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
Cerebrospinal Fluid and Central Nervous System Infections Extension From Cranial Structures
> 3rd ventricle > 4th ventricle (magendie, luschka) > subarachnoid space
> arachnoid granulations (absorbs) > sinuses
Infected thrombi may form in the diploic veins and spread
CSF Description along to the dural sinuses meningeal veins brain
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
Communicating type hydrocephalus - rounding of lateral ventricles border
Obstructive type
CSF Functions An osteomyelitic focus may form with erosion of the inner
It provides physical support and cushion for the brain which floats table of the skull and invasion of the dura, subdural space,
within the liquid pia-arachnoid layer and brain
It serves an excretory function and regulates the chemical
environment of the central nervous system Etiology
It acts as a channel for chemical communication within the central Most common organisms in adults: StrepNeiHiLi
nervous system o Streptococcus pneumoniae
Removes waste products of neuronal metabolism, drugs and o Neisseria meningitidis
other substances which diffuse into the brain from the blood o H. influenzae
o Listeria monocytogenes EG
Integrates brain and peripheral endocrine functions (hormone-
releasing factors) Most common organisms in neonates:
o E. coli
Influences microenvironment of neurons and glial cells (via pia-
o Group B Streptococcus
glial membrane)
Most common organism in children: Hi
CSF Production o H. influenzae controlled
Total cerebrospinal fluid production is approximately 500 ml per When septic embolus comes from lungs, congenital heart lesions,
day (450-600ml/day) ears and sinuses: Mixed flora
70% of the CSF is produced by the choroid plexus and the Iatrogenic infections: Staphylococcal Skin
remaining 30% is derived from metabolic water production
Of the 30%, 12% is produced by way of oxidation, 18% is capillary ACUTE BACTERIAL MENINGITIS
ultrafiltrate
Net production in man is about 0.35 ml/min Acute Bacterial Meningitis Dura & particularly subarachnoid
Inflammatory reaction in the pia, arachnoid and the CSF of the
INFECTIONS OF THE NERVOUS SYSTEM (CHAPTERS 32 & 33) brain and spinal cord
Initial hyperemia and permeability of vessels exudation of
Bacterial Infections protein and migration of neutrophils.
Acute meningitis Neutrophils disintegrate replaced by lymphocytes, histiocytes
Acute encephalitis and plasma cells
Cellular exudate forms and organizes resulting in fibrosis of the
Subdural empyema
arachnoid and loculation of pockets of exudates
Epidural abscess
Intracranial septic thrombophlebitis
Epidemiology
Brain abscess
75% of sporadic cases worldwide are due to:
Subacute and chronic meningitis StrepNeiHi
o H. influenzae, Streptococcus pneumoniae, N.
meningitidis
Pathways of Spread
o Predominating slightly in males 3:1
Bacterial infections reach the intracranial structures by:
4th most common is L. monocytogenes
Hematogenous spread (emboli of bacteria or infected thrombi)
H. influenzae getting less common in infants and children and
Extension from cranial structures (ears, sinuses)
getting more frequent in adults
Iatrogenic
Meningococcal more common in children and adolescents; low
incidence after age of 50
Hematogenous Spread
Pneumococcal predominates in the very young and the old
In most cases of bacteremia, the CNS seems spared Fatal > immediate prophylaxis
Direct injection of virulent bacteria into the brain seldom results Pathogenesis
in abscess The most common pathogens are all normal flora of the
Cranial epidural and subdural spaces are practically never the nasopharynx and depend on their antiphagocytic capsules for
sites of blood-borne infections survival
In humans, infarction of brain tissue by arterial or venous Postulated factors that predispose to disruption of the blood-CSF
occlusion appears to be common and perhaps a necessary barrier and invasion of the bloodstream and meninges include:
antecedent o VET Precedent viral infection, Trauma, Endotoxins

