CSF and CNS Infections

November 9, 2017 | Author: Jorelyn Frias | Category: Meningitis, Cerebrospinal Fluid, Diseases And Disorders, Immunology, Public Health
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trans from Warren MD...


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 > 3rd ventricle > 4th ventricle (magendie, luschka) > subarachnoid space > arachnoid granulations (absorbs) > sinuses

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 Communicating type hydrocephalus - rounding of lateral ventricles border Obstructive type

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 (hormonereleasing factors)  Influences microenvironment of neurons and glial cells (via piaglial 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: StrepNeiHiLi o Streptococcus pneumoniae o Neisseria meningitidis o H. influenzae o Listeria monocytogenes EG  Most common organisms in neonates: o E. coli o Group B Streptococcus  Most common organism in children: Hi o H. influenzae – controlled  When septic embolus comes from lungs, congenital heart lesions, ears and sinuses: Mixed flora  Iatrogenic infections: Staphylococcal Skin ACUTE BACTERIAL MENINGITIS Acute Bacterial Meningitis Dura & particularly subarachnoid  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: StrepNeiHi 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 Fatal > immediate prophylaxis

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 VET Precedent viral infection, Trauma, Endotoxins


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 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 

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

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

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, and 30% with pneumococcal meningitis Cranial nerve palsies tend to resolve after a few weeks or months Only half with deafness resolves Hydrocephalus BACTERIAL ENCEPHALITIS

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Mycoplasma pneumoniae – associated with neuritis, myositis, meningitis, encephalitis Listeria monocytogenes – focal, rhombencephalitis Legionella – often fatal, cerebellar and brainstem Catscratch Anthrax Brucellosis Whipple

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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

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


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


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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


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.

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

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

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


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:

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

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 

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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

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



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%)

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


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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



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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

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RABIES     

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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

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)

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


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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

Opportunistic Infections of the CNS in AIDS  Toxoplasmosis –most common focal infection  Cytomegalovirus most common non Cryptococcal infection focal infections  Varicella zoster  Tuberculosis  Neurosyphilis



Fatal Familial Insomnia – rare, familial o Intractable insomnia, sympathetic overactivity, leading to death in 7-15 months o SSE

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

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

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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


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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




Toxoplasma gondiio 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)


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 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)


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