rate 25-40% because of late diagnosis
EPIDURAL ABSCESS
Almost invariably associated with osteomyelitis in a cranial bone
Pus accumulate on the outer surface of the dura
Localizing neurologic signs are usually absent
Lumbar Puncture is not advisable
Usually due to Staphylococcus aureus
Antibiotics
Surgical drainage
SEPTIC THROMBOPHLEBITIS
Infection involving the dural sinuses, the ones usually involved are the lateral, cavernous and petrous sinuses
Extension from the middle ear, mastoid cells, paranasal sinuses and skin around the upper lip, nose and eyes
Streptococci and staphylococci
Fever, intracranial hypertension, cranial nerve palsies and gaze abnormalities
Prolonged antibiotic treatment is the mainstay of treatment
BRAIN ABSCESS
Encapsulated or free pus in the substance of the brain
40% come from infection of the middle ear, mastoid cells, and PNS
̴ 50% hematogenous from heart and lungs
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Etiology
Virulent streptococci, anaerobic and microaerophilic – most common (lungs and sinuses)
In combination with other anaerobes like Bacteroides,
Propionibacterium
E. coli, Proteus –Enterobacteriaceae (ears) Staphylococci
The type of organism depend on the source of abscess
Pathology
Septic thrombosis of vessels tissue necrosis local suppurative process
Within several days, the infection become delimited and the center of the infection takes on the character of pus
As the abscess becomes more chronic, the periphery grows granulation tissue and later on, collagenous connective tissue capsule
The capsule is thinner on the ventricular side
Diagnosis
Contrast enhanced CT and MRI – most important. If negative, there is almost no likelihood of abscess
Blood cultures, esp with acute endocarditis
ESR
Chest xray
Treatment
During the stage of cerebritis and early abscess formation: o Antibiotics: Pen G or third gen cephalosporin AND
either chloramphenicol or metronidazole
o For staphylococcal infection: Nafcillin or Vancomycin
If the abscess is solitary, superficial and encapsulated or associated with a foreign body, should total excision be attempted
If abscess is deep, stereotactic aspiration is the current method of choice.
Prognosis
If the treatment is started while the patient is alert, mortality is at 5-10%
If the patient is comatose before treatment, mortality is more than 50%
30% of survivors have neurologic residua, i.e., focal deficits or epilepsy
MENINGITIS Subacute and Chronic Meningitis
Induce an inflammation of the meninges of lesser intensity and chronicity
The organisms are more difficult to detect and culture o TB meningitis
o Neurosyphilis
Tuberculous Meningitis
Caused by the acid-fast Mycobacterium tuberculosis and exceptionally by M. bovis and M. fortuitum
There has been a steady decrease in the cases of TB since WW II, but since 1985, there has been a moderate increase again mainly, but not exclusively, because of HIV epidemic
Pathogenesis
First, a bacterial seeding of the meninges and subpial regions of the brain and formation of tubercles
Followed by the rupture of one or more of these tubercles and discharge of bacteria into the subarachnoid space
Pathologic Findings
Meningitis is most intense in the basal meninges
Unlike the typical bacterial meningitis, the disease is not confined to the subarachnoid space and invades the underlying brain (meningoencephalitis)
Cranial nerves are frequently involved
Arteries become inflamed and occluded leading to infarctions
Hydrocephalus forms because of blockage of basal cisterns
Multiple spinal radiculopathies and cord compression occurs if the exudate predominate around the spinal cord
Clinical Features
Occurs in persons of all ages
Initially, low grade fever, malaise, headaches, lethargy, confusion, and stiff neck with Kernig and Brudzinski signs
In the chronic stage, cranial nerve palsies, papilledema, FND because of infarction.
2/3 have evidence of active tuberculosis elsewhere
If untreated, it is usually fatal within 4-8 weeks of the onset
Diagnosis
CSF:
o Slightly cloudy or ground-glass appearance with formation of a clot on standing
o WBC 25-500 per cu. mm with lymphocytic predominance
o Sugar 20-40mg/dl o Increased protein o (+) AFB smear in 20-30% o (+) TB-PCR
o (-) serology for Cryptococcus and Syphilis
CT or MRI may show enhancing exudates, hydrocephalus, areas of infarction and tuberculomas
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Treatment
Quadruple anti-TB for 2 months (INH, RIF, PZA, ETH) then followed by 16-22 months of at least double anti-TB antibiotics (INH, RIF).
