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Lecture 17

Infections of the CNS

Definition of meningitis Inflammation of the leptomeninges
Classic triad of symptoms for meningitis (1)Fever (2)Headaches (3)Nuchal rigidity
Brudzinski's sign Sign of meningeal irritation. The sign is elicited by passive flexion of the neck induces flexion of the hip or knees.
Kernig's sign Sign of meningeal irritation. A positive sign is described as resistance to passive extension of the knee while the hip is flexed.
Clinical symptoms of CNS abscess (1)Headache (2)lethargy (3)fever (4)focal neurologic deficits
How are CNS abscesses diagnosed? Contrast-enhanced CT or MRI
Clinical symptoms of encephatlitis (1)Fever (2)headache (3)altered mental status (4)sezures (5)focal neurologic deficits
Diffuse or localized inflammation of the brain, resulting from direct viral invasion Encephalitis
Mode of transmission of CNS infections (1)Hematogenous (2)Direct extension from adjacent structures (3)Direct implantation(trauma or from surgeries) (4)Centripetal spread (retrograde from the PNS, axonal transportation)
Most common mode of transmission of CNS infections Hematogenous
Most common route of entry for bacterial meningitis Most common route is from hematogenous spread from upper respiratory tract
Most common agents responsible for bacterial meningitis infection of newborns (1)Group B streptococci (2)E. coli (3)Listeria
Most common agents responsible for bacterial meningitis in children (>1 mo) to adults (60 yrs) (1)Neisseria meningitides (2)Streptococcus pneumoniae (3)Haemophilus influenza type b
Most common agent responsible for bacterial meningitis in the elderly population Gram negative bacilli
Most common cause of bacterial meningitis associated with closed skull fractures S. pneumoniae
Most common cause of bacterial meningitis associated with open skull fractures S. aureus
Most common cause of bacterial meningitis associated with neurosurgical procedures S. aureus
How do most people acquire meningococcus meningitis? Meningococcous is present in the nasopharyns of 5% of people and spread by respiratory droplets and close contact
What populations are susceptible to H. influenzae meningitis? (1) Immunocompromised (2) unvaccinated individuals
CSF profile of acute bacterial meningitis (1)presence of PMN (2)High cellularity (10-10,000 cells/mm3) (3) low glucose (<40 mg/dl) (4) High protein (>50 mg/dl) (5) visualization of bacteria by gram stain
Complications of bacterial meningitis (1)Cerebral infarcts (2) Hydrocephalus (3) Abscesses (4) Hearing loss (5) Mental retardation
Mechanism of cerebral infarcts as a complication of bacterial meningitis The vasculitis elicited by bacterial meningitis affects the small cortical vessels resulting in thrombosis and eventual ischemic infarction
Mechanism of hydrocephalus secondary to bacterial meningitis Chronic phases of bacterial meningits causes leptomeningeal fibrosis, which results in obstruction of CSF flow
Disease characterized by inflammation of the meninges with CSF lymphocytic pleocytosis with negative CSF stains and bacterial cultures Aseptic meningitis
Most common cause of aseptic meningitis Viruses
CSF profile of viral meningitis (1)low cellularity (mainly mononuclear cells) (2)normal glucose (3)normal protein (4)negative gram stain
Most common agents for viral meningitis Enteroviruses: Coxsackie B, echovirus, poliovirus
Mode of transmission of viral meningitis (1) direct contact (2) oral-fecal transmission
Most common cause of viral menigitis worldwide Mumps (paramyxovirus)
(T or F) Tuberculous meningitis is primarly seen during primary infection in children. True. The most common type of CNS involvement by Mycobacterium tuberculosis manifests as menigitis. In children, most commonly occurs between birth and 5 years. In the US, it is most commonly seen in the elderly and immunocompromised patients.
Clinical symptoms of TB meningitis (1)low-grade fever (2)headache (3)nausea (4)drowsiness that may progress to stupor and coma (5) Positive Kernig's and Brudzinski's sign
What areas are involved in TB meningitis (1) base of the brain (2) cranial nerves
(T or F) TB meningitis is characterized by purulent subarachnoid exudates False. TB meningitis is characterized by gelatinous subarachnoidal exudates
Complications of TB meningitis (1) Focal or diffuse infarcts (2) Tuberculomas (3) Hydrocephalus
Infectious agent responsible for Lyme disease Borrelia burgdorferi
Neurological manifestations during the early phase of Lyme disease (1)Lymphocytic meningitis or meningoencephalitis (2) Cranial neuritis (Bell's palsy) (3) Senosry or motor radiculoneuropathies
Neurological manifestations during the late phase of Lyme disease (1) Mild encephalopathy (2) Peripheral polyneuropathy
(T or F) Majority of fungal infections of hte CNS are opportunistic. True. Major concern in fungal meningitis is in immunocompromised patients.
Most common fungal agent associated with meningitis in AIDS or immunocompromised patients Cryptococcus sp
Most common fungal agent associated with meningitis in Hodgkin's lymphoma patients Cryptococcus sp
Agents of fungal meningitis in immunocompetent patients Blastomyces dermatitidis and Coccidiodes immitis
Radiographic appearance of CNS abscesses Ring-enhancing lesion in contrast-enhanced CT and MRI
Pathogenesis of brain abscess Brain abscesses are most commonly a secondary infection spread by hematogenous dissemination, from direct extension from adjacent structures, introduced by trauma or surgical procedures, or cryptogenic.
Complications of brain abscesses (1) Herniations (2) Severe cerebral edema (3) Ventriculitis (4) CSF dissemination (5) Secondary abscess