1
 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

Clinical Features
Adults and children Treatment
o Fever, severe headaches, stiff neck, sometimes with Medical emergency
generalized convulsions and altered sensorium Sustain blood pressure and treat septic shock
o Nuchal rigidity, Kernig and Brudzinski signs Choose an antibiotic that is bactericidal and can penetrate the CSF
1. Meningococcal in effective amounts
o Extremely rapid evolution (hours), petechial and large Antibiotics for 10-14 days except when there is persistent
ecchymoses, circulatory shock, epidemic setting parameningeal focus, preferably intravenously
2. Pneumococcal Corticosteroids: before antibiotics
o Follows infection of lung, ears, sinuses, heart valves o In children- dexamethasone 0.15mg/kg QID X 4days
o Alcoholics, splenectomized, very elderly, sickle cell o In adults- only in pneumococcal
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
Prophylaxis
with meningitis
All household contacts of patients with meningococcal meningitis
Elevated pressure
Highest for those younger than 5yrs old, 2-4%
Pleocytosis 250-100,000/mm
Single dose of ciprofloxacin
Neutrophils predominate (85-95%)
Rifampicin 600mg every 12hrs for 2 days
Protein is higher than 45mg/dl
Vaccination vs. H. influenza, N. meningitidis
Glucose is usually 40mg/dl or 40% of RBS
Gram stain and cultures
Prognosis and Sequelae
High LDH particularly fractions 4 and 5
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

2
 Residual neurologic deficits are found in 25% of H. influenzae, and EPIDURAL ABSCESS
30% with pneumococcal meningitis
Almost invariably associated with osteomyelitis in a cranial bone
Cranial nerve palsies tend to resolve after a few weeks or months
Pus accumulate on the outer surface of the dura
Only half with deafness resolves
Localizing neurologic signs are usually absent
Hydrocephalus
Lumbar Puncture is not advisable
Usually due to Staphylococcus aureus
BACTERIAL ENCEPHALITIS Antibiotics
Mycoplasma pneumoniae associated with neuritis, myositis, Surgical drainage
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 SEPTIC THROMBOPHLEBITIS
followed by Bacteroides and anaerobic streptococci
Infection involving the dural sinuses, the ones usually involved are
Symptoms and signs: local pain and tenderness related to the
the lateral, cavernous and petrous sinuses
origin of the infection and its intracranial extension
Extension from the middle ear, mastoid cells, paranasal sinuses
o Chills, fever, severe headaches, stiff neck, sensorial
and skin around the upper lip, nose and eyes
change, focal seizures, neurologic deficits
Streptococci and staphylococci
o Intracranial hypertension and papilledema
Fever, intracranial hypertension, cranial nerve palsies and gaze
Diagnosis: should be considered whenever a patient with a
abnormalities
suppurative process in the sinuses or other cranial structures,
Prolonged antibiotic treatment is the mainstay of treatment
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

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
20% source cannot be ascertained

3
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
4

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
Lymes 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
Chronic viral infections
5
 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%
Treatment : Acyclovir 30mg/kg/day for 10-14 days
6
 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
RABIES untreated
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

AIDS Myelopathy
A form of vacuolar myelopathy that affects the posterior and
The survival of the infected person dependent on the institution
lateral columns of the cord, bearing a striking resemblance to
of specific therapeutic measures before the infection becomes
subacute combined degeneration because of Vit B12 deficiency
clinically evident
Peripheral neuropathy, mononeuropathy multiplex, cauda equina
Cleanse wound with soap and water
syndrome, myopathy
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 Opportunistic Infections of the CNS in AIDS
pox Toxoplasmosis most common focal infection
Dermatomal vesicular eruption, sometimes with fever and Cytomegalovirus most common non-
malaise Cryptococcal infection focal infections
Treatment Varicella zoster
o Vaccine to older adults Tuberculosis
o Analgesics and drying lotions Neurosyphilis
o Acyclovir, Famciclovir, or Valaciclovir for 7 days

7
 ACUTE ANTERIOR POLIOMYELITIS Fatal Familial Insomnia rare, familial
o Intractable insomnia, sympathetic overactivity, leading
Caused by poliovirus, but may also be caused by Coxsackie A and
to death in 7-15 months
B, Japanese encephalitis and West Nile virus
o SSE
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
FUNGAL INFECTIONS
May arise without any obvious predisposing cause but usually
complicate AIDS, transplantation, severe burns, leukemia,
lymphoma, diabetes, etc
Factors: Interference with the bodys 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

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 Mucormycosis
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

8
 PROTOZOAL DISEASES
Toxoplasma gondii- Nematodes:
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 Cestodes:
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)
WORM INFECTIONS
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
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

Cerebral Malaria

Thought is an infection. And in the case of certain thoughts, it becomes

an epidemic. Wallace Stevens

Prepared by: Paolo Warren (Med-3C)