Philippines – high rates of INH-resistant organisms
Corticosteroids, in conjunction with anti-TB drugs, may be used who have subarachnoid block or raised intracranial pressure
Tuberculomas that do not disappear with medication may be excised if there is a mass effect
Prognosis
Overall mortality is still significant at 10%, infants and the elderly being at greatest risk
HIV positive patients have higher mortality ̴ 21%
When coma has supervened before treatment, mortality is at 50%
20-30% of survivors have residual neurologic sequelae
NEUROSYPHILIS
Caused by a slender, spiral, motile Treponema pallidum
The treponeme invades the CNS within 3-18 months of inoculation
The initial event is a meningitis which occurs in 25%. The meningitis can be asymptomatic and can only be discovered by Lumbar Puncture!
Asymptomatic neurosyphilis is the most important form because treatment at this stage can prevent further symptomatic varieties.
Principal Types
Asymptomatic – abnormal CSF
Meningovascular – meningitis and strokes
Parenchymatous
o Tabetic – pain, paresthesia, ataxia caused by posterior spinal root and dorsal column changes
o Paretic – personality changes, convulsions, dementia (dementia paralytica)
o Optic atrophy – vision loss and pallor of optic discs o Spinal- chronic fibrosing myelitis or meningovascular
complications
o Nerve deafness and vestibulopathy
Diagnosis and Treatment
Syndrome consistent with neurosyphilis
o Abnormal blood titer of a treponemal antibody test o (+) nontreponemal antibody test in CSF
Treatment – high dose IV penicillin 18-24M U for 14 days o All forms of neurosyphilis should be reexamined every
3-4 months; CSF examination after 6 months
Other Spirochetal Infections
Lyme’s Disease – caused by Borrelia burgdoferi from tick bites o Erythema chronicum migrans
o Acute radicular pain followed by chronic lymphocytic meningitis and frequently with peripheral and cranial neuropathies
o Heart and articular surfaces are also affected
Leptospirosis – caused by Leptospira interrogans
o Rare cause of encephalitis, myelitis, optic neuritis, neuritis
Case:
19 year old female, college student, with 1-week history of fever and headaches.
With history of acne vulgaris over the forehead and above the bridge of the nose
Pertinent VS: temp 39 C
Pertinent neurologic exam: drowsy, utters incomprehensible words, spontaneously moves all extremities equally; Bilateral Babinski sign; (+) nuchal rigidity
Differential: Acute (1 week) Bacterial Meningitis (nuchal rigidity) due to Staphylococcus aureus (acne vulgaris)
VIRAL INFECTIONS
Viruses gain entrance to the body via:
o Respiratory passages – measles, mumps, VZV o Oral-intestinal route – polioviruses, enteroviruses o Oral or genital mucosa – HSV, HIV
o Bites of animals or mosquitoes – rabies, arboviruses o Transplacentally- CMV, HIV, rubella
Virus multiplies locally
In secondary sites usually gives rise to a viremia
Viruses are cleared from the body by the RES, but if the viremia is massive or other conditions are favorable, they invade the CNS probably via the cerebral capillaries and choroid plexus
Another pathway of infection is along peripheral nerves accomplished by the retrograde axoplasmic transport system
Mechanisms of Viral Infections
Viruses have a diverse clinical and pathologic effects:
o Different cells in the CNS vary in their susceptibility to different viruses
The cell must have membrane specific receptors sites to which the virus attaches The cell must have the metabolic capacity
to transcribe, translate virus-coated proteins, replicate viral nucleic acid, and to assemble virions
o For many of the rest, the affinity is less selective.
Clinical Syndromes
Acute aseptic meningitis
Recurrent meningitis
Acute encephalitis and meningoencephalitis
Ganglionitis
Chronic invasion of the nervous tissue by retroviruses
Acute anterior poliomyelitis
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ACUTE ASEPTIC MENINGITIS
Acute Aseptic Meningitis
“Bacterial cultures are negative”
Rarely fatal, limited to the meninges
Fever, headache, signs of meningeal irritation, a predominantly lymphocytic pleocytosis with normal CSF glucose
Photophobia, pain on movement of the eyes
Causes of Acute Aseptic Meningitis
Common – 11-27 cases per 100,000
Most commonly (80%) caused by the enteroviruses - echovirus and Coxsackievirus
2nd most common – HSV2
Varicella, HIV, mumps, LCM, HSV1, adenoviruses
Clinical Distinctions Between the Different Viral Causes
Enteroviruses (poliovirus) – fecal-oral route: family outbreaks, more common among children
Echovirus and group A Coxsackie – exanthemata, grayish vesicular oral herpangina
Group B coxsackie - pleurodynia, brachial neuritis, pericarditis, orchitis
Poliovirus – pain in the neck, back and muscles
LCM – house mouse and other rodents
Leptospira – wading in flood waters