Most common non-purulent bacterial agent of CNS abscesses Tuberculosis
Most common fungal agents of CNS abscesses Candida, Aspergillus, Cryptococcus, Zycomycosis, Blastomycosis, Coccidiodomycosis
Most common parasitic agent of CNS abscesses Toxoplasmosis, Amebiasis
Bacterial agents associated with brain abscesses secondary to otitis media and mastoiditis Streptococci, Bacteroides fragilis, Enterobacteria
Bacterial agents associated with brain abscesses secondary to frontoethomoidal and sphenoidal sinusitis Streptococci, Bacteroid spp, Enterobacteria, Staphylococcus aureus, Haemophilus sp
Bacterial agents associated with brain abscesses secondary to dental abscesses Mixed fusobacterium, Bacteroids, and Streptococcus sp
Bacterial agents associated with brain abscesses secondary to penetrating head trauma or post-surgical infection Staphylococcus aureus, Streptococci, Enterobacteria, Clostridium sp
Bacterial agents associated with brain abscesses secondary to congential heart disease Streptococci (viridans, anaerobic, or microaerophilic), Haemophilus sp
Bacterial agents associated with brain abscesses secondary to lung abscess, empyema, bronchiectasia Fusobacterium, Actinomyces, BActeroides, Streptococcus, Nocardia asteroides
Bacterial agents associated with brain abscesses secondary to bacterial endocarditis Stphylococcus aureus, Streptococcus sp
Diffuse or localized inflammation of the brain Encephalitis
Diffuse or localized inflammation of the brain and leptomeninges Meningoencephalitis
Diffuse or localized inflammation of the brain and spinal cord Encephalomyelitis
Symptoms of diffuse encephalopathy (1) Altered mental status (2) delirium (3) convulsions (4) coma
Route of infection for viral encephalitis (1) Hematogenous (2) Centripetal spread (retrograde form the PNS or retrograde from mucosal surface)
Four common pathological features of viral encephalitis (1)Mononuclear infiltrates (lymphocytic inflammation) (2)Microglia activaton (3) inclusion bodies (4) necrosis
(T or F) Some patients who recover from viral encephalitis have residual signs. True. 20% of cases have residual signs after resolution such as mental deterioration, amnesic defect, personality change, recurrent seizures, and hemiparesis
Most common type of HSV responsible for majority of encephalitis infections HSV-1
Population most affected by HSV-2 encephalitis Neonates
Mode of transmission of Herpes virus encephalitis Centripetal or retrograde spread
Anatomical distribution of Herpes Encephalitis infection Temporo-frontal and limbic distribution
What part of the year does arboviral encephalitis peak? Summer: June through September
Family of viruses that cause arboviruses encephalitis (1)Togaviridae (2) Flaviviridae (3) Bunyaviridae
Vector responsible for arbovirus encephalitis in the US Mosquitoes
Geographic distribution of St. Louis Encephalitis Nationwide, but especially along the Mississippi River
Geographic distribution of Eastern Equine Encephalitis Eastern states, Atlantic coast, Gulf coast
Geographic distribution of Western Equine Encephalitis West of Mississippi River
Geographic distribution of La Crosse Encephalitis Great lakes states
Arbovirus encephalitis characterized by poliomyelitis-like and Parkinsonian symptoms West Nile Encephalitis
Infectious agent responsible for Rocky Mountain Spotted Fever Rickettsia rickettsii
Disease characterized by a macular rash involving the trunk and limbs, fever, and arthralgia Rocky Mountain Spotted Fever
Neurologic manifestation of Rocky Mountain Spotted Fever (1) Progressive stupor leading to coma (2) sustained fever (3) focal neurologic signs (4) Optic neuritis
Infectious agent responsible for subacute sclerosing panencephalitis (SSPE) Measles
Infectious agent responsible for progressive multifocal leukoencephalopathy JC virus
Pathogenesis of Progressive Multifocal Leukoencephalopathy PML is caused by the reactivation of latent JC virus due to impaired cell-mediated immunity
A condition characterized by slowly or rapidly progressive dementia accompanied by abnormalities of motor function in AIDS/HIV patients HIV encephalitis or AIDS dementia complex
(T or F) Only adult HIV/AIDS patients develop HIV encephalitis or AIDS dementia complex False. Both pediatric and adult populations are affected by HIV encephalitis or AIDS dementia complex
Routes of infection of HIV encephalitis or AIDS dementia complex Hematogenous route carried by T lympocytes and macrophages or invasion and persistence in the CNS (HIV reservoir)
Pathologic features of HIV encephalitis or AIDS dementia complex (1)Mild diffuse cerebral atrophy (2)Diffuse and multifocal rarefaction of the cerebral white matter (3)diffuse lymphocytic infiltration (4)Macrophage reaction with microglial nodules, macrophages, multinucleated giant cells
(T or F) HIV genome/proteins can be detected in neurons False. There has been no demonstration of the virus in neurons. Only multinucleated giant cells and macrophages in the CNS have been detected to have HIV genome/proteins.
(T or F) In HIV encephalitis or AIDS dementia complex, neuronal death is a result of direct neuronal infection. False. Neuronal damage is not due to direct infection of the neuron. It is most likely due to secondary effects.
Infectious agents that make up the TORCH syndrome T=Toxoplasmosis O=other R=Rubella C=CMV H=Herpes (HSV-2) and HIV
(T or F) Most TORCH infections are due to transplacental transmission. True
Mode of transmission of HSV-2 meningoencephalitis in neonates Transvaginal
Modes of transmission of HIVmeningoencephalitis in neonates Transplacental and breast feeding
Created by: UVAPATH2



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