HSV-2 and HIV – Cauda equina, preceeding genital infection
EBV – sore throat, generalized lymphadenopathy, transient rash
ASEPTIC CHRONIC & RECURRENT MENINGITIS
Parameningeal infection (sinusitis)
Partially treated bacterial meningitis
Meningeal infections wherein the organism is difficult to isolate (NeuroSy, TB, fungal)
Neoplastic invasion (leukemias, lymphomas, carcinomatous)
Granulomatous, vasculitic and other inflammatory disease(Sarcoidosis, Behcet)
Chemical irritation (spinal administration of chemicals, leakage of a cystic tumor), drug-induced allergic reaction (IVIg, NSAID, antibiotics)
Idiopathic (33%)
ACUTE VIRAL ENCEPHALITIS
Core symptoms: acute febrile illness, with various combinations
of convulsions, delirium, confusion, stupor, coma, aphasia, hemiparesis, Babinski, involuntary movements, ocular palsies
Meningitis may also be intense
CSF: lymphocytic pleocytosis, mild protein elevation and normal
sugar values
Imaging is usually normal but may show diffuse edema, or cortical
enhancement
Perivascular cuffing by lymphocytes and other mononuclear leukocytes and plasma cells, as well as patchy infiltration of the meninges with similar cells
Viral Encephalitis VS Post-Infectious Encephalitis (ADEM)
True viral encephalitis – direct invasion of brain and meninges
ADEM post-infectious encephalomyelitis – presumably based on an autoimmune reaction to a systemic viral infection but in which no virus is present in neural tissue
o In children, they may present with fever but occurs only after a latency of several days, as the infection is subsiding
Differentiation may be very difficult
Epidemiology
CDC : approximately 20,000 cases are reported annually
5-20% mortality
20% with residual signs – mental deterioration, amnesia, epilepsy, personality changes, motor deficits
HSE- mortality is 50%
Diagnosis
Knowledge of epidemic setting and of seasonal occurrence of the different forms of infection.
Diagnosis can be made by a combination of virus isolation, serologic tests, and amplification of viral nucleic acids (PCR)
Arboviral Encephalitis
Flaviviruses
Have seasonal and geographic predilection
Incubation period after mosquito bite is 5-15 days
Signs and symptoms subside after 4-14 days
Japanese encephalitis – the most common type outside of North America
Herpes Simplex Encephalitis
The gravest and the most common
30-70% are fatal and most survivors are left with severe neurologic deficits
Almost always caused by HSV-1
Predilection for the inferomedial frontal and temporal lobes
Clinical Manifestations: olfactory, gustatory hallucinations; anosmia, temporal lobe seizures, personality change at the onset
Coma during the first few days means very poor prognosis
MRI: bilateral but not symmetrical temporal lobe lesions
EEG: periodic lateralizing epileptiform discharges (PLEDs)
CSF: PCR (+) in 95%
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RABIES
Almost invariably fatal when the clinical features appear
Transmitted by a bite of an infected animal
Rarely, inhalation of the virus shed by bats
Incubation: 2weeks to 2months
Clinical Manifestations: fever, headache, malaise, psychomotor overactivity, dysphagia, spasms of throat muscles, hydrophobia, numbness and tingling, seizures, coma, death in 4-10days
The survival of the infected person dependent on the institution of specific therapeutic measures before the infection becomes clinically evident
Cleanse wound with soap and water
Benzyl ammonium chloride inactivates the virus
Tetanus prophylaxis
Surveillance of the animal for 10 days
Post-exposure prophylaxis with HRIG (passive), and HDCV (active)
HERPES ZOSTER
3-5 cases per 10,000 persons per year and is more common in the elderly
Represents a spontaneous reactivation of VZV infection, which becomes latent in the neurons of the sensory ganglia following infection of chicken pox
It is not communicable except to those who have not had chicken pox
Dermatomal vesicular eruption, sometimes with fever and malaise
Treatment
o Vaccine to older adults o Analgesics and drying lotions
o Acyclovir, Famciclovir, or Valaciclovir for 7 days
o IV acyclovir for immunocompromised or disseminated zoster
Postherpetic neuralgia
o 5-10% of patients; treated with anticonvulsants
Incomplete interruption of the nerves result in a hyperpathic state wherein any stimulus can be painful
AIDS
Due to profound depression of cell-mediated immunity
Virtually all parts of the nervous system may be affected. Neurologic syndromes may occur at any stage from first infection and seroconversion to AIDS
Manifestations are likely transient in early infection and progressive in chronic infection.
Even without other manifestations of HIV infection, some are diagnostic of AIDS (dementia and myelopathy).
Neurologic abnormalities are noted in about 1/3 of AIDS patients.
But at autopsy, the nervous system is affected nearly all of them.
AIDS Dementia Complex
The most common neurologic complication in the later stages of HIV infection
Results from the direct invasion with HIV
Survival after the onset of dementia is generally 3-6months, if untreated
AIDS Myelopathy
A form of vacuolar myelopathy that affects the posterior and lateral columns of the cord, bearing a striking resemblance to subacute combined degeneration because of Vit B12 deficiency
Peripheral neuropathy, mononeuropathy multiplex, cauda equina syndrome, myopathy
Opportunistic Infections of the CNS in AIDS
Toxoplasmosis –most common focal infection
Cytomegalovirus most common non-
Cryptococcal infection focal infections
Varicella zoster
Tuberculosis
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ACUTE ANTERIOR POLIOMYELITIS
Caused by poliovirus, but may also be caused by Coxsackie A and B, Japanese encephalitis and West Nile virus
Highly communicable disease, humans are the only known natural hosts
Main route of infection is fecal-oral
Starts with a febrile illness followed in 3-4days by muscle weakening and pain
Lesions are found in the motor gyrus, brainstem and cord
Best prevented with Sabine vaccine
Mortality rate is 5-10%
SUBACUTE & CHRONIC VIRAL INFECTIONS
Caused by conventional virus
Chronic infection with progressive dementia, personality changes, seizures, ataxia
o Subacute sclerosing panencephalitis - measles o Progressive rubella panencephalitis
Usually in a patient with a neoplasm or immunodeficiency (AIDS) o Progressive multifocal leukoencephalopathy – JC virus
o With progressive dementia, hemi to quadriparesis. Blindness, ataxia in 3-6months
Progressive Multifocal Leukoencephalopathy
PRION DISEASES
Proteinacious infectious particle
The prion protein (PrP) is encoded by a gene in the short arm of ch.20 in humans, and mutations in the PrP or conversion to an abnormal isoform, are found in CJD and GSS
Genetic and infectious
Present with variable ataxia, weakness, dementia, seizures
Creutzfeldt-Jakob disease – rapid progressive and profound dementia with diffuse myoclonic jerks/seizures and visual or cerebellar signs
o Widespread neuronal loss and gliosis with striking vacuolation or spongy state of the brain (subacute spongiform encephalopathy SSE)
o Fatal within a year from onset
o Transmissible from humans to primates and iatrogenically from person to person with infected material
Gerstmann-Straussler-Scheinker – rare, strongly familial o Death in 5 years
o SSE
Kuru – transmitted by cannibalism in a group of natives of Papua New Guinea
o Death in 3-6months o SSE
Fatal Familial Insomnia – rare, familial
o Intractable insomnia, sympathetic overactivity, leading to death in 7-15 months
o SSE
FUNGAL INFECTIONS
May arise without any obvious predisposing cause but usually complicate AIDS, transplantation, severe burns, leukemia, lymphoma, diabetes, etc
Factors: Interference with the body’s normal flora and impaired T cell and humoral responses
Develops insidiuosly, similar to other subacute and chronic meningitis like TB
CSF: pressure elevated, lymphocytic pleocytosis, protein is high, sugar is subnormal
Cryptococcus neoformans
o Accounts for the most common, as a result of its association with AIDS
o (+)Latex agglutation test for the antigen in the CSF
Candida (severe burns, TPN), Aspergillus (sinusitis and otitis)
Mucormycosis
o Malignant infection of the cerebral blood vessels
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PROTOZOAL DISEASES
Toxoplasma gondii-
o Congenital – results from initial parasitemia of the pregnant mother
o Acquired –eating raw beef, contact with cat feces o In AIDS patients, it is the most common cause of focal
cerebral lesions
Naegleria fowleri, Acanthameoba –
o Acquired from swimming in contaminated waters o Inexorably progressive and practically always fatal
within a week
Plasmodium falciparum
o Great importance in tropical regions
o Cerebral malaria – rapidly fatal disease with fever,
headaches, seizures, coma, diffuse cerebral edema o Cerebral capillaries are packed with parasitized RBCs
Trypanosoma brucei
o Common in equatorial Africa, Central and South America
o Transmitted by the tsetse fly
o Chronic, progressive neurological deterioration with reversal or disruption of the circadian sleep pattern (sleeping sickness)
Cerebral Malaria
WORM INFECTIONS
Nematodes:
o Trichinella spiralis (intestinal) – from ingestion of uncooked or undercooked pork.
From the intestines, they invade the different organs but survive only in the muscle
Cestodes:
o Taenia solium – from ingestion of uncooked and undercooked pork
Multiple calcified lesions in the muscles and cerebrum
Seizures, multiple deficits
o Echinococcus – water and vegetables contaminated by canine feces
Trematodes:
o Schistosoma japonicum (cerebrum), Schistosoma mansoni (spinal cord) – direct invasion of the nervous system blood vessels
Acquired from swimming in lakes and rivers where the snail hosts are plentiful
Trichinella in Muscle
“Thought is an infection. And in the case of certain thoughts, it becomes an epidemic.” –Wallace Stevens